Postischemic Acute Renal Failure Research Articles

Theophylline in rats during maintenance phase of post-ischemic acute renal failure

We have shown previously that theophylline increases both renal plasma flow (RPF) and glomerular filtration rate (GFR) during the initiation phase of post-ischemic acute renal failure (ARF) in rats. The purpose of the present experiments was to determine the effects of theophylline during the maintenance phase of ARF, five days after initiation. Clearance techniques were used to measure renal function in a control group of pentobarbital anesthetized rats (group C) and in three experimental groups, five days after subjecting the left kidney to a thirty-minute period of complete ischemia. Group SS received saline during both the ischemic episode and the clearance measurements; group ST received saline during ischemia and theophylline, acutely, during the clearance measurements; group TS received theophylline during ischemia and saline during the clearance measurements. In comparison with the values for the control group (group C), RPF and GFR of the post-ischemic left kidneys of group SS were approximately half normal. In groups ST and TS, RPF and GFR of the left kidneys were higher than in group SS. Collectively, these results demonstrate that pretreatment with theophylline during the initiation phase of ischemia-induced ARF leads to increased RPF and GFR during the maintenance phase, and that acute theophylline treatment during the maintenance phase acutely increases RPF and GFR. Since increases in GFR were associated with increases in RPF, and since theophylline is an adenosine receptor antagonist, these results are consistent with the hypothesis that adenosine-mediated hemodynamic changes play a pathogenic role in ischemia-induced ARF in rats.

Urinary proteinase activity in patients with acute renal failure after trauma and kidney transplantation.

A pathophysiological stress that produced a “hypercatabolic” metabolic state often will cause an increased basal energy expenditure in addition to eccessive loss of body protein. This condition is further characterized by severe muscle wasting and increased urinary nitrogen excretion. Both protein synthesis and breakdown are stimulated in severe skeletal trauma (Birkhahn et al., 1981), sepsis (Long et al., 1977) and after burn (Kien et al. 1978). Under these conditions enhanced proteolytic activity in plasma ultrafiltrates and urine fractions of patients with severe trauma and acute renal failure has been reported (Hörl and Heidland, 1980; Hörl et al., 1981; 1982a; 1983; 1986). Until now, the effect of postischemic acute renal failure on urinary protease excretion has not been investigated. Therefore, the present study was undertaken to compare urinary protease activity in patients with acute renal failure after cadaveric kidney transplantation and following multiple traumatic injuries. Furthermore, the proteolytic enzymes involved were partly characterized.KeywordsAcute Renal FailureKidney TransplantationCyanogen BromideSubunit StructureNormal Kidney FunctionThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Protective effect of prostacyclin on postischemic acute renal failure in the rat

Infusion of prostacyclin (PGI2) reportedly attenuates renal ischemic injury in the dog and the rat. In the dog, PGI2 is a potent renal vasodilator; in the rat a direct action on the renal vasculature is not always apparent. To determine whether or not the protective effect of PGI2 on postischemic ARF was hemodynamically mediated, studies were performed in uninephrectomized Sprague-Dawley rats before and after a 40 minute period of complete renal artery occlusion. In response to the preischemic infusion of PGI2 for 30 minutes at 160 ng/kg body wt/min i.v. (N = 7), MAP and RBF fell to 86 +/- 7% (P less than 0.0001) and 84 +/- 9% (P less than 0.05) of baseline values, respectively. RVR initially declined to 81 +/- 9% of baseline values (P less than 0.025) but returned to 102 +/- 13% of baseline values prior to the period of ischemia. Following the period of ischemia, reflow of blood in the rats receiving PGI2 was delayed when compared to rats not receiving PGI2 (N = 7). RBF returned to only 76 +/- 19% of the initial values in PGI2-treated rats (P less than 0.01) but to 90 +/- 12% of the initial values in rats receiving buffer alone (NS).(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of dipyridamole on the initiation phase of postischemic acute renal failure in rats.

