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 effects of a protein-restricted diet on renal recovery following renal ischemia were studied. The renal function was assessed by measuring the inulin clearance (CIN), the p-aminohippurate clearance (CPAH), and the percent fractional sodium excretion (%FENa) 24 h after 45 min renal ischemia. In rats fed with a regular diet (containing 19.6% protein), CIN was 10.0 +/- 2.2 microL/min/100 g body weight (BW), CPAH 0.08 +/- 0.02 mL/min/100 g BW, and %FENa 14.8 +/- 2.0, 24 h after renal ischemia. In contrast, feeding rats with a no-protein diet (0% protein) for 1 week prior to the ischemic insult significantly improved renal recovery (CIN 48.0 +/- 9.3 microL/min/100 g BW, CPAH 0.16 +/- 0.04 mL/min/100 g BW, and %FENa 2.43 +/- 0.58). Feeding rats with a no-protein diet for 3 weeks prior to ischemic insult further improved the renal recovery (CIN 113 +/- 30 microL/min/100 g BW, CPAH 0.47 +/- 0.17 mL/min/100 g BW, and %FENa 1.55 +/- 0.29). When rats fed with a regular diet were exposed to 45 min of ischemia, the survival rate on day 7 was 16.7%. In rats fed with the no-protein diet for 1 week and for 3 weeks, the 7-day survival rate was 100% in each case. The survival rate of rats fed for 3 days instead of 7 days with the no-protein diet was 87.5%. When a no-protein feeding was shortened to 1 day, no beneficial effects were observed and survival rate was 14.3%. (ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Protein-restricted diet prior to renal insult improves the recovery of renal function following ischemia. 829 Jul 2

Rat experiments demonstrated that cystamine showed a dose-dependent effect in renal ischemia. Ischemia was induced by ligation of renal vessels and the ureter for 90 minutes. Unithiol given in a single dose before ischemia produced no protective effect. Preadministration of sodium nitrite in doses causing slight to moderate hemic hypoxia could not diminish reoxygenation ischemic lesions.
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PMID:[The action of sulfur-containing and methemoglobin-forming compounds in renal ischemia]. 831 3

After 45-min bilateral warm renal ischemia lethality amounted to 45% and 82% in 55- and 20-day-old rats, respectively (n = 176). Lethality rates were not significantly different after 20-min unilateral ischemia followed by contralateral nephrectomy after 24 hours (34 vs. 48% in young vs. adult rats; n = 168). The latter experimental approach was used to characterize age dependent differences in the susceptibility to ischemia. The degree of postischemic renal damage was the highest at the 1st and 2nd days after ischemia; at this time, lethality rates were similar in young and adult rats. However, urea concentration in serum was significantly more enhanced in young animals whereas that of creatinine was increased to the same extent in both age groups. The increase in protein excretion into urine was similar in young and adult rats, too. Furthermore, urine flow rates and GFR were significantly diminished after ischemia, independent of age. However, excretion of Na+ and K+ was distinctly more depressed in immature individuals. Finally, the glutathione content in kidney tissue of both age groups was reduced and lipid peroxidation was significantly higher after ligation of the renal arteries. The relative changes were similar in both age groups although the glutathione content was significantly lower in 20-day-old control rats. 4-5 days after ischemia, most parameters returned to baseline values. In 55-day-old rats, 45-min ischemia has more severe consequences on renal function compared to 20-min ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of methods indicating higher susceptibility of immature rats to renal ischemia. 832 66

In arterial hypertension associated with primary or secondary hyperaldosteronism myocardial fibrosis is an important determinant of pathologic hypertrophy. To further examine the relationship between elevations in plasma aldosterone (ALDO) and myocardial fibrosis, we analysed perivascular collagen area (PVCA) and interstitial collagen volume fraction (CVF) by videodensitometry and hydroxyproline concentration (HPro) by high-performance liquid chromatography. We examined both the left (LV) and right (RV) ventricles in the following rats models of primary or secondary hyperaldosteronism of eight weeks duration: unilateral renal ischemia (RHT); continuous ALDO administration via osmotic minipumps (0.75 microgram/h s.c.) and enhanced dietary sodium following uninephrectomy (AL); in RHT and AL after pre- and continuous treatment with either 20 (S) or 200 (SS) mg/kg/day s.c. of the aldosterone receptor antagonist, spironolactone; in AL after pre- and continuous treatment with 50 mg/kg/day oral captopril (AL + CAP); as well as in age and sex matched controls (C). Systolic arterial pressure was comparably elevated in RHT and AL (202 +/- 12 and 193 +/- 7 mmHg, respectively; P < 0.0005 vs C); it remained elevated with low dose spironolactone in either model of arterial hypertension, but was normalized with high dose spironolactone or captopril in AL. Left ventricular hypertrophy (LVH), expressed as significantly elevated LV/RV weight or LV/BW ratios, was present in all experimental groups, excluding AL + SS and AL + CAP, when compared with C (P < 0.005). In each ventricle, CVF and PVCA were increased (P < 0.005) in either model of hypertension and in AL + CAP, but were no different from C in all groups receiving either dose of spironolactone. Similar findings were observed for HPro. Thus, myocardial fibrosis was comparable in primary or secondary hyperaldosteronism, wherein elevations in plasma aldosterone, relative to increased sodium intake, are associated with arterial hypertension. The competitive ALDO receptor antagonist, spironolactone, was able to prevent fibrosis in either model irrespective of the development of LVH and the presence of hypertension. Captopril prevented hypertension and LVH, but not unexpectedly it did not prevent myocardial fibrosis in primary hyperaldosteronism. These findings provide further evidence that in these rat models increased plasma ALDO, relative to dietary sodium, plays a major role in the adverse accumulation of collagen that appears in the myocardium.
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PMID:Anti-aldosterone treatment and the prevention of myocardial fibrosis in primary and secondary hyperaldosteronism. 837 16

