The document discusses various pediatric kidney conditions including acute nephritis, acute kidney injury, hematuria, and nephrotic syndrome. It provides definitions, etiology, pathology, clinical features, diagnosis, treatment and complications for each condition. Acute nephritis is typically caused by immune complex mediated glomerulonephritis following a streptococcal infection. Acute kidney injury criteria include decreased estimated creatinine clearance and low urine output. Hematuria can have glomerular or extraglomerular causes such as glomerulonephritis, pyelonephritis, cystitis or tumors.
What is congenital nephrotic syndrome ,what is the definition of congenital nephrotic syndrome,what is the inheritance,what are the responsible genes ,what are the types of congenital nephrotic syndrome,what is the presentation ,diagnosis ,and treatment of congenital nephrotic syndrome, primary type and secondary type of congenital nephrotic syndrome
What is congenital nephrotic syndrome ,what is the definition of congenital nephrotic syndrome,what is the inheritance,what are the responsible genes ,what are the types of congenital nephrotic syndrome,what is the presentation ,diagnosis ,and treatment of congenital nephrotic syndrome, primary type and secondary type of congenital nephrotic syndrome
Objective Acute kidney injury
Know about definition of Acute kidney injury
Function of kidney
Sign and symptoms of AKI
Know about Risk factor of AKI
Understand about complication of AKI
Contents:
Introduction Of Acute kidney injury
Physiology Of Acute kidney injury
Pathophysiology Of Acute kidney injury
Clinical feature Of Acute kidney injury
Risk Factor Of Acute kidney injury
Diagnosis Of Acute kidney injury
Differential diagnosis Of Acute kidney injury
Complication Of Acute kidney injury
Management Of Acute kidney injury
Acute renal failure (ARF), characterized by sudden loss of the ability of the kidneys to excrete wastes, concentrate urine, conserve electrolytes, and maintain fluid balance, is a frequent clinical problem, particularly in the intensive care unit, where it is associated with a mortality of between 50% and 80%. In this review, the epidemiology and pathophysiology of ARF are discussed, including the vascular, tubular, and inflammatory perturbations. The clinical evaluation of ARF and implications for potential future therapies to decrease the high mortality are described.
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.
Pharmacology of commonly used antisep, disinfect, insecticideMr. Dipti sorte
Slides are prepared as per INC Syllabus Unit III Antiseptics & Disinfectants and it is most benefited for B sc Nursing students and faculty of the subject
Best Ayurvedic medicine for Gas and IndigestionSwastikAyurveda
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
- 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
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
CDSCO and Phamacovigilance {Regulatory body in India}NEHA GUPTA
The Central Drugs Standard Control Organization (CDSCO) is India's national regulatory body for pharmaceuticals and medical devices. Operating under the Directorate General of Health Services, Ministry of Health & Family Welfare, Government of India, the CDSCO is responsible for approving new drugs, conducting clinical trials, setting standards for drugs, controlling the quality of imported drugs, and coordinating the activities of State Drug Control Organizations by providing expert advice.
Pharmacovigilance, on the other hand, is the science and activities related to the detection, assessment, understanding, and prevention of adverse effects or any other drug-related problems. The primary aim of pharmacovigilance is to ensure the safety and efficacy of medicines, thereby protecting public health.
In India, pharmacovigilance activities are monitored by the Pharmacovigilance Programme of India (PvPI), which works closely with CDSCO to collect, analyze, and act upon data regarding adverse drug reactions (ADRs). Together, they play a critical role in ensuring that the benefits of drugs outweigh their risks, maintaining high standards of patient safety, and promoting the rational use of medicines.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
2. Dipti’s Page 2 of 22
11.1. Acute Nephritis.
1. Definition: Disease characterized by sudden onset of:
a) Hematuria.
b) Generalized edema.
c) Hypertension.
d) Oliguria.
e) Acute kidney injury.
2. Etiopathogenesis: Immune complex mediated nephritis: Most common form.
Typically follows infection of throat or skin with certain ‘Nephrogenic strains of
group A Beta hemolytic Streptococci (Pharyngitis or pyoderma)
Common strain-throat serotype 12, skin serotype 12, skin serotype 49.
May occur after infections with other organisms, infective endocarditis, shunt
nephritis.
Acute nephritis may also be seen in small vessel vasculitides (microscopic
polyangiitis, granulomatosis with polyangiitis) pauci-immune
glomerulonephritis, and anti-glomerular basement membrane disease.
Evidence in favor of immune complex disease.
a) Depression of serum complements C3 level.
b) Complement activation is primarily through alternative pathway rather than
classic pathway.
3. Pathology: Morphological features:
1) Kidney appears symmetrically enlarged.
2) By light microscopy.
A. All glomerular are enlarged and pale, relatively bloodless.
B. Glomerular hypercellularity:
a) Diffuse mesangial cell proliferation.
b) Increased mesangial matrix.
c) Crescents and interstitial inflammation may be seen in severe
cases.
3) Immunofluorescent microscopy.
Lumpy dumpy deposits of immunoglobulins and compliment on glomerular
basement membrane and mesangium.
4) Electron microscopy.
Electron dense deposit or humps are seen on epithelial side of GBM.
