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Query: UMLS:C0920646 (renal ischemia)
 2,515 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The delayed onset of anuria/oliguria in acute tubular necrosis has been theorized to represent a complicating compartment syndrome, i.e., parenchymal swelling within an unyielding capsule. To test this proposition, 12 monkeys had suprarenal aortic cross-clamping, followed by unilateral renal decapsulation to create an experimental as well as a control kidney unit in the same animal. Histologic examination uniformly confirmed tubular necrosis at death or sacrifice. Subsequent split renal function studies (creatinine, urea, and free water clearances) indicated significantly greater maintenance of renal function by the decapsulated kidney than by its paired control. Clinical evaluation in 21 hemorrhagic shock patients, with the capsule of one kidney stripped, revealed on follow-up that 15 developed a renal failure consistent with acute tubular necrosis. Although three patients with polyuric failure died before split studies could be run and two others have been too recent for computer analysis to have been completed, nine of the remaining ten had significantly greater renal plasma flows (194 versus 121 ml/min M(2), p < .01) and significantly greater urine flows (.99 versus .18 ml/min M(2), p < .01) on the decapsulated side than on the control, as determined by differential renal scans. No significant difference in these same lateralized renal functions was noted in the tenth patient with renal failure and in the six survivors without renal failure. Renal decapsulation as prophylaxis reduced the anticipated incidence of oliguria/anuria from an expected 75% to 7% (p < .01) in these 21 shock patients. Such data suggest that delayed renal ischemia, possibly based on a compartment syndrome, may be the cause for a progression of acute tubular necrosis from polyuria to oliguria and then to anuria.
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PMID:Renal decapsulation in the prevention of post-ischemic oliguria. 40 54

Cardiac output (CO) and renal blood flow (RBF) were simultaneously evaluated (microsphere method) in awake rats, 3, 6, and 24 h after induction of acute renal failure by mercuric chloride (HgCl2; 4.7 mg/kg body weight). 3 h after injection of HgCl2, CO and RBF decreased to 77 and 72% of respective control values of 32.0 +/- 2.4 and 4.65 +/- 0.44 ml/min/100 g. Renal vascular resistance (RVR) and total peripheral resistance (TPR) were significantly increased compared to control at this time. Similar results were observed 6 h after administration of HgCl2. Volume expansion with plasma (2% of body weight) restored CO, RBF, TPR, and RVR to normal 3 h after injection of HgCl2. Despite significantly elevated blood urea nitrogen 24h after injection of HgCl2 (103.7 mg%), all hemodynamic parameters were within control range. Plasma volume was normal 3 h after HgCl2 but was significantly elevated compared to control 24 h after HgCl2 (4.73 vs. 3.92 ml/100 g, p less than 0.01). These findings indicate that factors other than preferential renal vasoconstriction may be involved in the transient renal ischemia of HgCl2-induced acute renal failure.
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PMID:Systemic hemodynamics in nephrotoxic acute renal failure. 67 89

Out of 85 rabbits 2j received a purified 6% hemoglobin solution free of ghosts (1,8 gHb/Kg) and were compared to 14 animals receiving the same dose of a crude hemoglobin solution containing ghosts. 11 rabbits had 5 infusions with a daily dose of 1,2 g Hb/Kg of the stromafree solution. Controls were partly untreated partly infused with saline. Creatinin, urea, electrolytes, and haptoglobin were determined in the serum oxygen consumption was measured separately in cortex and medulla by Warburg technique, and all kidneys examined histologically. In both groups 20% of the animals died spontaneously. Both groups exhibited the typical morphological and functional signs of acute renal failure. There was an increase in creatinin, urea, and potassium in the serum and a gain in kidney weights. In cortex and medulla we found a 20% drop in O2 consumption in both groups. Thus there was no evidence that ghosts play any role in the pathogenesis of renal failure in hemolysis or in the course of Hb-infusions. even after 5 infusions with lower dose renal damage was demonstrable. The drop in haptoglobin levels indicates, that renal ischemia may be induced by a disturbance in hemoglobin breakdown. The pathogenesis of renal damage has to be elucidated before Hb-solutions come into therapeutical use.
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PMID:[Acute renal failure after the infusion of hemoglobin solutions with or without red cell ghosts in rabbits (author's transl)]. 123 60

