| Entity | Clinical Course | Prognosis |
|---|---|---|
| Postinfection glomerulonephritis (GN). Onset occurs 10–14 d after acute illness, commonly streptococcal. Characteristics include acute onset, tea-colored urine, mild to severe renal insufficiency, and edema. | Acute phase is usually over in 2 wk. Complete resolution occurs in 95% of cases. Severity of renal failure and hypertension varies. Microhematuria may persist to 18 mo. Hypocomplementemia resolves in 1–30 d. | Excellent. Chronic disease is rare. Severe proteinuria, atypical presentation or course, or persistent hypocomplementemia suggest another entity. |
| Membranoproliferative GN. Presentation ranges from mild microhematuria to acute GN syndrome. Diagnosis is made by renal biopsy. Etiology is unknown. Types I and II are most common. Lesion is chronic. | Course can be mild to severe (rapid deterioration in renal function); may mimic postinfection GN. Proteinuria can be severe. Complement depression is intermittent to persistent. Hypertension is usually significant. | Type I may respond to corticosteroids. Type II (dense deposit disease) is less treatable; function decrease varies from immediate to as long as 15 y in 30–50% of untreated cases. |
| IgA nephropathy. Classic presentation is asymptomatic gross hematuria during acute unrelated illness, with microhematuria between episodes. Occasional instances of acute GN syndrome occur. Etiology is unknown. Diagnosis is made by biopsy. | 90% of cases resolve in 1–5 y. Gross hematuric episodes resolve with recovery from acute illness. Severity of renal insufficiency and hypertension varies. Proteinuria occurs in more severe, atypical cases. | Generally good; a small percentage develops chronic renal failure. Proteinuria in the nephrotic range is a poor sign. There is no universally accepted medication. (Corticosteroids may be useful in severe cases.) |
| Henoch-Schönlein purpura GN. Degree of renal involvement varies. Asymptomatic microhematuria is most common, but GN syndrome can occur. Renal biopsy is recommended in severe cases; it can provide prognostic information. | Presentation varies with severity of renal lesion. In rare cases, may progress rapidly to serious renal failure. Hypertension varies. Proteinuria in the nephrotic range and severe decline in function can occur. | Overall, prognosis is good. Patients presenting with > 50% reduction in function or proteinuria exceeding 1 g/24 h may develop chronic renal failure. Severity of renal biopsy picture can best guide approach in such cases. There is no universally accepted medication. |
| GN of systemic lupus erythematosus (SLE). Microhematuria and proteinuria are rarely first signs of this systemic disease. Renal involvement varies, but severe GN may ensue with remissions and exacerbations throughout the course. | Renal involvement is mild to severe. Clinical complexity depends on degree of renal insufficiency and other systems involved. Hypertension is significant. Manifestations of the severity of the renal lesion guide therapeutic intervention. | Renal involvement accounts for most significant morbidity in SLE. Control of hypertension affects renal prognosis. Medication is guided by symptoms, serology, and renal lesion. End-stage renal failure can occur. |
| Hereditary GN (eg, Alport syndrome). Transmission is autosomal-dominant/X-linked, with family history marked by end-stage renal failure, especially in young males. Deafness and eye abnormalities are associated. | There is no acute syndrome. Females are generally less affected but are carriers. Hypertension and increasing proteinuria occur with advancing renal failure. There is no known treatment. | Progressive proteinuria and hypertension occur early, with gradual decline in renal function in those most severely affected. Disease progresses to end-stage renal failure in most males. |
Referensi : Current Diagnosis and Treatment Pediatrics 20th Edition (McGraw-Hill) 2010