Reduced renal blood flow in early cisplatin-induced acute renal failure in the rat

1985 ◽  
Vol 249 (4) ◽  
pp. F490-F496 ◽  
Author(s):  
J. A. Winston ◽  
R. Safirstein
Keyword(s):  
Renal Failure ◽  
Blood Flow ◽  
Acute Renal Failure ◽  
Renal Blood Flow ◽  
Plasma Flow ◽  
Volume Expansion ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Single Nephron ◽  
Renal Vascular

Studies were designed to determine the cause of the reduced glomerular filtration rate (GFR) in early cisplatin-induced acute renal failure. Rats were studied 72 h following a single intraperitoneal injection of cisplatin (5 mg/kg) or vehicle (0.9% NaCl). Whole kidney GFR and blood flow were lower in cisplatin-treated animals than in controls (0.30 +/- 0.06 vs. 1.17 +/- 0.06 ml X min-1 X g kidney wt-1 and 5.30 +/- 0.62 vs. 8.25 +/- 0.43 ml X min-1 X g kidney wt-1, respectively; P less than 0.001), as were superficial nephron GFR and stop-flow pressure (20.2 +/- 2.1 vs. 34.5 +/- 2.0 nl X min-1 X g kidney wt-1 and 29.0 +/- 1.9 vs. 39.8 +/- 1.3 mmHg, respectively; P less than 0.001). After volume expansion, renal plasma flow increased in control rats, whereas whole kidney and single nephron GFR did not change. In experimental animals, whole kidney filtration rate rose to 0.58 +/- 0.07 ml X min-1 X g kidney wt-1, single nephron filtration rate increased to 29.9 +/- 3.5 nl X min-1 X g kidney wt-1 (P less than 0.005), and renal plasma flow increased to 5.62 +/- 0.60 ml X min-1 X g kidney wt-1 (P less than 0.05). Intratubular hydrostatic pressure was not different in the two groups before or after volume expansion. The results of these studies show that the reduced GFR in early cisplatin-induced renal failure is due, in part, to reversible changes in renal blood flow and renal vascular resistance.

PAH extraction and estimation of plasma flow in human postischemic acute renal failure

1999 ◽  
Vol 277 (2) ◽  
pp. F312-F318 ◽  
Author(s):  
Geraldine Corrigan ◽  
Deepa Ramaswamy ◽  
Osun Kwon ◽  
F. Graham Sommer ◽  
Edward J. Alfrey ◽  
...  
Keyword(s):  
Renal Failure ◽  
Blood Flow ◽  
Acute Renal Failure ◽  
Renal Blood Flow ◽  
Plasma Flow ◽  
Renal Allograft ◽  
Renal Plasma Flow ◽  
Pah Clearance ◽  
Normal Controls

We determined the effect of postischemic injury to the human renal allograft on p-aminohippurate (PAH) extraction (EPAH) and renal blood flow. We evaluated renal function in 44 allograft recipients on two occasions: 1–3 h after reperfusion ( day 0) and again on postoperative day 7. On day 0 subsets underwent intraoperative determination of renal blood flow ( n = 35) by Doppler flow meter and EPAH( n = 25) by renal venous assay. Blood flow was also determined in another subset of 16 recipients on postoperative day 7 by phase contrast-cine-magnetic resonance imaging, and EPAH was computed from the simultaneous PAH clearance. Glomerular filtration rate (GFR) on day 7 was used to divide subjects into recovering ( n = 23) and sustained ( n = 21) acute renal failure (ARF) groups, respectively. Despite profound depression of GFR in the sustained ARF group, renal plasma flow was only slightly depressed, averaging 296 ± 162 ml ⋅ min−1 ⋅ 1.73 m−2 on day 0 and 202 ± 72 ml ⋅ min−1 ⋅ 1.73 m−2 on day 7, respectively. These values did not differ from corresponding values in the recovering ARF group: 252 ± 133 and 280 ± 109 ml ⋅ min−1 ⋅ 1.73 m−2, respectively. EPAH was profoundly depressed on day 0, averaging 18 ± 14 and 10 ± 7% in recovering and sustained ARF groups, respectively, vs. 86 ± 6% in normal controls ( P < 0.001). Corresponding values on day 7remained significantly depressed at 65 ± 20 and 11 ± 22%, respectively. We conclude that postischemic injury to the renal allograft results in profound impairment of EPAH that persists for at least 7 days, even after the onset of recovery. An ensuing reduction in urinary PAH clearance results in a gross underestimate of renal plasma flow, which is close to the normal range in the initiation, maintenance, and recovery stages of this injury.

