The clinicopathology and outcome of post-infectious glomerulonephritis: experience in 36 adults.

Post-infectious glomerulonephritis is one of the most common causes of acute glomerulonephritis. A retrospective study of post-infectious glomerulonephritis at King Chulalongkorn Memorial Hospital, Thailand was performed from January 1999 to December 2005. Among thirty six patients, eight cases were post-streptococcal glomerulonephritis and twenty eight cases were post non-streptococcal Glomerulo Nephritis (GN). Most cases present with edema, hypertension, gross hematuria and nephrotic-range proteinuria. C3 and CH50 commonly were low. Post-streptococcal glomerulonephritis had more aggressive pathology compared to the others. However the long term outcome was excellent. In the present study the authors found ESRD in only 14.3% (4 out of 28 cases) that reflects the excellent prognosis of post-infectious glomerulonephritis. Of interest, all of the ESRD patients were caused by post non-Streptococcal GN. Even though, no statistic was achieved; it might reflect the aggressiveness of non-Streptococcal pathogen.

The combination of thrombotic microangiopathy and nodular sclerosis in light chain deposition disease.

The authors reported the first case of nodular glomerulosclerosis, mesangiolysis, and thrombotic microangiopathy in a 69-year-old Thai man with chronic glomerulopathy from light chain deposition disease associated with multiple myeloma and kappa monoclonal gammopathy. He presented with subacute onset of generalized edema, hypertension, and renal insufficiency. Blood examinations revealed kappa monoclonal gammopathy. The diagnosis of multiple myeloma was confirmed by bone marrow aspiration and biopsy. The renal pathologies demonstrated specific findings for light chain deposition disease which were type II nodular glomerulosclerosis, strongly PAS-stained tubular basement membrane, monotypic-kappa light chain deposition along tubular and glomerular basement membranes, and granular electron dense deposits in electron microscopy. However the authors also found the concomitant findings of mesangial and endothelial injuries which were mesangiolysis and thrombotic microangiopathy. Of interest, type II nodular sclerosis and thrombotic microangiopathy were caused by the same cell injury. These might shed new light on the pathogenesis of glomerular injury in monoclonal immunoglobulin deposition disease (MIDD).