This document discusses clinical manifestations and evaluation of renal disease in children. Common signs of renal disorders include edema, hematuria, abnormalities in urination, and flank or abdominal pain. Evaluation of renal disease involves examination of urine for red blood cells, proteins, and casts. Imaging tests like ultrasound and IVU can identify structural abnormalities. Glomerular diseases commonly cause hematuria while tubular disorders present with electrolyte abnormalities. Renal biopsy may be needed to diagnose conditions like Alport syndrome.
The kidneys filter blood and regulate fluid levels in the body by selectively reabsorbing or secreting solutes. Urine passes from the kidneys through ureters into the bladder, then through the urethra. The kidneys contain nephrons which filter blood and reabsorb or excrete products. Hematuria, the presence of blood in urine, can indicate issues ranging from minor infections to serious conditions like cancer and requires medical evaluation.
This document discusses tubulo-interstitial pathology and chronic glomerulonephritis. It defines acute pyelonephritis, its causes and morphology. It describes chronic pyelonephritis and reflux nephropathy, including forms of chronic pyelonephritis and their gross and microscopic morphology. It also discusses drug-induced tubulo-interstitial nephritis, analgesic nephropathy, causes of chronic glomerulonephritis, and interpreting morphology of chronic glomerulonephritis.
Kidney disorders, Laboratory Investigation and Renal Function TestsMadhukar Vedantham
The document discusses kidney disorders, including their presentation, common diseases, and laboratory tests used in evaluation and diagnosis. It covers the functions of the kidneys, risk factors and symptoms of kidney failure, treatment options like dialysis and transplantation. Common kidney diseases described include polycystic kidney disease, hypertensive nephrosclerosis, glomerulonephritis, urinary tract infections, kidney stones, and diabetic kidney disease. Laboratory tests for kidney function include urine analysis, renal function tests of glomerular and renal blood flow, and renal biopsy.
Uremia develops as a result of chronic kidney disease and deterioration of renal function. It causes fluid, electrolyte, and hormone imbalances which can damage multiple organ systems. As kidney function declines to a creatinine clearance below 10 mL/min, waste products like nitrogen cannot be removed from the body and accumulate, disrupting water and electrolyte balance and causing pathological changes. Patients with end-stage renal disease experience fatigue, nutritional issues, and anxiety from their condition and treatment.
Dr. Sachin Verma is a young, diligent and dynamic physician. He did his graduation from IGMC Shimla and MD in Internal Medicine from GSVM Medical College Kanpur. Then he did his Fellowship in Intensive Care Medicine (FICM) from Apollo Hospital Delhi. He has done fellowship in infectious diseases by Infectious Disease Society of America (IDSA). He has also done FCCS course and is certified Advance Cardiac Life support (ACLS) and Basic Life Support (BLS) provider by American Heart Association. He has also done a course in Cardiology by American College of Cardiology and a course in Diabetology by International Diabetes Centre. He specializes in the management of Infections, Multiorgan Dysfunctions and Critically ill patients and has many publications and presentations in various national conferences under his belt. He is currently working in NABH Approved Ivy super-specialty Hospital Mohali as Consultant Intensivists and Physician.
The document discusses various kidney disorders including congenital anomalies, glomerular diseases, tubulointerstitial diseases, urinary stones, obstructive uropathy, and tumors. Specific conditions covered include polycystic kidney disease, glomerulonephritis, pyelonephritis, acute tubular necrosis, urolithiasis, hydronephrosis, and obstructive uropathy. The anatomy, functions, and histopathological features of the kidney are also summarized.
Glomerular disease is a group of diseases that affect the glomeruli in an inflammatory manner. They can be primary, arising from issues in the glomeruli themselves, or secondary, arising from other systemic diseases. Primary glomerular diseases include minimal change disease, membranous glomerulonephritis, and IgA nephropathy. Secondary glomerular diseases are often caused by systemic lupus erythematosus, diabetes, or amyloidosis. Glomerular diseases can present as nephrotic syndrome, with heavy proteinuria and edema, or nephritic syndrome, with hematuria and reduced kidney function. Rapidly progressive glomerulonephritis is characterized by a severe loss
This document discusses kidney failure caused by hypertension. It begins by defining blood pressure and the stages of hypertension. It then explains how high blood pressure can damage the kidneys over time by restricting blood flow. Specifically, it describes how narrowing of the renal arteries from conditions like atherosclerosis and fibromuscular dysplasia can lead to renal hypertension. Left untreated, this causes further kidney damage through activation of the renin-angiotensin system and fluid retention, eventually leading to kidney failure and the need for dialysis or transplantation. The document outlines symptoms, diagnostic tests, prevention methods like controlling blood pressure, and treatments including medications and revascularization.
The kidneys filter blood and regulate fluid levels in the body by selectively reabsorbing or secreting solutes. Urine passes from the kidneys through ureters into the bladder, then through the urethra. The kidneys contain nephrons which filter blood and reabsorb or excrete products. Hematuria, the presence of blood in urine, can indicate issues ranging from minor infections to serious conditions like cancer and requires medical evaluation.
This document discusses tubulo-interstitial pathology and chronic glomerulonephritis. It defines acute pyelonephritis, its causes and morphology. It describes chronic pyelonephritis and reflux nephropathy, including forms of chronic pyelonephritis and their gross and microscopic morphology. It also discusses drug-induced tubulo-interstitial nephritis, analgesic nephropathy, causes of chronic glomerulonephritis, and interpreting morphology of chronic glomerulonephritis.
Kidney disorders, Laboratory Investigation and Renal Function TestsMadhukar Vedantham
The document discusses kidney disorders, including their presentation, common diseases, and laboratory tests used in evaluation and diagnosis. It covers the functions of the kidneys, risk factors and symptoms of kidney failure, treatment options like dialysis and transplantation. Common kidney diseases described include polycystic kidney disease, hypertensive nephrosclerosis, glomerulonephritis, urinary tract infections, kidney stones, and diabetic kidney disease. Laboratory tests for kidney function include urine analysis, renal function tests of glomerular and renal blood flow, and renal biopsy.
Uremia develops as a result of chronic kidney disease and deterioration of renal function. It causes fluid, electrolyte, and hormone imbalances which can damage multiple organ systems. As kidney function declines to a creatinine clearance below 10 mL/min, waste products like nitrogen cannot be removed from the body and accumulate, disrupting water and electrolyte balance and causing pathological changes. Patients with end-stage renal disease experience fatigue, nutritional issues, and anxiety from their condition and treatment.
Dr. Sachin Verma is a young, diligent and dynamic physician. He did his graduation from IGMC Shimla and MD in Internal Medicine from GSVM Medical College Kanpur. Then he did his Fellowship in Intensive Care Medicine (FICM) from Apollo Hospital Delhi. He has done fellowship in infectious diseases by Infectious Disease Society of America (IDSA). He has also done FCCS course and is certified Advance Cardiac Life support (ACLS) and Basic Life Support (BLS) provider by American Heart Association. He has also done a course in Cardiology by American College of Cardiology and a course in Diabetology by International Diabetes Centre. He specializes in the management of Infections, Multiorgan Dysfunctions and Critically ill patients and has many publications and presentations in various national conferences under his belt. He is currently working in NABH Approved Ivy super-specialty Hospital Mohali as Consultant Intensivists and Physician.
The document discusses various kidney disorders including congenital anomalies, glomerular diseases, tubulointerstitial diseases, urinary stones, obstructive uropathy, and tumors. Specific conditions covered include polycystic kidney disease, glomerulonephritis, pyelonephritis, acute tubular necrosis, urolithiasis, hydronephrosis, and obstructive uropathy. The anatomy, functions, and histopathological features of the kidney are also summarized.
Glomerular disease is a group of diseases that affect the glomeruli in an inflammatory manner. They can be primary, arising from issues in the glomeruli themselves, or secondary, arising from other systemic diseases. Primary glomerular diseases include minimal change disease, membranous glomerulonephritis, and IgA nephropathy. Secondary glomerular diseases are often caused by systemic lupus erythematosus, diabetes, or amyloidosis. Glomerular diseases can present as nephrotic syndrome, with heavy proteinuria and edema, or nephritic syndrome, with hematuria and reduced kidney function. Rapidly progressive glomerulonephritis is characterized by a severe loss
This document discusses kidney failure caused by hypertension. It begins by defining blood pressure and the stages of hypertension. It then explains how high blood pressure can damage the kidneys over time by restricting blood flow. Specifically, it describes how narrowing of the renal arteries from conditions like atherosclerosis and fibromuscular dysplasia can lead to renal hypertension. Left untreated, this causes further kidney damage through activation of the renin-angiotensin system and fluid retention, eventually leading to kidney failure and the need for dialysis or transplantation. The document outlines symptoms, diagnostic tests, prevention methods like controlling blood pressure, and treatments including medications and revascularization.
1. Acute renal failure (ARF) is an acute, potentially reversible condition where the kidneys fail to maintain homeostasis. Causes include prerenal factors like shock, congestive heart failure, or intrarenal injury from toxins. Symptoms range from nonspecific like fever to specific kidney issues like electrolyte imbalances. Treatment focuses on fluid management, electrolyte replacement, and potentially dialysis.
2. Chronic renal failure is a permanent loss of kidney function that progresses to end stage renal disease. It is usually caused by congenital anomalies or acquired glomerular diseases. Symptoms emerge late and include fatigue, nausea, and cardiac/bone issues. Treatment manages complications and slows progression with a low protein
This document discusses liver cirrhosis, including its types, causes, pathophysiology, clinical manifestations, complications, nursing diagnoses, and interventions. Liver cirrhosis is a chronic, degenerative disease characterized by replacement of normal liver tissue with fibrosis that disrupts liver structure and function. Common types are alcoholic cirrhosis and postnecrotic cirrhosis resulting from viral hepatitis. Complications include ascites, hepatic encephalopathy, and esophageal varices, which can lead to life-threatening bleeding if ruptured. Nursing care focuses on reducing metabolic demands, providing adequate nutrition and hydration, preventing infection, and protecting patients from injury and further complications.
This document discusses various congenital abnormalities of the kidney and urinary tract that can occur during fetal development. It covers abnormalities in kidney formation such as renal agenesis, hypoplasia, and dysplasia. It also discusses abnormalities in kidney position and shape including ectopic kidneys, horseshoe kidneys, and crossed fused ectopia. Finally, it summarizes abnormalities of the collecting system like hydronephrosis, bladder extrophy, posterior urethral valves, and patent urachus. For each condition, it provides information on incidence, etiology, clinical manifestations, diagnosis, treatment, and nursing management.
This document discusses renal function tests (RFTs). It begins by describing the functions of the kidney including formation of urine, excretion of waste products, and regulation of water, electrolytes and acid-base balance.