Maintenance and recovery stages of postischemic acute renal failure in humans

2002 ◽  
Vol 282 (2) ◽  
pp. F271-F280 ◽  
Author(s):  
Deepa Ramaswamy ◽  
Geraldine Corrigan ◽  
Catherine Polhemus ◽  
Derek Boothroyd ◽  
John Scandling ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Control Group ◽  
Hydraulic Pressure ◽  
Structural Controls ◽  
Single Nephron

Postischemic injury in 38 recipients of 7-day-old cadaveric renal allografts was classified into sustained ( n = 15) or recovering ( n = 23) acute renal failure (ARF) according to the prevailing inulin clearance. Recipients of long-standing allografts that functioned optimally ( n = 16) and living transplant donors undergoing nephrectomy ( n = 10) served as functional and structural controls, respectively. A combination of physiological and morphometric techniques were used to evaluate glomerular filtration rate and its determinants 1–3 h after reperfusion and again on day 7 to elucidate the mechanism for persistent hypofiltration in ARF that is sustained. Glomerular filtration rate in the sustained ARF group on day 7 was depressed by 90% (mean ± SD); the corresponding fall in renal plasma flow was proportionately less. Neither plasma oncotic pressure nor the single-nephron ultrafiltration coefficient differed between the sustained ARF and the control group, however. A model of glomerular ultrafiltration and a sensitivity analysis were used to compute the prevailing transcapillary hydraulic pressure gradient (ΔP), the only remaining determinant of ΔP. This revealed that ΔP varied between 27 and 28 mmHg in sustained ARF and 32–38 mmHg in recovering ARF on day 7 vs. 47–54 mmHg in controls. Sustained ARF was associated with persistent tubular dilatation. We conclude that depression of ΔP, perhaps due partially to elevated tubule pressure, is the predominant cause of hypofiltration in the maintenance stage of ARF that is sustained for 7 days.

Current concepts on the pathophysiology of acute renal failure

1978 ◽  
Vol 234 (3) ◽  
pp. F171-F181 ◽  
Author(s):  
J. H. Stein ◽  
M. D. Lifschitz ◽  
L. D. Barnes
Keyword(s):  
Renal Failure ◽  
Blood Flow ◽  
Acute Renal Failure ◽  
Volume Expansion ◽  
Filtration Rate ◽  
Experimental Models ◽  
Tubular Epithelium ◽  
Norepinephrine Infusion ◽  
Glycerol Injection ◽  
Cellular Integrity

In the pase decade, several experimental models of acute renal failure (ARF) have been evaluated with micropuncture and hemodynamic techniques. Five of these models have been most extensively studied: glycerol injection, renal artery clamping, intrarenal norepinephrine infusion, uranyl nitrate, and mercuric chloride administration. In the first three models, renal ischemia is the initiating insult, whereas in the two nephrotoxic models a direct effect of the agent on cellular integrity is also seemingly operative. In all of these models, renal blood flow 24--48 h after the initial insult either spontaneously returns to normal or can be elevated to this level with volume expansion but without restoration of the glomerular filtration rate. Therefore, the maintenance of ARF in these various models is due to other factors, which include tubular obstruction, leakage of filtrate across damaged tubular epithelium, and a decrease in the glomerular capillary ultrafiltration coefficient. In a given model, one or all three of these alterations may be present. Although these various models may not be completely analogous to the clinical setting, they have provided powerful tools for the study of ARF and their use has greatly increased our knowledge in this field.

Human renal response to meat meal

1986 ◽  
Vol 250 (4) ◽  
pp. F613-F618 ◽  
Author(s):  
T. H. Hostetter
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Renal Plasma Flow ◽  
Statistical Significance ◽  
Prostaglandin E ◽  
Base Line ◽  
Meat Meal ◽  
Time Period ◽  
Beef Steak ◽  
Renal Vascular

Glomerular filtration rate (GFR) increases after a meat meal in several species. The mechanism of this phenomenon is unknown and the excretory and metabolic responses largely unexplored. We examined in humans the nature of the hemodynamic response to a meat meal, the role of salt and water load in this response, and the associated renal excretory responses. Ten normal volunteers were studied after eating an average of 3.5 g/kg body wt of lean cooked beef steak and, on a separate day, after ingesting an amount of sodium and water equivalent to that in the steak. Average GFR increased by 28% for the entire 3 h after the meat meal compared with the same time period after the control salt solution (90 +/- 8 vs. 114 +/- 6 ml X min-1 X 1.73 M-2, mean +/- SE, P less than 0.05) and by 15% compared with the base-line periods, although this difference was not of statistical significance. However, not all subjects demonstrated an increase, and in those eight who did the degree was variable from 5 to 46% for the 3-h mean above the basal value. During the hour of peak GFR, the increment was associated with a nearly proportional increase in renal plasma flow and renal blood flow (all P less than 0.05). The increase in renal blood flow was entirely due to a significant fall in renal vascular resistance. The vasodilation was not accompanied by any change in prostaglandin E excretion.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Dissociation of glomerular filtration and renal blood flow in HgCl2-induced acute renal failure

1982 ◽  
Vol 22 (2) ◽  
pp. 162-170 ◽  
Author(s):  
Raymond C. Vanholder ◽  
Marleen M. Praet ◽  
Piet A. Pattyn ◽  
Isidoor R. Leusen ◽  
Norbert H. Lameire
Keyword(s):  
Renal Failure ◽  
Blood Flow ◽  
Acute Renal Failure ◽  
Glomerular Filtration ◽  
Renal Blood Flow
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