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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal phospholipid metabolism was studied after ischemia was induced by occlusion of the left renal artery in the rat. There was no change in the rate of cellular [14C]choline uptake after 25 or 60 minutes of ischemia. However, [14C]choline incorporation into phospholipid was two to three times greater in slices from the ischemic kidney than in slices from the contralateral control kidney. The increase occurred after 25 minutes of ischemia plus 15 minutes of reflow, and after 60 minutes of ischemia with or without reflow. When [14C]choline was injected into rats after a 60-minute period of renal ischemia, the rate of incorporation into phospholipid in the ischemic kidney was almost twice that of the control kidney. These results were similar to those of the in vitro experiments. Since virtually all of the cellular phospholipids of the kidney are present in cellular membranes, renal ischemia affects membrane metabolism. The mean distribution ratio of alpha-aminoisobutyric acid in slices of kidneys ischemic for 60 minutes was similar to that of control slices: 4.11 +/- 0.2 (SEM) vs. 4.30 +/- 0.30. The normal uptake of alpha-aminoisobutyric acid indicates that the increased incorporation of choline is associated with functional integrity of the membrane.
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PMID:Choline uptake into renal phospholipids following renal ischemia in rats. 75 33

Seventy patients undergoing renal arteriography were studied prospectively to define optimal techniques of renal venous sampling and to establish the most appropriate methods for interpretation of renal vein renin and activity (RVRA). Plasma renin activity values from the aorta, the antecubital vein and the lower inferior vena cava were nearly identical. The relationship between renal vein renin activity in the two renal veins was not influenced by lack of simultaneous sampling or by contrast administration. Thirty-one patients with normal arteriograms had a mean RVRA ratio (right over left) of 1.12 +/- .11 (mean +/- SEM) but RVRA difference (right minus left) of only 0.02 +/- .11 ng/ml/hr. In contrast 16 patients with "significant" (greater than 70%) narrowing of the main renal artery had a mean RVRA ratio (involved over uninvolved) of 4.3 +/- 1.2 and a mean RVRA difference (involved minus uninvolved) of 3.9 +/- 1.4 ng/ml/hr. Seven patients (22%) with normal arteriograms had "abnormal" RVRA ratios (greater than or equal 1.5) but corresponding RVRA differences within one standard deviation of the group mean. Thus the difference inRVRA between both renal veins may more accurately reflect a patient's renovascular status than does the corresponding RVRA ratio. An "abnormal" RVRA ratio alone inadequately indicates the presence of renal ischemia.
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PMID:Renal vein renin activity: a prospective study of sampling techniques and methods of interpretation. 89 53

Renal ischemia has been implicated as a major factor in the pathogenesis of acute renal failure. Despite several differences between the intrarenal norepinephrine infusion and renal artery occlusion models, they have been assumed to be prototypic models of ischemic renal injury. In our previous studies, an intrarenal infusion of norepinephrine caused a marked reduction in inulin clearance 3 hours after infusion. This reduction could be significantly attenuated by the concurrent infusion of mannitol, furosemide, or bradykinin. The effects of these three protective agents were evaluated before and after variable durations of renal artery occlusion to establish the similarities between the models and the magnitude of versatility of these protective agents. In the renal artery occlusion model, capsular fascia was stripped to eliminate collateral flow and ensure maximal renal ischemia. Three hours after 120 minutes of renal artery occlusion (n = 7), inulin clearance returned to 5.7% +/- 2.2% (SEM) of the control values and was not statistically different from that observed in the norepinephrine model. Intrarenal infusion of mannitol, furosemide, or bradykinin prior to and during the occlusion period, however, had no protective effect. Shorter durations of renal artery occlusion were evaluated to ensure an equivalent or decreased severity of acute renal failure compared with the norepinephrine model. After 90 or 60 minutes of renal artery occlusion, the clearance of inulin returned to 10.9% +/- 3.3% (n = 8) and 31.1% +/- 8.2% (n = 4) of control values, respectively. An intrarenal infusion of mannitol, furosemide, or bradykinin still had no significant protective effect, despite the decreased insult in the 60-minute renal artery occlusion studies. In summary, these findings demonstrate fundamental differences between renal artery occlusion and the norepinephrine model of renal functional impairment, and they suggest that the insult associated with norepinephrine infusion may involve factors other than cessation of blood flow.
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PMID:Renal ischemic injury in the dog: characterization and effect of various pharmacologic agents. 643 74

