Exaggerated fractional sodium excretion in hypertension with advanced renal disease: the role of renal prostaglandin and kallikrein.
1. The role of renal prostaglandin E (PGE) and kallikrein in the mechanism of the exaggerated fractional sodium excretion in hypertensive patients with advanced renal disease was investigated. 2. Urinary excretion of PGE and kallikrein was significantly decreased in patients with sustained hypertension. 3. Four times higher values for fractional sodium excretion and four or five times higher values for the urinary excretion of PGE corrected for creatinine clearance were found in patients with sustained hypertension. There was a significant positive correlation (r = 0.677) between the two, suggesting that PGE in the renal tubular compartment may be involved in the mechanism of the exaggerated fractional Na excretion in patients with advanced renal disease. 4. The urinary excretion rate of kallikrein corrected for creatinine clearance was three times greater in patients with borderline hypertension, but not significantly increased in those with sustained hypertension, compared with that in healthy volunteers.
D000328:Adult; D005260:Female; D005921:Glomerulonephritis / Q000652:urine; D006801:Humans; D006977:Hypertension, Renal / Q000652:urine*; D007610:Kallikreins / Q000652:urine*; D007668:Kidney / Q000503:physiopathology; D008297:Male; D011458:Prostaglandins E / Q000652:urine*; D012964:Sodium / Q000652:urine*
D011458:Prostaglandins E; D012964:Sodium; D007610:Kallikreins