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Professional dialysis recruitment| 23 year old man with hematuria and proteinuria |
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... http://www.nature.com/isn/education/articles/cpc/fullview.html?content_id=74603 Michael B Stokes MD Columbia University Medical Center, New York, NY Clinical History A 23-year-old Asian male presented with edema, new-onset hypertension, hematuria, and proteinuria. He reported a sore throat 8 days prior. There was no history of hypertension or diabetes mellitus. Physical examination revealed BP 168/100, 1+ lower extremity edema, and no rash. Lab tests revealed a serum creatinine of 1.9 mg/dL, 24hr urine protein 2.5 g/day, positive ASLO, microhematuria, negative ANA, depressed C3, normal C4, negative HBsAg & HCV Ab, hct 36%, and serum albumin 3 g/dL. SPEP and UPEP showed no evidence of a monoclonal spike. Kidneys measured 12.6 & 12.4 cm in length by ultrasound. Renal biopsy findings: Figure 1 PAS stain. Full size image(1.1 MB) Figure 2 H&E stain. Full size image(1008.9 KB) Figure 3 Immunofluorescence staining for C3. Full size image(393 KB) Figure 4 Immunofluorescence staining for IgG. Full size image(468.7 KB) Figure 5 Electron photomicrograph (12,000 X magnification). Full size image(1.9 MB) What is your diagnosis? Membranoproliferative glomerulonephritis (19) Dense deposit disease (4) Membranous nephropathy (3) Acute post-infectious glomerulonephritis (136) Lupus nephritis, class IV (7) Total Votes (169) Figure 1 Light microscopy shows global endocapillary hypercellularity. Full size image(1.1 MB) Figure 2 Higher power shows numerous intracapillary neutrophils. Full size image(1008.9 KB) Figure 3 IF shows granular mesangial and capillary wall staining for C3. Full size image(393 KB) Figure 4 IF shows granular mesangial and capillary wall staining for IgG. Full size image(468.7 KB) Figure 5 EM shows "hump-like" subpithelial electron dense deposits and a few subendothelial deposits. Full size image(1.9 MB) PATHOLOGIC DIAGNOSIS Acute post-infectious glomerulonephritis. DISCUSSION ]]>Acute post-infectious glomerulonephritis (APIGN) is an immune complex-mediated glomerular disease which classically follows group A streptococcal infection of the upper respiratory tract or skin in children, but may also occur after other bacterial infections, in both children and adults. Childhood APIGN typically presents with nephritic syndrome, hypocomplementemia and elevated anti-streptolysin O (ASO) titer, and generally has a good prognosis. The clinical spectrum and prognosis in adults are more variable, reflecting the frequency of co-morbid conditions that predispose to infection, such as alcoholism, diabetes, and intravenous drug abuse(1-4).The incidence of childhood APIGN has steadily declined in the United States and in Europe over the last several decades, but it remains high in tropical countries. This decline has been attributed to a reduction in the nephritogenic potential of certain streptococcal strains, and improved host immunity. The attack rate of APIGN following streptococcal infection varies from 1-33%, depending on the site of infection and the bacterial strain. APIGN may also occur concomitantly with rheumatic fever, and with streptococcal pneumonia. In adults with APIGN, non-streptococcal and gram negative infections are more commonly identified (1, 3, 4). In a recent review of 86 cases from Columbia University Medical Center in New York, one-third of patients were older than 64 years, and approximately 38% had underlying risk factors for infection, including diabetes (21%), malignancy (5%), alcoholism (2%), AIDS (2%) and IVDU (1%)(3). Streptococcal and staphylococcal infections were equally prevalent (28% and 24%), and most common sites of infection were upper respiratory tract (23%), skin (17%), lung (17%) and heart valves (12%). Most biopsies (72%) showed a diffuse proliferative pattern, with focal endocapillary proliferation and mesangial proliferation seen in the remaining cases. Cellular crescents were present in a minority of cases, and only affected >50% of glomeruli in 4% of cases. Outcomes were poor in the 11 cases with coexistent diabetic glomerulosclerosis, with persistent renal dysfunction in 2 and progression to ESRD in the remaining 9 patients. In the non-diabetic patients with APIGN, 56% had complete remission, 27% had persistent renal dysfunction and 17% developed ESRD(3). ]]>1. Montseny JJ, Meyrier A, Kleinknecht D, Callard P. The current spectrum of infectious glomerulonephritis. Experience with 76 patients and review of the literature. Medicine (Baltimore) 1995;74:63-73. 2. Moroni G, Pozzi C, Quaglini S, Segagni S, Banfi G, Baroli A, Picardi L, Colzani S, Simonini P, Mihatsch MJ, Ponticelli C. Long-term prognosis of diffuse proliferative glomerulonephritis associated with infection in adults. Nephrol Dial Transplant 2002;17:1204-1211.3. Nasr SH, Markowitz GS, Stokes MB, Said SM, Valeri AM, D'Agati VD. Acute postinfectious glomerulonephritis in the modern era: experience with 86 adults and review of the literature. Medicine (Baltimore) 2008;87:21-32.4. Wen YK. The spectrum of adult postinfectious glomerulonephritis in the new millennium. Ren Fail 2009;31:676-682 |
