The document discusses the management of urinary calculi in children. It begins by introducing the topic and noting that renal calculus disease is becoming more common in children. It then covers the clinical features, diagnostic evaluation including urine analysis and imaging, identification of underlying metabolic causes, and general and specific management approaches. Specific causes discussed include hypercalciuria, renal tubular acidosis, hyperoxaluria, hyperuricosuria, cystinuria, and infective stones. Treatment involves identifying the etiology and approaches like dietary modifications, medications to modify urine composition, medical expulsive therapy for passing stones, and surgical interventions if needed.
This document discusses nephrolithiasis (kidney stones). It notes that kidney stones are common, affecting around 12% of men and 5% of women by age 70. Low urine volume is a major risk factor. Risk factors include diet, with high animal protein, sodium, and sucrose/fructose intake associated with stone formation. Treatment involves increasing fluid intake to dilute urine and reducing risk factors like dietary oxalate, animal protein, salt, and sucrose/fructose.
Calcium oxalate and calcium phosphate stones are the most common types in children. Risk factors include hypercalciuria, hyperoxaluria, hypocitraturia, cystinuria, and renal tubular acidosis. Struvite stones form due to urinary tract infections while uric acid stones are caused by hyperuricosuria. Treatment depends on stone location and size, and involves medications to address the underlying metabolic abnormality, increased fluid intake, and sometimes surgical removal by lithotripsy or ureteroscopy. Ongoing management focuses on prevention of recurrence through dietary modifications and medications that reduce stone-forming substance levels in urine.
The document discusses renal stones (kidney stones). It defines renal stones as hard mineral deposits that form inside the kidneys. Risk factors include dehydration, family history, obesity, and certain medical conditions. The most common types of stones are calcium and uric acid stones. Symptoms include severe back and abdominal pain, painful urination, and blood in the urine. Diagnosis involves blood and urine tests, along with imaging like ultrasound or CT. Treatment depends on the size and location of the stone but may include increased fluid intake, pain medication, surgery to remove large stones, or lithotripsy to break up stones. Preventing recurrence involves drinking plenty of water and eating a diet low in salt and oxalates
This document discusses the classification, pathophysiology, presentation, imaging, laboratory evaluation and treatment of nephrolithiasis in pediatric patients. The main types of stones include calcium, uric acid, cystine and struvite. Important risk factors are hypercalciuria, hypocitraturia, hyperoxaluria and low urine volume. Treatment depends on stone size and location but may include extracorporeal shock wave lithotripsy, ureteroscopy, percutaneous nephrolithotomy or open surgery. Diet and medical management target the underlying metabolic abnormalities promoting stone formation.
This document summarizes the composition, causes, and pathophysiology of kidney stone formation. The majority of kidney stones are composed of calcium oxalate (70%) or calcium phosphate (20%). Stone formation can be caused by genetic factors like primary hyperoxaluria or environmental factors like diet, obesity, and geography. Stones form when substances in urine like calcium, oxalate, and phosphate become supersaturated and precipitate out to form crystals and stones. The pathophysiology depends on the stone composition, but involves factors like urinary pH, crystal nucleation, and substances that promote or inhibit precipitation.
The document describes the anatomy and physiology of the urinary tract and kidney, risk factors and types of kidney stones, and methods for diagnosing and treating stones, including increasing fluid intake, altering diet, using medications to change urine composition, and surgically removing stones with procedures like ureteroscopy and lithotripsy. Kidney stones form when substances like calcium, oxalate, and uric acid become supersaturated in the urine and crystallize into solid masses.
1. The kidneys maintain water and electrolyte balance, blood pH, excrete waste products and toxins, filter the blood, produce erythropoietin, and reabsorb desirable elements.
2. Renal function can be impaired acutely (acute renal failure) or chronically (chronic renal failure). Tests like urea, creatinine, and uric acid help diagnose and monitor kidney function.
3. Kidney diseases include acute tubular necrosis, renal calculi, and gout caused by uric acid crystals. Treatment depends on the underlying cause but may include fluid management, dialysis, and transplantation.
This document discusses nephrolithiasis (kidney stones). It notes that kidney stones are common, affecting around 12% of men and 5% of women by age 70. Low urine volume is a major risk factor. Risk factors include diet, with high animal protein, sodium, and sucrose/fructose intake associated with stone formation. Treatment involves increasing fluid intake to dilute urine and reducing risk factors like dietary oxalate, animal protein, salt, and sucrose/fructose.
Calcium oxalate and calcium phosphate stones are the most common types in children. Risk factors include hypercalciuria, hyperoxaluria, hypocitraturia, cystinuria, and renal tubular acidosis. Struvite stones form due to urinary tract infections while uric acid stones are caused by hyperuricosuria. Treatment depends on stone location and size, and involves medications to address the underlying metabolic abnormality, increased fluid intake, and sometimes surgical removal by lithotripsy or ureteroscopy. Ongoing management focuses on prevention of recurrence through dietary modifications and medications that reduce stone-forming substance levels in urine.
