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 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 m g/kg/day) and methylprednisolone 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 m g/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...

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Because glomerular diseases have an unforeseeable course during pregnancy, appropriate counseling is al ways compromised. Opposed evidence has been re ported without firm conclusions, and some risk factors are only considered as reference, e.g. serum creatinine (sCr) higher than 2 mg/dl, especially in the presence of severe hypertension.We report of a young female known to have membran oproliferative glomerulonephritis (MPGN) with stable renal function, controlled arterial pressure and moderate proteinuria, who developed a renal thrombotic microan giopathy in the later part of her second pregnancy. Case ReportA 24-year-old female, who had never taken oral contraceptives, presented at the age of 13 years with microscopic hematuria but no nephrotic proteinuria. She had normal renal function (sCr 0.6 mg/ dl) and blood pressure was 110/70 mm Hg. A percutaneous renal biopsy was performed 3 months later due to persistent urinalysis disorders. It contained 23 glomeruli, all of which were impaired, with lobulation of the tufts and marked mesangial hypercellulariiy. The capillary walls were thickened to a variable degree, and doublecontoured basement membranes were present. With Masson trich rome. deposits on the subendothelial side of the basement mem brane were observed. There were no sclerosis, crescents, nor intersti tial or vascular damage. An immunofluorescence technique was not performed. In short, it was a membranoproliferative glomerulo nephritis type 1, with subendothelial deposits.After treatment with steroids, her condition remained stable with 24-hour proteinuria 1.4 g. Seric C3 and C4 levels were normal and ANA and anti-ds-DNA antibodies negative. In 1982, she had her first pregnancy and the course as well as the delivery in February 1983 were normal without detrimental effects on nephropathy. Des pite an intrauterine device that was fitted in August 1983, she became pregnant in September. 2Vi months later, she developed high blood pressure (160/100 mm Hg) and proteinuria increased to 3 g/day without edema, but renal function was normal. Oral methyldopa I g/day was initiated. At 30 weeks of pregnancy, hematocrit was 36%, sCr 1.0 m g/dl and arterial pressure 160/105 mm Hg; hydralazine and propanolol were associated. 2 weeks later she was admitted to hospital for worsening of renal function (sCr 2.2 mg/dl), hematocrit (30%) and severe hypertension (170/120 mm Hg). The next week (33nd), sCr was 3.1 mg/dl, hematocrit 26%, and hyperten sion persisted with fundi examination grade III (K-W). A cesarean section was undertaken at this point and a premature, viable female infant of low weight (1,530 g) was born. A tubal ligature was also performed. In the postoperative course, diazoxide was prescribed and an increase of anemia (Hb 8.1 g/dl, hematocrit 23%) was observed. Signs of hemolytic activity were present: absent hapto globin level, reticulocyte count 109 x 109/l (40%o) and schistocytes 6-10%. White cell count (10 x I0V1), platelet count (138 x I0V1) and coagulation factors were normal, with plasma fibrin degrad...