Several previous observations support the hypothesis that increased adenosine production and release mediate, at least in part, the reductions in renal blood flow and glomerular filtration rate in ischemic acute renal failure (ARF). If this hypothesis is correct, dipyridamole should potentiate these changes, since it blocks cellular adenosine uptake, thereby increasing the concentration and potentiating the effects of extracellular adenosine. Moreover, theophylline should block the effects of dipyridamole, since it is an adenosine receptor antagonist. These predictions were tested in three groups of anesthetized rats. All rats were subjected to 30 min of left renal artery occlusion; 30 min after relieving the occlusion, a 45-min clearance period was begun. The control group was given saline i.v.; the two experimental groups received either dipyridamole (24 micrograms X min-1 X kg-1) or dipyridamole plus theophylline i.v. (111 mumol/kg as a prime, 1.1 mumol X min-1 X kg-1 as an infusion). In the control group, the previously ischemic left kidneys exhibited decreased clearances of para-aminohippurate and inulin (CPAH and CIn), filtration fraction (FF), and urine/plasma inulin concentration (U/PIn), and increased urine flow (V), Na excretion (UNaV), and fractional Na excretion (FENa) in comparison with the contralateral right kidney. Dipyridamole pretreatment did not affect the right kidney, but it intensified the reductions in left kidney CPAH, CIn, and FF. Theophylline blocked all these effects of dipyridamole on the left kidney, and increased renal plasma flow (CPAH/PAH extraction), despite a decrease in systemic arterial blood pressure. These results are further support for the hypothesis that adenosine mediates, at least in part, the hemodynamic changes in postischemic ARF in rats.

Protective effect of prostacyclin on postischemic acute renal failure in the rat

Protective effect of prostacyclin on postischemic acute renal failure in the rat

Prevention of Delayed Graft Function in Cadaver Kidney Transplants by Diltiazem

Calcium entry blockers have a protective effect on experimental postischemic acute renal failure (ARF). Since delayed graft function (DGF) in cadaver kidney transplants is in part due to an ischemic damage to the kidney, we initiated two prospective, randomized clinical trials of human kidney transplants. Study I (control: n = 22; diltiazem: n = 20): Diltiazem (D) was added to Eurocollin's solution at a dose of 20 mg/l. If the donor had been treated with D, the graft recipient got a bolus injection of 0.28 mg/kg D and a continuous infusion of 0.002 mg/min/kg D for the first two days. A dose of 60 mg D was then given orally twice daily. Study II (control: n = 11; diltiazem: n = 10): We used the same regimen without donor pretreatment. All patients had immunosuppression with cyclosporine A (CsA) and low-dose steroids. Primary graft function (PGF) was defined as vital kidney function without hemodialysis (HD) during the first week. In both studies the incidence of PGF was higher in the D groups (I: 90% vs. 59%, p less than 0.05; II: 70% vs. 55%). In the control groups, 3.6 +/- 0.4 (I) and 4.9 +/- 0.7 (II) HD per patient was necessary, compared to 0.6 +/- 0.2 (I), p less than 0.05) and 1.9 +/- 0.4 (II) HD in the treatment groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of captopril on the intrarenal hemodynamics of postischemic acute renal failure in anesthetized dogs.

Effects of captopril on the intrarenal hemodynamics of postischemic acute renal failure in anesthetized dogs.

Microdissection studies of the structural alterations induced in rat kidneys by experimental postischemic acute renal failure.

A unique opportunity presented itself for a morphologic study of experimental unilateral acute renal failure (ARF) in male rats. The ARF had been induced in the rats by temporary occlusion (1h) of the left renal artery. Twenty-nine rats were divided into subsets as follows: 2-3 h, 24 h, 1 week, 2, 4, 8, and 12 weeks following release of occlusion. Microdissection showed a heterogeneous population of abnormally structured proximal tubules in which the regressive lesions of tubular necrosis were combined with the progressive reaction of repair. The lesions demonstrated are reminiscent of those which have been described in ARF in the human and in experimental animals. Many proximal tubules in the 2- to 3-hour subset presented 1-3 disruptive lesions (DLs) while greater numbers of proximal tubules from the 24-hour group presented 1-5 DLs. Many proximal tubules presented no DLs, but nearly all from the 24-hour subset (97-100%) displayed a squamate appearance which paralleled and was caused by acute tubular necrosis. At 1 week, a dilated pars recta was common, but by this time, the squamate pattern had disappeared. Many casts were present. At 2 weeks, many fewer casts were present in proximal tubules and none were seen at 4, 8 or 12 weeks. The nephrons, particularly the proximal tubules, presented a variety of structural alterations at 2, 4, 8 and 12 weeks. Changes of special interest include (1) the presence of swan-necks; (2) a distinctive squamate appearance of the proximal tubules in the animals killed at 24 h; (3) a spiral, curled appearance caused by differential hyperplasia in animals at 4, 8 and 12 weeks, and (4) a tendency for ischemic lesions to involve all layers of the renal cortex.

