Nephron heterogeneity in ischemic acute renal failure

Nephron heterogeneity in ischemic acute renal failure. To uncover the reasons for reported internephron heterogeneity in acute renal failure (ARF) serial micropuncture experiments in norepinephrine-induced ARF and sham-infused control rats were carried out to investigate this phenomenon. Proximal tubular pressures (P T ) were scattered at 24, 48, and 72 hr in ARF rats ranging from 4 to 42 mm Hg, but the majority were greater than the mean control values (10 ± 1 mm Hg). One week ARF P T were less variable than on previous days (5 to 17 mm Hg). The decreased variability was the result of a reduced number of P T values that were greater than controls. When single nephron filtration rates (SNGFR) were measured with spontaneous flow collections without maintaining the existent tubular pressures, results were widely scattered on each day. When SNGFR were measured at the existent P T , individual determinations were tightly clustered on each experimental day, clearly different from controls (all P T ranging below as well as above controls, suggested that a mechanism in addition to tubular obstruction was operative in reducing SNGFR. Recoveries of microperfused 14 C-inulin were similar to controls excluding significant backleak of tubular fluid. Glomerular filtration capacity (GFC) determined by performing tubular fluid collections at measured reductions in pressure (P D ) from stop-flow varied as a function of the initial P T indicating that obstruction was the dominant pathogenetic factor in nephrons with the highest P T values, while glomerular dysfunction was the major pathogenetic mechanism in nephrons with the lowest P T values. Intermediate P T and GFC values represented nephrons with both tubular obstruction and glomerular dysfunction operating to reduce SNGFR. Heterogeneite nephronique au cours de l'insuffisance renale aigue ischemique. Decouvrir les raisons de l'heterogeneite inter-nephronique rapportee au cours de l'insuffisance renale aigue (ARF) des experiences de microponctions repetees chez des rats en ARF induite par l'adrenaline et des controles ayant recu un simulacre de perfusion ont ete enterprises pour etudier ce phenomene. Les pressions tubulaires proximales (P T ) etaient variables a 24, 48, et 72 hr chez les rats en ARF, comprises entre 4 et 42 mm Hg, mais la majorite etait plus elevee que la moyenne des valeurs controles (10 ± 1 mm Hg). ARF P T a une semaine etait moins variable que les jours preceedents (5 a 17 mm Hg). Cette diminution de variabilite etait due a une reduction du nombre des valeurs de P T qui etaient plus elevees que les controles. Lorsque les debits de filtration nephronique individuels (SNGFR) etaient mesures par des collections du flux spontane sans conserver les pressions tubulaires existantes, les resultats etaient tres variables chaque jour. Lorsque SNGFR etait mesure aux P T existantes, les determinations individuelles etaient tres serrees pour chaque jour experimental, nettement differentes des controles (tous les P T situees au-dessous comme au-dessus des controles suggeraient qu'un mechanisme de plus que l'obstruction tubulaire contribuait a reduire SNGFR. Les recuperations de 14 C-inuline microperfusee etaient identiques aux controles, excluant une fuite retrograde de liquide tubulaire. La capacite de filtration glomerulaire (GFC) determinee en collectant du liquide tubulaire pour des reductions mesurees de la pression (P D ) a partir de l'interruption de flux variait en fonction de P T initiale indiquant que l'obstruction etait le facteur pathogenique dominant dans les nephrons dont les valeurs de P T etaient les plus hautes, alors que le dysfonctionnement glomerulaire etait le facteur pathogenique principal dans les nephrons aux plus faibles valeurs de P T . Les valeurs intermediaires de P T et de GFC correspondaient a des nephrons dans lesquels l'obstruction tubulaire et le dysfonctionnement glomerulaire contribuaient ensemble a reduire SNGFR.