The document discusses renal stones (kidney stones). It defines renal stones as hard mineral deposits that form inside the kidneys. Risk factors include dehydration, family history, obesity, and certain medical conditions. The most common types of stones are calcium and uric acid stones. Symptoms include severe back and abdominal pain, painful urination, and blood in the urine. Diagnosis involves blood and urine tests, along with imaging like ultrasound or CT. Treatment depends on the size and location of the stone but may include increased fluid intake, pain medication, surgery to remove large stones, or lithotripsy to break up stones. Preventing recurrence involves drinking plenty of water and eating a diet low in salt and oxalates
This document discusses the classification, pathophysiology, presentation, imaging, laboratory evaluation and treatment of nephrolithiasis in pediatric patients. The main types of stones include calcium, uric acid, cystine and struvite. Important risk factors are hypercalciuria, hypocitraturia, hyperoxaluria and low urine volume. Treatment depends on stone size and location but may include extracorporeal shock wave lithotripsy, ureteroscopy, percutaneous nephrolithotomy or open surgery. Diet and medical management target the underlying metabolic abnormalities promoting stone formation.
This document summarizes the composition, causes, and pathophysiology of kidney stone formation. The majority of kidney stones are composed of calcium oxalate (70%) or calcium phosphate (20%). Stone formation can be caused by genetic factors like primary hyperoxaluria or environmental factors like diet, obesity, and geography. Stones form when substances in urine like calcium, oxalate, and phosphate become supersaturated and precipitate out to form crystals and stones. The pathophysiology depends on the stone composition, but involves factors like urinary pH, crystal nucleation, and substances that promote or inhibit precipitation.
The document describes the anatomy and physiology of the urinary tract and kidney, risk factors and types of kidney stones, and methods for diagnosing and treating stones, including increasing fluid intake, altering diet, using medications to change urine composition, and surgically removing stones with procedures like ureteroscopy and lithotripsy. Kidney stones form when substances like calcium, oxalate, and uric acid become supersaturated in the urine and crystallize into solid masses.
1. The kidneys maintain water and electrolyte balance, blood pH, excrete waste products and toxins, filter the blood, produce erythropoietin, and reabsorb desirable elements.
2. Renal function can be impaired acutely (acute renal failure) or chronically (chronic renal failure). Tests like urea, creatinine, and uric acid help diagnose and monitor kidney function.
3. Kidney diseases include acute tubular necrosis, renal calculi, and gout caused by uric acid crystals. Treatment depends on the underlying cause but may include fluid management, dialysis, and transplantation.
Nephrolithiasis refers to stones (calculi) in kidney when urinary concentration of substances such as calcium oxalate, calcium phosphate and uric acid increases, but they can form in or migrate to the lower urinary system. They are typically asymptomatic until they pass into the lower urinary tract.
A 44-year-old male presented with hematuria, polyuria, and polydipsia for 8 days. He has a history of hypertension. Evaluation showed nephrocalcinosis, which is a condition where calcium levels in the kidneys are increased. This can be caused by hypercalcemia and leads to impaired kidney function and calcium deposits that can rupture and cause stones. Workup includes labs to check calcium levels and imaging like CT or x-ray to identify calcium deposits. Management focuses on hydration and treating the underlying cause to reverse hypercalcemia and protect kidney function.
This document provides an overview of pediatric urolithiasis (urinary stones in children). Some key points:
- Infection and metabolic abnormalities are major causes of stones in children.
- Metabolic evaluation is essential for every child to identify underlying conditions.
- Stones are most commonly calcium-containing, struvite, or uric acid.
- Common metabolic abnormalities include hypercalciuria, hyperoxaluria, cystinuria, and hypocitraturia.
- Treatment involves managing the underlying condition, increasing fluid intake, and sometimes surgery or lithotripsy as in adults. Thorough evaluation is needed to identify causes and guide management.
The document discusses renal stones (nephrolithiasis), including their definition, etiology, risk factors, pathophysiology, types, clinical manifestations, diagnostic studies, management, nursing management, prevention, and questions. Renal stones are formed by crystallization of substances in the urine, and can be caused by metabolic, lifestyle, or genetic factors. Common types include calcium oxalate, calcium phosphate, uric acid, cystine, and struvite stones. Treatment may involve medical management, extracorporeal shock wave lithotripsy (ESWL), or surgical procedures like ureteroscopy. Nursing focuses on pain management, education, and preventing infection and recurrence.
Nephrolithiasis, commonly known as kidney stones, refers to the formation of hard mineral and salt deposits within the kidneys or urinary tract. These stones can vary in size, ranging from tiny grains to larger, more substantial formations. Nephrolithiasis is a relatively common condition and can affect people of all ages, although it is more prevalent in adults.
This document provides a classification and overview of the diagnostic criteria for nephrolithiasis (kidney stones). It classifies the causes of nephrolithiasis into calcium based calculi, uric acid based calculi, cystinuria, infective (struvite) calculi, and low urine volumes. For each category, it describes the underlying metabolic abnormalities and risk factors that can lead to stone formation, such as hypercalciuria, hyperoxaluria, hypocitraturia, and urinary tract infections. It also discusses specific conditions like renal tubular acidosis and cystinuria that are associated with stone formation.
