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 hypothesis that dietary fish oil would protect dogs from ischemic acute renal failure was tested. Fish oil (eicosapentaenoic acid, 55 mg/kg per day, and docosahexaenoic acid, 40 mg/kg per day was given to eight instrumented, female, beagle dogs for 6 wk, while seven control dogs received vehicle. After 3 wk, unilateral nephrectomy was performed and a pneumatic cuff with flow probe was placed around the remaining renal artery of each dog. Three weeks thereafter, the cuff was inflated for 120 min. Renal function, RBF, and prostanoid excretion were measured 24 and 72 h after ischemia. In dogs receiving fish oil, blood pressure, GFR, RBF, renal vascular resistance (RVR), cholesterol, triglycerides, and prostanoid excretion were measured weekly for 6 wk. Further, cytosolic calcium was measured before and five times after fish oil. Blood pressure decreased, serum cholesterol and triglycerides decreased, and the cytosolic calcium within platelets decreased. The urinary excretion (expressed as picograms per milligram of creatinine) of the thromboxane (TX) metabolite TXB2 and the excretion of prostaglandin (PG)E2, as well as the excretion of the PGI2 metabolite 6-keto PGF1 alpha were decreased. GFR, RBF (Cl inulin and Cl para-aminohippuric acid), and RVR were not influenced by fish oil. Unilateral nephrectomy decreased GFR and RBF and increased RVR as expected, whereas it further decreased prostanoid excretion. Acute renal ischemia caused a significant, reversible decrease in GFR and urine volume in vehicle-treated animals, whereas no significant effect on renal function or urine volume was observed in animals pretreated with fish oil.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Amelioration of ischemic acute renal failure by dietary fish oil administration in conscious dogs. 147 27

Aortic and renal vascular reconstruction often involve significant renal ischemia. Profound hypothermia during renal ischemia preserves renal tissue. However, in the clinical setting of vascular reconstruction specific attempts at cooling the kidney are often impractical, and renal ischemia frequently occurs at physiologic temperatures. This study demonstrates that minimal temperature changes during renal ischemia alter the functional and morphologic outcome. Rats anesthetized with halothane underwent a right nephrectomy and placement of a snare around the left renal pedicle for 45 minutes to produce renal ischemia. Seventy-five adult male Sprague-Dawley rats, weighing 250 to 350 gm were divided into three groups based on the body temperature maintained during renal ischemia (35 degrees C, 37 degrees C, 39 degrees C). Body temperature was continuously monitored with a rectal thermistor and maintained by adjustment of a heating pad and lamp. Two postischemic protocols were followed including a creatinine assessment protocol with blood samples collected at 24, 48, and 72 hours and a histologic assessment protocol with biopsy of the kidney at 30 hours. At 24 hours after ischemia plasma creatinine concentrations were increased in rats with elevated body temperatures (35 degrees C vs 37 degrees C; [p = 0.001], 37 degrees C vs 39 degrees C; [p = 0.150]). The 30-hour histologic assessment indicated a difference in morphologic outcome (35 degrees C vs 37 degrees C; [p = 0.063], 37 degrees C vs 39 degrees C; [p = 0.016]), with proximal tubular morphology being better maintained at lower temperatures.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Minimal physiologic temperature variations during renal ischemia alter functional and morphologic outcome. 156 May 50

A retrospective investigation was undertaken in which the rate of decline of residual renal function (RRF), estimated from creatinine clearance, was compared in 55 continuous ambulatory peritoneal dialysis (CAPD) and 57 hemodialysis (HD) patients for whom a minimum of four (mean of 7.6) well-spaced historic measurements of residual clearance were available. Because of the intrinsic variability that attends such data, specialized nonlinear, growth curve statistical methods were employed. Residual function was found to decline exponentially after the onset of therapy in both cohorts. The rate of decline in the HD group was twice that of the CAPD group (5.8% +/- 0.4% per month for HD vs 2.9% +/- 0.3% per month for CAPD; difference significant at p less than 0.0001). This difference remained highly significant (p less than 0.01) when corrected for other potential risk factors such as age, gender, hypertensive status, and use of angiotensin converting enzyme inhibitors in patients with diabetic or other forms of glomerular nephropathy. Differences between cohorts were not significant for patients with other diagnoses (p greater than 0.1) although the size of some of these subsets was very small. The physiologic mechanism for the more rapid fall-off of RRF on HD remains speculative, but could be related to renal ischemia secondary to intratreatment hypovolemia and/or to nephrotoxic effects of the inflammatory mediators of extracorporeal circulation.
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PMID:The influence of dialysis treatment modality on the decline of remaining renal function. 176 96

