Schistosomal glomerulonephritis: is it more prevalent in hepatosplenic patients when cor pulmonale is present?

S. mansoni infection can produce damage in several organs, in some due to immunological altera­ tions such as the development of glomerulopathy2 and in others, at least in great part, due to vascular obstruction related to egg deposition, such as chronic cor pulmonale 1. Both situations are essentially obser­ ved in patients with the hepatosplenic form of the parasitic infection. There are reports in the literature suggesting that a chronic increase in renal vein pressure may favour the development of glomerulopathy and/or nephrotic syndrome, such as has been described in chronic congestive pericarditis, renal vein thrombosis or chronic congestive heart failure3 4 5. Even though the increase in renal vein pressure may not be a cause of glomerulopathy, there is some agreement that it could exacerbate a previously exis­ tent proteinuria3. In chronic cor pulmonale due to S. mansoni infection, besides the immunological alte­ rations related to the parasitic infection, there is frequently heart failure, with severe systemic conges­ tion. It would be logical to assume, then, that patients with hepatosplenic schistosomiasis and cor pulmonale should have more frequent (or, perhaps more intense) glomerulopathy or proteinuria than similar patients without cor pulmonale. To investigate this question, a total of 20 (twenty) patients with hepatosplenic schis­ tosomiasis and cor pulmonale (Group I) were compa­ red with 20 others with schistosomal hepatospleno­ megaly without cor pulmonale (Grupo II), matched ac­ cording to ager and sex. All cases had been autopsied at the University Hospital of Federal University of Bahia. Schistosomal cor pulmonale was defined as hypertrophy of the right ventricle (> 0 .5 cm thickness), with a normal left ventricle, pulmonary arteritis with multiple granulomas around eggs of the parasite, and systemic venous congestion. In each group, 10 (ten) patients were male and 10 (ten) female with an average of 15.3 ± 14.2 years for Group I and 26.5 ± 14.3 for Group II. There was no significant difference in the occurrence of arterial hypertension, microscopic hematuria nor the nephrotic syndrome (Table 1).