Renal tubular acidosis (RTA) is a disease characterized by a normal anion gap metabolic acidosis caused by impaired acid excretion in the kidney tubules. There are four main types: distal (type I) RTA which involves impaired hydrogen ion secretion; proximal (type II) RTA which involves impaired bicarbonate reabsorption; combined proximal and distal (type III) RTA; and hyperkalemic (type IV) RTA caused by impaired aldosterone production or responsiveness. Treatment involves bicarbonate replacement and monitoring for complications like nephrocalcinosis, nephrolithiasis, and bone disease depending on the type of RTA.
This document discusses renal calculi (kidney stones). It defines renal calculi as stones formed from increased concentrations of substances like calcium, oxalate, and uric acid in the urine. Risk factors include a sedentary lifestyle, dehydration, metabolic disturbances, and certain foods/medications. Symptoms include pain, nausea, hematuria, and urinary issues. Diagnosis involves tests like CT scans, ultrasounds, and urine analysis. Treatment includes increasing fluid intake, pain medications, dietary changes, and medications to prevent future stones. Surgical options for removing stones include endourologic procedures, lithotripsy, and open surgeries like ureterolithotomy.
Primary hyperoxaluria and renal hypercalciuriaPrateek Laddha
This document discusses primary hyperoxaluria and renal hypercalciuria. It defines hyperoxaluria and describes the four main types: primary hyperoxaluria types I and II, enteric hyperoxaluria, dietary hyperoxaluria, and idiopathic/mild hyperoxaluria. It explains oxalate production, absorption, and excretion in the body. For primary hyperoxaluria, it covers the genetic defects, pathophysiology, clinical manifestations, prognosis, treatment including pyridoxine, orthophosphate, magnesium, and sometimes combined liver-kidney transplantation. The document provides details on evaluation, management, and treatment of the different types of hyperoxaluria.
This document discusses renal calculi (kidney stones). It begins by listing learning objectives about the renal system, renal calculi, types of stones, clinical manifestations, diagnosis, medical and surgical management, and nursing management. It defines renal calculi as stones formed from crystallization of substances excreted in urine. Risk factors include slow urine flow and decreased inhibitors. Types of stones include calcium, uric acid, cystine, and struvite. Diagnosis involves urinalysis, urine culture, cystoscopy, ultrasound and x-rays. Treatment involves medications, hydration, diet changes, and sometimes surgery. Nursing focuses on pain management, education, and preventing infections.
Renal calculi, also known as kidney stones, form when minerals in urine crystallize and deposit on the inner surfaces of the kidneys. The most common types are calcium-containing stones, uric acid stones, struvite-carbonate stones, and cystine stones. Risk factors include dehydration, genetics, diet high in purines or oxalates, and urinary tract infections. Symptoms include flank pain, nausea, and blood in the urine. Diagnosis involves urine analysis, blood tests, imaging like ultrasounds or CT scans. Treatment focuses on pain relief, preventing recurrence through increased fluid intake and dietary changes, and removing stones through extracorporeal shockwave lithotripsy, surgery
Urolithiasis and comparison between Urosinal Syrup and zyloric TabletAamir Sharif
This document discusses kidney stones, their causes, types, and treatments. It provides details on the main types of stones:
- Calcium stones, which account for 80% of cases, form in alkaline urine and can be calcium oxalate or calcium phosphate.
- Uric acid stones form in acidic urine and account for 5-10% of cases. They are associated with hyperuricemia.
- Struvite (magnesium ammonium phosphate) stones form due to urinary tract infections and account for 10-15% of cases.
- Cystine stones are very rare and due to a genetic disorder causing cystine to leak into the urine.
It also covers laboratory investigations for kidney
Urolithiasis pathophysiology , medical management Banda Gopal
This document discusses the pathophysiology and medical management of urolithiasis. It covers calcium metabolism and factors affecting calcium absorption. It then discusses the different types of stones including calcium, struvite, uric acid, and cystine stones. For each type, it outlines the underlying causes and medical management strategies. Conservative measures include diet modifications and increasing fluid/citrate intake, while medications used include thiazides, citrate supplements, allopurinol, and others to treat specific metabolic abnormalities causing stone formation. Imaging techniques for evaluating stones and indications for metabolic stone evaluation are also reviewed.
This document discusses nephrolithiasis (kidney stones). It begins with a case of a 78-year-old man who presented with gross hematuria and was found to have a kidney stone. The stone was removed, and analysis showed it was calcium oxalate. The document then reviews epidemiology, natural history, stone formation process, clinical presentation, evaluation, etiologies including calcium, uric acid, struvite and cystine stones, and treatment options including medical management and urological interventions.
Acute renal failure and chronic renal failure are discussed. Acute renal failure can be prerenal, renal, or postrenal and is characterized by a sudden reduction in urine output. Chronic renal failure is a permanent loss of kidney function that progresses to end stage renal disease. It has multiple etiologies including glomerular diseases. Both present with electrolyte imbalances, fluid retention, and other complications. Treatment focuses on fluid management, diet modification, and dialysis or transplantation as needed.
