Albumin-Induced Primary Disorders in Nephrotic Syndrome: Experimental and Clinical Data

Abstract

Increased albumin concentration in primary urine leads to apoptosis and fbrosis of podocytes and tubule cells and is a main cause of functional deterioration in chronic kidney disease. Here we show that excessive albumin uptake into rat primary renal cells causes an almost immediate mitochondrial accumulation of the apoptotic factor Bax. We show that nephrotic patients reveal a high level of marker of cellular hypoxia HIF-1αand its dependence on the level of kidney function impairment and proteinuria. The progression of the sclerosis as a sign of irreversible kidney damage is accompanied by gradual increase in expression of proapoptotic factor Bax. We conclude that albumin-induced disorders in nephrotic children are presented by disturbances in apoptosis controlling system and accompanied by cellular hypoxia.