Urine activity of cathepsin B, collagenase and urine excretion of TGF-beta(1) and fibronectin in membranous glomerulonephritis

In 30% of cases nephrotic syndrome is caused by membranous glomerulonephrit is (MG). Protein accumulation in glomeruli leads to progressive loss of kid ney function and damage of structure in MG, The role of tissue proteolytic systems and growth factors in this process is not known. The purpose of the study was to estimate urine cathepsin B, collagenase activity and urine ex cretion of TGF-beta(1) and fibronectin in MG, Cathepsin B activity was grea ter in the urine of MG patients than in the control group (10.58+/-8.73 pmo l AMC/mg creatinine per min(-1) vs control 7.11+/-2.05 pmol AMC/mg creatini ne per min(-1); P<0.05). Urine collagenase activity was higher in the group of patients than in the control group (8.59+/-4.26 pmol AMC/mg creatinine per min(-1) vs control 3.84+/-2.09 pmol AMC/mg creatinine per min(-1) P < 0 .02). Urine excretion of fibronectin (45.60 ng/mg creatinine vs control 10. 30 ng/mg creatinine P < 0.04) and TGF-beta(1) levels in the urine were high er than in controls (283.55+/-248.13 pg/ml vs 36.11+/-48.01 pg/ml; P < 0.01 ). Results suggest glomerular overproduction of TGF-beta(1) and urinary lea k of proteolytic enzymes (PE). This may result in decreased glomerular PE a ctivity in MG and, with time, may lead to protein accumulation in renal glo meruli and to progressive loss of kidney function and damage of structures as the course of MG progresses. PE urine composition as well as ECM protein and cytokine urine excretion may alow noninvasive glomerulopathy course mo nitoring in humans in the future.