Thirty-eight recipients of nineteen pairs of cadaveric kidneys were entered into a double-blind randomized study in which one recipient received a 12-hour intravenous infusion of Atriopeptin III (AP-3), a synthetic analogue of atrial natriuretic factor, commencing at release of the vascular clamps, and the other received a placebo infusion. In an initial dose ranging study, successive groups of six kidneys (3 pairs) were randomized to receive each of 0.0125, 0.025, 0.05 micrograms/kg/min AP-3 or placebo. Thereafter 20 kidneys (10 pairs) received 0.1 micrograms/kg/min or placebo. There was no discernable effect of AP-3 on allograft creatinine clearance or sodium excretion either when the highest dose of AP-3 was considered alone or when all doses were considered together. Averaged creatinine clearance over the period 0 to 24 hours after transplantation was 20.1 +/- 14.7 ml/min in patients receiving active treatment and 18.2 +/- 13.7 ml/min in those receiving placebo. Thus, despite the documentation of a protective effect of atrial natriuretic factor in animal models of renal ischemia, it is unlikely that intravenous infusion of AP-3 in this dose range will be of benefit in improving immediate renal allograft graft function.
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PMID:Effect of intravenous infusion of atriopeptin 3 on immediate renal allograft function. 182 57

Water soluble ionic contrast media (CM) and glucose 5% were administered to Sprague-Dawley rats 36 hours after bilateral warm renal ischemia for 45 min. In all animals (n = 28) the renal ischemia caused a decrease of the absolute urinary creatinine output. Intra-arterial injection of glucose 5% or CM did not produce different patterns of absolute urinary creatinine output. The serum creatinine increased after 36 hours of reflow. When compared by means of a Mann-Whitney U-test to a normal median serum creatinine obtained in a separate group of 22 normal rats, the increase was statistically significant (p less than or equal to 0.01). The serum creatinine medians returned to a normal level after 24 hours. It seems therefore that 45 min of warm renal ischemia and 36 hours of reflow is an insufficient challenge to the rat kidney for the detection of the nephrotoxic properties of CM as opposed to when CM are injected during ischemia.
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PMID:Absence of functional renal effects of uro-angiographic contrast media on post-ischemic rat kidneys. 186 6

Spontaneous renal artery dissection is an uncommon cause of renovascular hypertension, usually associated with fibromuscular dysplasia. Among reported nonautopsy cases (N = 80), arterial reconstruction has seldom been attempted (N = 21) and the outcome has frequently been poor (48% clinical failure rate). This is attributed in part to the frequent involvement of renal artery branches by the dissection. Furthermore, the report of spontaneous reversion to normotension among patients treated medically has also clouded the role of surgery in this disease. Since progress in the technique of renal artery repair now allows successful treatment of anatomically complex lesions, we reviewed our experience with arterial reconstruction in the management of spontaneous renal artery dissection to determine the frequency of and factors correlating with cure after operative repair. Ten patients (eight men, two women; mean age, 39.3 +/- 5.9 years) were admitted with severe hypertension (10/10), often associated with neurologic symptoms, hematuria, or flank pain (8/10). Serum creatinine was elevated in only two patients. Angiography demonstrated changes consistent with fibromuscular dysplasia in 7 of 10 patients and evidence of dissection in 6 of 10. Bilateral disease was present in three patients. Only five patients had a single renal artery on the involved side. The dissection extended into the primary branches in 8 of 10 patients and involved both renal arteries in four of the five patients with two arteries. Histologic study confirmed fibromuscular dysplasia in six and intramural dissection in all operative specimens. Five patients underwent revascularization (in one case requiring the ex vivo technique), with use of hypogastric artery as a conduit in four of five or resection and primary reanastomosis in one of five. Three patients became normotensive, and two returned to their previous level of blood pressure control. Follow-up averaged 14.5 years. Two patients underwent nephrectomy after exploration demonstrated nonreconstructible vessels, and two underwent nephrectomy when intraoperative assessment of the kidney showed that revascularization had failed to adequately reverse extensive renal ischemia. After a mean follow-up of 14.6 years these patients remain normotensive, although two require antihypertensive medications. One patient was treated medically and is currently hypertensive off all medications. Nine of 10 patients have maintained a normal serum creatinine during follow-up. We conclude that renal revascularization is frequently successful in spontaneous renal artery dissection (five of seven, 71.4%) and results in sustained relief of hypertension with maximal conservation of renal tissue. This is important because of the young age at onset and the not infrequent occurrence of bilateral fibromuscular dysplasia, and even of dissection.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The role of arterial reconstruction in spontaneous renal artery dissection. 192 Jun 44

The effect of timing of cyclosporine administration on functional recovery from renal ischemia was studied in Sprague-Dawley rats. Animals were given cyclosporine and subjected to renal ischemia by temporarily occluding both the renal artery and vein. Our data demonstrate no significant difference in serum creatinine among rats subjected to renal ischemia, cyclosporine, or cyclosporine-vehicle cremophor EL administration, or the control group. On the other hand, renal ischemia in combination with cyclosporine resulted in rapid and marked deterioration in renal function with serum creatinine peaking on Day 2. The most significant rise was in rats that received cyclosporine 4 hr prior to induction of renal ischemia (4.7 +/- 0.5 mg/dl), followed by those that received cyclosporine 4 and 24 hr postischemia (2.8 +/- 0.5 and 3.2 +/- 0.7 mg/dl, respectively). Cyclosporine administration 24 hr prior to renal ischemia resulted in the least elevation of the serum creatinine (2.1 +/- 0.5 mg/dl) and the earliest return to the baseline value. Our data suggest that the timing of cyclosporine administration in rats subjected to renal ischemia influences the extent of renal injury and the subsequent recovery of renal function.
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PMID:Effect of timing of cyclosporine administration on recovery from renal ischemia in rats. 192 74

