Glomerulonephritis (GN)is the most frequent acquired progressive nephropathy of child age.The rate of progression up to renal insufficiency depends in addition to the intensity of immune mechanisms also on genetic and metabolic factors.The authors examined in children with chronic GN TH1/TH2 cytokines,renal excretion MCP-1,TGF-beta and PDGF.With the level of creatinaemia TH1 cytokines correlated (p <0.05);MCP-1 (p < 0.05)and TGF-beta (p <0.05)which supports the pathogenetic importance of these cytokines in the development of GN progression.In severe forms of GN they found a significantly higher incidence of apoptic cells (p <0.01). As to genetic markers they investigated the polymorphism of the ACE gene and ATR1 gene in 75 children.CC and/or CA genotype AT1R was found more frequently (54.05%,p =0.02)in children with impaired renal functions and represented a threefold risk of progression (OR =2.88,CI =1.03 -8.09). Among selected metabolic indicators they examined homocysteine in serum and advanced glycation end-pro- ducts (AGEs)which may hasten sclerosis of the glomerular and tubular cells.In children with impaired renal functions they found hyperhomocysteinaemia (p <0.01).AGEs correlated directly with serum creatinine (r =0.898, p <0.001). The assembled results support the complexity of the pathogenesis of progressive GN.In the first stage a dominant part is played by immune mechanisms,independently on them genetic factors are involved and during progression of the disease to renal insufficiency metabolic factors come to the foreground.

        Key words: glomerulonephritis in children,immune mechanisms,genetic and metabolic factors