Metabolic workup and medical management of urolithiasis aims to prevent recurrent stone formation through identifying underlying causes. The goals are to prevent further stone growth and extrarenal complications. Evaluation involves medical history, blood and urine tests, imaging, and stone analysis to guide targeted therapy. First-line management includes increased fluid intake, dietary modifications like reduced sodium and animal protein, and medications depending on the metabolic abnormality identified, such as thiazides for hypercalciuria. Selective long-term medical management can normalize urinary risk factors and prevent further stone episodes in many patients.
This document summarizes renal (kidney) stones, including their epidemiology, composition, risk factors, pathophysiology, clinical presentation, diagnosis, and management. Some key points:
- Kidney stones are common and recurrent in many patients. Calcium oxalate and uric acid stones account for over 75% of cases.
- Risk factors include dietary factors, anatomical abnormalities, certain drugs, and metabolic conditions like hypercalciuria.
- Patients present with flank pain, hematuria, and sometimes fever. Diagnosis involves medical history, imaging like ultrasound or CT, and urine/blood tests.
- Treatment depends on stone size and includes increased fluid intake, medications to modify risk factors, procedures like
The document discusses hyperuricemia and gout. It defines hyperuricemia as a plasma urate concentration greater than 7.0 mg/dl and can result from increased urate production, decreased urate excretion, or a combination. Gout is caused by the deposition of monosodium urate crystals in the joints and other tissues, which can cause acute inflammatory arthritis. The first metatarsophalangeal joint is commonly affected. Treatment involves medications like colchicine, NSAIDs, or glucocorticoids for acute attacks and urate-lowering therapies for long-term management.
Renal calculi, or kidney stones, are solid mineral deposits that form in the kidneys from supersaturated urine. They are typically classified based on their location in the urinary tract or their chemical composition. Risk factors include a family history, certain diets or medical conditions that cause urine to become supersaturated. Symptoms include flank pain, painful urination, and bleeding in the urine. Complications can arise if stones cause blockages and damage to the kidneys.
This document discusses the evaluation and workup of patients presenting with renal stones. It outlines the importance of obtaining a detailed history regarding lifestyle, diet, medical history and risk factors. A physical exam can reveal signs of renal colic or obstruction. Metabolic testing and stone analysis help determine the stone composition and underlying abnormalities. Radiological investigations including ultrasound, CT and occasionally IVP are used to identify stones and assess for complications like hydronephrosis. Proper evaluation guides management and treatment of kidney stone disease.
Nephrolithiasis refers to stones (calculi) in kidney when urinary concentration of substances such as calcium oxalate, calcium phosphate and uric acid increases, but they can form in or migrate to the lower urinary system. They are typically asymptomatic until they pass into the lower urinary tract.
A 44-year-old male presented with hematuria, polyuria, and polydipsia for 8 days. He has a history of hypertension. Evaluation showed nephrocalcinosis, which is a condition where calcium levels in the kidneys are increased. This can be caused by hypercalcemia and leads to impaired kidney function and calcium deposits that can rupture and cause stones. Workup includes labs to check calcium levels and imaging like CT or x-ray to identify calcium deposits. Management focuses on hydration and treating the underlying cause to reverse hypercalcemia and protect kidney function.
This document provides an overview of pediatric urolithiasis (urinary stones in children). Some key points:
- Infection and metabolic abnormalities are major causes of stones in children.
- Metabolic evaluation is essential for every child to identify underlying conditions.
- Stones are most commonly calcium-containing, struvite, or uric acid.
- Common metabolic abnormalities include hypercalciuria, hyperoxaluria, cystinuria, and hypocitraturia.
- Treatment involves managing the underlying condition, increasing fluid intake, and sometimes surgery or lithotripsy as in adults. Thorough evaluation is needed to identify causes and guide management.
The document discusses renal stones (nephrolithiasis), including their definition, etiology, risk factors, pathophysiology, types, clinical manifestations, diagnostic studies, management, nursing management, prevention, and questions. Renal stones are formed by crystallization of substances in the urine, and can be caused by metabolic, lifestyle, or genetic factors. Common types include calcium oxalate, calcium phosphate, uric acid, cystine, and struvite stones. Treatment may involve medical management, extracorporeal shock wave lithotripsy (ESWL), or surgical procedures like ureteroscopy. Nursing focuses on pain management, education, and preventing infection and recurrence.
Nephrolithiasis, commonly known as kidney stones, refers to the formation of hard mineral and salt deposits within the kidneys or urinary tract. These stones can vary in size, ranging from tiny grains to larger, more substantial formations. Nephrolithiasis is a relatively common condition and can affect people of all ages, although it is more prevalent in adults.
This document provides a classification and overview of the diagnostic criteria for nephrolithiasis (kidney stones). It classifies the causes of nephrolithiasis into calcium based calculi, uric acid based calculi, cystinuria, infective (struvite) calculi, and low urine volumes. For each category, it describes the underlying metabolic abnormalities and risk factors that can lead to stone formation, such as hypercalciuria, hyperoxaluria, hypocitraturia, and urinary tract infections. It also discusses specific conditions like renal tubular acidosis and cystinuria that are associated with stone formation.