Dietary protein prior to renal ischemia dramatically affects postischemic kidney function

Male Sprague-Dawley rats were maintained on high protein (60%), normal protein (20%), low protein (5%), or no protein (0%) diets for two or four weeks prior to 45 minutes of renal ischemia induced by renal pedicle clamping. Most (93%) of the rats on the high protein diet died within three days following renal ischemia. In addition, 69% of the rats on normal protein diets also died, most before the fourth day following ischemic insult. In contrast, 88% of the rats on the low protein diet lived, although some exhibited elevated serum creatinine levels for up to one to two weeks following ischemia. Finally, all of the rats on no protein diets lived, and most (75%) exhibited normal serum creatinine levels by the fourth day following ischemia. Shifting the diets of high protein and normal protein adapted rats to no protein diets immediately following ischemia did not improve postischemic survival. Also, changing the diets of no protein adapted rats to high protein diets immediately following ischemia did not significantly affect postischemic recovery. When rats were maintained on no protein diets for shorter periods of time prior to ischemia, it was found that approximately a week on this diet is necessary to provide maximum protection from postischemic acute renal failure. These findings demonstrate a dramatic effect of dietary protein prior to ischemic induced acute renal failure, and suggests that preoperative dietary protein intake should be an important consideration in those situations which are predisposed to postoperative acute renal failure.

Pathophysiology of Protracted Acute Renal Failure in Man

Postischemic acute renal failure (ARF) induced by cardiac surgery is commonly prolonged and may be irreversible. To examine whether persistence of postischemic, tubular cell injury accounts for delayed recovery from ARF, we studied 10 patients developing protracted (36 +/- 4 d) ARF after cardiac surgery. The differential clearance and excretion dynamics of probe solutes of graded size were determined. Inulin clearance was depressed (5.0 +/- 1.7 ml/min), while the fractional urinary clearance of dextrans (radii 17-30 A) were elevated above unity. Employing a model of conservation of mass, we calculated that 44% of filtered inulin was lost via transtubular backleak. The clearance and fractional backleak of technetium-labeled DTPA ([99mTc]DTPA, radius = 4 A) were identical to those of inulin (radius 15 A). The time at which inulin or DTPA excretion reached a maximum after an intravenous bolus injection was markedly delayed when compared with control subjects with ARF of brief duration, 102 vs. 11 min. Applying a three-compartment model of inulin/DTPA kinetics (which takes backleak into account) revealed the residence time of intravenously administered inulin/DTPA in the compartment occupied by tubular fluid and urine to be markedly prolonged, 20 vs. 6 min in controls, suggesting reduced velocity of tubular fluid flow. We conclude that protracted human ARF is characterized by transtubular backleak of glomerular ultrafiltrate, such that inulin clearance underestimates true glomerular filtration rate by approximately 50%, and by sluggish tubular fluid flow, which strongly suggests the existence of severe and generalized intraluminal tubular obstruction. Because all patients also exhibited extreme hyperreninemia (16 +/- 2 ng/ml per h) that was inversely related to inulin clearance (r value = -0.83) and urine flow (r value = -0.70), we propose that persistent, angiotensin II-mediated renal vasoconstriction may have delayed healing of the injured tubular epithelium.

The influence of long-term infusion of the calcium antagonist diltiazem on postischemic acute renal failure in conscious dogs.

The influence of long-term infusion of the calcium-entry blocker diltiazem on postischemic acute renal failure was investigated in conscious dogs monitored by implanted instruments. In 18 uninephrectomized beagle dogs on a salt-rich diet, an electromagnetic flow probe and an inflatable plastic cuff were placed around the renal artery. Acute renal failure was induced by inflating the cuff for 180 min in the conscious animal. Group A (n = 5, control) received an intraaortic injection of 0.9% NaCl (5 ml/day) from the 3rd day before until the 7th day after ischemia and group B (n = 6, posttreatment) an intra-aortic injection of diltiazem (5 micrograms X min-1 X kg-1) beginning at the end of ischemia until the 7th day. Group C (n = 7, pre- and posttreatment) received diltiazem from the 3rd day before until the 7th day after ischemia. In group A, renal blood flow dropped from 149 +/- 16 (preischemic) to 129 +/- 29 ml X min-1 on the 1st day after ischemia. In contrast, renal blood flow increased on the 1st postischemic day in both treatment groups by 29 +/- 15% (group B, P 0.05) and 14 +/- 13% (group C). In the following days, there was no significant difference in renal blood flow between groups A, B and C. In group B, the reduction of the glomerular filtration rate was similar to that in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium Channel Blocker Nisoldipine Limits Ischemic Damage in Rat Kidney