It then explains that RFTs are used to assess renal damage, monitor progression of renal disease, and adjust dosing of nephrotoxic drugs. RFTs provide information on renal blood flow, glomerular filtration rate, tubular function, and urine output. Tests include urine analysis, measurements of glomerular function like creatinine clearance, and tests of tubular function like concentration and dilution tests. The document describes several RFTs in detail.
This document discusses acute and chronic renal failure. It defines renal failure and describes how acute failure has a sudden onset and may be reversible, while chronic failure progresses slowly over months and can lead to permanent damage. Causes of acute failure include reduced blood flow or obstruction, while chronic failure may result from conditions like diabetes, hypertension, or glomerulonephritis. Symptoms depend on the type and stage of renal failure. Treatment involves managing fluid, electrolytes, diet, and potentially dialysis or transplantation.
The document discusses proteinuria and hematuria in children. It covers the definition, causes, evaluation, and treatment of both conditions. Proteinuria can be caused by glomerular, tubular, or overflow mechanisms and is evaluated through urine dipsticks, 24-hour urine collection, and urine protein to creatinine ratio. Hematuria can be gross or microscopic and is seen in conditions like UTI, nephrolithiasis, glomerulonephritis, IgA nephropathy, and Alport syndrome. Evaluation of hematuria involves urinalysis, urine culture, imaging, and considering familial causes. Specific renal diseases like post-streptococcal glomerulonephritis
This document discusses renal function tests which are divided into three groups: glomerular function tests, tubular function tests, and urine analysis.
Glomerular function tests include clearance tests such as creatinine clearance test which measures glomerular filtration rate (GFR). Tubular function tests assess kidney's concentrating and diluting abilities through urine concentration and dilution tests. Urine analysis examines physical properties, chemical components, and microscopic contents of urine to detect abnormalities.
Pyelonephritis is an infection and inflammation of the kidneys that is usually caused by bacteria ascending from the lower urinary tract. It is more common in females than males, especially between ages 15-35. Common symptoms include flank pain, fever, nausea, and urinary symptoms like dysuria and hematuria. Diagnosis involves urinalysis showing white blood cells and a urine culture. Treatment focuses on antibiotics and prevention emphasizes frequent urination and hydration to maintain bladder health.
Approach to the Patient with Renal DiseasePatrick Carter
This document provides an overview of renal disease for medical students. It defines key terms related to renal function and urine findings. It describes tools for detecting renal disease including history, physical exam, urinalysis, and bloodwork. It discusses uremic syndrome and its effects on multiple organ systems. It differentiates between acute and chronic renal failure, nephritic and nephrotic syndrome based on causes, labs, and physical findings. The goal is to review approaches for evaluating and classifying patients with possible renal disease.
This document provides information on how to approach and evaluate a patient presenting with proteinuria. It defines proteinuria and normal albumin excretion rates. It describes the composition of urinary protein and mechanisms of proteinuria. It discusses classification of proteinuria according to quantity, nature, and selectivity. It outlines the clinical evaluation including history, physical exam, urine dipstick testing, quantifying proteinuria, and microscopic urine analysis. It provides guidance on when to refer to nephrology and how to evaluate transient and orthostatic proteinuria.
Liver cirrhosis is a chronic, progressive disease of the liver characterized by diffused damage to liver cells with fibrosis and nodular regeneration. It is caused by many forms of liver disease and conditions like hepatitis and chronic alcohol abuse. This leads to scarring of the liver and loss of liver function. Common complications of cirrhosis include ascites, bruising/bleeding, jaundice, and portal hypertension which can lead to esophageal or gastric varices. Management involves promoting rest, improving nutrition, preventing infection, and treating complications medically or through procedures like TIPS or liver transplantation.
Proteinuria – early indicator of renal disease
Increases the risk of renal impairment, hypertension & cardiovascular disease.
Proteinuria of 1+ or more persisting on 2 subsequent dipstick tests at weekly intervals – requires further investigations.
Causes of transient proteinuria to be excluded
This document provides information on proteinuria (abnormal amounts of protein in the urine) including its history, physiology, detection, quantification, causes, and diagnostic evaluation. It details the normal mechanisms by which the kidneys filter and reabsorb albumin and other proteins from the blood. Common causes of proteinuria include benign causes like exercise as well as pathological glomerular, tubular, and overflow proteinuria due to various kidney diseases and disorders. The diagnostic approach involves urinalysis, urine protein creatinine ratio, and ruling out transient causes through repeated testing.
Malabsorption refers to disorders that disrupt digestion and nutrient absorption in the small intestine. This can lead to malnutrition and various anemias from deficiencies. Diagnosis involves tests like fecal fat analysis, D-xylose absorption tests, and vitamin B12 absorption (Schilling) tests. Treatment focuses on correcting nutritional deficiencies through supplements and treating any underlying diseases through measures like gluten-free diets for celiac disease or antibiotics for bacterial overgrowth.
A 12-year-old boy presented with fever, edema, and decreased urine output. He was diagnosed with mesangiocapillary glomerulonephritis (GN) with cellular crescents based on investigations showing hematuria, proteinuria, hypertension, and renal biopsy. He was initially treated with calcium channel blockers, ACE inhibitors, and methylprednisolone + cyclophosphamide IV. His renal function improved and he was discharged on azathioprine and prednisone for maintenance. At last follow up 34 months later, he had normal renal function while continuing immunosuppressants, indicating a good prognosis with aggressive treatment.
This document discusses glomerular disease and glomerulonephritis. It begins by defining glomerular disease and glomerulonephritis, noting that glomerulonephritis is a type of glomerular disease involving inflammation of the glomeruli. It then discusses the main clinical presentations of glomerular disease, including nephrotic syndrome, acute glomerulonephritis, and asymptomatic urinary abnormalities. The causes, symptoms, investigations, and management of various glomerular diseases are subsequently outlined. Throughout, examples are provided of specific diseases like post-streptococcal glomerulonephritis, membranous nephropathy, and crescentic glomerulone
The document provides information about renal biopsies, including their definition, history, indications, contraindications, preparation, procedure, post-procedure care, complications, and discharge/follow-up. A renal biopsy is a procedure that obtains kidney tissue, typically using a needle, to help diagnose kidney diseases. It has become safer since the 1950s with the development of needle biopsies and imaging guidance. Key indications include unexplained kidney issues like proteinuria or injuries. Risks include bleeding, but most complications are minor and self-limiting. Patients are monitored after the procedure and advised on follow-up care.
This presentation comprises of congenital anomalies of kidney and urinary tract made concise and in depth for PG preparation. It contains all important topics of the regarding subject covered in detail.
This document provides an overview of glomerulonephritis (GN), including its definition, types, causes, pathophysiology, clinical manifestations, diagnostic evaluation, management, complications, and nursing care. GN involves inflammation or damage to the glomeruli in the kidneys. It discusses the anatomy of the nephron and causes of GN, including infections and immune or genetic factors. Types of GN include acute and chronic forms. Treatment depends on severity and may include medications, lifestyle changes, and dialysis. Complications can include renal failure, hypertension, and fluid overload. Nursing care focuses on pain management, fluid balance, breathing exercises, and patient education.
This document discusses renal function tests and their importance in assessing kidney function. It covers urine analysis including physical, chemical and microscopic examination. It also discusses various blood tests like serum creatinine, blood urea, uric acid and electrolytes to evaluate glomerular function. Tests of tubular function examined include urine concentration, vasopressin and water load tests. The significance of renal function tests in acute kidney injury is also highlighted. An addendum discusses cystatin C as a novel marker for non-invasive estimation of glomerular filtration rate and early renal impairment.
This document discusses renal function tests. It describes why renal function is tested, such as to assess kidney function and detect impairment. It outlines when renal function should be assessed, such as in older age, diabetes, or hypertension. The document then describes the different types of renal function tests, including urine analysis, blood tests like creatinine and urea, and glomerular function tests. Urine analysis involves examining color, volume, specific gravity, pH, and microscopic sediment. Blood tests evaluate substances that are normally excreted by the kidneys. Glomerular function tests directly measure the glomerular filtration rate.
1. Acute renal failure (ARF) is an acute, potentially reversible condition where the kidneys fail to maintain homeostasis. Causes include prerenal factors like shock, congestive heart failure, or intrarenal injury from toxins. Symptoms range from nonspecific like fever to specific kidney issues like electrolyte imbalances. Treatment focuses on fluid management, electrolyte replacement, and potentially dialysis.
2. Chronic renal failure is a permanent loss of kidney function that progresses to end stage renal disease. It is usually caused by congenital anomalies or acquired glomerular diseases. Symptoms emerge late and include fatigue, nausea, and cardiac/bone issues. Treatment manages complications and slows progression with a low protein
This document discusses liver cirrhosis, including its types, causes, pathophysiology, clinical manifestations, complications, nursing diagnoses, and interventions. Liver cirrhosis is a chronic, degenerative disease characterized by replacement of normal liver tissue with fibrosis that disrupts liver structure and function. Common types are alcoholic cirrhosis and postnecrotic cirrhosis resulting from viral hepatitis. Complications include ascites, hepatic encephalopathy, and esophageal varices, which can lead to life-threatening bleeding if ruptured. Nursing care focuses on reducing metabolic demands, providing adequate nutrition and hydration, preventing infection, and protecting patients from injury and further complications.
This document discusses various congenital abnormalities of the kidney and urinary tract that can occur during fetal development. It covers abnormalities in kidney formation such as renal agenesis, hypoplasia, and dysplasia. It also discusses abnormalities in kidney position and shape including ectopic kidneys, horseshoe kidneys, and crossed fused ectopia. Finally, it summarizes abnormalities of the collecting system like hydronephrosis, bladder extrophy, posterior urethral valves, and patent urachus. For each condition, it provides information on incidence, etiology, clinical manifestations, diagnosis, treatment, and nursing management.
This document discusses renal function tests (RFTs). It begins by describing the functions of the kidney including formation of urine, excretion of waste products, and regulation of water, electrolytes and acid-base balance.
It then explains that RFTs are used to assess renal damage, monitor progression of renal disease, and adjust dosing of nephrotoxic drugs. RFTs provide information on renal blood flow, glomerular filtration rate, tubular function, and urine output. Tests include urine analysis, measurements of glomerular function like creatinine clearance, and tests of tubular function like concentration and dilution tests. The document describes several RFTs in detail.
This document discusses acute and chronic renal failure. It defines renal failure and describes how acute failure has a sudden onset and may be reversible, while chronic failure progresses slowly over months and can lead to permanent damage. Causes of acute failure include reduced blood flow or obstruction, while chronic failure may result from conditions like diabetes, hypertension, or glomerulonephritis. Symptoms depend on the type and stage of renal failure. Treatment involves managing fluid, electrolytes, diet, and potentially dialysis or transplantation.
