The influence of increased tubular hydrostatic pressure on renal function.
The effect of tubular obstruction on renal function has been understood poorly at the tubular level and from the clinical standpoint. In our review the evidence for a direct influence of hydrostatic pressure on tubular transport and glomerular filtration is examined. The data generated to date indicate a direct influence of hydrostatic pressure on tubular transport only at the level of the distal convoluted tubule and collecting duct. With respect to glomerular filtration increased tubular pressure reduces the net driving force for filtration and reduces glomerular filtration rate in the absence of a compensatory increase in glomerular hydrostatic pressure. We next review physiological data concerning the mechanism of post-obstructive diuresis. Available information suggests 4 factors that play a significant role in the clinical syndrome of post-obstructive diuresis: 1) medullo-papillary washout, 2) decreased fractional and absolute salt and water reabsorption in the collecting duct, presumably secondary to direct influence of hydrostatic pressure on transport mechanisms, 3) osmotic diuresis secondary to retention of urea and other osmotic solutes during the period of obstruction and 4) prior salt and water administration in the absence of excretion, resulting in extracellular fluid volume expansion.
D004231:Diuresis; D005919:Glomerular Filtration Rate; D006801:Humans; D006874:Hydrostatic Pressure; D007668:Kidney / Q000502:physiology*; D007674:Kidney Diseases / Q000503:physiopathology; D007684:Kidney Tubules / Q000502:physiology*; D007686:Kidney Tubules, Distal / Q000502:physiology*; D008954:Models, Biological; D009995:Osmosis; D011312:Pressure; D012964:Sodium / Q000378:metabolism; D014508:Urea / Q000378:metabolism
D014508:Urea; D012964:Sodium