Rapidly Progressive Glomerulonephritis and Pulmonary Tuberculosis

Abstract

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...

A rare case of coexistence of Wegener’s granulomatosis and pulmonary tuberculosis with subsequent development of thrombosis of the cerebral veins

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Coexistence of Pulmonary Thromboembolism, Pulmonary Tuberculosis and Granulomatosis with Polyangiitis

“…Moreover, combined treatments for both vasculitis and TB shows positive patient response, according to published case reports. 9,10 Authors' Contribution STP and AK conceptualized the work. AK, KK and AG managed the patient.…”

Caso clínico en el Hospital Nacional Arzobispo Loayza.

“…Se ha descrito diferentes tipos de glomerulonefritis asociadas a TBC (8)(9)(10)(11)(12)(13)(14)(15); en los que la expresión clínica ha sido proteinuria, síndrome nefrótico o insuficiencia renal. En estos casos se ha propuesto que el daño glomerular es producido por un mecanismo inmunológico iniciado por la TBC, sin embargo no se ha podido demostrar ningún antígeno tuberculoso a nivel del glomérulo.…”