A retrospective analysis of clinicopathology and plasma complement activation in C3 glomerulonephritis / 中华肾脏病杂志

ABSTRACT

Objective To study the clinicopathological features of C3 glomerulonephritis and the associations between plasma complement fragments level and clinical manifestations.Methods The clinical and pathological data of the 12 patients with C3 glomerulonephritis in our division from January 1999 to June 2010 were analyzed retrospectively.Concentrations of plasma factor B,Ba,C3,C3a,C4a and C5a were detected by commercial available sandwich ELISA kits on the day of renal biopsy.Results Ten of the 12 patients were C3 glomerulonephritis without MPGN,and the rest 2 were C3 glomerulonephritis with MPGN.All the patients presented proteinuria.Two of the 10 C3 glomerulonephritis patients without MPGN presented nephrotic range proteinuria,6 with microhematuria,1 with gross hematuria,and 2 with renal insufficiency.One of the 2 C3 glomerulonephritis patients with MPGN presented nephrotic range proteinuria,accompanied by microhematuria,hypertension and renal insufficiency.The other patient showed moderate proteinuria with normal renal function.Most of C3 glomerulonephritis patients without MPGN showed mild mesangial proliferative glomerulonephritis,and 4/10 patients had various degree cresentic formation.One C3 glomerulonephritis patient with MPGN had 47.1％ cresentic formation.The concentration of plasma C3 in C3 glomerulonephritis patients was normal,while the plasma factor B was significantly decreased,and the concentrations of plasma Ba,C3a,C4a and C5a were significantly elevated.The concentration of plasma Ba was positively correlated with the proteinuria level,while the concentrations of plasma C3a,C4a and C5a were not correlated with the levels of proteinuria or plasma creatinine.Conclusions Majority of these 12 patients were C3 glomerulonephritis without MPGN,manifests as nephritic syndrome clinically and mild mesangial proliferative glomerulonephritis histopathologically.Complement activation via alternative pathway may play an important role in the pathogenesis of C3 glomerulonephritis.