The document discusses proteinuria and hematuria in children. It covers the definition, causes, evaluation, and treatment of both conditions. Proteinuria can be caused by glomerular, tubular, or overflow mechanisms and is evaluated through urine dipsticks, 24-hour urine collection, and urine protein to creatinine ratio. Hematuria can be gross or microscopic and is seen in conditions like UTI, nephrolithiasis, glomerulonephritis, IgA nephropathy, and Alport syndrome. Evaluation of hematuria involves urinalysis, urine culture, imaging, and considering familial causes. Specific renal diseases like post-streptococcal glomerulonephritis
This document discusses renal function tests which are divided into three groups: glomerular function tests, tubular function tests, and urine analysis.
Glomerular function tests include clearance tests such as creatinine clearance test which measures glomerular filtration rate (GFR). Tubular function tests assess kidney's concentrating and diluting abilities through urine concentration and dilution tests. Urine analysis examines physical properties, chemical components, and microscopic contents of urine to detect abnormalities.
Pyelonephritis is an infection and inflammation of the kidneys that is usually caused by bacteria ascending from the lower urinary tract. It is more common in females than males, especially between ages 15-35. Common symptoms include flank pain, fever, nausea, and urinary symptoms like dysuria and hematuria. Diagnosis involves urinalysis showing white blood cells and a urine culture. Treatment focuses on antibiotics and prevention emphasizes frequent urination and hydration to maintain bladder health.
Approach to the Patient with Renal DiseasePatrick Carter
This document provides an overview of renal disease for medical students. It defines key terms related to renal function and urine findings. It describes tools for detecting renal disease including history, physical exam, urinalysis, and bloodwork. It discusses uremic syndrome and its effects on multiple organ systems. It differentiates between acute and chronic renal failure, nephritic and nephrotic syndrome based on causes, labs, and physical findings. The goal is to review approaches for evaluating and classifying patients with possible renal disease.
This document provides information on how to approach and evaluate a patient presenting with proteinuria. It defines proteinuria and normal albumin excretion rates. It describes the composition of urinary protein and mechanisms of proteinuria. It discusses classification of proteinuria according to quantity, nature, and selectivity. It outlines the clinical evaluation including history, physical exam, urine dipstick testing, quantifying proteinuria, and microscopic urine analysis. It provides guidance on when to refer to nephrology and how to evaluate transient and orthostatic proteinuria.
Liver cirrhosis is a chronic, progressive disease of the liver characterized by diffused damage to liver cells with fibrosis and nodular regeneration. It is caused by many forms of liver disease and conditions like hepatitis and chronic alcohol abuse. This leads to scarring of the liver and loss of liver function. Common complications of cirrhosis include ascites, bruising/bleeding, jaundice, and portal hypertension which can lead to esophageal or gastric varices. Management involves promoting rest, improving nutrition, preventing infection, and treating complications medically or through procedures like TIPS or liver transplantation.
Proteinuria – early indicator of renal disease
Increases the risk of renal impairment, hypertension & cardiovascular disease.
Proteinuria of 1+ or more persisting on 2 subsequent dipstick tests at weekly intervals – requires further investigations.
Causes of transient proteinuria to be excluded
This document provides information on proteinuria (abnormal amounts of protein in the urine) including its history, physiology, detection, quantification, causes, and diagnostic evaluation. It details the normal mechanisms by which the kidneys filter and reabsorb albumin and other proteins from the blood. Common causes of proteinuria include benign causes like exercise as well as pathological glomerular, tubular, and overflow proteinuria due to various kidney diseases and disorders. The diagnostic approach involves urinalysis, urine protein creatinine ratio, and ruling out transient causes through repeated testing.
Malabsorption refers to disorders that disrupt digestion and nutrient absorption in the small intestine. This can lead to malnutrition and various anemias from deficiencies. Diagnosis involves tests like fecal fat analysis, D-xylose absorption tests, and vitamin B12 absorption (Schilling) tests. Treatment focuses on correcting nutritional deficiencies through supplements and treating any underlying diseases through measures like gluten-free diets for celiac disease or antibiotics for bacterial overgrowth.
A 12-year-old boy presented with fever, edema, and decreased urine output. He was diagnosed with mesangiocapillary glomerulonephritis (GN) with cellular crescents based on investigations showing hematuria, proteinuria, hypertension, and renal biopsy. He was initially treated with calcium channel blockers, ACE inhibitors, and methylprednisolone + cyclophosphamide IV. His renal function improved and he was discharged on azathioprine and prednisone for maintenance. At last follow up 34 months later, he had normal renal function while continuing immunosuppressants, indicating a good prognosis with aggressive treatment.
This document discusses glomerular disease and glomerulonephritis. It begins by defining glomerular disease and glomerulonephritis, noting that glomerulonephritis is a type of glomerular disease involving inflammation of the glomeruli. It then discusses the main clinical presentations of glomerular disease, including nephrotic syndrome, acute glomerulonephritis, and asymptomatic urinary abnormalities. The causes, symptoms, investigations, and management of various glomerular diseases are subsequently outlined. Throughout, examples are provided of specific diseases like post-streptococcal glomerulonephritis, membranous nephropathy, and crescentic glomerulone
The document provides information about renal biopsies, including their definition, history, indications, contraindications, preparation, procedure, post-procedure care, complications, and discharge/follow-up. A renal biopsy is a procedure that obtains kidney tissue, typically using a needle, to help diagnose kidney diseases. It has become safer since the 1950s with the development of needle biopsies and imaging guidance. Key indications include unexplained kidney issues like proteinuria or injuries. Risks include bleeding, but most complications are minor and self-limiting. Patients are monitored after the procedure and advised on follow-up care.
This presentation comprises of congenital anomalies of kidney and urinary tract made concise and in depth for PG preparation. It contains all important topics of the regarding subject covered in detail.
This document provides an overview of glomerulonephritis (GN), including its definition, types, causes, pathophysiology, clinical manifestations, diagnostic evaluation, management, complications, and nursing care. GN involves inflammation or damage to the glomeruli in the kidneys. It discusses the anatomy of the nephron and causes of GN, including infections and immune or genetic factors. Types of GN include acute and chronic forms. Treatment depends on severity and may include medications, lifestyle changes, and dialysis. Complications can include renal failure, hypertension, and fluid overload. Nursing care focuses on pain management, fluid balance, breathing exercises, and patient education.
This document discusses renal function tests and their importance in assessing kidney function. It covers urine analysis including physical, chemical and microscopic examination. It also discusses various blood tests like serum creatinine, blood urea, uric acid and electrolytes to evaluate glomerular function. Tests of tubular function examined include urine concentration, vasopressin and water load tests. The significance of renal function tests in acute kidney injury is also highlighted. An addendum discusses cystatin C as a novel marker for non-invasive estimation of glomerular filtration rate and early renal impairment.
This document discusses renal function tests. It describes why renal function is tested, such as to assess kidney function and detect impairment. It outlines when renal function should be assessed, such as in older age, diabetes, or hypertension. The document then describes the different types of renal function tests, including urine analysis, blood tests like creatinine and urea, and glomerular function tests. Urine analysis involves examining color, volume, specific gravity, pH, and microscopic sediment. Blood tests evaluate substances that are normally excreted by the kidneys. Glomerular function tests directly measure the glomerular filtration rate.
This document discusses several causes of hematuria (red blood cells in the urine) in children, including glomerular diseases like acute poststreptococcal glomerulonephritis and hemolytic uremic syndrome. Acute poststreptococcal glomerulonephritis typically occurs 1-2 weeks after a streptococcal infection and presents with edema, hypertension and hematuria. Hemolytic uremic syndrome is commonly caused by E. coli infection and presents with bloody diarrhea, decreased urination, anemia and thrombocytopenia. Both conditions can potentially lead to acute kidney injury and require careful fluid management and treatment of complications.
The document provides information on performing a general urine examination. It discusses testing the urine as part of a medical examination. The urine specimen should be collected without additives and tested as soon as possible after collection. Normal urine output in adults is between 750-2500mL per day. Urine color can indicate various conditions like bile pigments, blood, or myoglobin. Specific gravity and osmolality measurements provide information about urine concentration. Urine pH typically ranges from 4-8. Glycosuria is commonly caused by elevated blood glucose or during pregnancy. Normal daily urine protein excretion is less than 150mg. Microbiological examination of a midstream urine sample can detect a urinary tract infection if there are over 105 bacteria per
Nephrotic syndrome may be caused by primary (idiopathic) renal disease or by a variety of secondary causes. Patients present with marked edema, proteinuria, hypoalbuminemia, and often hyperlipidemia.
Nephrotic syndrome is a primary glomerular disease characterized by the following:
Marked increase in protein in the urine (proteinuria)
Decrease in albumin in the blood (hypoalbuminemia)
Edema (The swelling (edema), can be most noticeable on the face, around the eyes, around the feet and ankles, and in the belly area (or the abdomen).
High serum cholesterol and low-density lipoproteins (hyperlipidemia)
Nephrotic syndrome is a clinical disorder characterized by marked increase of protein in the urine ( proteinuria ), decrease in albumin in the blood (hypoalbuminemia ),edema, & excess lipids in the blood ( hyperlipidemia )
Pathophysiology
Nephrotic syndrome can occur with almost any intrinsic renal disease or systemic disease that affects the glomerulus.
Although generally considered a disorder of childhood, nephrotic syndrome does occur in adults, including the elderly. Causes include:
Chronic glomerulonephritis
Diabetes mellitus with intercapillary glomerulosclerosis
Amyloidosis of the kidney
Systemic lupus erythematosus
Multiple myeloma and renal vein thrombosis.
NSAIDs
Pre eclampsia
Hematuria in children can be detected by urinary dipstick or microscopic examination. Common causes include glomerular disease, hypercalciuria, and nutcracker syndrome. Evaluation depends on whether hematuria is isolated, accompanied by proteinuria, or symptomatic. For isolated hematuria, follow-up includes urine culture and screening for hypercalciuria if persistent. Hematuria with proteinuria warrants further testing including serum creatinine. Symptomatic hematuria evaluation includes history, physical exam, and urinalysis to determine glomerular vs extraglomerular cause. Renal biopsy is considered if hematuria is substantial or progressive.
The document discusses various methods for evaluating renal function and structure, including urinalysis, tests of glomerular function like GFR and protein excretion, tests of renal tubular function, imaging procedures like ultrasound and radionuclide scanning, renal biopsy, and the limitations of renal function at birth. Renal function encompasses filtration, clearance, excretion, fluid/electrolyte balance, and production of hormones, while structure can be examined through imaging and biopsy. A range of tests are used to evaluate both function and structural abnormalities.
pediatrics.Evaluation of renal function and structure.(dr.adnan hamawandi)student
The document discusses various methods for evaluating renal function and structure, including urinalysis, tests of glomerular function like GFR and protein excretion, tests of renal tubular function, imaging procedures like ultrasound and radionuclide scanning, renal biopsy, and the limitations of renal function at birth. Renal function encompasses filtration, clearance, excretion, fluid/electrolyte balance, and production of hormones, while structure can be examined through imaging and biopsy. A range of tests are used to evaluate both function and structural abnormalities.
pediatrics.Evaluation of renal function and structure.(dr.adnan hamawandi)student
The document discusses various methods for evaluating renal function and structure, including urinalysis, tests of glomerular function like GFR and protein excretion, tests of renal tubular function, imaging procedures like ultrasound and radionuclide scanning, renal biopsy, and the limitations of renal function at birth. Urinalysis provides a non-invasive indicator of renal function while tests of glomerular and tubular function assess filtration, concentration, dilution and acidification abilities. Imaging can evaluate kidney size, shape, blood flow and reflux while biopsy offers definitive histological diagnosis. Renal function is significantly limited at birth with low GFR and impaired concentration, sodium handling and acid-base regulation.