4. Clinical features:
Age: Rare before 3years of age, common age 5-12 years.
Onset: 1-2 weeks after antecedent streptococcal infection for post streptococcal
nephritis.
Clinical presentation: Six clinical presentation.
1) Asymptomatic: microscopic hematuria.
2) Hematuria: cola cored urine.
3) Anasarca: (Generalized edema)
4) Rapidly progressive glomerulonephritis (RPGN): Acute kidney injury,
oliguria, deranged renal functions.
5) Hypertension presenting as:
a) Hypertensive CHF: Dyspnea, Tachycardia, tachypnoea.
3. Dipti’s Page 3 of 22
b) Hypertensive encephalopathy: Seizures, Headache.
Nonspecific symptoms: Malaise, Lethargy, abdominal pain, fever.
Resolution: Usually within 6-8 weeks following onset. Urinary abnormalities
especially microscopic hematuria may persist for more than 1 year.
5. Diagnosis:
1) Urine Examination:
a) RBC, RBC casts.
b) Proteinuria: Mild to moderate.
c) Polymorphs can be seen.
2) Blood:
a) Normochromic anemia because of hemodilution and low-grade
hemolysis.
b) C3 level decrease.
3) Throat culture positive for streptococcus suggests carrier stage.
4) Antibody titer to DNA se B antigen (streptozyne test)
5) Biochemical – Elevated blood urea & Sr. creatinine.
6) ECG: Changes of hyperkalemia.
Indication for Biopsy Presence of systemic features: Fever, Rash, Joint pain, heart
diseases.
• Normal levels of C3.
• Mixed nephritic-Nephrotic features.
• Azotemia requiring dialysis (suspected rapidly progressive GN)
Atypical course:
• Persistence of oliguria, hypertension and/or Azotemia beyond 7-10 days.
• Persistence of gross hematuria beyond 3-4 weeks or nephrotic range
proteinuria beyond 2weeks
• Low C3 level beyond 12 weeks.
• Persistent proteinuria beyond 6months persistent microscopic hematuria
beyond 12-18 months.
6. Differential Diagnosis
a) Hematuria:
1) Glomerular disease.
a. IgA Nephropathy.
b. Idiopathic hematuria.
c. Membranous Glomerulopathy.
d. Hemolytic uremic syndrome.
2) Infection (UTI).
a. Bacterial.
b. Tubercular.
c. Viral.
3) Blood.
a. Bleeding disorder.
b. Thrombocytopenia.
c. Renal vein thrombosis.
d. Sickle cell disease.
4) Renal stone.
4. Dipti’s Page 4 of 22
5) Hypercalciuria.
6) Anatomic Abnormalities.
a. Polycystic kidney.
b. Tumors.
c. Vascular abnormality.
d. Congenital abnormality.
7) Trauma.
8) Exercise.
9) Drug.
b) Edema:
Nephrotic syndrome, Hypoproteinemia, CHF.
7. Complications:
1) Uremia.
2) Hypertensive CHF.
3) Hypertensive encephalopathy.
4) Hyperkalemia.
5) Hyperphosphatemia.
6) Hypokalemia.
7) Acidosis.
8) Seizures.
8. Treatment:
I. General measures:
Diet – Salt restricted, in case of clinical edema, restrict fluid.
II. Daily monitoring of:
Blood pressure.
Intake output chart (sply urine output).
Weight.
Edema. (Diuretics for management of edema.)
III. Treatment of complications:
a. Renal failure.
b. Hypertension.
c. Acidosis.
d. Hyponatremia.
e. Seizures.
11.2. Acute kidney injury.
1. Treatment of AKI.
There have been various definitions for AKI over the years. The acute dialysis quality
initiative group (ADQI)proposed a definition of AKI for the adults using the RIFILE
criteria. RIFILE is an acronym where each letter means a level of severity of AKI
(R=risk, I=injury, F=failure, E=end stage kidney disease.) This is modified as pediatric
scale or is modified as the pediatric scale or ‘pRIFILE’ scale. The proposed ‘pRIFILE
criteria is based on the decrease in estimated creatinine clearance (eCCI) and the child’s
urine output based on body weight as shown in Table
Classification Estimated creatinine
clearance (Eccl)
Urine output
5. Dipti’s Page 5 of 22
Risk Decreased by 25% <0.5mL/kg/hr ×8hrs.
Injury Decreased by 50% <0.5mL/kg/hr×16hrs.
Failure Decreased by 75% or Eccl
<35mL/min/1.73m2
<0.5mL/kg/hr×24hrs or
Anuric×12hrs.
Loss Persistent failure >4/52weeks.
End stage renal disease. End stage renal failure (Persistent failure
>3/12months)
Modified Schwartz
formula5
for
Eccl(ml/min/1.73m2
)
Height (cm)×0.413
Serum Creatinine (mg/dL)
Treatment of Acute kidney injury”
I. Assess patient’s volume status
• If hypovolemic rapidly establish euvolemia with 0.9% NS boluses.
• If urine output remains low after euvolemia is established, begin fluid
restriction (insensible loss and urine output)
Impending renal failure – furosemide may be tried but it does not
change the outcome of AKI and may cause toxicity. Mannitol may
be harmful in AKI and low dose dopamine has been shown to be
ineffective in improving kidney function.