The effects of the calcium channel blocker nisoldipine on renal function after 60 min. normothermic ischemia and contralateral nephrectomy were studied in male Wistar rats. Nisoldipine (300ppm) was given in a standard diet as well as one hour prior to ischemia (10mg./kg. orally). Survival, serum urea, serum creatinine, urine volume and creatinine clearance were used to test the effectiveness of the drug. Nisoldipine treatment resulted in the survival of all animals (compared to 66.6 per cent in the untreated group) and improved immediate and long term (14 days) renal function. The drug given post ischemia only was not effective, suggesting that nisoldipine must be present in the kidney during ischemia. The beneficial effects of the drug in postischemic acute renal failure may be attributed in part to effects on postischemic renal hemodynamics. Additional direct effects on ischemic renal epithelial cells, presumably by inhibiting transmembrane calcium fluxes, cannot be excluded.

Pathophysiology of protracted acute renal failure in man.

Postischemic acute renal failure (ARF) induced by cardiac surgery is commonly prolonged and may be irreversible. To examine whether persistence of postischemic, tubular cell injury accounts for delayed recovery from ARF, we studied 10 patients developing protracted (36 +/- 4 d) ARF after cardiac surgery. The differential clearance and excretion dynamics of probe solutes of graded size were determined. Inulin clearance was depressed (5.0 +/- 1.7 ml/min), while the fractional urinary clearance of dextrans (radii 17-30 A) were elevated above unity. Employing a model of conservation of mass, we calculated that 44% of filtered inulin was lost via transtubular backleak. The clearance and fractional backleak of technetium-labeled DTPA ([99mTc]DTPA, radius = 4 A) were identical to those of inulin (radius 15 A). The time at which inulin or DTPA excretion reached a maximum after an intravenous bolus injection was markedly delayed when compared with control subjects with ARF of brief duration, 102 vs. 11 min. Applying a three-compartment model of inulin/DTPA kinetics (which takes backleak into account) revealed the residence time of intravenously administered inulin/DTPA in the compartment occupied by tubular fluid and urine to be markedly prolonged, 20 vs. 6 min in controls, suggesting reduced velocity of tubular fluid flow. We conclude that protracted human ARF is characterized by transtubular backleak of glomerular ultrafiltrate, such that inulin clearance underestimates true glomerular filtration rate by approximately 50%, and by sluggish tubular fluid flow, which strongly suggests the existence of severe and generalized intraluminal tubular obstruction. Because all patients also exhibited extreme hyperreninemia (16 +/- 2 ng/ml per h) that was inversely related to inulin clearance (r value = -0.83) and urine flow (r value = -0.70), we propose that persistent, angiotensin II-mediated renal vasoconstriction may have delayed healing of the injured tubular epithelium.

Nitroprusside (NP) on Post-Ischemic Acute Renal Failure

Nitroprusside (NP) on Post-Ischemic Acute Renal Failure

Evaluation of a Flushing Solution Designed to Protect Kidneys From In Situ Ischemia

An in situ flushing solution was evaluated with regard to the following: (1) its ability to protect the kidney during 60, 90, and 120 minutes of normothermic ischemia; (2) the effects of using an intracellular versus extracellular electrolyte composition in the flushing solution; and (3) the ability of the flushing solution to complement in situ hypothermia as a protective measure during long-term ischemia. Rat kidneys were briefly flushed in situ with an isotonic phosphate buffered solution (pH 7.2) containing 50 milliosmole of sucrose. The left renal pedicle was then immediately clamped to render the kidney ischemic and to hold the flushing solution in the kidney. Following removal of the pedicle clamp, a contralateral nephrectomy of the right kidney was performed and daily serum creatinine levels determined to evaluate postischemic renal function. The results indicate the following: (1) the flushing procedure is very effective in preventing postischemic acute renal failure following 60 minutes of normothermic ischemia, but is considerably less effective for ischemic times of 90 minutes or more; (2) an intracellular electrolyte composition in the flushing solution does not improve the protective effects of this solution; and (3) the flushing procedure can significantly improve on the protection otherwise provided by in situ hypothermia.