Poststreptococcal acute glomerulonephritis (AGN) is a common condition in childhood caused by a Streptococcus pyogenes infection. It involves an immune response that leads to inflammation of the glomeruli in the kidneys. Symptoms include edema, gross hematuria, hypertension, and acute renal insufficiency. Treatment focuses on controlling blood pressure, restricting fluid and salt intake, and administering antibiotics. While early AGN is often temporary and reversible, chronic glomerulonephritis can lead to permanent kidney damage if not properly managed.
Glomerular diseases account for a significant proportion of acute and chronic kidney disease and can have various causes including immune system problems, inherited conditions, and protein deposition in the glomeruli. The response of the glomerulus depends on the type of injury and may cause blood or protein in the urine, as well as high blood pressure or impaired kidney function. Diagnosis involves urine and blood tests to examine for blood, protein, and kidney function. Common glomerular diseases include minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy, and IgA nephropathy.
1. Acute glomerulonephritis is a common kidney disease in children that often presents with red urine caused by blood in the urine. It typically results from a prior streptococcal infection of the throat or skin.
2. The disease is characterized by sudden onset of hematuria, decreased urine output, edema, and high blood pressure. It involves inflammation of the capillary loops in the kidneys caused by antigen-antibody complexes depositing in the glomeruli.
3. Treatment focuses on monitoring for hematuria, edema, and hypertension. Fluid intake is restricted if urine output decreases significantly. Antibiotics may be given if a streptococcal infection preceded the acute glomerulone
Hematuria, or blood in the urine, can be caused by diseases of the urinary system or other systemic disorders. It is classified as microscopic or gross based on visibility, and as early, terminal, or diffuse based on timing during urination. Common causes include glomerular diseases, infections, cancers, trauma, and stones. Diagnosis involves urinalysis, microscopy, imaging, and sometimes kidney biopsy. Treatment focuses on the underlying condition causing the hematuria. Prognosis depends on associated clinical or laboratory abnormalities, with isolated microscopic hematuria generally having a good prognosis.
This document discusses primary biliary cirrhosis (PBC), a chronic disease that slowly destroys bile ducts in the liver. It begins by describing a 45-year-old patient presenting with fatigue, itching, jaundice, and an enlarged spleen. Test results and liver biopsy are needed to diagnose PBC, which is characterized by antibodies and inflammation of bile ducts. Ursodeoxycholic acid is the standard treatment and improves liver tests, though transplantation may be needed for advanced cases. The document then provides further details on symptoms, causes, complications, diagnostic tests, treatment goals, and managing specific complications of PBC.
Kidney infection or pyelonephritis is an infection of the kidney that can be acute or chronic. Acute pyelonephritis causes symptoms like fever, flank pain, nausea, and painful urination. It is usually treated with antibiotics to control the bacterial infection. Chronic pyelonephritis can cause permanent kidney damage if not properly treated. Prompt treatment and prevention of recurrent urinary tract infections can help reduce the risk of chronic pyelonephritis.
This document discusses renal function tests and their importance in assessing kidney function and detecting impairment. It describes various tests including urine analysis, blood tests of creatinine and urea, and glomerular function tests. Common indications for evaluating renal function are listed, such as older age, diabetes, and hypertension. The document also outlines approaches to interpreting test results and diagnosing different kidney conditions like acute injury, nephritic syndrome, and nephrotic syndrome.
This document provides an overview of hematuria and glomerular causes of hematuria. It defines macroscopic and microscopic hematuria and discusses various glomerular diseases that can cause hematuria including IgA nephropathy, Alport syndrome, thin basement membrane disease, post-infectious glomerulonephritis, and Henoch–Schönlein purpura. It describes the clinical presentations, pathologies, diagnoses, and treatments of these conditions. Key investigations for glomerular hematuria are outlined.
Jaundice otherwise called icterus, which may occurs due to high bilirubin level in blood. The slides here explains the epidemiology, metabolism of bilirubin, types of jaundice, their etiology, risk factors involved, symptoms diagnosis and treatment.
Acute-Liver-Failure-2012 power point presentationNishanthTR
- Acute liver failure has a high mortality rate between 56-80%. The main role of intensive care is providing multi-organ support.
- The most common cause in the western world is paracetamol toxicity. Hepatic encephalopathy no longer the main cause of death but its detection and management require sophisticated monitoring.
- Hepatorenal failure results from complex circulatory changes due to liver failure. Terlipressin may help treat it. Novel replacement therapies are under development but more studies are still needed on their efficacy.
This document summarizes common viral infections including measles, varicella, mumps, and viral hepatitis. Measles is caused by a paramyxovirus and causes a rash and respiratory symptoms. Varicella (chickenpox) is caused by varicella zoster virus and presents with a pruritic vesicular rash that spreads. Mumps is caused by a paramyxovirus and presents with painful swelling of the salivary glands. Hepatitis A and B viruses are described as common causes of viral hepatitis transmitted through fecal-oral and blood-borne routes respectively.
Principles of acute management of diabetic ketoacidosisEric General
This document provides guidelines for managing diabetic ketoacidosis (DKA) in children. It outlines recommendations for initial fluid bolus and hydration, monitoring of electrolytes and glucose during treatment, use of bicarbonate and insulin therapy, and monitoring of vital signs and lab values. It also describes cerebral edema as a potential complication of DKA and recommends reducing fluid administration rates and using mannitol or hypertonic saline if cerebral edema develops.
This document discusses pediatric anemia. It defines anemia based on hemoglobin and hematocrit levels below certain thresholds defined by age and sex. Anemia results in physiological adaptations like increased cardiac output to maintain oxygen delivery to tissues. Causes of anemia vary by age and can be multifactorial, including nutritional deficiencies, blood loss, infections, and genetic disorders. Iron deficiency is a common cause, presenting with microcytic indices and low iron studies. Evaluation involves a complete blood count and smear to classify anemia, along with testing to identify the underlying cause.
Congenital heart disease (CHD) refers to structural heart defects present at birth. Diagnosis involves history, physical exam, chest X-ray, ECG, and echocardiogram. Most CHDs can be corrected with surgery if done in a timely manner. Echocardiography can identify and determine severity of specific lesions. Pediatricians must also identify any associated conditions that could impact outcomes.
This document discusses congestive cardiac failure in infants and children. It describes the causes, signs, and management of cardiac failure. The main causes in infants include congenital heart disease, arrhythmias like supraventricular tachycardia, and myocarditis. Signs of left-sided failure include tachypnea and hepatomegaly while signs of right-sided failure include hepatomegaly and facial edema. Management involves reducing cardiac workload, improving contractility, and treating the underlying cause. Diuretics, vasodilators, inotropes, and drugs that suppress the renin-angiotensin system are used. Prognosis depends on the cause, with mortality from cardiac failure being high
1. Tracheoesophageal fistula occurs due to deviation or altered cellular growth in the septum that separates the respiratory and esophageal primordia during development. It has an incidence of 1 in 4,000 live births.
2. Clinical features include excessive drooling, choking, and cyanosis during feeding as well as aspiration pneumonia from overflow of secretions into the lungs.
3. Diagnosis is made by passing a stiff catheter into the esophagus and obtaining an x-ray, which will show an air bubble in the stomach if there is a communication between the esophagus and trachea.
The document summarizes information about malaria, including that it is caused by Plasmodium parasites and can range from uncomplicated to severe. Severe malaria affects multiple organ systems and has a 20% mortality rate if not properly treated. Diagnosis involves examining thick and thin blood films under a microscope. Treatment depends on the severity of the case, with uncomplicated malaria typically treated with artemisinin-based combination therapy and severe malaria requiring hospitalization and parenteral antimalarial drugs along with supportive therapies.
This document provides information on various types of acyanotic congenital heart defects, including their anatomy, physiology, clinical features, diagnosis, treatment and prognosis. It discusses atrial septal defects (ASD), ventricular septal defects (VSD), and patent ductus arteriosus (PDA). ASDs are classified based on their location. VSDs account for one-quarter of all congenital heart defects and result in left-to-right shunting. PDA causes left-to-right shunting between the aorta and pulmonary artery. Surgical or catheterization closure is often recommended for larger defects.
Neonatal sepsis refers to systemic bacterial infections in newborns. Early-onset sepsis occurs within 72 hours of birth and is usually caused by maternal genital tract organisms. Late-onset sepsis occurs after 72 hours and is often caused by environmental organisms acquired in the hospital or home. Treatment involves supportive care and empiric antibiotics targeting common causes like E. coli, S. aureus, and Klebsiella spp. Prompt treatment is important but overuse of antibiotics risks emerging resistance, so diagnosis is confirmed using blood cultures and sepsis screening tests when possible. Outcomes depend on the infant's health and prompt, appropriate treatment.
This document provides guidance on performing a newborn history and examination. It outlines key components to include in the history such as the mother's obstetric history, antenatal care, labor/delivery details, and newborn's immediate care and current problems. The examination section describes assessing the newborn's appearance, vital signs, measurements, and performing a full physical exam including the neurological exam and evaluating primary reflexes like the Moro reflex. The goal is to obtain a thorough history and perform an examination of all body systems to identify any issues in the newborn.
Respiratory distress in neonates can be caused by pulmonary issues like respiratory distress syndrome, pneumonia, or transient tachypnea of the newborn, or non-pulmonary issues like cardiac problems, hypoglycemia, or central nervous system conditions. Early recognition and prompt treatment is essential to improve outcomes. Respiratory distress is characterized by tachypnea, chest retractions, and/or grunting. Causes and management should be considered based on gestational age, time of onset, and associated clinical features.
This document discusses acute kidney injury (AKI), formerly known as acute renal failure, in pediatrics. It defines AKI, describes the causes and pathophysiology, presents approaches to evaluation and management, and outlines treatment of complications. The key points are:
- AKI is defined as an abrupt reduction in kidney function over 48 hours, seen as a rise in creatinine or decrease in urine output.
- Common causes include prerenal failure from hypovolemia, intrinsic renal failure like acute tubular necrosis, and postrenal failure from urinary tract obstruction.
