Showing papers on "Obstructive Nephropathy published in 1988"

Pathophysiology of obstructive nephropathy

Abstract: Obstruction of the urinary tract is a common and often reversible cause of renal failure. Partial chronic obstruction of the urinary tract may lead to progressive atrophy and destruction of nephrons resulting in chronic renal failure; in contrast complete obstruction occurring suddenly may result in the development of acute renal failure. The mechanisms by which obstructive diseases affect renal function are incompletely understood. Much information has been obtained using animals models of obstruction, ranging from studies using whole animal to those using single nephrons. In this review, the effect of either unilateral or bilateral obstruction on renal blood flow, glomerular filtration rate and tubular function is presented. The possible involvement of angiotensin II, thromboxan A2, macrophage-derived products and platelet-activating factor in the pathophysiology of obstruction is discussed.

[Obstructive nephropathy; kidney function and renal excretion of prostaglandin (E)2 and Thromboxane B(2) following percutaneous decompression nephropyelostomy].

Abstract: In patients with chronic urinary obstruction the excretion of prostaglandin E(2) (PGE2) and thromboxane B(2) (TXB2) was measured. During obstruction signs of an increased vasoconstrictor (TXB2)- and a decreased vasodilator (PGE2) activity were found. After percutaneous nephropyelostomy a reverse pattern with decrease of the initially high (TXB2) excretion and increase of the PGE(2)excretion was observed. It is suggested that these changes of the arachidonic acid metabolism previously found in animals also take part in the pathophysiological changes in humans after relief of urinary obstruction having significant effect of renal blood flow, glomerular filtration rate and tubular function in obstructive nephropathy in humans.