RESUMO
Renal failure is a rare complication associated with the use of rifampin. Intravascular hemolysis leading to acute renal failure following rifampin therapy is extremely rare. Two patients with leprosy who developed hemolysis and acute renal failure following rifampin are reported.
Assuntos
Injúria Renal Aguda/induzido quimicamente , Anemia Hemolítica/induzido quimicamente , Hemólise , Hanseníase/tratamento farmacológico , Rifampina/efeitos adversos , Adulto , Humanos , Hanseníase Dimorfa/tratamento farmacológico , Hanseníase Tuberculoide/tratamento farmacológico , Masculino , Rifampina/uso terapêuticoAssuntos
Nefropatias/epidemiologia , Clima Tropical , Amiloidose/epidemiologia , Anemia Falciforme/epidemiologia , Filariose/epidemiologia , Glomerulonefrite por IGA/epidemiologia , Glomerulonefrite Membranosa/epidemiologia , Hepatite B/epidemiologia , Humanos , Hanseníase/epidemiologia , Nefrite Lúpica/epidemiologia , Malária/epidemiologia , Nefrose Lipoide/epidemiologia , Prevalência , Esquistossomose Urinária/epidemiologia , Esquistossomose mansoni/epidemiologiaRESUMO
Sixty consecutive patients with leprosy were investigated for renal involvement. Clinically overt renal disease was present in 4 patients; 3 presented with a nephrotic state and one patient with progressive renal failure. Urinalysis showed daily protein loss ranging from 0.4 to 8.9 g in 8 patients and microscopic haematuria in 4 cases. Elevated levels of blood urea and creatinine were seen only in one patient with diffuse proliferative glomerulonephritis. Of the 36 patients in whom distal tubular functions were evaluated, concentration and/or acidification defects were detected in 9 patients (25%). Renal histology revealed no abnormality in any of these patients. Serum C3 levels were decreased in 5 patients with lepromatous leprosy and 3 patients with borderline leprosy. Histological evidence of renal involvement was detected in 9 patients (15%). Amyloid deposits were seen in 3 (5%) patients of whom 2 had lepromatous leprosy and one had tuberculoid leprosy with chronic trophic ulcers. Mesangial proliferative lesions were seen in 5 (8.3%) and diffuse proliferative lesions (with crescents in more than 70% of glomeruli) in one patient. All of them had lepromatous leprosy. Three of the 5 patients with mesangial proliferative glomerulonephritis had erythema nodosum leprosum at the time of biopsy. Immunofluorescence studies revealed granular deposits of IgA, IgM and C3 in one patient with mesangial proliferation and IgA/IgM with or without C3 in 3 more patients in whom renal histology was normal. Glomerulonephritis associated with leprosy appears to be immune mediated but confirmation requires identification of lepra antigen in the glomerular immune complex deposits.
Assuntos
Nefropatias/etiologia , Hanseníase/complicações , Adolescente , Adulto , Amiloidose/etiologia , Eritema Nodoso , Feminino , Glomerulonefrite/etiologia , Humanos , Túbulos Renais , Masculino , Pessoa de Meia-IdadeRESUMO
Two hundred and thirty-three patients with renal amyloidosis were studied in an attempt to identify the incidence and pattern of the disease in northern India. The incidence of amyloidosis was 1.01% of 6431 post-mortems and 8.4% of 1980 renal biopsies from patients who presented with clinical evidence of glomerular disease. Two hundred and three patients (87.1%) had secondary amyloidosis, 22 (9.4%) had primary amyloid and 8 patients (3.5%) had amyloidosis associated with multiple myeloma. Tuberculosis of various organs was the commonest predisposing disease accounting for 59.1% of secondary amyloidosis, followed by chronic suppurative lung disease in 24.1%. Rheumatoid arthritis, chronic osteomyelitis and lepromatous leprosy were seen in a small percentage of patients (2 to 8%). Proteinuria of varying degree was present in all the 233 patients and 12.9% of them had a daily protein excretion of more than 10 g. Post-mortem examination of 65 patients with renal amyloidosis showed that 75.3% also had amyloid deposit in the spleen, 63% in the liver, and 50.8% in the adrenals. Clinical evidence of disappearance of proteinuria was observed in 3 patients with secondary amyloidosis; in 2 of them, the regression of amyloidosis was confirmed by serial renal biopsy performed 3 and 5 years after the initial diagnosis.