Course of acute renal failure studied by a model of creatinine kinetics

A computerized model of creatinine kinetics was developed to predict the relationship between creatinine clearance [G(t)] and plasma creatinine concentration [C(t)] in patients with postischemic acute renal failure (ARF). A comparison of predicted to measured values in 35 episodes of ARF in 27 patients revealed three patterns of declining G(t) following an ischemic insult. Pattern A, characterized by an abrupt step decrement in G(t) following an isolated renal ischemic episode lasting minutes or hours, was observed in nine patients. It was followed invariably by an immediate ramp increment in G(t), despite which C(t) continued to increase for several days. Urinary indices during the period of increasing azotemia were consistent with the resolving stage of ARF. Patterns B (N = 15) and C (N = 11) were associated with persistent renal ischemia of long (days to weeks) duration and were respectively characterized by prolonged ramp or exponential decrements in G(t). A concurrent increase in C(t) was associated with urinary indices typical of the maintenance or sustained stage of ARF. Recovery of G(t) was observed in only two-thirds of patterns B and C cases and took the form of a ramp or exponential increment. Because G(t) and total body water were changing rapidly in ARF, changes in measured plasma creatinine levels alone failed to identify these patterns of deteriorating or improving renal function. However, when the computerized model was used in conjunction with daily measured values of C(t) and body weight and occasional estimates of G(t), the course and prognosis of ARF in individual patients were illuminated.

Metabolic studies of postischemic acute renal failure in the rat

Postischemic acute renal failure was induced by 1 hr of clamping of the renal vasculature. Adenine nucleotide (ATP, ADP, AMP) and lactate (Lac) levels were measured after 0, 0.25, 1, 6, 24, and 48 hr of reflow to determine the time necessary for recovery to control levels. After 1 hr of ischemia with no reflow, [ATP] was 18% and [Lac] was 10-fold control levels. Control levels were restored after 24 hr of reflow. Variable ischemic times (5, 15, 30, 60, 90, and 120 min) followed by (1) no reflow or (2) 24 hr of reflow were also studied. [ATP] decreased to 25 and 13% of controls after 5 and 120 min of ischemia, respectively, and [Lac] increased to 5- and 13-fold controls after 5 and 120 min. Five to ninety minutes of ischemia followed by 24 hr of reflow resulted in a trend toward restoration of ATP and Lac levels; whereas, 120 min of ischemia followed by 24 hr of reflow resulted in death. The results indicate that: (1) In vivo ischemia results in a drastic and rapid shift in the ATP-ADP-AMP equilibrium; (2) the absolute concentration of ATP is not a reliable criterion of cell viability, but the ability to resynthesize ATP may be determinant in the reversibility of the lesion; (3) 1 hr of ischemia is reversible with respect to restoration of [ATP] and [Lac], but 24 hr of reflow are needed for restoration; and (4) ischemia for 90 min results in a metabolic derangement which is partially reversible in that metabolite levels are partially restored after 24 hr of reflow. However, 90 min of vascular clamping is not functionally reversible since the majority of animals exhibit severe azotemia and do not survive.

Glomerular filtration and tubular reabsorption during anuria in postischemic acute renal failure

