Tuberculosis-Associated Collapsing Glomerulopathy: Remission after Treatment

Nephrology Division of University of São Paulo School of Medicine, São Paulo, Brazil.
Renal Failure (Impact Factor: 0.94). 02/2010; 32(1):143-6. DOI: 10.3109/08860220903368567
Source: PubMed


Collapsing glomerulopathy (CG) is a severe form of nephrotic syndrome and has been mostly associated with human immunodeficiency virus (HIV) infection. Treatment response is poor, and the disease frequently leads to end-stage renal disease. More recently, CG has been described in association with other conditions, such as drug exposure and other infections, but renal prognosis remains unfavorable. This paper reports an interesting case of an HIV-negative patient with tuberculosis-related CG who needed dialysis for five months but presented full renal recovery after tuberculosis (TB) treatment and corticotherapy.

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    ABSTRACT: BACKGROUND: Collapsing glomerulopathy (CG) is a glomerulonephritis seen in association with human immunodeficiency virus (HIV) infection, known as HIV-associated nephropathy (HIVAN), and less frequently observed in non-HIV-infected patients. Method. The aim of this study was to review the histological and clinical findings of all CG diagnosed since 1981 in our laboratory. Result. Since 1981, 18 kidney biopsies with collapsing features were diagnosed among 6130 biopsies performed: 72.2% (n = 13) males, mean age 33.8 ± 9.7 years, 61.1% (n = 11) of black ethnic origin. HIV infection was present in 10 patients. Mean serum creatinine (Scr) was 4.7 ± 2.5 mg/dL, and mean proteinuria was 6.1 ± 5 g/24 h. Both HIVAN and non-HIVAN patients were similar in terms of age, gender and dialysis requirement. In the HIVAN population, African origin was predominant and more frequent than in the non-HIVAN population, Scr was higher and proteinuria was less severe. Interstitial infiltrate, interstitial fibrosis and tubular atrophy were severe, and the presence of microcystic dilatation of renal tubules was more common. Immunofluorescence was positive in six patients. In the non-HIVAN population, this histological lesion was related to an infectious illness in 6/8 patients and to the use of illegal oral drugs in one patient. Interstitial infiltrate, interstitial fibrosis and tubular atrophy presented as moderate to severe, and tubular atrophy correlated with dialysis requirement. Mesangial proliferation was present in 3/8 patients, with C3 and IgA deposits. CONCLUSION: CG is a rare podocytopathy. In this study, the association between infection and CG is evident, and we may suggest that infections could, in a direct or indirect manner, be a trigger of podocyte injury.
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    ABSTRACT: Collapsing glomerulopathy is a rare form of glomerular injury, characterized by segmental or global collapse of the glomerular capillaries, wrinkling and retraction of the glomerular basement membrane, and marked hypertrophy and hyperplasia of podocytes. Prognosis is usually poor, with most cases developing end-stage renal disease, in spite of treatment. The association of collapsing glomerulopathy and systemic lupus erythematosus is very unusual. In this report, we describe the first case of a simultaneous diagnosis of collapsing glomerulopathy and diffuse proliferative lupus nephritis. The case presented with acute kidney injury and nephrotic syndrome and evolved with partial remission of nephrotic syndrome and recovery of renal function after aggressive treatment with intravenous cyclophosphamide and methylprednisolone.
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