- Management involves treating complications, maintaining fluid/electrolyte balance, and considering dialysis for issues like fluid
This document discusses jaundice in newborns. It describes physiological jaundice as normal and temporary, while pathological jaundice requires treatment. Pathological jaundice is defined as a total serum bilirubin level exceeding certain thresholds depending on the baby's age. Causes of jaundice include hemolytic issues and problems with feeding. Treatment may involve phototherapy or exchange transfusions in severe cases. Monitoring, prevention, and ensuring proper breastfeeding are also discussed.
This document discusses acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML). It describes the epidemiology, pathogenesis, classification, clinical presentation, diagnosis, prognostic factors, management and outcomes of both ALL and AML in children. ALL is more common and has a better prognosis than AML. Prognostic factors for ALL include age, white blood cell count, specific genetic mutations and response to initial treatment. Treatment involves induction, consolidation, central nervous system prophylaxis and maintenance therapy over 2-3 years.
This document discusses encephalitis and encephalopathies in pediatrics. Encephalitis involves inflammation of the brain parenchyma, while encephalopathy implies cerebral dysfunction due to toxins or metabolic disorders without inflammation. Etiologies include various viruses, bacteria, fungi, parasites, toxins and metabolic disorders. Clinical manifestations depend on severity, localization, and presence of increased intracranial pressure, and can range from mild illness to severe encephalomyelitis. Diagnosis involves ruling out treatable causes through examinations, tests, and imaging. Management focuses on emergency treatment, controlling seizures and pressure, and treating the underlying cause.
This document discusses cerebral palsy (CP), a nonprogressive neuromotor disorder of cerebral origin. CP can be caused by factors operating prenatally, during delivery, or postnatally. It is classified based on topographic distribution, neurological findings, and etiology, with the main types being spastic, hypotonic, extrapyramidal, and cerebellar CP. Evaluation of patients with CP includes assessing eyes, ears, speech, sensory function, seizures, intelligence, and other issues. The diagnosis is made based on signs of increased muscle tone, feeding difficulties, and developmental delays. Differential diagnoses need to be considered. Management aims to improve posture, reduce muscle tone, prevent contractures, and provide early
Perinatal asphyxia is caused by lack of oxygen or poor perfusion to organs in fetuses or newborns. It is defined by criteria like low umbilical cord pH, low Apgar scores, seizures or multiorgan dysfunction in newborns. It can cause neurological injuries like selective neuronal necrosis or periventricular leukomalacia. Management involves maintaining normal temperature, oxygenation, blood pressure, blood glucose and treating seizures. Outcomes are predicted by factors like lack of breathing at birth or severe hypoxic ischemic encephalopathy.
This document summarizes HIV infection in pediatric patients. It describes the natural history of the disease, including three patterns of progression. It discusses clinical manifestations, opportunistic infections like Pneumocystis pneumonia, and respiratory diseases seen in HIV-infected children. It also outlines the WHO clinical staging criteria for pediatric HIV/AIDS.
This document provides information on acute bacterial meningitis in pediatrics, including epidemiology, clinical features, diagnosis, treatment and other types of meningitis such as tuberculous, cryptococcal and pneumococcal meningitis. It describes the typical presentation of acute bacterial meningitis in children including fever, irritability, headache and altered mental status. Diagnosis is made through lumbar puncture and examination of cerebrospinal fluid. Treatment involves administration of antibiotics such as ceftriaxone intravenously for 10-14 days. Complications, steroid use, and other types of meningitis are also summarized.
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Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
2. Common manifestations of renal disorders include edema,
hematuria, oligoanuria, dysuria and abnormalities of
micturition, flank pain and ureteric colic.
With
improvements in techniques and widespread availability
of antenatal ultrasonography, several congenital anomalies
of kidney and urinary tract (CAKUT) are detected.
Appropriate imaging procedures are needed to confirmWith
improvements in techniques and widespread availability
of antenatal ultrasonography, several congenital anomalies
of kidney and urinary tract (CAKUT) are detected.
Appropriate imaging procedures are needed to confirm and
define their severity.
3. Abnormal urinary stream or
dribbling of urine suggests an anomaly of the distal
urinary tract. The causes of acute kidney injury in the
newborn are different from those in older children.
During infancy, unexplained fever may be the only
feature of urinary tract infection (UTI). UTI may be
suggested by other nonspecific symptoms such as failure
to thrive, diarrhea and vomiting. It is important to diagnose
these infections since urinary tract anomalies may
be present. An abdominal mass at this age is likely to be
Wilms' tumor, hydronephrosis or multicystic renal
dysplasia.
An important cause of acute kidney injury, at
this age, is hemolytic uremic syndrome. About 20%
patients with minimal change nephrotic syndrome have
onset of the disease between 2 and 3 yr. Renal tubular
disorders such as renal tubular acidosis and Fanconi syndrome
are usually diagnosed at this age.
4. Acute poststreptococcal glomerulonephritis (GN), rare
below the age of 3 yr, is usual in older children. Rickets at
this age is rarely due to vitamin D deficiency, unless there
is malabsorption or chronic liver disease. Nephrotic
syndrome beginning in adolescence may be of the
nonminimal
type. Acute-on-chronic renal failure, previously
undetected chronic renal failure, symptomatic
hypertension
and collagen vascular diseases are common.
5. Clinical Features of Renal Disease
Hematuria
Gross hematuria in acute GN is typically smoky brown
or cola colored. Bright red blood suggests a nonglomerular
cause, as in renal or vesical calculi. Gross hematuria is
rare in UTI. Other conditions, which might impart a red
color to urine include hemoglobinuria, myoglobinuria,
porphyria and ingestion of beetroot.
Edema
Acute GN presents with facial puffiness and gross
hematuria; the edema does not pit readily on pressure. If
fluid intake is not restricted, the edema may increase and
involve hands, feet and legs. In nephrotic syndrome,
edema develops insidiously, starting with eyelid puffiness
most noticeable in the morning. Over a period of several
days, there is pitting edema over the feet and legs. Facial
swelling is often mistaken for allergy or insect bite.
6. Oliguria
Oliguria, defined as urine volume less than 0.5 ml/kg per
hr, commonly results from gastroenteritis and hypovolemia.
Oliguria is an important feature of moderate or
severe acute GN, acute tubular necrosis and conditions
causing severe glomerular injury (e.g. HUS, vasculitis).
Abnormalities of Micturition
A poor urinary stream in boys, especially in presence of a
full bladder, suggests obstruction, most commonly dueto posterior
urethral valves. Persistent dribbling indicates
abnormal ureteric insertion distal to bladder neck. Infants
with meningomyelocele should be evaluated for bladder
dysfunction. Dysuria, flank pain or ureteric colic suggest
UTI or urinary tract calculi.
7. Polyuria, Polydipsia
Impaired urinary concentration is a feature of
obstructive
uropathy and primary or secondary tubulointerstitial
disorders. Polyuria is also present in conditions
associated
with deficiency or resistance to antidiuretic hormone,
diabetes mellitus, hypokalemia (e.g. distal renal
tubular
acidosis) and hypercalcemia.
8. Enuresis
Primary monosymptomatic enuresis needs to be distinguished
from patients with dysfunctional voiding. Most
children with nocturnal enuresis have no evidence of renal
disease. Urinalysis and culture are recommended in
patients with secondary enuresis.
Hypertension
Assessment of blood pressure is necessary in all children,
and especially those with disorders of the kidneys or
urinary tract. Symptomatic hypertension is chiefly due to
a renal parenchymal or renovascular cause; endocrine
conditions are uncommon
9. Growth Retardation, Anemia
Physical retardation is a feature of chronic kidney disease
(stage 3-5) and tubular disorders. Normocytic
normochromic
anemia is striking in patients with chronic kidney
disease (stage 3-5). Patients with unexplained anemia
should be evaluated for a renal disease.
Abdominal Mass
Multicystic renal dysplasia, polycystic kidneys, renal vein
thrombosis, hydronephrosis (due to pelviureteric or lower
urinary tract obstruction) and Wilms' tumor may result
in palpable masses.
10. Examination of Urine
Urinalysis is an important step for diagnosis of renal
disease. Evaluation includes microscopic examination of
the uncentrifuged as well as centrifuged specimen and
semiquantitative or quantitative detection of different
substances.
Collection of Specimen
The first morning specimen is preferred since it is
relatively concentrated. While a clean container is
sufficient, specimens for culture should be collected in a
sterile container. After cleaning the perineum with soap
and water, a 'clean catch' sample is collected. If facilities
for immediate processing are not available, the specimen
is stored at 4°
C for 12-14 hr.
11. It is difficult to obtain satisfactory specimens in children
below 2-yr-old. Urine may be collected using a sterile bag
that is applied after local cleaning and removed soon after
the void. These specimens should not be used for culture.
Other reliable ways for obtaining urine specimens in
infants include percutaneous suprapubic aspiration or
transurethral catheterization
Specific Gravity
Specific gravity is measured using either refractometer or
hydrometer; the former is convenient, requires less volume
of urine and gives accurate values. The early morning
urine specific gravity should exceed 1015.
12. pH
Urine is collected in a capped syringe if pH can be
measured promptly. If measurement is likely to be
delayed, urine should be collected under paraffin. Urine
pH is lowest in the fasting, early morning specimen and
increases following meals.
Protein
Proteinuria is an important marker of renal injury. Detection
of 3-4+ albuminuria suggests glomerular disease.
Low molecular weight proteinuria, including lysozyme,
2 microglobulin, neutrophil gelatinase associated
lipocalin and retinol binding protein, suggest tubular
injury. Dipstick methods (Uristix) for proteinuria are
convenient and reliable. Composite strips for pH, glucose,
hematuria, leukocyte esterase and nitrite are also available.
Proteinuria can also be semiquantitatively tested using
the boiling and the sulfosalicylic acid tests
13. Microscopic Examination
A fresh, well-mixed specimen is examined for cellular
elements, crystals and casts. Alternatively, urine is
centrifuged at 1500 rpm for 10 min; urine is decanted and
the cell pellet resuspended in 0.3-0.5 ml urine. Evaluation
for hematuria, defined as more than 5 red cells/hpf in a
centrifuged specimen is abnormal. Red cell casts indicate
glomerular inflammation. Leukocytes may occasionally
be absent despite significant bacteriuria. On the other
hand, isolated presence of leukocytes is not specific for
UTI, and may be noted in interstitial nephritis, stones and
high fever. The detection of bacteriuria in fresh,
uncentrifuged urine is significant.
14. Blood Tests
Blood levels of creatinine and urea are used to assess
renal
function. The normal levels of serum creatinine are
0.2-0.5
mg/ dl in children below 6 yr and 0.4-0.8 mg/ dl in
older
children. Blood urea ranges between 20-35 mg/ dl
during
childhood.
