GLOMERULONEPHRITIS DUE TO IMMUNE-COMPLEXE S ASSOCIATED WITH PULMONARYTUBERCULOSIS

A 32 year old man was admitted for dyspnea, hemoptysis, macroscopic he maturia, hypertension (140/100), peripheral edema and hemodynamic deco mpensation. Lung Xrays revealed pulmonary edema and a cavity in the le ft apex. Laboratory determinations revealed an altered renal function with increased creatinine and urea levels and nephrotic syndrome. Ther e was leucocyturia, hematuria and cylindruria. The sputum showed a lar ge number of acid-fast bacilli. The patient began anti-tuberculosis tr eatment with three drugs (isoniacid, rifampicin, pirazinamide). On ult rasonography, both kidneys revealed ecogenic lesions with size, shape and cortico-medular relationship preserved. The patient persisted with altered renal function, steady levels of urea nitrogen, creatinine an d potassium, preserved diuresis and hypertension. Bidimensional echoca rdiogram: LVDD 55 mm, hypoquinetic septum, pericardic effusion, thicke ned pericardium, pleural effusion, shortening fraction decreased. He r eceived treatment for this congestive cardiac failure and hypertension with enalapril, nifedipine and fursemide. A percutaneous renal biopsy was performed with anatomopathologic diagnosis of diffuse encocapilla r proliferative glomerulonephritis with crescents (15%) and total glom erular sclerosis (33%). Immunofluorescence: positive, immune-complexes with IgM and C3. The patient gradually recovered his normal renal fun ction, improved his pleural effusions and normalized his cardiac funct ion. He was discharged in good clinical condition on the 69th day of a nti-tuberculosis treatment. An association between pulmonary tuberculo sis and glomerulonephritis is discussed. It is proposed that renal les ions might be the consequence of the tuberculosis due to the sedimenta tion of circulating immune-complexes.