Aminopeptidase A (= angiotensinase A) in human progressive renal disease

To elucidate factors possibly involved in adaptive cell responses due to progressive deterioration of glomerular structure and function, the activity of angiotensinase A (ATA), a glycoprotein of the glomerular tuft and of the proximal tubule, was analyzed on human kidney sections applying quantitative image analysis. Based on the software the exclusive glomerular expression of ATA was assessed in normal controls and 34 kidneys of patients with various stages of renal insufficiency (1.3-12 mg/dl serum creatinine). The data from diseased kidneys revealed a reduced total ATA-positive glomerular compartment, a larger area of remaining glomeruli, and a rise of the ATA-negative renal interstitium. Irrespective of the progression of the disease, hypertrophic glomeruli of remnant nephrons exhibited a high and homogeneous expression of ATA. Survival of glomeruli in patients with chronic renal failure correlated with the capability of glomerular cells to synthesize ATA at an increased rate, which may prevent angiotensin II-mediated growth effects, the accumulation of extracellular matrix proteins, etc., thus escaping final glomerulosclerosis.