15. The level of serum
creatinine is dependent on muscle mass and is,
therefore
low in malnutrition. Bilirubin may interfere with
creatinine
measurements. Blood urea levels are low on a protein
deficient diet and high with tissue breakdown, trauma,
gastrointestinal bleeding and use of corticosteroids.
Estimation of blood levels of cystatin C, which does not
depend on the nutritional status, is considered a sensitive
indicator of glomerular function.
16. Other specific investigations include albumin,
cholesterol,
antistreptococcal antibody titers, complement,
imrnunoglobulins and autoantibodies. Estimation of
blood
pH, bicarbonate, electrolytes and osmolality are
important
in patients with tubular disorders and/ or renal failure.
17. Glomerular Filtration Rate (GFR)
While clearance of inulin is regarded as the reference
for
estimating GFR, the test involves its accurate IV
infusion
followed by measurement of levels in timed urine and
blood samples. Measurement of the creatinine
clearance
is adequate for assessing GFR in most cases.
18. Creatinine Clearance
Creatinine clearance depends on the body size; the values
are normalized to surface area. The normal
creatinineclearance is 80-120 ml/minute per 1.73 m2
• GFR can be
estimated from serum creatinine (mg/ dl) and patient
height (cm). The value of the constant k ranges between
0.41-0.43.
GFR (ml/minute per 1.73 m2) = k x height
Serum creatinine
19. Investigations for evaluation of suspected tubular
diseases
Substrate Test
Phosphate Blood parathormone Tubular reabsorption of
phosphate Tubula maximum for reabsorption/GFR
Glucose Renal threshold and tubular maximum for
glucose r eabsorption
Amino acids Clearance of amino acid
Bicarbonate Blood anion gap
Fractional excretion of
bicarbonate
H+ Minimum urinary pH Urine
anion gap; urine osmolal gap U-B
CO2 gradient Water Maximum urine
osmolality Water deprivation test Plasma ADH
Sodium Urinary sodium excretion Plasma renin,
aldosterone
20. Imaging of the Urinary Tract
Plain X-Ray
A plain film of abdomen provides information on renal
size, shape and outline and radiopaque calculi. The
length of normal kidney approximates the height of
first four
lumbar vertebrae. A small kidney may indicate
hypoplasia
or chronic damage. The opposite kidney, unless
diseased,
shows compensatory hypertrophy.
21. Ultrasonography
Ultrasonography is the initial modality for imaging
kidneys and urinary tract in renal diseases. This
investigation
is readily available, noninvasive and performed
even in uncooperative patients, infants and those with
renal failure. Anatomic details of the kidneys, ureters and
bladder are examined. Doppler ultrasonography is useful
for studying renal blood flow
22. Intravenous Pyelogram (/VP)
The patient is prepared as for plain X-ray. The
radiocontrast
is injected and films taken at 2, 5, 10 and 30 min.
IVP provides satisfactory details on renal size, shape,
cortical outlines and calyceal pattern. The use of IVP
has
declined following the availability of radionuclide
imaging.
23. HEMATURIA
The presence of blood in urine imparts it a color, which
includes various shades of deep red, smoky brown, colacolor
and faint pink. Parents may mistake very concentrated
urine for that containing blood. Microscopic
examination of urine will show red blood cells. Reagent
coated dipsticks detect free hemoglobin and myoglobin.
Red urine may be present in porphyria and following
beetroot ingestion. Urine appears orange-colored after
administration of rifampicin or pyridium. Uric acid
crystals may also impart a pink tinge to the nappy. In children, the commonest
cause of gross hematuria is
postinfectious GN. Urinary tract stones are not infrequent Gross hematuria is
rare in acute pyelonephritis.
Conditions that cause persistent microscopic
hematuria include idiopathic hypercalciuria, benign
familial hematuria, Alport syndrome, IgA nephropathy
and membranoproliferative GN.
24. Diagnostic Evaluation
A history of pain in the flank or supra pubic region,
dysuria
and edema should be obtained. Physical examination
includes assessment of growth and features of acute or
chronic kidney disease such as edema, hypertension,
unexplained pallor, bony abnormalities and abdominal
mass. An audiogram and a detailed eye examination
may
be needed.
25. A fresh specimen is examined for red cells, red cell casts
and protein. Absence of large number of red cells in bloody
urine suggests hemoglobinuria (intravascular hemolysis)
or myoglobinuria. In glomerular disease, urine shows
dysmorphic red cells, of different shapes, whereas in
bleeding from renal pelvis or the lower urinary tract, the
red cells maintain normal morphology . Presence of
significant proteinuria (2+ or
more) and/or red cell casts suggests glomerular disease.
Hypercalciuria should be excluded by determination of
urinary calcium to creatinine ratio on one or more random
samples.
26. A plain X-ray film of the abdomen and abdominal
ultrasound is done to exclude major renal and urinary
tract
anomalies and calculi. Blood levels of creatinine are
measured; other specialized blood tests depend on the
likely
clinical etiology. Surgical conditions that cause
hematuria
can be diagnosed by appropriate imaging. Invasive
procedures such as cystoscopy are rarely indicated.
27. In a significant proportion, mild microscopic
hematuria
spontaneously disappears over a period of several
years.
Other family members may have similar urinary
abnormalities. If there is no family history, a renal
biopsy is not urgently indicated and the patient kept
under
observation.
28. Causes of hematuria
Glomerular
Postinfectious glomerulonephritis (GN)
IgA nephropathy
Henoch-Schonlein nephritis
Membranoproliferative GN
Rapidly progressive GN
30. Renal Biopsy
Renal biopsy should be done if hematuria is associated
with persistent or heavy (3+ or more) proteinuria, history of
renal disease in the family or evidence of chronic kidney
disease in the patient, or if renal impairment or hypertension
are seen on followup. A biopsy is also considered
in children showing persistent microscopic hematuria for
two or more years even in the absence of the above
features. This procedure is necessary to diagnose
IgAnephropathy, Alport syndrome, thin basement membrane
disease (typically presents as familial, benign hematuria)
and chronic GN. The biopsy is evaluated by light,
immunofluorescence and electron microscopy.
31. Alport Syndrome
This condition is inherited in an X-linked manner,
although autosomal transmission is known. Mutations in
the gene encoding alpha subunit of collagen IV (COL4A5)
result in persistent microscopic hematuria, moderate
proteinuria and progressive kidney failure. A significant
proportion show high frequency sensorineural deafness;
ocular defects (lenticonus, cataract, macular changes) are
often associated. Ultrastructural examination of renal
biopsy shows variable thickness of glomerular basement
membrane with lengths of marked attenuation to areas of
lamination. Therapy is supportive, including the use of
angiotensin converting enzyme inhibitors. The majority
of male patients show progression to end stage kidney
disease.
32. Quantitation of Proteinuria
Protein concentration of 100-1000 mg/ m2 / day
indicates
mild to moderate proteinuria; more than that is heavy
(nephrotic range) proteinuria. Accurate quantitative
measurements of 24 hr urinary protein are not needed, if
semiquantitative tests are done on a concentrated (first
morning) specimen. Normally the protein to creatinine
ratio, in the first morning urine specimen, is below
0.1 (mg/mg); a ratio of 0.1-2 indicates mild to moderate
and >2 heavy proteinuria. The latter usually corresponds
to 3+ or 4+ reaction on boiling or dipstick test.
33. Fever, dehydration and heavy exercise may cause
transient and mild proteinuria. Mild proteinuria may
occur in UTI, hydronephrosis and renal tuberculosis.
Mild
proteinuria in proximal tubular defects (e.g. Fanconi
syndrome) is composed of low molecular weight
proteins,
while heavy proteinuria (predominantly albumin)
indicates glomerular disease.
34. Important causes of asymptomatic proteinuria include
orthostatic proteinuria, chronic glomerular diseases, reflux
nephropathy, renal hypoplasia and rarely renal tubular
Disorders
In orthostatic (postural) proteinuria,
protein is absent in urine specimen collected after
overnight recumbence. The pathogenesis of this condition
is not clear but longterm outcome is good. Continued
followup is necessary until proteinuria disappears.
Chronic renal damage from vesicoureteric reflux and UTI
may manifest with proteinuria. Several forms of glomerular
diseases, especially focal segmental glomerulosclerosis,
may cause persistent asymptomatic proteinuria; microscopic hematuria is often
associated. A renal biopsy is
indicated in presence of persistent or heavy proteinuria.
Longterm observation is necessary to monitor clinical
course and renal function. Low salt diet and prolonged
treatment with angiotensin converting enzyme inhibitors
or angiotensin receptor blockers are effective in reducing
glomerular proteinuria.
35. ACUTE GLOMERULONEPHRITIS
Acute glomerulonephritis (GN) is characterized by abrupt
onset of hematuria, oliguria, edema and hypertension. The
clinical severity varies, depending on histological
involvement, salt and water retention and glomerular
filtration rate. Mild disease may go undetected; severe
cases have anuria, hypertensive encephalopathy and heart
failure. The most common cause of acute GN is that
following streptococcal infection. Key
investigations include renal function tests, urinalysis,
serum complement C3 and titers of
antistreptolysin. Renal
biopsy is required if the presentation or course suggest a
diagnosis other than poststreptococcal GN
36. Poststreptococcal Glomerulonephritis
Acute GN following infection by group A beta-
hemolytic
streptococci is a common disorder. Streptococcal
infection
of the throat or skin precedes the onset of nephritis by
1
to 4 weeks. Only a few strains of streptococci are
nephritogenic, e.g. types 4 and 12 causing pharyngitis
and
type 49 causing pyoderma.
37. Etiology of the acute nephritic syndrome
Postinfectious
Streptococci, staphylococci, pneumococci, meningococci,
Treponema pallidum, Salmonella, leptospira
Plasmodium malariae, P. falciparum, toxoplasma, filaria
Hepatitis B and C, cytomegalovirus, parvovirus, Epstein-Barr
virus, coxsackievirus, echovirus, varicella
Associated with severe infections; infection of shunts,
prostheses, bacterial endocarditis
Systemic vasculitis
Henoch-Schonlein purpura
Microscopic polyarteritis, Wegener granulomatosis
Others
Membranoproliferative glomerulonephritis
IgA nephropathy
Hereditary nephropathy
Systemic lupus erythematosus
38. Indications for renal biopsy in acute glomerulonephritis
Systemic features. Fever, rash, joint pain, heart disease
Absence of serologic evidence of streptococcal infection;
normal levels of C3 in the acute stage of illness
Mixed features of glomerulonephritis and nephrotic syndrome
High blood levels of urea or presence of anuria requiring
dialysis (rapidly progressive GN)
Delayed resolution
Oliguria, hypertension and/ or azotemia persisting past
7-10 days
Gross hematuria persisting past 3-4 weeks
Nephrotic range proteinuria beyond 2 weeks
Low C3 levels beyond 12 weeks
Persistent proteinuria beyond 6 months
39. Pathology
On light microscopy, glomeruli are enlarged and ischemic
and capillary loops narrowed, making glomeruli appear
Bloodless 16.8A); there is proliferation of mesangial
cells and neutrophil infiltration. Immunofluorescence
shows granular deposits of IgG and complement (C3)
along capillary walls. Electron microscopy
shows deposits (humps) on the subepithelial side of the
glomerular basement membrane.
