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ACUTE NEPHRITIC SYNDROME By Hakimah KhaniBintiSuhaimi
Introduction Synonyms: acute nephritis, acute nephritic syndrome An immunologic mechanism: the result of an immune process that injures the glomeruli of the kidney. Clinical features: A sudden onset of hematuria, Proteinuria, Edema, Oliguria and volume overload, Hypertension, Azotemia is another common but inconstant finding.
Outline Definition Epidemiology Etiology and Pathogenesis Clinical Features Complication Investigation Diagnosis Differential Diagnosis Treatment and Management Prognosis
Definition AGNthat follows an infection with a nephritogenic strain of group A beta hemolytic streptococci. The classic example of the acute nephriticsyndrome. Nelson Textbook of Pediatrics, 7th Edition
Etiology and Pathogenesis The child gets gets throat or skin infection bynephritogenic strain of group A beta hemolytic streptococci - serotype 12 , 4 and 1 Antibodies to streptoccocus (egantistreptolysin O) are formed in his circulation Antigen-antibody circulating immune complexes are subsequently deposited along the glomerular basement membrane (GBM).
Streptococcal infection immune complex formation + deposited in GBM complement system activated immune injuriescellular proliferation GBM fracturecapillary lumen narrowed hematuriaglomerular blood flow decreased proteinuriaoliguria GFR distal sodium reabsorptionretention of water & sodiumblood volume edema hypertension Low serum complement
Typical Manifestation Develop acute nephritic syndrome 1–2 wk after an antecedent streptococcal pharyngitis or 3–6 wk after a streptococcal pyoderma. Edema 75% of the patients Face,periorbital area lowerextremities generalized (ascites, pleural effusions) 2. Proteinuria– usu. normalize after 4 weeks 3. Oliguria school child < 400ml/day preschool child < 300ml/day infant & toddler < 200ml/day
Typical Manifestation (2) Gross hematuria(65% of patients) Smoky, tea-colored, cola-colored, or fresh bloody urine Microscopical hematuria (almost all patients) The urine appears normal, but >3 RBCs/HP are found in centrifuged urine sediment examined microscopically. Hypertension (50%) – mild to moderate, typically subsides promptly after diuresis Nonspecific symptoms: Such as anorexia, vomiting, general malaise, lethargy, abdominal or flank pain, low-grade fever and weight gain.
Clinical course Spontaneous improvement typically begins within 1 wk with resolution of edema in 5-10 days and hypertension in 2-3 wk, but urinalysis may be abnormal (persistent microscopic hematuria) for a year.
Treatment Treatment of APSGN is largely that of supportive care. Usually, patients undergo a spontaneous diuresis within 7 to 10 days after the onset of their illness - strict monitoring – nephrotic chart + fluid restriction until diuresis Management is directed at treating the acute effects of renal insufficiency and hypertension
Diuretics Diet Fluid restriction – during oliguric phase Sodium restriction is necessary Protein restriction is unnecessary Antibiotics A 10-day course of systemic antibiotic therapy with penicillin V is recommended to limit the spread of the nephritogenic organisms. Antibiotic therapy does not affect the natural history of glomerulonephritis. Paediatric Protocols, 12th Edition
Treatment for complications Significant asymptomatic hypertension symptomatic, severe hypertension or hypertensive emergency / encephalopathy Paediatric Protocols, 12th Edition
Follow-up • for at least 1 year. • monitor BP at every visit • do urinalysis and renal func on to evaluate recovery. • repeat C3 levels 6 weeks later if not already normalised by time of discharge Paediatric Protocols, 12th Edition
Prognosis short term outcome: excellent, mortality <0.5%. long term outcome: 1.8% of children develop chronic kidney disease following post streptococcal AGN. These children should be referred to the paediatric nephrologists for further evaluation and management. Paediatric Protocols, 12th Edition