II. Renal failure:
a) Fluid restriction.
I.V. fluid quantity: Insensible losses (400mL/m2
/24hy) + Amount of
urine output/day + any additional losses.
Type – Glucose solution – 10to30% without electrolyte, without K+
.
b) Measure to reduce hyperkalemia.
i. Serum K+ >5.5 mEq/L
1) High concentration of IV glucose (10-50%)
2) Resin – Sodium polystyrene sulphonate resin
(Kayexalate)
Dose – 1gm/kg, route orally, rectal enema.
Method – suspended in 70% sorbitol 2ml/kg, repeat
2hrly.
M.O.A. – Resin exchanges Na+ for K+
Sorbitol causes osmotic diarrhea leading to K+
loss.
ii. Serum k+>7mEq/L
1) Calcium gluconate:
a) 10% solution.
b) Dose – 0.5ml/kg.
c) Duration: 10 mins.
d) Route – I.V.
e) Monitor H.R. if fall 20bts/min – stop.
M.O.A. Counteract K+
induced myocardial
irritability.
2) NaHCO3 – 7.5%
a) Dose – 3mEq/kg.
b) Route – I.V.
6. Dipti’s Page 6 of 22
c) Complication – B.P. increase tetany.
d) M.O.A. – decreases K+
.
3) 50% Glucose + Insulin.
Dose: 1gm/kg glucose with
Insulin 1unit/5gm of glucose.
Route – I.V.
Duration – 1hr.
Precaution – monitor hypoglycemia
M.O.A. – Shifts k+
from extracellular to intracellular.
M.O.A. – (Mechanism of action)
4) ꞵ Adrenergic receptor agonists: Salbutamol Route
aerosol.
5) Dialysis:
i. Indications: - Acidosis, Hyperkalemia, CNS
involvement, increase B.P., fluid overload, CHF.
ii. Types:
1. Hemodialysis.
2. Peritoneal Dialysis.
3. Continuous renal replacement therapy.
2. Acidosis treatment:
a) pH< 7.15 or bicarbonate < 8mEq/L require treatment.
b) Corrected partially by I.V. bicarbonate up to pH 7.2.
c) Side effect: Precipitates tetany (Reduces ionic Ca+2
)
3. Treatment of Hypertension:
A. Fluid and salt restriction
B. Diuretics – Hydrochlorothiazide – 1-2 mg/kg/24hr orally.
Furosemide – 1-6mg/kg/24hr. orally, I.V. 1mg/kg.
C. Antihypertensive Drugs:
i. Propranolol – Vasodilator (1-3mg/kg dose)
ii. Hydralazine – (Vasodilator) – 0.1 – 0.4 mg/kg/dose I.V.
0.25 – 1.0 mg/dose 6-8 hrly orally.
iii. Nifedipine – 0.25 – 0.5 mg/kg/dose.
iv. I.V. diazoxide – 1-3 mg/kg/dose I.V. (max. 150mg)
4. Treatment of Hyponatremia: Fluid restriction.
5. Treatment of Seizures: Treat cause of Seizures:
i. Electrolyte imbalance.
ii. Cerebral edema.
iii. Uremia.
iv. Hypertension.
Treatment: Diazepam 0.3mg/kg/I.V.
Prognosis: The like hood of recovery from AKI depends on the underlying
causes.
AKI may result in full recovery, or incomplete recovery leading to
chronic kidney disease. In severe cases, non-recovery may lead to End stage
disease (ESRD).
Long term follow-up to monitor renal function is recommended.
7. Dipti’s Page 7 of 22
11.3. Hematuria.
1. Definition: Microscopic hematuria is defined as the presence of at least five RBC per
high power field in freshy voided and centrifuged urine.
2. Causes:
I. Glomerular causes:
1) Isolated renal disease.
a) IgA Nephropathy.
b) Post streptococcal Glomerular Nephritis.
c) Membranous Nephropathy.
d) Membranoproliferative GN.
e) Focal segmental GN.
f) Alport syndrome.
2) Multisystem diseases.
a) SLE Nephritis.
b) Henoch – Schoenlein purpura nephropathy.
c) Polyarthritis nodosa.
d) Good pasture’s syndrome.
e) Sickle cell glomerulopathy.
f) HIV nephropathy.
g) Wegener granulomatosis.
II. Extraglomerular Hematuria:
1) Upper urinary tract:
a) Pyelonephritis.
b) Interstitial nephritis.
c) Acute tubular necrosis.
d) Papillary necrosis.
e) Nephrocalcinosis.
f) Vascular
g) Crystal urea.
h) Hemoglobinopathy.
i) Hydronephrosis.
j) Polycystic kidney disease.
k) Hydronephrosis.
l) Polycystic kidney disease.
m) Tumors – Wilms, Rhabdomyosarcoma, angiomyolipoma.
n) Trauma.
2) Lower urinary tract:
a) Cystitis.
b) Urethritis.
c) Urolithiasis.
d) Trauma.
e) Coagulopathy
f) Heavy exercise.