40. Clinical Features
Poststreptococcal GN involves school-age children, more
commonly boys and is uncommon below 3 yr. Subclinical
episodes are more common than overt disease, especially
during epidemics. Patients may have mild proteinuria and
microscopic hematuria. The onset is rapid, with puffiness
around the eyes and pedal edema. Urine is cola-colored;
hematuria is brief, often lasting only a few hours and does
not persist beyond 1-2 weeks. While the degree of oliguria
usually correlates with the disease severity, anuria is
uncommon. Hypertension, present in over half the patients,
resolves with loss of edema. Atypical presentations
include (i) convulsions due to hypertensive encephalopathy;
(ii) left ventricular failure and pulmonary edema,
due to malignant hypertension and hypervolemia; (iii)
acute kidney injury; and (iv) nephrotic syndrome
41. Laboratory Findings
Urine shows 1-2+ protein with red cells, and red cell and
granular casts. White cells indicate glomerular inflammation
and should not be regarded as evidence of UTI.
Hemodilution may result in normocytic anemia; ESR is
raised. Blood levels of urea and creatinine are elevated
reflecting renal impairment; hyponatremia and hyperkalemia
occur with continuing oliguria. Chest X-ray may
show prominent vascular markings suggesting hypervolemia.
Serologic evidence for streptococcal infection is
present in most patients with pharyngitis, though
antibiotic therapy may blunt this response.
42. Management
Patients with mild oliguria and normal blood pressure
can be managed at home. Close attention to blood
pressure
and dietary intake is essential. Once acute GN has
occurred, treatment with penicillin has no effect on the
course of the disease, but may be given if active
pharyngitis or pyoderma is present. The principles of
management of patients with severe oliguria and acute
kidney injury are discussed later.
43. Diet. The intake of sodium, potassium and fluids should
be restricted until blood levels of urea reduce and urine
output increases. Overhydration is a dangerous
complication
as it may increase hypertension and precipitate left
ventricular failure. Patients with azoternia require accurate
measurement of urine output and daily weight, and
restriction of fluid intake to an amount equal to insensible
losses and 24 hr urine output.
44. Diuretics. Patients showing modest edema are treated
with
oral frusemide at a dose of 1-3 mg/kg; the edema
disappears with the return of renal function. Therapy
with
IV frusernide (2-4 mg/kg) is necessary in subjects with
pulmonary edema.
45. Hypertension. Mild hypertension may be controlled
by
restriction of salt and water intake. Effective
antihypertensive
agents include arnlodepine, nifedipine or
diuretics. Beta-blockers and angiotensin converting
enzyme inhibitors carry risk of hyperkalemia. Patients
with hypertensive emergencies need prompt treatment
with IV nitroprusside or labetalol
46. Left ventricular failure. Hypertension should be controlled
and IV frusemide given to induce diuresis, leading to
improvement in heart failure. If diuresis is not noted,
dialysis is initiated. Respiratory support with positive
endexpiratory
pressure may be needed.
Prolonged oliguria. Treatment, as outlined above, should
be continued and levels of blood urea and electrolytes
monitored. Dialysis is required in children with severe renal
failure and prolonged oligoanuria, fluid overload and
lifethreatening
electrolyte disturbances. Occurrence of secondary
infections should be avoided.
47. Outcome and Prognosis
Acute poststreptococcal GN has an excellent prognosis in
childhood. The symptoms begin to resolve in the first week
with loss of edema and fall in blood pressure. Gross
hematuria and significant proteinuria disappear within
2-weeks, although microscopic hematuria and slight
proteinuria may persist for several months. Hypertension
subsides within 2-3 weeks, but rarely may persist for
several weeks. Patients with acute GN of nonstreptococcal
etiology have variable and unpredictable outcome. These
cases need close followup over several years with periodic
urinalyses and measurements of blood pressure.
48. lmmunoglobulin A Nephropathy
Predominant deposition of IgA in the glomeruli, chiefly
in the mesangium and occasionally in capillary walls is
characteristic. The usual clinical manifestation is recurrent
episodes of gross hematuria following upper respiratory
infections; each episode lasts for 2-5 days. In between
these episodes, microscopic hematuria and mild proteinuria
may persist. An acute nephritic or nephrotic
syndrome is rarely the initial manifestation. Renal histology
shows mesangial proliferation of varying severity.
Patients with hematuria and non-nephrotic proteinuria
are treated using angiotensin converting enzyme inhibitors.
Therapy with corticosteroids and alkylating agents
is indicated in patients with nephrotic range proteinuria
or deranged renal function.
49. NEPHROTIC SYNDROME
Nephrotic syndrome is characterized by massive
proteinuria,
hypoalbuminemia and edema; hyperlipidemia
is often associated. Some patients show hematuria and
hypertension. Heavy proteinuria (more than 1 g/m2 per
day) is the underlying abnormality, leading to
hypoalbuminemia (serum albumin below 2.5 g/ dl). The
resultant fall in plasma oncotic pressure leads to interstitial
edema and hypovolemia.
50. This stimulates the reninangiotensin-
aldosterone axis and antidiuretic hormone
secretion that enhances sodium and water retention.
The
pathogenesis of edema may however be different in
patients with significant glomerular lesions, who show
primary sodium retention and expanded intravascular
volume. Hypoalbuminemia also induces hepatic
synthesis
of -lipoproteins resulting in hypercholesterolemia
51. More than 90% of childhood nephrotic syndrome is
primary (or idiopathic). Other causes such as amyloidosis,
vasculitis, systemic lupus erythematosus, postinfectious
GN and hepatitis B nephropathy are infrequent. Nephrotic
syndrome in children can be divided into two groups
based on renal histological characteristics: (i) minimal
change nephrotic syndrome (MCNS); and (ii) nephrotic
syndrome with significant lesions
52. STEROID SENSITIVE NEPHROTIC
SYNDROME
MCNS accounts for 80% cases of nephrotic syndrome in
children. Renal biopsy does not show
significantabnormalities on light microscopy. Electron
microscopy shows nonspecific obliteration of epithelial
foot processes. Immunofluorescence studies do not
demonstrate deposition of immune reactants except
occasional mesangial IgM. On the other hand, patients
with focal segmental glomerulosclerosis (FSGS) show
evidence of sclerosis involving a segment of the glomerular
Tuft.
53. The pathogenesis of MCNS is
obscure. There is evidence to suggest perturbation of
cell
mediated immunity, which through yet undefined
mechanisms alters the permselectivity of the
glomerular
filter, resulting in massive proteinuria. A proportion of
patients have a primary abnormality of the epithelial
foot
processes (podocytes).
54. Clinical Features
The onset is insidious with edema first noticed around
the eyes and subsequently on legs. It is soft and pits easily
on pressure. Gradually edema becomes generalized, with
ascites, hydrothorax and hydrocele. With
increasing edema, urine output may fall. The blood
pressure is usually normal; sustained elevation suggests
the possibility of significant glomerular lesions. The
bloated appearance and relative well-being of the child is
misleading and after the loss of edema, severe muscle
wasting is revealed. Infections may be present at the onset
and during relapses.
55. Laboratory Findings
Urine examination shows heavy (3-4+) proteinuria. Gross
hematuria or persistent microscopic hematuria suggests
the likelihood of significant glomerular lesions; hyaline
and granular casts are present. Serum albumin is low and
values below 1 g/ dl are often obtained.
Hypercholesterolemia
may impart a milky appearance to the plasma.blood
urea and creatinine values are within the normal range
except when there is hypovolemia and fall in renal
perfusion.
56. Blood levels of IgG are low and those of IgM elevated;
C3 level is normal. The severity of glomerular damage is
reflected in the passage of proteins of large molecular
weight, chiefly globulin. Protein selectivity is the ratio of
clearance of high molecular weight (e.g. IgG) to low
molecular weight proteins (e.g. transferrin, albumin). A
low ratio indicates highly selective proteinuria, as in
MCNS. However, this infor mation does not offer
diagnostic help.
57. An 8-yr-old boy with steroid dependent nephrotic
syndrome. Anasarca is seen affecting upper limbs (including dorsa
of hands), trunk and ascites. Note the cushingoid features and striae
on lower abdominal wall and upper legs
58. Evaluations considered at onset of nephrotic syndrome
include: (i) urinalysis for proteinuria, red cells, casts;
(ii) blood levels of urea, creatinine, albumin, cholesterol;
(iii) complete blood counts and (iv) tuberculin test. Depending
on clinical and laboratory findings, the following
additional tests may be required: (i) C3 and antistreptolysin
O (gross or persistent microscopic hematuria); (ii)
chest X-ray (positive tuberculin test; history of contact with
tuberculosis); (iii) hepatitis B surface antigen (recent
jaundice, raised levels of transaminases); (iv) antinuclear
antibodies (suspected systemic lupus erythematosus); and
(v) urine culture (suspected urinary tract infection).
59. A
renal biopsy is not required to confirm the diagnosis of
MCNS prior to starting treatment. A biopsy is
recommended
in children with atypical features at the onset (age
below 12 months, gross or persistent microscopic
hematuria,
low blood C3, hypertension or impaired renal
function). Patients who continue to show nephrotic range
proteinuria despite appropriate steroid therapy require a
biopsy to determine the underlying disorder.
60. Management of Initial Episode
The child should receive a high protein diet. Salt is restricted
to the amount in usual cooking with no extra salt given.
Any associated infection is treated. The presence of
tuberculosis should be looked for. Diuretics are administered
only if edema is significant. F ruse mi de (1-4 mg/ kg/
day in 2 divided doses) alone or with an aldosterone
antagonist, spironolactone (2-3 mg/kg/ day in 2 divided
doses) is adequate. Diuretics should be used cautiously and
overzealous fluid loss avoided. Therapy with corticosteroids
results in abolition of proteinuria (remission)
usually by 10-14 days, diuresis and loss of edema
61. The first episode of nephrotic syndrome should be
treated adequately, both in terms of dose and duration of
corticosteroids, since this is considered an important
determinant of longterm course. Only prednisolone and
prednisone are of proven benefit in the treatment of
proteinuria. Either of these agents is given at a dose of
2 mg/kg per day (maximum 60 mg) in single or divided
doses for 6 weeks, followed by 1.5 mg/kg (maximum
40 mg) as a single morning dose on alternate days for the
next 6 weeks. Therapy with corticosteroids is then
stopped. While some experts propose that therapy with
corticosteroids should not be stopped abruptly and
tapered over the next 8-12 weeks, the benefits of prolonged
therapy need to be balanced by the risk of steroid
adverse effects.