Renal tubular acidosis (RTA) is a disease characterized by a normal anion gap metabolic acidosis caused by impaired acid excretion in the kidney tubules. There are four main types: distal (type I) RTA which involves impaired hydrogen ion secretion; proximal (type II) RTA which involves impaired bicarbonate reabsorption; combined proximal and distal (type III) RTA; and hyperkalemic (type IV) RTA caused by impaired aldosterone production or responsiveness. Treatment involves bicarbonate replacement and monitoring for complications like nephrocalcinosis, nephrolithiasis, and bone disease depending on the type of RTA.
This document discusses renal calculi (kidney stones). It defines renal calculi as stones formed from increased concentrations of substances like calcium, oxalate, and uric acid in the urine. Risk factors include a sedentary lifestyle, dehydration, metabolic disturbances, and certain foods/medications. Symptoms include pain, nausea, hematuria, and urinary issues. Diagnosis involves tests like CT scans, ultrasounds, and urine analysis. Treatment includes increasing fluid intake, pain medications, dietary changes, and medications to prevent future stones. Surgical options for removing stones include endourologic procedures, lithotripsy, and open surgeries like ureterolithotomy.
Primary hyperoxaluria and renal hypercalciuriaPrateek Laddha
This document discusses primary hyperoxaluria and renal hypercalciuria. It defines hyperoxaluria and describes the four main types: primary hyperoxaluria types I and II, enteric hyperoxaluria, dietary hyperoxaluria, and idiopathic/mild hyperoxaluria. It explains oxalate production, absorption, and excretion in the body. For primary hyperoxaluria, it covers the genetic defects, pathophysiology, clinical manifestations, prognosis, treatment including pyridoxine, orthophosphate, magnesium, and sometimes combined liver-kidney transplantation. The document provides details on evaluation, management, and treatment of the different types of hyperoxaluria.
This document discusses renal calculi (kidney stones). It begins by listing learning objectives about the renal system, renal calculi, types of stones, clinical manifestations, diagnosis, medical and surgical management, and nursing management. It defines renal calculi as stones formed from crystallization of substances excreted in urine. Risk factors include slow urine flow and decreased inhibitors. Types of stones include calcium, uric acid, cystine, and struvite. Diagnosis involves urinalysis, urine culture, cystoscopy, ultrasound and x-rays. Treatment involves medications, hydration, diet changes, and sometimes surgery. Nursing focuses on pain management, education, and preventing infections.
Renal calculi, also known as kidney stones, form when minerals in urine crystallize and deposit on the inner surfaces of the kidneys. The most common types are calcium-containing stones, uric acid stones, struvite-carbonate stones, and cystine stones. Risk factors include dehydration, genetics, diet high in purines or oxalates, and urinary tract infections. Symptoms include flank pain, nausea, and blood in the urine. Diagnosis involves urine analysis, blood tests, imaging like ultrasounds or CT scans. Treatment focuses on pain relief, preventing recurrence through increased fluid intake and dietary changes, and removing stones through extracorporeal shockwave lithotripsy, surgery
Urolithiasis and comparison between Urosinal Syrup and zyloric TabletAamir Sharif
This document discusses kidney stones, their causes, types, and treatments. It provides details on the main types of stones:
- Calcium stones, which account for 80% of cases, form in alkaline urine and can be calcium oxalate or calcium phosphate.
- Uric acid stones form in acidic urine and account for 5-10% of cases. They are associated with hyperuricemia.
- Struvite (magnesium ammonium phosphate) stones form due to urinary tract infections and account for 10-15% of cases.
- Cystine stones are very rare and due to a genetic disorder causing cystine to leak into the urine.
It also covers laboratory investigations for kidney
Urolithiasis pathophysiology , medical management Banda Gopal
This document discusses the pathophysiology and medical management of urolithiasis. It covers calcium metabolism and factors affecting calcium absorption. It then discusses the different types of stones including calcium, struvite, uric acid, and cystine stones. For each type, it outlines the underlying causes and medical management strategies. Conservative measures include diet modifications and increasing fluid/citrate intake, while medications used include thiazides, citrate supplements, allopurinol, and others to treat specific metabolic abnormalities causing stone formation. Imaging techniques for evaluating stones and indications for metabolic stone evaluation are also reviewed.
This document discusses nephrolithiasis (kidney stones). It begins with a case of a 78-year-old man who presented with gross hematuria and was found to have a kidney stone. The stone was removed, and analysis showed it was calcium oxalate. The document then reviews epidemiology, natural history, stone formation process, clinical presentation, evaluation, etiologies including calcium, uric acid, struvite and cystine stones, and treatment options including medical management and urological interventions.
Acute renal failure and chronic renal failure are discussed. Acute renal failure can be prerenal, renal, or postrenal and is characterized by a sudden reduction in urine output. Chronic renal failure is a permanent loss of kidney function that progresses to end stage renal disease. It has multiple etiologies including glomerular diseases. Both present with electrolyte imbalances, fluid retention, and other complications. Treatment focuses on fluid management, diet modification, and dialysis or transplantation as needed.