3. Diagnostic Approach:
I. Glomerulo Hematuria.
Features:
8. Dipti’s Page 8 of 22
1) Brown color.
2) Significant proteinuria may be present.
3) RBC cast, dysmorphic RBS’s.
Investigations:
a) CBC with differential count.
b) Electrolytes – Na+
, K+
, Ca+2
.
c) BUN/Creatinine.
d) Sr. protein/ albumin.
e) Cholesterol.
f) C3 /C4.
g) ASO/Anti DNASE B
h) Urine protein/Creatinine Ratio.
II. Extra Glomerular Hematuria.
Step I:
Urine culture.
Step II:
a) Urine Ca+2
Creatinine.
b) Ultrasonography.
Step III:
a) Urine analysis.
b) Serum electrolytes.
c) If Crystalluria – Urolithiasis or Nephrocalcinosis, 24-hour urine for Ca+2
,
Creatinine, Uric acid and oxalate.
d) If hydronephrosis:
Cystogram.
Renal scan.
I.V.P.
Voiding cystourethrogram.
11.4. Proteinuria:
1. Definition: Normal protein secretion in healthy children is 150mg/day or 4mg/m2/hr.
Abnormal protein excretion 4 – 40 mg/m2/hr. Nephrotic Range 40mg/m2/hr.
2. Diagnosis:
Dipstick is reported as:
a) Negative or trace – 10 – 20mg%.
b) 1+ = 30mg%.
c) 2+ = 100mg%
d) 3+ = 300mg%
e) 4+ = 1000 – 2000 mg%
More than 1% is clinically significant.
3. Causes:
1) Transient proteinuria: Fever, Exercise, Dehydration, CHF, Seizures, stress.
2) Postural proteinuria.
3) Glomerular Diseases:
a) Acute Nephritis.
9. Dipti’s Page 9 of 22
b) Nephrotic syndrome.
c) IgA Nephropathy.
d) Lupus Nephritis.
e) Henoch – Schoenlein purpura Nephritis.
f) Sickle cell Nephropathy.
g) Diabetic Nephropathy.
h) Alport Syndrome.
4) Tubular Diseases:
a) Reflux Nephropathy.
b) Polycystic kidney diseases.
c) Renal dysplasia.
d) Acute tubular necrosis.
e) Galactosemia.
f) Cystinosis.
g) Wilson disease.
h) Heavy metal poisoning.
4. Nephrotic Syndrome.
1. Definition: It is a syndrome characterized by:
1) Heavy proteinuria: >3.5gm/24 hr. in adult and >40gm/m2/hr. in children.
2) Hypoalbuminemia: <2.5 gm%.
3) Edema.
2. Etiology:
1) 90% cases are idiopathic nephrotic syndrome:
Causes
a) Minimal changes disease – 75%.
b) Mesangial proliferation – 5%.
c) Focal segmental glomerulosclerosis – 5to20%
d) Membranous nephropathy 1-2%
e) Membrano-proliferative glomerulonephritis 4-5%.
2) 10% secondary nephrotic syndrome:
a) Systemic diseases: SLE, HSP, Diabetes, Amyloidosis.
b) Leukemia, Lymphoma, Sickle cell disease.
c) Infectious diseases: Hepatitis B, Hepatitis C, HIV, Malaria,
Toxoplasmosis.
d) Drugs: Gold, Penicillamine, Heroin.
3. Pathophysiology:
1) Underlying abnormality in Nephrotic syndrome is increase in
permeability of glomerular capillary wall, which leads to massive
proteinuria and hypoalbuminemia.
2) Causes of increased permeability:
a) In minimal lesion NS T dysfunction leads to alteration of cytokines
which causes loss of negatively charged glycoproteins within the
glomerulo capillary wall.
b) In focal segmental glomerular sclerosis – A plasma factor
produced by lymphocyte may responsible.
10. Dipti’s Page 10 of 22
3) Mechanism of edema:
a) Urinary protein loss leads to hypoalbuminemia Decrease oncotic
pressure Transudation of fluid in interstitial space.
b) Reduction in intravascular volume and decrease renal perfusion
pressure which:
i. Activate renin angiotensin and aldosterone system increases
tubular reabsorption of Na+.
ii. Also stimulate ADH – increase reabsorption of water.
c) Primary renal avidity for sodium water.
4) Cause of lipid elevation:
a) Hypoalbuminemia stimulates generalized hepatic protein synthesis
including lipoproteins.
b) Lipid catabolism is diminished due to decrease lipoprotein lipase by
increase loss of enzymes in urine.
11.5.3. Idiopathic Nephrotic syndrome.
1) Incidence: - 90% children have idiopathic Nephrotic syndrome.
2) Types: Commen histological types:
A. Minimal changes disease (85%).
B. Mesangial proliferation (5%).
C. Focal segmental glomerulosclerosis (10%).
3) Pathology:
A. Minimal change disease (85%).
a) Glomeruli appear normal.
b) Minimal increase in mesangial cells and matrix.
c) Immunofluorescent microscopy – No abnormality detected.
d) Electron microscopy – Effacement of epithelial cell foot
processes.
