Which are common clinical manifestations of acute Poststreptococcal glomerulonephritis?
Postinfectious glomerulonephritis occurs after infection, usually with a nephritogenic strain of group A beta-hemolytic streptococcus. Diagnosis is suggested by history and urinalysis and confirmed by finding a low complement level and sometimes by antibody testing. Prognosis is excellent. Treatment is supportive. Show Most cases are caused by nephritogenic strains of group A
beta-hemolytic streptococci, most notably type 12 (which causes pharyngitis
Tonsillopharyngitis Tonsillopharyngitis is acute infection of the pharynx, palatine tonsils, or both. Symptoms may include sore throat, odynophagia, cervical lymphadenopathy, and fever. Diagnosis is clinical, supplemented... read more
Less common pathogens are nonstreptococcal bacteria, viruses, parasites, rickettsiae, and fungi (see table
Causes of Glomerulonephritis
Causes of Glomerulonephritis The mechanism is unknown, but microbial antigens are thought to bind to the glomerular basement membrane and activate primarily the alternate complement pathway both directly and via interaction with circulating antibodies, causing glomerular damage, which may be focal or diffuse. Alternatively, circulating immune complexes could precipitate on the glomerular basement membrane. Symptoms and SignsSymptoms and signs range from asymptomatic hematuria (in about 50%) and mild proteinuria to full-blown nephritis with microscopic or gross hematuria (cola-colored, brown, smoky, or frankly bloody urine), proteinuria (sometimes nephrotic-range), oliguria, edema, hypertension, and renal insufficiency. Fever is unusual and suggests persistent infection. Renal failure that causes fluid overload with heart failure and severe hypertension requiring dialysis affects 1 to 2% of patients. Uncommonly, nephrotic syndrome may persist after resolution of severe disease. Clinical manifestations of nonstreptococcal PIGN may mimic other disorders (eg, polyarteritis nodosa, renal emboli, antimicrobial drug–induced acute interstitial nephritis).
Tests done to confirm the diagnosis depend on clinical findings. Antistreptolysin O, antihyaluronidase, and antideoxyribonuclease (anti-DNAase) antibodies are commonly measured. Serum creatinine and complement levels (C3 and total hemolytic complement activity) are also usually measured; however, in patients with typical clinical findings, some tests can be omitted. Sometimes other tests are done. Biopsy confirms the diagnosis but is rarely necessary. Antistreptolysin O level, the most common laboratory evidence of recent streptococcal infection, increases and remains elevated for several months in about 75% of patients with pharyngitis and in about 50% of patients with impetigo, but it is not specific. The streptozyme test, which additionally measures antihyaluronidase, antideoxyribonuclease, and other titers detects 95% of recent streptococcal pharyngitis and 80% of skin infections. Urinalysis typically shows proteinuria (0.5 to 2 g/m2/day); dysmorphic RBCs; WBCs; renal tubular cells; and possibly RBC, WBC, and granular casts. Random (spot) urinary protein/creatinine ratio is usually between 0.2 and 2 (normal, < 0.2) but may occasionally be in the nephrotic range (≥ 3). C3 and total hemolytic complement activity (CH50) levels fall during active disease and return to normal within 6 to 8 weeks in 80% of PIGN cases; C1q, C2, and C4 levels are only minimally decreased or remain normal. Cryoglobulinemia may appear and persist for several months, whereas circulating immune complexes are detectable for only a few weeks. Biopsy specimens show enlarged and hypercellular glomeruli, initially with neutrophilic infiltration and later with mononuclear infiltration. Epithelial cell hyperplasia is a common early, transient feature. Microthrombosis may occur; if damage is severe, hemodynamic changes due to cellular proliferation and edema of the glomerulus cause oliguria, occasionally accompanied by epithelial crescents (formed within Bowman space from epithelial cell hyperplasia). Endothelial and mesangial cells multiply, and the mesangial regions often are greatly expanded by edema and contain neutrophils, dead cells, cellular debris, and subepithelial deposits of electron-dense material. Immunofluorescence microscopy usually shows immune complex deposition with IgG and complement in a granular pattern. On electron microscopy, these deposits are semilunar or hump-shaped and are located in the subepithelial area. The presence of these deposits and of small subendothelial and mesangial deposits initiates a complement-mediated inflammatory reaction that leads to glomerular damage. The major antigen is probably Zymogen cysteine proteinase exotoxin B (Zymogen/SPE B).
Treatment is supportive and may
include restriction of dietary protein, sodium, and fluid and, in more severe cases, treatment of edema
Treatment Edema is swelling of soft tissues due to increased interstitial fluid. The fluid is predominantly water, but protein and cell-rich fluid can accumulate if there is infection or lymphatic obstruction... read more
Click here for Patient Education Which of the following is a clinical manifestation of post streptococcal glomerulonephritis?The clinical presentation of PSGN varies from asymptomatic, microscopic hematuria to the full-blown acute nephritic syndrome, characterized by red to brown urine, proteinuria (which can reach the nephrotic range), edema, hypertension, and acute kidney injury.
What is acute Poststreptococcal glomerulonephritis?Acute post streptococcal glomerulonephritis is an immunologic response of the kidney to infection, characterized by the sudden appearance of edema, hematuria, proteinuria and hypertension . It is essentially a disease of childhood that accounts for approximately 90% of renal disorders in children.
What are the signs and symptoms of acute glomerulonephritis?These are the most common symptoms:. Fatigue.. High blood pressure.. Swelling of the face, hands, feet, and belly.. Blood and protein in the urine (hematuria and proteinuria). Decreased urine output.. What is the most common finding in acute glomerulonephritis?Acute glomerulonephritis is characterized by the sudden onset of painless dark, cola- or tea-colored urine; proteinuria; and cellular casts on urine microscopy. Edema, HTN, and renal dysfunction are common clinical findings and together constitute the nephritic syndrome.
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