Renal function and morphology were studied before and after 60 min of renal ischemia and contralateral nephrectomy in two groups of rabbits. The animals were pretreated with ginsenosides (n = 22) and saline (n = 22) respectively, the latter as control. Results showed that ginsenosides (30 mg/kg body wt.) pretreatment by intravenous injection 10 min before warm ischemia resulted in the survival of all the animals with better renal function, 1, 3 and 7 days after blood urea nitrogen, fraction of excreted sodium and urine protein were observed in the control rabbits and a less pronounced increase was noted (P less than 0.05) after pretreatment with ginsenosides. The appearance of kidney tissue taken from surviving rabbits with Ginsenosides pretreatment was found to be normal under light microscope. Severe tubular necrosis was observed in kidneys of the control group. Tissues were examined with a transmission electron microscope. ginsenosides have protective effects on the epithelial cells of the proximal convoluted tubules, and microvilli and mitochondria were less damaged by ischemia than those of the control animals. There was also a large amount of ribosome on rough surfaced endoplasmic reticulum in the cells of ginsenosides-treated kidney, reflecting their ability to stimulate ribonucleic acid and protein synthesis. This is considered to be the basis of improvement of renal function.
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PMID:[Protective effects of ginsenosides on warm ischemic damages of the rabbit kidney]. 132 38

This article reports the case of a rapidly severe stenosis of the right renal artery, causing uncontrolled hypertension. After failure of a percutaneous transluminal renal angioplasty, which provoked the thrombosis of the vessel, a surgical revascularization was performed after +/- eighteen hours of renal ischemia. Blood pressure, blood urea nitrogen and serum creatinine returned to normal values. A dramatic improvement of the right renal function was attested at the hippuran scintigraphy after a dose test of captopril. The results of renographic studies obtained in this clinical case underline the role of the captopril radionuclide test in detection and follow-up after treatment of renovascular hypertension.
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PMID:Role of the captopril test in renovascular hypertension: a case report. 144 67

The spin-trapping agent alpha-phenyl-N-tert-butyl nitrone (PBN) reduced the ischemia-reperfusion induced acute renal failure in the rat. Renal ischemia was produced in unilateral nephrectomized rats by complete occlusion of the left renal artery for 60 min. Perfusion of the kidney was then reestablished, and the rats were sacrificed 48 h later. PBN (100 mg/kg i.p.) administered 30 min prior to renal artery occlusion significantly reduced the increase in serum creatinine and urea and renal failure index, as well as the decrease in urine/plasma creatinine ratio and creatinine clearance compared to saline-injected ischemic rats. PBN injected to control rats had no effect on these parameters. These data support the hypothesis of an involvement of reactive free radicals in the pathogenesis of ischemia-reperfusion induced acute renal failure in the rat and suggest that PBN may be a useful agent for the prevention of renal ischemia-reperfusion damage.
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PMID:Ischemia-reperfusion induced acute renal failure in the rat is ameliorated by the spin-trapping agent alpha-phenyl-N-tert-butyl nitrone (PBN). 146 97

Renal failure was produced in rats by unilateral clamping of the left renal artery for 60 min, followed by reperfusion and contralateral nephrectomy. Prophylactic administrations of benidipine (10, 30 micrograms/kg, i.v.) significantly ameliorated the development of renal failure as estimated by histological examination as well as by the measurements of serum creatinine and blood urea nitrogen. ATP content of the ischemic kidney dropped immediately after renal ischemia, and this decline persisted for more than 48 hr after reperfusion. The content of lipid peroxide in the kidney was increased 15 min after reperfusion following renal ischemia. Calcium content of the kidney progressively increased after reperfusion and reached the peak level 24 hr after reperfusion, whereas calcium content scarcely changed during 60 min of renal ischemia. The decline of ATP, the lipid peroxidation, and the increase in calcium content of the kidney observed after reperfusion were significantly inhibited by pretreatment of the rats with benidipine (30 micrograms/kg, i.v.). These results suggest that lipid peroxidation and Ca-overload play causative roles in the pathogenesis of acute ischemic renal failure and that benidipine protects the ischemic kidney by inhibiting these deteriorating consequences.
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PMID:Protection by benidipine hydrochloride (KW-3049), a calcium antagonist, of ischemic kidney in rats via inhibitions of Ca-overload, ATP-decline and lipid peroxidation. 234 26

