Nephron 1991;57:251-252 © 1991S. Karger AG. Basel 0028- 2766/91/0572 0251S2.75/0 Rapidly Progressive Glomerulonephritis and Pulmonary Tuberculosis Bernardo Sopeñaa, José SobradoA. Javier Pérez*. Josefina Oliverb, Miguel CoureP, Luisa Palomaresa. Luis González* 'Nephrology Section and ’’Pathology Service, Hospital Xeral Vigo, Vigo, Spain Dear Sir, Rapidly progressive glomerulonephritis accounts for 2-7% of renal biopsies. A number of etiologic factors have been incriminated, including drugs, malignancy, immune mechanism and viral and bacterial infections [1], So far, a possible relationship between tuberculosis and glomerulonephritis has been suggested in a small number of cases, whose authors postulated that renal lesions could be the consequence of immune complex deposi tion [2, 3], A 55-year-old man was initially hospitalizated for fever and productive cough. A chest radiograph showed bilateral localized consolidations. In sputum cultures no abnormal flora grew, and by the Ziehl-Neelsen tinction there was no evidence of acid-fast bacilli in the specimens processed. Lowenstein culture was simultaneously performed in the smears obtained by bronchial washings. A clinical partial radiological improvement was observed after therapy with broad spectrum antibiotics. The arterial pressure, renal function and urinalysis were normal. The patient was allowed to leave hospi tal and he was well for 3 weeks. After this period of time, he began to develop edema and progressive oliguria. After 2 more weeks, he was again admitted to hospital for edema and oliguria. The arterial pressure was 180/110 mm Hg: the serum creatinine was 1,594 mmol/1 (18 mg/dl), the serum total hemolytic complement 54 U 100/ml complement C3: 63 mg/dl were both reduced, and complement C4 was normal. Circulating immune complexes 1.8 pg/ml, measured by nephelometry, were slightly elevated (normal level up to 1.5 jig/ml). ANA, HBsAg and cryoglobulins were negative. Hemoglobin was 8.4 g/dl. Urinalysis showed microscopic hematuria and mild pro teinuria (0.7 g/day). Urine culture was sterile and there was no evidence of acid-fact bacilli in urine. On ultrasonography, the kid neys were of normal size and shape. At this phase of the evolution, the process of the Lowenstein culture in the specimens taken by bronchial washings 6 weeks before was ended with positive evi dence of acid-fast bacilli. An open renal biopsy revealed diffuse mesangial proliferation and the formation of crescents involving 40% of the glomeruli (fig. I). No vasculitis or interstitial abnormalities were present. Immunofluorescence was positive with complement C3 antisera in Fig. t. Glomerulus with epithelial crescent and mesangial proli feration. PAS. x40. a granular ditribution within the glomeruli. He was promptly treated with regular hemodialysis for a time period of 21 days. Ten days after the second admission, antituberculous treatment with rifampicin, INH and ethambutol was simultaneously initiated together with a combination of corticosteroids and cytotoxic agents, consisting of oral cyclophosphamide (1.5 mg/kg/day) and methyl- prednisolone given intravenously in three pulses (1 g/day) followed by oral prednisolone (1.5 mg/kg/day). Over an ll-day period we observed a progressive increase of diuresis with an initial improve ment of renal function, and dialysis was discontinued. The patient became normotensive. Over a 1-month period, serum creatinine was 443 mmol/l (5 mg/dl) and over a 6-month period it was 168 mmol/l (1.9 mg/dl). After this 6-month period the prednisone dose was 15 mg/day and the cyclophosphamide dose was 75 mg/day, and he was still receiving rifampicin and INH. At this time, serum comple ment and the level of circulating immune complexes were within the normal limits. During the 6-month follow-up period, there was no new evidence of acid-fast bacilli and therapy was well tolerated.