Metabolic workup and medical management of urolithiasis aims to prevent recurrent stone formation through identifying underlying causes. The goals are to prevent further stone growth and extrarenal complications. Evaluation involves medical history, blood and urine tests, imaging, and stone analysis to guide targeted therapy. First-line management includes increased fluid intake, dietary modifications like reduced sodium and animal protein, and medications depending on the metabolic abnormality identified, such as thiazides for hypercalciuria. Selective long-term medical management can normalize urinary risk factors and prevent further stone episodes in many patients.
This document summarizes renal (kidney) stones, including their epidemiology, composition, risk factors, pathophysiology, clinical presentation, diagnosis, and management. Some key points:
- Kidney stones are common and recurrent in many patients. Calcium oxalate and uric acid stones account for over 75% of cases.
- Risk factors include dietary factors, anatomical abnormalities, certain drugs, and metabolic conditions like hypercalciuria.
- Patients present with flank pain, hematuria, and sometimes fever. Diagnosis involves medical history, imaging like ultrasound or CT, and urine/blood tests.
- Treatment depends on stone size and includes increased fluid intake, medications to modify risk factors, procedures like
The document discusses hyperuricemia and gout. It defines hyperuricemia as a plasma urate concentration greater than 7.0 mg/dl and can result from increased urate production, decreased urate excretion, or a combination. Gout is caused by the deposition of monosodium urate crystals in the joints and other tissues, which can cause acute inflammatory arthritis. The first metatarsophalangeal joint is commonly affected. Treatment involves medications like colchicine, NSAIDs, or glucocorticoids for acute attacks and urate-lowering therapies for long-term management.
Renal calculi, or kidney stones, are solid mineral deposits that form in the kidneys from supersaturated urine. They are typically classified based on their location in the urinary tract or their chemical composition. Risk factors include a family history, certain diets or medical conditions that cause urine to become supersaturated. Symptoms include flank pain, painful urination, and bleeding in the urine. Complications can arise if stones cause blockages and damage to the kidneys.
This document discusses the evaluation and workup of patients presenting with renal stones. It outlines the importance of obtaining a detailed history regarding lifestyle, diet, medical history and risk factors. A physical exam can reveal signs of renal colic or obstruction. Metabolic testing and stone analysis help determine the stone composition and underlying abnormalities. Radiological investigations including ultrasound, CT and occasionally IVP are used to identify stones and assess for complications like hydronephrosis. Proper evaluation guides management and treatment of kidney stone disease.
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2. INTRODUCTION
Renal calculus disease is uncommon in children, although it is being
detected more frequently.
An underlying metabolic cause can be identified in a significant
proportion of cases.
Vesical (bladder) calculi, endemic in some parts of India and other
developing countries, are chiefly related to dietary factors
Crystallization and calculus formation depends upon a number of
factors.
The point at which urine is saturated with a solute is called its
‘solubility product’
The point at which the solute can no longer remain in solution is
termed the ‘formation product.’
3. CONTD…
Between these two indices there is a metastable zone in which the
existing crystals grow but precipitation does not occur.
At the formation product, spontaneous nucleation takes place.
The role of inhibitors of calculus formation is poorly understood.
Substances such as magnesium, citrate, pyrophosphate, uropontin,
nephrocalcin, ribonucleic acid and zinc have been suggested to
inhibit formation of calcium crystals.
Citrate forms soluble complexes with calcium and reduces its free ion
concentration
Increased excretion of solutes, low urinary citrate and abnormal pH
are more important in calculus formation.
Urinary infection with urea-splitting organisms such as Proteus is
also an important cause of urolithiasis.
4. Metabolic calculi results commonly from primary metabolic disorders like
hypercalciuric states, distal RTA, hyperoxaluria, cystinuria and hyperuricosuria.
Stone promoting factors :-
Low intake of fluids causes increased supersaturation of stone forming salts.
Dairy products cause hypercalciuria and animal products increase the uric acid
production.
Increased oxalate content in vegetarian diet increases urinary excretion of
oxalate.
Immobilization leads to hypercalcemia and hypercalciuria.
Hypocitraturia resulting in reduced complexing of calcium with citrate causes
increased calcium oxalate super saturation.
Hypomagnesiuria results in reduced magnesium oxalate complexing,
producing increased calcium oxalate super saturation.
5. CLINICAL FEATURES
The usual symptoms are recurrent flank pain, renal colic, repeated
attacks of urinary tract infections and gross or microscopic hematuria.
The child may pass gravel or a small stone.
Occasionally the stone may be ‘silent’ and lead to obstructive
uropathy.
A stone in the urethra or in both ureters may rarely precipitate acute
renal failure
Noncalculi presentation as hematuria is seen in hypercalicuria and
even in hyperoxaluria and hyperuricosuria
Most of the times stones are identified during investigations for UTI,
hematuria, renal colic or renal failure
6. RADIOLOGICAL DIAGNOSIS
Radiological conformation is important
Plain X-ray of the abdomen shows radio-opaque stones like calcium oxalate
and calcium phosphate stones.
Radiolucent stones (uric acid, xanthine and cystine) are not seen in plain X-ray
abdomen.