B. Mesangial proliferation (5%).
a) Diffuse increase mesangial cells and matrix.
b) Immunofluorescent microscopy reveals trace to 1+ mesangial
IgM and or IgA staining.
c) Electron microscopy:
i. Increase mesangial cells matrix.
ii. Effacement of epithelia cells. Foot process.
C. Focal segmental glomerulosclerosis (10%).
Light microscopy:
a) Mesangial proliferation.
b) Segmental scarring.
Immunofluorescent microscopy: May be normal.
Electron microscopy:
a) Segmental scarring of glomeruli tuft.
b) Obliteration of glomeruli capillary lumen.
Disease progress and ultimately involves all glomeruli.
4) Clinical features: Age 2-6 yrs. (6months to childhood)
i. Sex: - More in males (M:F – 2:1)
ii. Edema (Anasarca):
11. Dipti’s Page 11 of 22
Initially mild edema around eyes and lower extremities with time it
becomes generalized with development of ascites, pleural effusion and
genital edema.
iii. Anorexia, Irritability, abdominal pain and diarrhea.
iv. Rarely hypertension and hematuria.
5) Diagnosis:
1. Urine exam: Proteinuria exceeds 3.5 gm/24hr in adults, 40mg/m2/he in
children.
2. Random urine protein to creatinine ratio exceeds – 2.
3. Sr. Albumin - <2,5gm%.
4. C3 and C4 normal.
5. Renal biopsy normally not required.
6) Treatment:
1. Diet: Salt restriction when edema present, High protein diet.
2. Drug therapy:
a) Initial episode therapy:
Drug of choice – Prednisolone.
Dose – 60mg/m2
/day given in 2 divided doses.
Or
2mg/kg/day (Max. 80mg)
Duration: 6weeks.
Followed by 40mg /m2
/day or 1.5mg/kg/day on alternate day
for 6weeks.
b) Alternate day medication is given as a single dose in the
mornings. The initial episode is treated with 6weeks daily and
6weeks alternate day steroids as described above.
3. Remission: Urine protein should be negative ore trace for three
consecutive days.
• Relapse: Urinary protein ≥3+ by Dipstick for 3 consecutive
days.
• Frequent relapse: two or more relapses in 6months of initial
response 4 relapses in any 12 months period.
• Steroid dependence: Occurrence of two consecutive relapses
during steroid therapy or within two weeks of its cessation.
• Steroid resistance: Failure to achieve remission after 4weeks
of daily therapy with oral prednisolone at a dose of 2mg
/kg/day.
4. Treatment of relapse: Relapse treated with daily prednisolone
(2mg/kg/day) Until remission i.e. Urine negative for protein for three
consecutive days, followed by alternate day steroids (1.5mg/kg/day)
for 4weeks.
5. Treatment of steroid dependent or frequent relapses.
a) Cyclophosphamide: Along with alternate day prednisolone
therapy.
Dose: 2mg/kg/day.
Duration: 12 weeks.
12. Dipti’s Page 12 of 22
Side effects: Neutropenia, Hemorrhagic Cystitis, Alopecia,
Sterility, increase risk of future malignancy.
b) Levamisole: 2mg/kg on alternate days for 18-24 months.
Wean steroids to 0.25 to 0.5 mg/kg on alternate day slowly.
Side effects: Common – Leukopenia, Rarely – Liver toxicity,
convulsions and skin rash.
c) Mycophenolate mofetil: Dose 800-1200 mg/m2
in BID dosing
with tapering prednisolone for 12-24 months.
Side effects: Pain, Diarrhea, Leukopenia.
d) Cyclosporine: Dose: 3-5mg/kg/day for 12-24 months; with
weaning dose of steroids.
Side effects: Nephrotoxicity, Hypertension, Hyperkalemia,
hyperlipidemia.
Cosmetic symptoms: Gum hypertrophy, Hirsutism.
7) Complications:
A. Infections: Spontaneous bacterial peritonitis is most common
complication.
Organism: Streptococcus pneumonia. Is common. E. Coli may be
encountered.
B. Thromboembolic Events: Both arterial and venous thrombosis are
seen.
Cause:
a) Increase fibrinogen.
b) Thrombocytosis.
c) Hemoconcentration.
d) Relative immobilization.
e) Decrease fibrinolytic factors.
C. Vitamin D Deficiency Rickets.
D. Prognosis: Majority of patients have Relapses up to 2nd decade of
life but, overall prognosis is good.
11.5.4. Congenital Nephrotic syndrome:
1) Definition: Infants who develop nephrotic syndrome in the first three months
of life.
2) Type: (Finnish type)
a) Autosomal recessive disorder.
b) Caused by mutation in NPHS 2 Gene located on chromosome 19.
This gene encodes protein nephrin.
c) Pathology.
i. Dilation of proximal tubules.
ii. Mesangial hypercellularity.
iii. Glomerular sclerosis.
d) Features:
i. Massive proteinuria.
ii. Large placenta.
iii. Marked edema.
iv. Prematurity.
13. Dipti’s Page 13 of 22
v. Respiratory Distress.
vi. Separation of cranial sutures.
e) Course – Progressive renal failure with death by the age of 5yrs.
f) Treatment:
i. ACE inhibitor.
ii. Indomethacin.
iii. Unilateral nephrectomy.
iv. Bilateral nephrectomy.
v. Dialysis.
vi. Aggressive nutritional support.
vii. Kidney transplantation.
g) Antenatal Diagnosis:
Increase amniotic protein α fetoprotein.
