In type and distribution the renal changes that follow dietary exposure to diphenylamine (DPA) in rats resemble those seen in human polycystic and medullary cystic kidney disease: local tubular dilation and cyst formation occurring in the absence of demonstrable tubular occlusion. The pathogenesis of such changes remains unexplained. Using a servo nulling pressure recording device and routine micropuncture techniques to examine the DPA exposed rat kidney, the authors documented higher pressure (52.1 vs 29.7 cm H2O; p<0.05) (Mann Whitney U test) but similar glomerular filtration rates (NGFRs) (48.4 vs 50.6 nliter/min; p>0.80) and tubular fluid to plasma inulin ratios (TF/Pin) (3.73 vs 3.42; p>0.60) in dilated vs nondilated nephrons in the same DPA exposed kidneys. NGFRs do not correlate with initial or mean collection pressures, nor with the degree of pressure change monitored during TH collections. In relation to % proximal tubular length, TF/Pin are the same in DPA exposed and normal control kidneys. These observations are interpreted as showing that higher pressures occur as a consequence of increased resistance to flow, not of increased fluid entry into or decreased fluid removal from dilated nephrons. Microscopical examination of latex injected dilated nephrons confirm segments of apparent focal narrowing, sites of potential increased resistance to flow. It is concluded that increased intralumenal pressure, a consequence of increased intrarenal resistance to flow, plays a significant role in the pathogenesis of some forms of mammalian cystic kidney disease.
|Original language||English (US)|
|State||Published - Jan 1 1975|
ASJC Scopus subject areas