But mixed uric acid and calcium oxalate stones as well as cystine stones with
more sulfur content can be radio-opaque. Infective stones exhibit varying
radio-opacity.
Ultrasonogram can identify the stones. They also detect hydronephrosis and
ureterohydronephrosis, which are the secondary effects. They also identify
associated anomalies of the tract.
Intravenous urography is useful in radiolucent stones by documenting the
filling defect. IVU is also useful to identify other anomalies of the tract.
7. Identification of etiology
Management of renal stone disease in children involves identification
of the etiology of urolithiasis as management depends on the
etiology.
Urine analysis is done for:
RBCs and pus cells in urine
Study of crystals in urine:
Calcium oxalate crystals Pyramid / Envelope shaped
Magnesium ammonium phosphate
crystals
Coffin lids (Triple phosphate)
Cystine crystals Flat hexagonal plates
Urate crystals Diamond /Trapezoid shaped
8. Urine culture is essential, as UTI may be secondary to a stone or
primary as in infective stones.
Renal function studies are mandatory for basal renal evaluation.
Acute renal failure may indicate bilateral ureteric obstruction or
obstruction to the single functioning kidney.
It signifies urgency in the management of obstruction
Serum electrolytes and arterial blood gas analysis are useful.
Normal anion gap hyperchloremic acidosis is the feature of Type I
RTA.
One has to look for hypercalcemia and hypercalciuria in every
stone disease.
Then look for hyperuricemia, hyperuricosuria, hyperoxaluria and
hypocitraturia
9. GENERAL STEPS OF MANAGEMENT
Increase the fluid intake to increase the urine volume.
Avoid unwanted intake of vitamin D, vitamin C and calcium
containing antacids.
Needed oral intake of milk should be advised in children.
Avoidance of oxalate rich substances is useful.
Colicky pain is usually treated with narcotic analgesics.
Surgical care for obstruction should be always considered.
Associated UTI, renal failure and obstruction modify the care to an
emergency one.
Liberal use of USG for monitoring is very much ideal.
10. SPECIFIC MANAGEMENT
HYPERCALCIURIA
Hypercalciuria is suspected when spot urine calcium/creatinine ratio in
the second morning urine sample is more than 0.21 and is confirmed by
24 hours urine calcium excretion of more than 4 mg/kg/day.
Hypercalciuria may be normocalcemic or hypercalcemic variety.
Conditions commonly seen with normocalcemic hypercalciuria are
idiopathic hypercalciuria and distal RTA.
Conditions usually seen with hypercalcemic hypercalciuria are
hyperparathyroidism, vitamin D intoxication and malignancy.
Idiopathic hypercalciuria is one of the common causes of renal calculi in
children.
11. In renal hypercalciuria, hydrochlorothiazide (2-3 mg/kg/day in 1-2 divided
doses) for increasing the tubular reabsorption of calcium is done.
Low sodium intake is mandatory for optimal effect.
In absorptive type of hypercalciuria decrease in calcium intake is needed but is
usually impossible in children.
Cellulose phosphate to bind calcium in the gut can be tried but there is
reduced calcium to complex with oxalate leading to increased oxalate
absorption and oxaluria.
Overall in hypercalicuria recommended dietary allowance of calcium and
protein should be allowed.
Gross reduction in calcium intake will lead to increased oxalate absorption due
to non-availability of adequate calcium to complex with oxalate leading to
hyperoxaluria.
Administration of potassium citrate (1.5-2 mEq/kg/day) results in reduction of
calcium excretion and an increase of urinary citrate and potassium
12. RENAL TUBULAR ACIDOSIS
About two thirds of children with distal RTA have nephrocalcinosis
and nephrolithiasis.
Calcium phosphate is the basic content of the stones with distal RTA.
High urine calcium, high urine pH and decreased citrate excretion are
the factors involved in stone formation in this condition.
Rickets can occur and growth may be poor.
Correction of acidosis with alkali therapy is done.
A child needs 3-5 mEq/kg/day of alkali.
Potassium citrate is better than sodium citrate.
Hydrochlorothiazide may also be needed to treat the associated
hypercalciuria
13. HYPEROXALURIA
Hyperoxaluria is defined as urine oxalate more than 0.7 mg/kg/day
or > 45 mg/1.73 m2 /day.
To cause a stone usually more than 1.4 mg/kg/day is needed.
This may be due to inherited or acquired disorder
Usual steps include reduction in intake of oxalate rich food,
administration of high dose pyridoxine, increasing the fluid intake,
normal dietary calcium intake to fascilitate calcium to bind to
oxalate in the gut and alkalinisation of urine with potassium citrate.
Citrate therapy reduces calcium oxalate supersaturation.
Reducing intake of spinach, cocoa, roasted coffee, peanuts etc
reduces dietary intake of oxalate.
14. In primary hyperoxaluria large doses of pyridoxine, maintaining
good hydration, hemodialysis to reduce oxalate burden are needed.
Combined liver and renal transplantations is the only real answer.
Acquired enteral variety is due to malabsorption of fat.
