Mesangio-Capillary Glomerulonephritis and the Nephrotic Syndrome in the Course of Disseminated Tuberculosis

Prof. Alain Meyrier, Service de néphrologie et d’hémodialyse, Hôpital Avicenne, 125, route de Stalingrad, F-93009 Bobigny (France) Dear Sir, Murray et al. [1] reported in the July issue of this Journal a case of rapidly progressive glomerulonephritis in a patient with pulmonary tuberculosis treated with rifampicin. In the light of a recent personal case we wish to present an alternative physiophathology of glomerular disease associated with tuberculosis. Case Report A 46-year-old man was hospitalized for pitting edema and hypertension (230/120 mm Hg). His temperature was normal. Physical examination disclosed liver and spleen enlargement. His past history was unremarkable. Mantoux test was strongly positive. Laboratory investigations disclosed nephrotic syndrome: urinary protein output 8 g/24 h, serum albumin 2.4 g/dl and serum globulins 1.9 g/dl. He had microscopic hematuria (24,000 red cells/minute) and mild renal insufficiency (serum creatinine 120 μmol/l, creati-nine clearance 55 ml/min). The following tests were within normal limits: serum complement fractions, Waaler-Rose, circulating immune complexes (polyethylene-glycol) and antinuclear antibodies. Lung radiographs revealed a cavity in the upper right lobe, and acid-fast bacilli were present in the sputum. Liver biopsy disclosed epithelioid granulomas. Liver specimen culture was negative. Percutaneous renal biopsy showed mesangiocapillary glomerulonephritis, and immunofluorescence was positive with anti-IgG, IgM, Clq, C4 and C3 antisera. Hypertension was controlled with ß-block-ers and dihydralazine, nephrotic syndrome was symptomatically treated with indomethacin (3 mg/kg for 2 months, tapered to a stop by 6 months), and tuberculosis was treated with INH, rifampicin and myambutol. The lung lesion healed within 3 months. Proteinu-ria gradually subsided and disappeared after one year. After a 4-year follow-up, there was no proteinuria, no blood cells in the urine and renal function was unchanged. Persisting mild hypertension was controlled with ßblockers. On light microscopy, a control renal biopsy yielding 25 glomeruli showed 8 sclerotic glomeruli, disappearance of proliferation, persisting modification of basement membranes by focal thickening, double contours and a few spikes on the outer aspect, and some capsular adhesions. Immunofluorescence revealed mostly fixation of anti-IgM antiserum along some basement membranes but no significant staining by anti-IgG, anti-IgA, anti-C3, anti-Clq and antifibrinogen antisera.