AbstractGlomerular filtration and tubular reabsorption during anuria in postischemic acute renal failure. Complete occlusion of the left renal artery for 60min in the rat produced anuric acute renal failure after 1 day. Using fluorescence microscopy, a television system combined with double slit densitometry, and micropuncture techniques, tubular pressure and tubular flow rates were determined in different segments of superficial nephrons. Intratubular pressures in proximal convolutions of the postischemic kidney were largely heterogeneous due to abnormally increased flow resistance in proximal tubules which were filled with loose obstructive material. Proximal tubular pressure in the control kidney was independent of the site of its measurement and had a mean value of 14.1mm Hg. In the postischemic kidney pressure decreased gradually along the proximal tubule, its value in the early and late segments being 16.3 and 9.7mm Hg, respectively. Low pressure in late proximal convolutions excludes a significant flow impediment due to obstruction in more distal segments. The mean nephron filtration rate (SNGFR) obtained by extrapolation of tubular flow data was 62% of the control value, whereas tubular reabsorption was estimated to be 50% above normal. Reduced SNGFR and increased outflux caused a total reabsorption of tubular fluid within 60% of proximal convoluted tubule length. The partial reduction of SNGFR can be explained by increased pressure in early proximal convolutions and reduced glomerular plasma flow known for these kidneys, without postulating a change in glomerular permeability. Tubular obstruction and increased passive outflux in proximal tubules due to cellular damage appear to be crucial mechanisms responsible for the loss of renal function in this model of acute renal failure.Filtration glomérulaire et réabsorption tubulaire pendant l'anurie due à une insuffisance rénale aiguë postischémique. Une occlusion complète de l'artère rénale gauche pendant 60min chez le rat a entraîné une insuffisance rénale aiguë anurique après 1 jour. En utilisant la microscopie par fluorescence, un système de télévision combiné avec une densitométrie à double faisceau, et des techniques de microponction, la pression tubulaire et les débits tubulaires ont été déterminés dans différents segments de néphrons superficiels. Les pressions intratubulaires dans les convolutions proximales du rein postischémique étaient largement hétérogènes, en raison d'une augmentation anormale de la résistance au flux dans les tubules proximaux qui étaient remplis avec un matériau lâche obstructif. La pression tubulaire proximale dans le rein contrôle était indépendante du lieu de sa mesure et avait une valeur moyenne de 14,1mm Hg. Dans le rein postischémique, la pression diminuait graduellement le long du tubule proximal, ses valeurs dans les segments proximal et terminal étant 16,3 et 9,7mm Hg, respectivement. La faible pression dans les convolutions proximales tardives exclut un ralentissement significatif du flux par obstruction dans les segments plus distaux. La filtration glomérulaire moyenne par néphron (SNGFR), obtenue par extrapolation des valeurs de flux tubulaire était de 62% de la valeur contrôle, tandis que la réabsorption tubulaire était estimée à 50% au-dessus de la normale. La réduction de SNGFR et l'augmentation du flux sortant entraînaient une réabsorption totale du liquide tubulaire dès 60% de la longueur du tubule contourné proximal. Cette réduction partielle de SNGFR peut être expliquée par l'augmentation de pression dans les convolutions proximales précoces et la réduction du flux plasmatique glomérulaire connue dans ces reins, sans postuler de modification de la perméabilité glomérulaire. L'obstruction tubulaire et l'augmentation passive du flux sortant dans les tubules proximaux par l'altération cellulaire semblent être des mécanismes cruciaux responsables de la perte de la fonction rénale dans ce modèle d'insuffisance rénale aiguë.

The influence of an angiotensin II antagonist, saralasin, given before donor nephrectomy, on kidney function after transplantation. A controlled prospective study.

Kidneys from cadaver donors who had been treated during the last 10 min before bilateral nephrectomy with an infusion of 10 micrograms/kg-1/min-1 (Sar1, Val5, Ala8)-angiotensin II had a remarkable, significantly lower percentage of acute renal failure (25%) after renal transplantation than untreated kidneys (58.3%). Anuria was seen in the treated group only in 4.2%, although it occurred in the untreated control group in 16.6%. The role of the activated renin-angiotensin system in postischemic acute renal failure is discussed.

Renal hemodynamics and oxygen consumption during postischemic acute renal failure in the rat

Acute renal failure in the rat was induced by occluding the left renal artery for 1 hour. The kidneys were examined 1, 3, 10, and 40 days after temporary ischemia. Inulin clearance was essentially zero in oligoanuric kidneys on days 1 and 3, and regained 14% and 63% of the control value on days 10 and 40, respectively. Mean cortical blood flow remained almost constant at 75% of control up to day 10 and normalized subsequently on day 40. Renal oxygen consumption during anuria on days 1 and 3 was 53% and 46% of the control value and increased thereafter concurrently with the restoration of renal function. With a single linear correlation being assumed to exist between sodium reabsorption and oxygen consumption for all kidneys, the sodium reabsorption and oxygen consumption for all kidneys, the sodium transport estimated from oxygen consumption on day 1 was about 40% of control value. The difference between the sodium transport calculated from oxygen consumption and that from inulin clearance decreased with time in the recovery phase. The results indicate only a partial reduction of GFR due to the reduced blood flow in this model. The data are consistent with the hypothesis that tubular leakage and tubular obstruction play an important role in the loss of renal function during the manifestation of acute renal failure.