Normally good amount of oxalate is excreted as calcium oxalate, in
stool
For enteric hyperoxaluria, treatment of precipitating gastrointestinal
conditions and reducing the fat intake are needed
15. HYPERURICOSURIA
Low urine pH favours uric acid ionization resulting in crystalisation,
concretion formation, ending in stone formation.
Increased uric acid production (Gout due to enzyme defect, myelo-
lymphoproliferative diseases or excessive purine intake) and decreased
urinary volume as in chronic diarrhoea and ileostomy are the common
etiologies.
Uric acid further forms the nidus for calcium oxalate stone and it decreases
the concentration of inhibitors of calcium oxalate lithiasis in urine.
A value more than 750 mg/1.73 m2 or more than 11 mg/kg/ day is taken as
hyperuricosuria.
Reducing the dietary purine intake, urinary alkalinisation with potassium
citrate or with acetazolamide, increasing the fluid intake and allopurinol
administration if hyperuricemia is present are useful steps.
Diet rich in purine include majority of the animal protein, mushroom and
drybeans.
16. CYSTINURIA
Cystinuria is an autosomal recessive disorder with increased excretion
of cystine and dibasic amino acid ornithine, arginine and lysine.
There is a defective cystine transport across renal tubules and GI tract.
Cystine is usually insoluble in acid medium and hence crystal
precipitation occurs leading to urolithiasis.
Cystine is detected by the purple color reaction with cyanide
nitroprusside testing
Cystine stones are non radio-opaque unless the sulfur content and
calcium makes it radio-opaque
Beyond a urine pH above 7.5 the solubility is more and is difficult to
maintain this with alkali therapy.
Normal cystine values in urine is 30-50 mg/ 1.73 m2 or <
75 mg/gm of creatinine.
17. An increased fluid intake spread over 24 hours to reduce the
supersaturation along with adequate alkali therapy is the mainstay
of treatment.
D-Penicillamine therapy by forming cysteine-penicillamine
disulfide and excretion of it is useful but for its toxicity.
Surgical care may be needed for staghorn calculus or for removal
of bladder stones
18.
19. INFECTIVE STONES
Recurrent urinary infection with Proteus (rarely K. pneumoniae and
Serratia marcescens), such as in patients with obstructive uropathy
or urinary stasis, may cause stone formation.
Bacterial urease activity leads to formation of ammonium from urea,
which raises the urine pH causing precipitation of calcium
phosphate-carbonate (carbonate apatite) and magnesium
ammonium phosphate (struvite)
These amorphous stones mould easily into the renal calyces, grow
rapidly and fill the renal collecting system with staghorn calculi.
Surgical stone removal is difficult and recurrence of stone
formation is common
20. Acidification of urine and long-term chemoprophylaxis are the
usual post surgical care for infective stones
Conservative management is not advised, as infective calculi if left
untreated calculus pyonephrosis leading to destruction of kidney
can occur.
Percutaneous nephrolithotomy is employed to completely remove
struvite calculi, but some patients might require open surgery to
repair associated renal anomalies.
21. MEDICAL EXPULSIVE THERAPY
In a child with a renal or ureteral calculus, the decision whether to remove
the stone depends on its location, size, and composition (if known) and
whether obstruction and/or infection is present.
Pain is managed with nonsteroidal antiinflammatory drugs or, less often,
opiates.
Small ureteral calculi often pass spontaneously, although the child might
experience severe renal colic.
The narrowest segment of the ureter is the ureterovesical junction. Calculi
<5 mm will pass 80–90% of the time.
An α-adrenergic blocker, such as tamsulosin, 0.4 mg at bedtime, may
facilitate stone passage by decreasing ureteral pressure below the stone and
decreasing the frequency of the peristaltic contractions of the obstructed
ureter.
This intervention is termed medical expulsive therapy.
In many cases, passage of a ureteral stent past the stone endoscopically
relieves pain and dilates the ureter sufficiently to allow the calculus to pass.
22. SURGICAL MANAGEMENT
If the calculus does not pass or seems unlikely to pass or if there is
associated urinary tract infection, removal is necessary
Lithotripsy of bladder, ureteral, and small renal pelvic calculi using the
holmium laser through a flexible or rigid ureteroscope is quite effective.
Extracorporeal shock wave lithotripsy has been successfully applied to
children with renal and ureteral stones, with a success rate of > 75%
Another alternative is percutaneous nephrostolithotomy, in which access to
the renal collecting system is obtained percutaneously and the calculi are
broken down by ultrasonic lithotripsy.
In cases in which these modalities are unsuccessful, an alternative is
laparoscopic removal.
This procedure can be performed using the da Vinci robot.
23. Cystoscopic crushing or removal of the stones and basketing out
the VUJ junction stones are popular.
Lower ureteric stones are removed by ureteroscope.
Upper ureteric and pelvic stones are removed by percutaneous
nephrolithotomy.
ESWL alone or in combination with percutaneous nephrolithotomy
is useful in stones larger than 2.5 cms.
Open surgery is useful in difficult stones.
24.
25. REFERENCES
Nelson textbook of pediatrics
Principles and practice of pediatric nephrology by Nammalwar
Pediatric nephrology by Arvind bagga