Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0920646 (renal ischemia)
 2,515 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of FK 506 pretreatment on renal ischemia and reperfusion (I/R) injury was investigated. Adult male rats were assigned to one of two groups (20 animals each). Group 1 (controls) received 0.5 mL saline while group 2 received FK 506 (0.3 mg/kg) intravenously 24 h prior to the induction of renal ischemia. After a 60-min period of ischemia of the right kidney, a left nephrectomy was performed. Blood for BUN, creatinine, and tumor necrosis factor (TNF) was obtained prior to ischemia and on days 1, 2, 3, 5, 7, and 10. All surviving animals were sacrificed at day 10. FK 506 pretreatment reduced the serum levels of BUN (p less than .02), creatinine (p less than .02) and TNF (p less than .05) as compared to that seen in controls. Based upon these data, it appears that: (a) renal ischemia induces the release of TNF; (b) FK 506 pretreatment inhibits TNF production; and (c) FK 506 reduces renal injury association with I/R.
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PMID:FK 506 reduces the injury experienced following renal ischemia and reperfusion. 138 Jul 20

8-epi-prostaglandin F2 alpha (8-epi-PGF2 alpha) and related compounds are novel prostanoid produced by a noncyclooxygenase mechanism involving lipid peroxidation. Renal ischemia-reperfusion injury increased urinary excretion of these compounds by 300% over baseline level. Intrarenal arterial infusion at 0.5, 1, and 2 micrograms/kg per min induced dose-dependent reductions in glomerular filtration rate (GFR) and renal plasma flow, with renal function ceasing at the highest dose. Micropuncture measurements (0.5 microgram/kg per min) revealed a predominant increase in afferent resistance, resulting in a decrease in transcapillary hydraulic pressure difference, and leading to reductions in single nephron GFR and plasma flow. These changes were completely abolished or reversed by a TxA2 receptor antagonist, SQ 29,548. Competitive radioligand binding studies demonstrated that 8-epi-PGF2 alpha is a potent competitor for [3H]SQ 29,548 binding to rat renal arterial smooth muscle cells (RASM) in culture. Furthermore, addition of 8-epi-PGF2 alpha to RASM or isolated glomeruli was not associated with stimulation of arachidonate cyclooxygenase products. Therefore, 8-epi-PGF2 alpha is a potent preglomerular vasoconstrictor acting principally through TxA2 receptor activation. These findings may explain, in part, the beneficial effects of antioxidant therapy and TxA2 antagonism observed in numerous models of renal injury induced by lipid peroxidation.
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PMID:Glomerular actions of a free radical-generated novel prostaglandin, 8-epi-prostaglandin F2 alpha, in the rat. Evidence for interaction with thromboxane A2 receptors. 138 85

Radiocontrast-induced nephropathy (RCIN), a leading cause of in-hospital acute renal failure, is an acute decrease in renal function related to intravascular administration of iodinated radiocontrast agents. Though RCIN is relatively uncommon in patients without predisposing factors, patients with preexisting renal dysfunction, diabetes mellitus and severe congestive heart failure are at increased risk for acute renal failure following radiocontrast. Three recently developed animal models have provided important insights into the pathophysiology of RCIN. Specifically, these studies have implicated transient renal ischemia, direct renal tubular toxicity and changes in glomerular capillary permeability as possible mediators of RCIN, and these pathophysiologic mechanisms are not mutually exclusive. There is currently no effective treatment for RCIN. Assuring adequate hydration may reduce the risk of RCIN. In addition, synthetic atrial natriuretic factor and/or mannitol are promising, but as yet unproven, approaches to the prophylaxis of RCIN.
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PMID:Radiocontrast-induced nephropathy: current status and future prospects. 138 89

The role of neutrophils (PMN) in acute renal failure (ARF) is controversial. Although the development of acute renal failure (ARF) frequently occurs in situations where there is partial activation of PMN (primed PMN) and mild renal ischemia, the interaction between primed PMN and ischemic organs has not been studied in any biological system. To define the interaction between primed PMN and mild renal ischemia, kidneys were made ischemic for 10 minutes in situ and reperfused by the isolated kidney technique with untreated PMN or PMN primed with low concentrations of lipopolysaccharide (LPS) or phorbol myristate acetate (PMA). We found that primed PMN had no effect on control (non-ischemic) kidneys and that untreated PMN did not cause injury to kidneys previously subjected to mild ischemia. However, addition of primed PMN to mildly ischemic kidneys caused severe injury. To determine the nature of renal injury, ischemic kidneys were reperfused with primed PMN and catalase (CAT) or the elastase inhibitor, Eglin C. In ischemic kidneys reperfused with LPS-primed PMN, Eglin C (but not CAT) was partially protective while in ischemic kidneys reperfused with PMA-primed PMN, CAT (but not Eglin C) was partially protective. Reperfusion with both CAT and Eglin C completely prevented the damaging effects of either LPS- or PMA-primed PMN. In conclusion, addition of primed but not untreated PMN causes ARF in mildly ischemic kidneys by PMN oxidant- and/or protease-mediated mechanisms. This synergism could account for the high frequency of ARF in conditions associated with prerenal azotemia and primed PMN.
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PMID:Mild renal ischemia activates primed neutrophils to cause acute renal failure. 140 39