62. Complications in Nephrotic Syndrome
The patient should be maintained in remission, as far
as
possible. Relapses should be promptly treated so that
the
child does not develop more than minimal edema.
Several
complications that are associated with massive edema
and
ascites.
63. Edema
Edema is controlled with salt restriction and oral
hydrochlorothiazide
or frusemide for a few days. Salt must not
be totally stopped and the usual amounts used in cooking
should be allowed. For massive edema, higher doses of
frusemide along with spironolactone are needed. Infusion
of albumin may be necessary in intractable cases where
serum albumin levels are extremely low causing poor
renal perfusion and oliguria.
64. Infections
Nephrotic syndrome and steroid therapy render children
susceptible to infections. Infection with S. pneumoniae,
gram-negative organisms and varicella are common.
Children present with serious infections, e.g. peritonitis,
cellulitis, pneumonia and meningitis. Peritonitis may
manifest with low grade fever, diarrhea and abdominal
discomfort. Patients with varicella should receive oral
acyclovir for 7 days; severe illness requires administration
of IV acyclovir. Immunization with pneumococcal and
varicella vaccines is advised once the patient is off steroids
for 4 weeks.
65. Thrombotic Complications
Patients with nephrotic syndrome are at risk for
thrombosis
involving renal, pulmonary and cerebral veins.
Aggressive use of diuretics, venepuncture of deep veins
and hypovolemia increase the risk of this complication.
Treatment with low molecular weight heparin followed
by oral anticoagulants is recommended.
66. Hypovolemia and Acute Renal Failure
Hypovolemia may occur during a severe disease relapse
or following administration of diuretics, particularly in
children with poor oral intake, diarrhea and vomiting.
Features include abdominal pain, lethargy, dizziness and
leg cramps, tachycardia, hypotension, delayed capillary
refill, low volume pulses and clammy distal extremities.
Elevated ratio of blood urea to creatinine, high hematocrit,
urine sodium <20 mEq/1, fractional excretion of sodium
0.2-0.4% and urinary potassium index [urineK+ /(urineK+
+ urine Na+)] >0.6 suggest the presence of hypovolemia.
Therapy with diuretics should be discontinued. Patients
require admission and rapid infusion of normal saline
(10-20 ml/kg) over 20-30 min. Those who do not respond
to two boluses of saline should receive infusion of 5%
albumin (10-15 ml/kg) or 20% albumin (0.5-1 g/kg).
67. Congenital Nephrotic Syndrome
Congenital nephrotic syndrome present in the first
3 months of life with anasarca, hypoalbuminemia and
oliguria. The etiology of congenital nephrotic syndrome
is heterogeneous. The 'Finnish' form of the disease is
inherited in an autosomal recessive manner, with
mutations in the gene encoding nephrin (NPHSl). The
characteristic renal histology with microcystic dilation
of proximal tubules is seen after a few months of life,
although ultrastructural abnormalities of the glomerular
basement membrane are present at birth. Elevated levels
of alpha-fetoprotein (AFP) in maternal serum and
amniotic fluid enable antenatal screening. The clinical
course is complicated by failure to thrive, recurrentinfections,
hypothyroidism and progression to renal
failure by 2-3 yr.
68. Other causes of congenital nephrotic syndrome include
infections (congenital syphilis, cytomegalovirus disease,
toxoplasmosis) and mutations in PLCEl or NPHS2 genes;
rarely renal histology may be normal (minimal change
nephrotic syndrome) or show focal segmental
glomerulosclerosis.
Therapy of patients with congenital nephrotic
syndrome is supportive with appropriate nutrition,
control of edema, thyroxin supplements and reduction of
proteinuria through ACE inhibitors and/ or indomethacin.
69. CHRONIC GLOMERULONEPHRITIS
Chronic GN is not a single disease entity, but comprises
advanced stages of several forms of GN. In most cases, the
glomerular disease is primary and not part of a systemic
disorder. However, chronic GN may occur in systemic
lupus erythematosus, microscopic polyarteritis, familial
nephropathies and nephropathies due to drugs and toxins.
Variable glomerular deposition of immunoglobulin,
complement and fibrin is found on irnrnunofluorescence
studies. Renal biopsy examination in early stages shows
several patterns, while later the histologic changes are
nonspecific. Most glomeruli are sclerosed with
corresponding
tubular, interstitial and vascular changes.
Poststreptococcal GN seldom leads to chronic GN.
70. Clinical Features
The patient may be asymptomatic and the disease
detected
on routine urine examination. Others may show failure
to thrive, persistent anemia, moderate to severe
hypertension,
edema, nocturia, microscopic or gross hematuria,
bone pains and deformities.
71. Management
There is no specific treatment for chronic GN.
Treatment
with steroids and immunosuppressive drugs does not
offer any benefit. The blood pressure should be
controlled
and infections treated. If renal function is
compromised,
the treatment is that of advanced chronic kidney
disease
72. INTERSTITIAL NEPHRITIS
This is focal or diffuse inflammatory reaction of renal
interstitiurn with secondary involvement of tubules and
rarely, glomeruli. Acute interstitial nephritis is usually due
to infections or drugs (e.g. ampicillin, cephalosporins).
Common causes of chronic interstitial nephritis include
urinary tract obstruction and vesicoureteric reflux.
Interstitial nephritis may be a feature of a systemic
disorder (e.g. systemic lupus, vasculitis, associated with
uveitis); autoantibodies to tubular basement membrane
are found in some cases. In many instances, no cause is
determined.
73. The clinical features are nonspecific and include
abdominal pain, anorexia, pallor, headache and edema.
Hypertension is absent. The presence of progressive renal
insufficiency associated with satisfactory urine output,
and urinary abnormalities such as hyposthenuria and mild
proteinuria suggest the diagnosis. Leukocytes and
eosinophils are frequently seen in the urine, the latter a
feature of drug-associated disease.
A renal biopsy establishes the diagnosis and helps assess
severity. Drug-related interstitial nephritis is treated with
stoppage of the offending drug; treatment with corticosteroids
is beneficial. Systemic illness, if any, should be
appropriately managed. The treatment of chronic
interstitial nephritis is symptomatic.
74. URINARY TRACT INFECTIONS
Urinary tract infection (UTI) is a common medical problem
in children, affecting 3-10% girls and 1-3% boys. They
are an important cause of morbidity and might result in
renal damage, often in association with vesicoureteric
reflux (VUR). Beyond infancy, the incidence of UTI is
higher in girls. During infancy, UTI are equally common
in boys and girls because the route of infection is often
hematogenous and boys have a higher incidence of
urinary tract anomalies.
75. Microbiology
In most cases, UTI are caused by E. coli that forms the
predominant periurethral flora, and uncommonly by
Klebsie/la, Enterobacter and Staphylococci
epidermidis. Proteus
and Pseudomonas infections occur following
obstruction
or instrumentation, while Candida infection occurs in
immunocompromised children or after prolonged
antimicrobial therapy.
76. Predisposing Factors
Recurrent UTI are observed in 30-50% children, usually
within 3 months of the first episode. Predisposing factors
for recurrent UTI include female sex, age below 6 months,
obstructive uropathy, severe vesicoureteric reflux (VUR),
habitual postponement of voiding (voiding dysfunction),
constipation and repeated catheterization, e.g. for
neurogenic bladder. Children with malnutrition and
those receiving immunosuppressive therapy are also
susceptible.
77. Clinical Features
The clinical features depend upon the age and the
severity
of UTI. Neonates show features of sepsis with fever,
vomiting, diarrhea, jaundice, poor weight gain and
lethargy. The older infant has unexplained fever,
frequent
micturition and occasionally convulsions.
78. Gross hematuria is uncommon. The presence of crying or
straining during
voiding, dribbling, weak or abnormal urine stream and
palpable bladder suggest urinary obstruction. It is difficult to
distinguish between infection localized
to the bladder (cystitis) and upper tracts (pyelonephritis).
The distinction is not necessary since radionuclide studies
show that most UTI in children below 5 yr of age involve
the upper tracts. Hence, all children should be managed as
if they have pyelonephritis. Patients with high fever (>39°C),
systemic toxicity, persistent vomiting, dehydration, renal
angle tenderness or raised creatinine are considered as
having complicated UTI.
79. Patients with low grade fever,
dysuria, frequency and urgency and absence of symptoms
of complicated UTI are considered to have simple UTI.
This
distinction is important for purposes of therapy.
Important features on evaluation include history of
straining at micturition, incontinence or poor urinary
stream, voiding postponement and surgery for
meningomyelocele
or anorectal malformation. Finding of palpable
kidney(s), distended bladder, tight phimosis or vulval
synechiae and neurological deficit in lower limbs suggest
a predisposing cause.a
80. Diagnosis
The diagnosis of UTI is based on growth of significant
number of organisms of a single species in the urine.
Significant bacteriuria is defined as a colony count of > 105
/
ml of a single species in a clean catch sample. Urine is
obtained by suprapubic bladder aspiration or urethral
catheterization in children below 2 yr. Any colonies on
suprapubic aspiration and >50,000/ml on urethral
catheterization are considered significant. The occurrence
of significant bacteriuria in absence of symptoms is termed
asymptomatic bacteriuria.
81. The presence of >10 leukocytes per mm3 in fresh
uncentrifuged sample, or >5 leukocytes per high power
field in centrifuged sample is useful for screening.
Dipstick
examination, combining leukocyte esterase and nitrite,
has
moderate sensitivity and specificity for detecting UTI.
82. Treatment
Once UTI is suspected, a urine specimen is sent for culture
and treatment started. Infants below 3 months of age and
children
with complicated UTI should initially receive p arenter al
antibiotics. The initial choice of antibiotics is empiric and
is
modified once culture result is available. While a third
generation cephalosporin is preferred, therapy with a
single
daily dose of aminoglycoside is also safe and Once oral
intake improves and symptoms abate,
usually after 48-72 hr, therapy is switched to an oral
antibiotic.
83. The duration of treatment for complicated UTI
should be 10-14days. Older infants and patients with
simple
UTI should receive treatment with an oral antibiotic
for
7-10 days. Adolescents with cystitis may receive
shorter
duration of antibiotics, lasting 72 hr. Patients with
asymptomatic
bacteriuria do not require treatment
84. All children with UTI are encouraged to take enough
fluids and empty the bladder frequently to prevent stasis
of urine. Routine alkalization of the urine is not necessary.
With appropriate therapy, fever and systemic toxicity
reduce and urine culture is sterile within 24-36 hr. Failure
to obtain such a result suggests either lack of bacterial
sensitivity to the medication or presence of an underlying
anomaly of the urinary tract. A repeat urine culture is not
required during or following treatment, unless symptoms
fail to resolve despite 72 hr of therapy; symptoms recur,
suggesting recurrent UTI, or contamination of the initial
urine culture is suspected.