ABSTRACT
This study was carried out on 12 patients with essential hypertension without micro or macroalbuminuria [group I] and 15 patients with chronic glomerulonephritis with mean 24-hour urinary protein = 4.3 + 3.l g/24 hours, [group II], 7 patients had hypertension [group IIa] and 8 patients had normal blood pressure [group IIb]. Ten healthy subjects were taken as controls. Blood urea, serum creatinine, fasting and 2-hour postprandial plasma glucose, urine analysis, 24-hour urinary protein and serum TGF-beta 1 were measured in diseased groups and controls. TGF-beta 1 was significantly higher in group I with essential hypertension [mean +/- SD 80.4 +/- 18.2 ng/dl] and group II with glomerulonephritis. [387.2 +/- 89.0 ng/dl], compared to control group [36.3 +/- 12.9 ng/dl]. In group II, patients with glomerulonephritis mean serum TGF-beta 1 was significantly higher than group I patients with essential hypertension [p <0.001]. In group II, TGF-beta 1 was not significantly different in hypertensive [group IIa] or normotensive patients [group IIb] [mean serum TGF-beta l = 393.3 +/- 92.0 and 379.0 +/- 84.l ng/dl, respectively]. Patients with glomerulonephritis received the angiotensin converting enzyme inhibitor ACE-I [captopril 25-75 mg/day] for four weeks then blood urea, serum creatinine, 24-hour urinary protein and serum TGF-beta 1 were re-estimated. There was significant reduction in both 24-hour urinary protein and TGF-beta 1 after captopril with no significant changes in urea and creatinine. It might be concluded that serum TGF-beta 1is elevated in patients with essential hypertension and glomerulonephritis. In patients with glomerulonephritis the use of ACE-I may reduce proteinuria and serum TGF-beta 1. Reduction of TGF-beta 1 might be a possible mechanism in the reduction of proteinuria in patients with glomerulonephritis, however, other mechanisms cannot be ruled out