DNA Analysis.
3) Other Causes:
i. Congenital infection:
a) Syphilis, Toxoplasmosis.
b) Rubella, CMV, HIV, Hepatitis B.
ii. Diffuse mesangial sclerosis.
Difference between Acute Nephritis and Acute Nephrotic
syndrome. is as follows:
S.
No.
Acute Nephritis Nephrotic Syndrome
I Definition: Characterized by:
A Hematuria Heavy proteinuria >3.5 gm / day.
B Edema Hypo-albuminemia.
C Hypertension Edema
D Oliguria/Renal failure Hyperlipidemia.
II Etiology
A 90% Post infective, Immune complex
disease.
90% Idiopathic.
III Relapses
A Usually only one attack Relapses common.
IV Pathology
Immune complex deposits on basement
membrane.
Minimal changes, retraction of epithelial foot
processes.
V Clinical features
A Mainly presenting as mild to moderate
edema.
Gross massive edema.
B Hypertension is present. Usually absent.
C Renal failure common. Uncommon.
D Hematuria commonly present No Hematuria.
VI Urine Examination:
A Albumin 1, 2+ proteinuria <2gm% Massive proteinuria (<3.5 gm%) with selective
albuminuria.
B Hematuria (RBC) No RBC
C RBC Cast, granular cast No RBC.
VII Blood Urea
14. Dipti’s Page 14 of 22
A Raised Usually not raised
VIII Treatment:
A Penicillin/Erythromycin.
Corticosteroid is drug of choice for minimal LNS.B Treatment of Hypertension.
C Treatment of Renal failure.
IX Diet:
Protein restriction High protein diet.
5. Urinary tract infection.
1. Incidence:
Girls – 3-5%
Boy’s 1%
In newborn period it is more commen in males, beyond newborn period more in
females.
2. Predisposing factors:
1) Vesicoureteric reflux, Neurogenic bladder.
2) Obstructive uropathy, Renal calculi.
3) Urinary instrumentation.
4) Female sex, Pregnancy, Sexual activity, malnutrition.
5) Uncircumcised males, Labial adhesions.
6) Children on immunosuppressive therapy.
7) Diabetes.
8) Constipation.
3. Route of infection:
A. During neonatal period:
• Blood stream.
• Urethra.
B. During childhood: Usually from bellow ascending UTI.
4. Etiology:
Mainly caused by Colonic bacteria.
In females – 75 to 90% cases, it is caused by E coli (Escherichia coli) followed by
klebsiella, proteus, and staphylococcusaprophyticus.
Viral – Especially Adenovirus causing cystitis.
5. Pathology:
1) Acute bacterial cystitis:
a. Mucosal congestion, edema, petechiae, hemorrhages.
b. Functional capacity of bladder is decreased.
2) Chronic cystitis: Cystitis cystica.
3) Acute pyelonephritis:
a. Kidney are enlarged.
b. Renal micro abscesses.
4) Chronic pyelonephritis:
a. Renal scar:
Cortical scar with underlying calyceal deformity is diagnostic.
b. Microscopic:
i. Lesions are patchy with Glomerular fibrosis.
15. Dipti’s Page 15 of 22
ii. Interstitial chronic inflammation and fibrosis.
iii. Atrophy of tubules.
5) Proteus infection can cause stone formation.
6. Clinical features: Three basic forms of UTI.
a. Asymptomatic bacteriuria.
b. Pyelonephritis.
c. Cystitis.
A. Infancy: Fever, weight loss, failure to thrive, nausea, vomiting, acute
diarrhea and Jaundice.
B. Children:
i. PUO.
ii. Urinary frequency.
iii. Painful micturition.
iv. Urinary incontinence.
v. Urinary urgency.
vi. Bed wetting in dry child.
vii. Abdominal pain.
viii. Foul smelling urine.
C. Chronic recurrent cystitis: Day time incontinence.
D. Hemorrhagic cystitis: Hematuria at the end of urination.
E. Acute pyelonephritis:
i. Fever with chills.
ii. Flank pain and tenderness.
iii. Kidney’s enlarge and palpable.
7. Investigations:
I. Urine Examination: Mild stream urine is collected after clearing urethral
meatus with povidone, iodine with rinsing.
a) In females’ labia should be spread manually.
b) In male’s prepuce should be retracted.
c) Urine can also be collected by catheterization or suprapubic aspiration.
d) Urine should be transported immediately to the laboratory to the
laboratory or stored at 4⁰C for 12-14hours.
Result: Uncentrifuged samples of urine suggest infection when:
a. On microscopy: More than 10WBC /Cumm.
b. On Gram’s staining:
c. Positive dipstick test:
d. Centrifuged urine - > 4WBCs/ Cumm Suggest UTI.
II. Urine culture:
a) Colony count ≥105/mL of single organism is Diagnostic of UTI.
b) Colony count ≥ 104
/mL – 105
mL with symptomatic UTI.