The objective of this study was to evaluate the renal tolerance of a new magnetic resonance contrast agent, AMI 25. This agent has an affinity for the reticuloendothelial system and is used for the detection of focal liver lesions. A combination of renal ischemia and intra-arterial iodinated contrast agent infusion (diatrizoate) leads to a reproducible and reversible model of acute renal failure in the rat. Using this model, AMI 25 was perfused directly into the aorta at the dose of 1 ml/kg--ten times the dose used in humans. AMI 25 induced no change in serum creatinine (45 +/- 7, 40 +/- 6, 40 +/- 9 mumol/L before infusion and at 24 and 48 hours, respectively), in creatinine clearance (2.1 +/- 0.6, 2.1 +/- 0.6, 2.1 +/- 0.6 mL/mn), or in urinary N-acetyl glucosaminidase (NAG) excretion (72 +/- 16, 98 +/- 12, 58 +/- 9.8 mumol hour-1/mmol creatinine). Blinded histologic analysis of 11 kidneys perfused with AMI 25 revealed no abnormalities, whereas diatrizoate induced acute tubular necrosis in four of the seven kidneys examined. In our animal model, AMI 25 has no nephrotoxicity, even at ten times the expected clinical dose for humans.
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PMID:Renal tolerance of AMI 25. 196 29

The objectives of this study were first to develop a reproducible and reversible model of acute renal failure following contrast medium infusion in the rat; second to use that method to compare the nephrotoxicity of low- and high-osmolar contrast agents. Contrast media or saline were perfused in the aorta while a clamp was applied on the aorta just above the renal artery. Three minutes of renal ischemia with or without infusion of isotonic saline induced no change in serum creatinine and a slight and transient decrease in creatinine clearance at 24 h. Urinary N-acetyl glucosaminidase (NAG) excretion was not modified in this control group. All 17 kidneys which were examined were normal. 2,100 mosm/kg hypertonic saline induced a significant increase in serum creatinine and a significant decrease in creatinine clearance (from 1.8 +/- 0.1 to 0.8 +/- 0.1 and 1.0 +/- 0.2 ml/min at 24 and 48 h, respectively). Urinary NAG excretion increased from 23 +/- 18 to 48 +/- 20 and 8 +/- 4 mumol h-1/mmol creatinine at 24 and 48 h, respectively (p less than 0.05). Histologic analysis of 5 kidneys revealed acute tubular necrosis (n = 3) and no histologic abnormalities (n = 2). Diatrizoate induced an acute and reversible renal failure. Creatinine clearance decreased from 1.6 +/- 0.1 to 0.4 +/- 0.1 and 0.8 +/- 0.1 ml/min at 24 and 48 h, respectively (p less than 0.01). Urinary NAG excretion increased also significantly from 43 +/- 9 to 352 +/- 79 and 64 +/- 23 mumol h-1/mmol creatinine at 24 and 48 h, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal effects of radiocontrast agents in rats: a new model of acute renal failure. 207 9

The effects of chronic dietary protein restriction on ischemic renal failure were evaluated in rats subjected to 90 min of bilateral renal clamping. The rats were kept on either 20% casein (regular) diet or casein-free (protein-free) diet 10 days before and 21 days after renal injury. Rats on regular protein diet showed higher levels of BUN and serum creatinine and had a lower inulin clearance (microliter/min/100 g BW) than animals on protein-free diet (289 +/- 34 vs 582 +/- 103, p less than 0.05) 2 days after ischemia. However, the inulin clearance measured 21 days following ischemia was significantly higher in rats on regular diet (1468 +/- 181) than those maintained on protein-free diet after ischemia (560 +/- 167). When unilateral 90 min ischemia was performed in rats on regular diet, the postischemic kidneys showed an incomplete recovery of the inulin clearance (226 +/- 35) compared to the contralateral kidney (900 +/- 116), 21 days after ischemia; whereas in rats on a protein-free diet the inulin clearance averaged 106 +/- 17 in the postischemic kidney and 345 +/- 41 in the right kidney. When left renal ischemia and contralateral nephrectomy were performed, the inulin clearance was 1149 +/- 74 in rats on regular diet and 534 +/- 60 in rats on protein-free diet, 21 days following renal insult. These results suggest that protein restriction can play a protective role against renal ischemia in an initial phase, but it limits the late recovery from ischemia. The presence of a normal contralateral kidney inhibits the functional recovery of the postischemic kidney and a contralateral nephrectomy produces a compensatory functional hypertrophy of the postischemic kidney, even in rats on a protein-free diet.
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PMID:The effect of protein restriction on the severity and recovery from ischemic renal failure. 210 Aug 29


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