P-fimbriated Escherichia coli, which cause nonobstructive pyelonephritis, adhere to a specific urothelial glycolipid receptor. In either the presence or absence of reflux (in the area of turbulent urine flow) these bacteria ascend the ureter and cause a decrease in ureteral motility. Endotoxin causes peristalsis to cease, leading to ureteral dilatation and change in papillary shape, thus allowing intrarenal reflux and adherence of the bacteria to renal tubules. Bacterial infection of a refluxing ureter may cause reflux to persist. Once the bacteria reach the kidney rapid effects occur at the cellular level with activation of complement followed by granulocytic aggregation and capillary obstruction, causing renal ischemia and damage during reperfusion. In addition, during phagocytosis the respiratory burst occurs, releasing toxic oxygen molecules, which leads to renal tubular death, invasion of the interstitium, microabscess and renal scar formation, that is chronic pyelonephritis, which equates with reflux nephropathy.
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PMID:Vesicoureteral reflux and pyelonephritis in the monkey: a review. 143 97

Acute renal failure (ARF) is a serious complication in clients who have undergone bone marrow transplantation (BMT). The majority of cases develop as a result of intrarenal damage. Renal ischemia or nephrotoxic drugs, free hemoglobin, and free myoglobin contribute to acute tubular necrosis (ATN), which is the most likely cause of ARF in BMT clients. Nursing care of hospitalized BMT clients is directed toward the prevention of ARF by identifying clients who are at risk, the early diagnosis of renal impairment, and the administration of comprehensive treatment. Nurses play a vital role in the early diagnosis of renal impairment by assessing the client's fluid status, serum and urine electrolyte levels, and daily weights. The nursing role in managing clients with ARF includes preventing drug nephrotoxicity, maintaining fluid and electrolyte balance, preventing infection, and providing emotional support.
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PMID:Acute renal failure in bone marrow transplantation. 143 67

To determine whether heat shock proteins (HSPs) might be active in cellular recovery following transient ischemia, we examined rat kidneys for 70-kDa HSP (HSP-70) mRNA expression, protein elaboration, and intracellular localization after 45 min of renal ischemia and reflow of 15 min, 2, 6, and 24 h. Inducible HSP-70 mRNA is present at 15 min of reperfusion, peaks between 2 and 6 h, and falls by 24 h. Inducible 72-kDa HSP (HSP-72) protein accumulates progressively through 24 h and is found in both soluble and microsomal fractions following ischemia. Within proximal tubules, immunofluorescent localization of HSP-72 is restricted to the apical domain at 15 min, is dispersed through the cytoplasm in a vesicular pattern at 2 and 6 h, and has migrated away from the apical domain at 24 h. A portion of the vesicular HSP-72 is associated with lysosomes; no intranuclear HSP-72 is detected. The course of mRNA induction, protein elaboration, and HSP-72 localization coincides with previously described changes in proximal tubule morphology and polarity following sublethal ischemic injury. HSP-72 may be instrumental in cellular remodeling and restitution of epithelial polarity during recovery from ischemic renal injury.
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PMID:Induction and intracellular localization of HSP-72 after renal ischemia. 144 67

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

Renal artery perfusion is usually unnecessary during resection of an abdominal aortic aneurysm, because most of these aneurysms are situated below the renal arteries. The authors report the interesting case of a patient with a solitary functioning kidney, who had undergone previous bypass grafting from the right iliac artery to the right renal artery and in whom the kidney was perfused with the Biomedicus pump during the repair of an abdominal aortic aneurysm. This technique may be useful in special situations in which any period of renal ischemia might be hazardous to renal function.
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PMID:Renal perfusion with the Biomedicus pump during resection of an abdominal aortic aneurysm. 145 90

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


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