III. Computed topography:
IV. Renal cortical 99m Tc DMSA or glucoheptonate scan. It detects cortical
scars.
V. Blood examination: TLC increase, Neutrophilia, increase ESR, C-reactive
proteins. Marked leukocytosis in renal abscess.
VI. Approach to a child with first episode of UTI is shown in table:
16. Dipti’s Page 16 of 22
Age < 1year 1 – 5Years >5Years.
USG USG & DMSA USG
MCU If abnormal If abnormal
DMSA Scan MCU MCU/DMSA
USG – Ultrasonogram, MCU – Micturating Cystourethrogram, DMSA –
Dimercapto succinic acid.
8. Differential diagnosis:
i. Vulvitis.
ii. Vaginitis.
iii. Eosinic cystitis.
9. Treatment:
1) Send urine culture first.
2) Drug used for cystitis.
a) Trimethoprim – Sulfamethoxazole.
Dose – 8to10mg of trimethoprim for 5-10 days.
b) Nitrofurantoin.
Dose – 5to7 mg/kg/day × 7days not used for febrile UTI.
c) Amoxicillin: Dose 50mg/kg/day. × 7days.
3) Pyelonephritis treatment:
A. Parenteral treatment: Duration depends on depends on severity of illness
and age of patient.
a) Ceftriaxone
Dose 50-75 mg /kg/day.
b) Ampicillin
Dose: 100mg/kg/day.
+
Aminoglycosides (Gentamycin)
Dose: 3-5 mg/kg/day in two divided doses.
B. Oral third generation cephalosporins such as cefixime is also effective
except for pseudomonas.
C. Fluoroquinolones: Ciprofloxacin uses for resistant microorganism especially
for pseudomonas for patient older than 17years.
D. Surgical treatment
Renal and perirenal abscess.
Obstructive uropathy.
E. No need for follow up urine culture to document cure.
F. Find out predisposing factors if recurrent UTI then treat.
G. Prophylaxis for recurrent UTI.
a. Sulfamethoxazole + Trimethoprim combination (1/3rd
Dose –
1to2mg/kg/day.)
b. Nitrofurantoin (1to2mg/kg/day)
6. Chronic kidney disease.
1. Definition:
Presence of structural or functional abnormalities of the kidney for ≥ 3months with or
without decreased GFR, manifested by ≥ 1 of the following features:
17. Dipti’s Page 17 of 22
o Abnormalities in the blood or urine tests.
o Abnormalities in imaging tests.
o Abnormalities on kidney biopsy.
GFR ≤ 60 mL/min/1.73 m2
for ≥ 3months with or without other signs of
kidney damage.
2. Etiology:
1) Causes in younger than 5yrs. Of age.
a. Congenital anomalies – renal hypoplasia, dysplasia.
b. Obstructive uropathies.
2) After 5yrs. Of age.
a. Glomerulonephritis.
b. Inherited disorders – familial juvenile nephrolithiasis, Alport
syndrome.
3) Metabolic disorders.
a. Cystinosis.
b. Hyperoxaluria.
4) Polycystic kidney disease.
3. Pathogenesis:
Progressive renal injury is caused by following mechanisms:
1) Hyperfiltration injury.
2) Persistent proteinuria.
3) Systemic hypertension.
4) Intrarenal hypertension.
5) Renal calcium, phosphorus deposition
6) Hyperlipidemia.
A. Final common pathway is hyperfiltration injury as the populations
of sclerosed nephrons increase, surviving nephrons have increased
excretory burden and ultimately hyperfiltration injury.
B. Proteinuria is other factor causing renal injury by transversing across
glomerular capillary wall and have direct toxic effect causing
glomerular sclerosis.
C. Hyperphosphatemia may increase the progression of disease.
Staging of chronic kidney disease. (Normal GFR – 90 – 120 mL/min/1.73m2
)
a. Stage 1 With normal or high GFR (GFR >90m L / min).
b. Stage 2 Mild CKD (GFR = 60to89 mL/min)
c. Stage 3 A moderate CKD (GFR = 39to59 mL/min).
d. Stage 4 Severe CKD (GFR = 15to29 mL/min).
e. Stage 5 End stage CKD (GFR = 60to89 mL/min)
4. Clinical features:
1) Neonatal period (Congenital disorders)
Presents as failure to thrive, dehydration, UTI, Overt renal insufficiency.
2) Patients with familial juvenile nephropathies:
They present as headache, fatigue, lethargy, anorexia, vomiting, polydipsia,
polyuria, and Growth failure.
3) CRF form of glomerulonephritic origin:
18. Dipti’s Page 18 of 22
It presents as edema, hypertension, hematuria and proteinuria.
4) Renal osteodystrophy:
Muscle weakness, bone pain, fractures, with minor trauma, rachitic changes.
5) Physical examination:
a. Pallor, Anemia.
b. Sallow appearance of skin.
c. Short stature
d. Renal osteodystrophy.
e. Edema.
f. Hypertension.
5. Lab Diagnosis:
1) BUN increases.
2) Serum creatinine increases.
3) GFR – K × height in cms/serum creatinine (mg%) K = 0,413.
4) Serum K+
increase, Serum Na+2
decrease, Sr. Ca+2
decrease.