In animals models, exposure of the brain, heart, or kidneys to sublethal ischemia induces tolerance for subsequent ischemia. However, the ability of human renal cells to undergo hypoxic preconditioning has not been evaluated. In addition, it is unclear if renal ischemic preconditioning induces resistance at the cellular level, or if preconditioning is a result of altered postischemic hemodynamics or the azotemic environment. In this study, we tested the ability of cultured human proximal tubular epithelial cells (PTEC) to undergo hypoxic preconditioning at the cellular level. Hypoxia was induced by incubating cells in an anaerobic incubator in glucose-free buffer (combined oxygen-glucose deprivation; COGD). Cell injury was assessed by lactate dehydrogenase (LDH) efflux, release of arachidonic acid metabolites, and light microscopy. PTEC preconditioned with 12 h of COGD and a 24-h recovery period had less LDH efflux than control PTEC after subsequent exposure to 20 h of COGD (15.0 +/- 2.5% vs. 44.0 +/- 3.4%, p < 0.05). Preconditioned PTEC also retained relatively normal morphology and had less release of arachidonic acid metabolites than control PTEC. Because renal ischemia is characterized predominately by tubular injury with relative sparing of the glomerulus, we determined if PTEC are more susceptible to hypoxic injury than glomerular cells. For further comparison, we also assessed the susceptibility to hypoxia of the porcine tubular epithelial cell line LLC-PK1. After exposure to 18 h of COGD, LDH efflux from PTEC (25.5 +/- 3.3%, mean +/- SEM) was lower than from LLC-PK1 cells (47.6 +/- 4.0%; p < 0.01), but not mesangial cells (22.7 +/- 5.0%) or glomerular endothelial cells (38.2 +/- 6.2%). In conclusion, we have demonstrated that cultured PTEC are as resistant to hypoxic injury as glomerular cells, and that PTEC attain cytoresistance after hypoxic preconditioning. Characterization of the molecular changes that occur in human PTEC after hypoxic preconditioning may reveal innate survival mechanisms that can be manipulated to promote protection from renal ischemia in patients.
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PMID:Susceptibility of human proximal tubular cells to hypoxia: effect of hypoxic preconditioning and comparison to glomerular cells. 904 51

Lipoxins are endogenous lipoxygenase-derived eicosanoids, generated during inflammatory, hypersensitivity, and vascular events, that display vasodilatory, antiinflammatory, and pro-resolution activity. Here, we evaluated the efficacy of 15-epi-16-(para-fluorophenoxy)-lipoxin A(4)-methyl ester (15-epi-16-(FPhO)-LXA(4)-Me), a stable synthetic analogue of aspirin-triggered 15-epi-lipoxin A(4) in ischemic acute renal failure (ARF) in NIH Swiss mice. ARF was induced by 30-min crossclamping of renal pedicles and was associated with elevated serum creatinine, morphologic injury, polymorphonuclear leukocyte (PMN) recruitment, and increased mRNA levels for adhesion molecules (intercellular adhesion molecule-1 [ICAM-1] and vascular cell adhesion molecule-1 [VCAM-1]), chemokines (growth regulated oncogene-1 [GRO1]), and cytokines (interleukin-1beta [IL-1beta] and IL-6) after 24-h reperfusion. A single bolus of 15-epi-16-(FPhO)-LXA(4)-Me afforded striking functional (mean +/- SEM creatinine in mg/dl: sham-operated, 0.77 +/- 0.04; ARF + vehicle, 2.49 +/- 0.19; ARF + 15-epi-16-(FPhO)-LXA(4)-Me, 0.75 +/- 0.12; P < 0.001) and morphologic protection and reduced PMN infiltration. Treatment with 15-epi-16-(FPhO)-LXA(4)-Me was also associated with lower IL-1beta, IL-6, and GRO1 mRNA levels, whereas ICAM-1 and VCAM-1 mRNA levels were unchanged. Compatible with these results, LXA(4) blunted chemoattractant-stimulated PMN migration across HK-2 renal epithelial cell monolayers in vitro, but it did not inhibit cytokine-induced HK-2 ICAM-1 expression or adhesiveness for PMN. Interestingly 15-epi-16-(FPhO)-LXA(4)-Me-treated animals also displayed increased renal mRNA levels for suppressors of cytokine signaling-1 (SOCS-1) and SOCS-2, but not CIS-1, endogenous inhibitors of cytokine-elicited Jak/Stat-signaling pathways. These results indicate that 15-epi-16-(FPhO)-LXA(4)-Me is protective in renal ischemia reperfusion injury in vivo, at least partially by modulating cytokine and chemokine expression and PMN recruitment, and provides a rationale for further exploration of the efficacy of LXA(4) structural analogues in ischemic ARF and other renal diseases.
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PMID:15-Epi-16-(para-fluorophenoxy)-lipoxin A(4)-methyl ester, a synthetic analogue of 15-epi-lipoxin A(4), is protective in experimental ischemic acute renal failure. 1203 96