Acute glomerulonephritis in children

2,068 views 20 slides Apr 26, 2021
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About This Presentation

Renal disorders are very common in children


Slide Content

Dr. Sunil Natha Mhaske Dean And Professor (Paediatrics) Dr. Vithalrao Vikhe Patil Foundation’s Medical College And Hospital, Ahmednagar, Maharashtra, India in children

Glomerulonephritis (GN) is inflammation of the glomeruli of Kidney. GN can be both acute, chronic and Rapidly progressive. This condition used to be known as Bright’s disease. The symptoms and signs of Bright's disease were first described in 1827 by the English physician Richard Bright, after whom the disease was named.

Poststreptococcal acute Glomerulonephritis or Acute glomerulonephritis (AGN) is a common condition in childhood. Immune mediated inflammation of glomerules in childhood. Typical age is 2-12 years. Patients usually have streptococcal pharyngitis or impetigo 5-21 days before AGN manifestation. It is caused by Streptococcus pyogenes infection. Incidence is 6–20:1,00,000 in western countries Risk factors : gender (more frequent in boys) Lower hygienic standard malnutrition. Genetic predisposition Nephritogenic beta- hemolytic streptococcus, group A, type M 12 and 49 -originator.

Antigens produced by Streptococcus pyogenes - NSAP-streptokinase ( nephritogen strains associated protein), M-protein and endostreptosin . These antigenes are binded by specific antibodies. So created immunocomplexes are taken up in capillaries of glomerules as deposites . It is mediated by activation of complement too. Finally, it leads to proligerative glomerulonephritis with decreased glomelural filtration, higher natrium resorption in tubules (→ edema ), increased renin secretion (→ hypertension). Pathophysiology

Edema - 75% of patients Acute onset. Mild to modest severity. Pitting edema. Starts in the eyelids and face then the lower and upper limbs then generalized (Hydrocele, ascites. Pericardial and pleural effusion.) It may be migratory: appear in eyelid in the morning, disappear in the afternoon and reappear around the ankle in the ambulant patients by the end of the day. Gross hematuria (65%) - tea colored or cola colored urine; Hypertension (50%) Acute renal insufficiency Oliguria - Urine output is less than 400 ml/day - 0 .5ml/hour/day Hypertension. General- Fever, Pallor, headache, malaise, anorexia, nausea and vomiting. C linical features-

Illnesses which triggers acute GN- Strep throat Systemic lupus erythematosus (lupus) Goodpasture syndrome- a rare autoimmune disease in which antibodies attacks kidneys and lungs. Amyloidosis - when abnormal proteins harms organs and tissues. Granulomatosis with polyangiitis (Wegener’s granulomatosis)- inflammation of the blood vessels. Polyarteritis nodosa-cells attack arteries. Heavy use of nonsteroidal anti-inflammatory drugs-ibuprofen and naproxen.

develop over several years with no or very few symptoms. This can cause irreversible damage to your kidneys and ultimately lead to complete kidney failure. Chronic GN doesn’t always have a cause. Hereditary nephritis Other possible causes include: certain immune diseases a history of cancer exposure to some hydrocarbon solvents acute form of GN may make you more likely to develop chronic GN later on. Clinical features- blood or excess protein in urine. high blood pressure. swelling in ankles and face. frequent night time urination. abdominal pain. frequent nosebleeds. Chronic GN

Urine assay- Hematuria Urine color - “coke,” “tea,” or “smoky” colored . Urine color in agn is uniform throughout the stream. Mild to moderate proteinuria- 1 + to 2+ protein. Concentrated urine Presence of casts Urine culture. Creatinine clearance Urine specific gravity Urine osmolality Diagnosis

2 . Blood examination - Elevated creatinine . ASO antibodies Reduced serum C3 level Elevated serum IGM and IGG Anemia – hemodilution Abnormal albumin levels E.S.R. increased. Blood of urea elevated 3. Immunology - Antiglomerular basement membrane antibodies Antineutrophil cytoplasmic antibodies Antinuclear antibodies Complement levels

CT scan Kidney ultrasound Chest X-ray Intravenous pyelogram Renal biopsy is not indicated.

Hematuria in Children Hematuria means that red blood cells are in the urine. Urine does not normally contain red blood cells because the filters in the kidney prevent blood from entering the urine. In hematuria , the filters or other parts of the urinary tract allow blood to leak into the urine. Gross hematuria -urine appears red or the color of tea or cola. Microscopic hematuria -urine microscopic examination findings of red blood cells (RBCs) of more than 5/µL in a fresh uncentrifuged midstream urine specimen or more than 3 RBCs/high-power field (HPF) in the centrifuged sediment from 10 mL of freshly voided midstream urine.

Causes of hematuria - A. Glomerular diseases - 1) Recurrent gross hematuria (IgA nephropathy, benign familial hematuria and Alport’s syndrome); 2) acute poststreptococcal glomerulonephritis; 3) membranoproliferative glomerulonephritis; 4) systemic lupus erythematosus; 5) membranous nephropathy; 6) rapidly progressive glomerulonephritis, Henoch- Schonlein purpura and Goodpasture’s disease. B. Interstitial and tubular - 1) acute pyelonephritis; 2) acute interstitial nephritis; 3) tuberculosis. C. Hematologic causes - Sickle cell disease, coagulopathies, von Willebrand’s disease, renal vein thrombosis and thrombocytopenia. D. Urinary tract - 1) bacterial or viral infection, 2) nephrolithiasis; 3) hypercalciuria. E. Structural anomalies - Congenital anomalies and polycystic kidney disease. F. Trauma, tumors and exercise . G. Medications - Aminoglycosides, amitryptiline , anticonvulsants, aspirin, chlorpromazine, coumadin, cyclophosphamide, diuretics, penicillin and thorazine .

Hospitalization Monitor blood pressure and urine output Checking of weight daily Blood for urea, creatinine, sodium and potassium. Anti-hypertensive drugs Restrict fluid intake till urine output improves. Intake of salt needs to be restricted Avoid intake of substances containing high potassium like fruits and tender coconut. A course of appropriate antibiotic is needed to eradicate infection. Management-

Acute kidney failure Chronic kidney disease Electrolyte imbalances, such as high levels of sodium or potassium Chronic urinary tract infections Congestive heart failure due to retained fluid or fluid overload Pulmonary edema due to retained fluid or fluid overload High blood pressure Malignant hypertension, which is rapidly increasing high blood pressure Increased risk of infections Complications -

Early, acute GN can be temporary and reversible. Chronic GN may be slowed with early treatment. Complete remission is in 95% of patients . only 5% of all patients can progress to end stage renal disease. Prognosis-

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