5) Acidosis.
6) Hyperphosphatemia.
7) Uric acid increases.
8) Hypoalbuminemia in heavy proteinuria patients.
9) CBC – normochromic, normocytic anemia.
10) Sr. Cholesterol increase, increase triglycerides.
11) Urine examination – Hematuria, Proteinuria, low specific gravity.
6. Treatment: Principles of treatment.
1) Renal replacement therapy dialysis when indicated.
2) Slow progression of disease.
I. Monitoring clinical and laboratory status:
a. Routine testing of HB, Sr. Electrolyte, BUN, Creatinine, Ca++
,
P, Albumin, alkaline phosphate.
b. Periodic assessment of parathyroid hormone. (PTH)
II. Fluid electrolyte management:
a. In renal dysplasia patients require high volume, low calorie
density feedings with sodium supplementation.
b. Patients with edema, hypertension and CHF.
• Sodium restriction.
• Diuretic therapy.
c. K+
Mostly K+
positive balance is maintained but hyperkalemia
may be treated by:
• Restricting K+
intake.
• Oral alkalinizing agent.
• Kayexalate – Resin.
III. Acidosis:
→ Sodium bicarbonate tablet 650mg daily. (1=8mEq bases.)
IV. Nutrition:
a. Restriction of phosphorus, K+
, Na+2
, may be required according
to blood levels.
b. Calorie – Daily requirement as per age.
19. Dipti’s Page 19 of 22
c. Proteins – 2.5 gm/kg/day. Quality proteins, high biological
values should be given.
Example: - Egg, meat, milk, fish.
d. Vitamin supplementation, water soluble vitamins only.
V. Growth: Recombinant Human growth hormone may be used. Start
with 0.05mg/kg/day S.C. till final height is achieved.
VI. Anemia:
• Erythropoietin:
Dose – 50 – 150mg/kg/dose.
Routes – Subcutaneous.
Erythropoietin should be supplemented with oral and IV iron.
Packed cell transfusion if required may be given.
VII. Renal Osteodystrophy:
o Vitamin D therapy Calcitriol 0.01 – 0.5 mg/kg/day.
o Phosphate binders: Calcium carbonate and calcium acetate.
VIII. Treatment of hypertension: Hypertension with volume overload.
a. Salt restricted diet.
b. Furosemide.
c. ACE inhibitor – Enalapril, Lisinopril.
d. Angiotensin II blockers in diabetic nephropathy – losartan.
e. In resistant cases use following drugs:
a) Calcium channel blockers.
o Nifedipine.
o Amlodipine.
b) Clonidine.
c) ꞵ Blockers – Atenolol.
IX. Immunization: Immunization should be completed.
X. Drug dosage adjustment: Either decrease the dose or increase the
drug interval or both.
XI. Prompt treatment of infection.
XII. Dialysis indications:
a. If GFR < 15ml/min/1.73m2
b. Refractory fluid overload.
c. Electrolyte imbalance.
d. Acidosis.
e. Growth failure.
f. Uremic symptoms.
XIII. Renal transplantation: Indicated in end stage renal disease.
7. Peritoneal Dialysis.
1. Principle:
a) Peritoneal membrane acts as dialyzer.
b) Excess body water is removed by osmotic gradient created by high dextrose
concentration.
c) Metabolic wastes are removed by diffusion from peritoneal capillaries into
dialysate.
20. Dipti’s Page 20 of 22
2. Methods:
Entry to peritoneal cavity is achieved by surgical inserted tunneled Tenckhoff
catheter.
3. Types:
a) CAPD: Continuous ambulatory peritoneal dialysis.
b) CCPD: Continuous cyclic peritoneal dialysis.
c) IPD: Intermittent peritoneal dialysis.
d) NIPD: Nocturnal Intermittent peritoneal dialysis
4. Advantages:
1) Can be performed at home.
2) Technically easier.
3) Freedom to attend school and after school activities.
4) Less restrictive diet.
5. Disadvantages:
1) Catheter malfunction.
2) Infections.
3) Impaired appetite.
4) Negative body image.
5) More Expensive.
8. Hemolytic Uremic Syndrome
1. Definition:
HUS is characterized by:
a) Microangiopathic hemolytic anemia.
b) Thrombocytopenia.
c) Uremia.
2. Etiology:
a) Acute diarrhea caused by shiga toxin producing Escherichia coli 0157:
H7 precedes the disease.
b) Toxin is absorbed from intestine and initiates endothelial injury.
c) Rarely association with shigella, salmonella, campylobacter, Streptococcus
Pneumonae and Bartonella.
d) Virus: Coxsackie, Echo, Influenza, Varicella, HIV and Epstein bar.
e) It may develop with use of oral contraceptives, mitomycin and cyclosporin.
f) Also reported with SLE, malignant, hypertension, preeclampsia, Post partum
renal failure.
g) Radiation nephritis.
3. Pathology:
Glomeruli:
a) Thickening of capillary wall, narrowing of capillary lumen, widening of
mesangium.
b) Fibrin thrombi are seen in glomerular capillaries.
c) Glomerular sclerosis in severe cases.
Pathogenesis:
i. Primary event
Endothelial cell injury