Recently we reported that maintaining rats on restricted dietary protein regimens prior to renal ischemia will significantly improve postischemic survival rates. This effect required a week or more of maintenance on a restricted protein diet prior to the renal insult and appeared to be independent of the postischemic dietary protein regimen. The present study was designed to evaluate the role of systemic toxicity in this protection. Adult male Sprague-Dawley rats were pair-fed by weight on restricted or high isocaloric protein diets for 8-10 days prior to 45 min of renal ischemia induced by renal pedicle clamping. When placed on a normal dietary protein regimen immediately following ischemia, the rats preconditioned to restricted dietary protein exhibited significantly less acidosis, less hyperkalemia, lower blood urea nitrogen values, and improved survival rates compared with rats preconditioned on a high dietary protein regimen. In order to separate the possible effects of prior dietary protein regimen on acute tubular necrosis suffered during renal ischemia from its effects on the uremic response, bilateral nephrectomies were performed on rats preconditioned for 14 days to low, normal, and high dietary protein regimens. Although all of the rats were placed on the same dietary protein regimen immediately following bilateral nephrectomy, those that had previously been on a lower dietary protein regimen exhibited a significantly reduced uremic response and lived longer. These findings indicate that dietary protein regimen prior to renal ischemia is a risk factor which can have a significant lingering effect on the severity of postischemic systemic toxicity.
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PMID:Dietary protein regimen prior to renal ischemia significantly affects the postischemic uremic response. 237 Sep 27

In this randomized, double-blind, placebo-controlled trial the renal function was studied in 60 patients recovering from coronary artery bypass surgery treated with a daily dose of 800 mg sulphinpyrazone (SP) or 880 mg acetylsalicylic acid (ASA) or placebo. Serum creatinine level increased (p less than 0.05) during the first 2 days of SP treatment, but returned to its baseline level within 4 days under maintained therapy; during ASA and placebo therapy no significant changes occurred. Serum urea levels decreased (p less than 0.01) during ASA and placebo treatments as time from surgery subsided; the decrease of serum urea level was delayed in the SP group compared with the ASA and placebo groups. Urinary excretion of prostaglandin E2 (PGE2) was significantly decreased (p less than 0.01) during ASA treatment; in the SP group, urinary PGE2 excretion tended also to decrease during the first days of treatment, the decrease being significant only on the 4th day (p less than 0.01). The urinary excretion of kallikrein decreased significantly only in the SP group (p less than 0.01), while the changes in the ASA and placebo group were not significant. We suggest that the rapidly reversible acute renal impairment during SP therapy was probably due to a transient renal ischemia caused by a drug-related decrease in urinary kallikrein excretion rather than by renal prostaglandin inhibition.
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PMID:Impairment of renal function due to sulphinpyrazone after coronary artery bypass surgery: a prospective double-blind study. 242 79

To determine the timing and location of renal cell regeneration after ischemic injury to the kidney and to assess whether exogenous epidermal growth factor (EGF) enhances this regenerative repair process to accelerate recovery of renal function, experiments were undertaken in rats undergoing 30 min of bilateral renal artery clamp ischemia followed by reperfusion for varying time intervals. Renal cell regeneration, as reflected by incorporation of radiolabeled thymidine within the kidney, began between 24 to 48 h and reached a peak at 72 h after renal ischemia. As demonstrated by histoautoradiography, renal thymidine incorporation was essentially confined to tubule cells. Morphometric analysis of histoautoradiograph sections of renal tissue demonstrated that the majority of labeled cells were found in renal cortex, but some labeled cells were also located in the inner stripe of the outer medulla, suggesting that injury to medullary thick ascending limbs also occurs in this ischemic model. Exogenous EGF administration produced increases in renal thymidine incorporation compared with non-treated animals at 24, 48, and 72 h after ischemic injury. This accelerated DNA replicative process was associated with significantly lower peak blood urea nitrogen (BUN) and serum creatinine levels, averaging 63 +/- 20 and 3.1 +/- 0.4 mg/dl in EGF-treated ischemic rats compared with 149 +/- 20 and 5.1 +/- 0.1 mg/dl, respectively, in nontreated ischemic rats, and was also associated with a return to near normal BUN and serum creatinine levels in EGF-treated animals approximately 4 d earlier than that observed in nontreated animals. This report is the first demonstration that EGF accelerates the repair process of a visceral organ after an injurious insult.
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PMID:Epidermal growth factor enhances renal tubule cell regeneration and repair and accelerates the recovery of renal function in postischemic acute renal failure. 259 59


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