Studies in experimental models of renal ischemia have shown that calcium antagonists are effective in the protection from the ischemic insult. Thirty-five patients who received a kidney graft over a 2-year period (nifedipine group) were compared with 35 consecutive transplanted patients (control group). The two groups were compatible with regard to age, sex, duration of hemodialysis, graft matching, and total number of blood transfusions. The patients in the nifedipine group were given 0.2 mg nifedipine (10% solution) through the renal artery immediately after revascularization, and also nifedipine per os during all the study periods. Adequate diuresis (1 mL/min) was obtained in 14.5 +/- 37.2 and 43.9 +/- 46.8 h after transplantation in the nifedipine and control groups respectively (p < 0.01). The frequency of acute tubular dysfunction and the mean serum creatinine concentrations were found to be higher in the control group. Fractional excretion of sodium was not found to be different in the two groups on the first day, but it was significantly lower by the first week after transplantation in the nifedipine group (p < 0.05). Acute rejection episodes were found to be more frequent in the control group during the first 6 months after transplantation (p < 0.05). It is suggested that nifedipine is effective in the protection of renal function after transplantation.
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PMID:Effect of calcium antagonist on renal graft function. 844 43

We investigated the effects of renal ischemia with reperfusion on the reactivity of rabbit renal vasculature. The main renal and arcuate arteries were isolated and studied as ring preparations. In the renal artery, concentration-response curves for potassium chloride (KCl), noradrenaline (NA), serotonin (5-HT), angiotensin II (AII), acetylcholine (ACh), A23187 or sodium nitroprusside (SNP) were unaltered after ischemia and reperfusion. Under the same conditions, the relaxation of arcuate arteries elicited by ACh was reduced when vessels were precontracted with methoxamine but not with KCl, whereas SNP-induced responses were unaffected. In anesthetized rabbits, renal blood flow and corresponding renal vascular resistances (RVR) were not modified by ischemia and reperfusion. ACh (1, 3 and 10 micrograms/kg per min) reduced RVR (maximally -24 +/- 8%) and this response was unchanged after ischemia and reperfusion (maximally -25 +/- 10%). These results demonstrate that the rabbit renal vasculature is relatively resistant to an ischemic insult and is probably not involved in the development of postischemic renal failure.
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PMID:Endothelium-dependent control of vascular tone in the rabbit kidney after ischemia and reperfusion. 845 77

NSAIDs pose little threat of renal insult in normal, healthy persons at therapeutic dosages. However, NSAID administration to susceptible persons may cause decrements in renal plasma flow and glomerular filtration rate within hours. Such acute noxious renal effects are mediated by products of arachidonic acid metabolism. Precipitous decrements in glomerular filtration and renal ischemia, manifested by increased serum creatinine and urea nitrogen, are possible. However, these effects are usually fully reversible with prompt discontinuation of the offending NSAID. Risk factors for the development of these acute renal effects are known. Acute interstitial nephritis with or without nephrotic syndrome is a rare form of renal toxicity that typically occurs between 2-18 months of use. Renal impairment may be so severe as to require temporary hemodialysis; however, renal function usually returns to normal upon discontinuation of the NSAID. The mechanism of acute interstitial nephritis is presumed to be of allergic origin but could also be caused by a reactive metabolite. Fenoprofen use appears to be associated with a much higher risk for its development. In contrast to the acute effects of NSAIDs, irreversible, analgesic-associated nephropathy manifested by papillary necrosis and chronic interstitial nephritis may occur following months to years of high doses of analgesic mixtures. The mechanism by which combination analgesics produce this form of renal injury is unknown and could be either a result of medullary ischemia or a direct effect of a reactive metabolite. An important issue to be resolved is the relationship between the acute, reversible, prostaglandin-mediated renal effects of the NSAIDs and chronic, irreversible destruction, if such a relationship exists. Theoretically, continual or repeated decrements in renal function in patients with predisposing risk factors could cause or contribute to progressive deterioration in renal function. Elevations in blood pressure or interference with the effects of antihypertensive medications could theoretically also contribute to long-term renal deterioration. In addition to renal syndromes caused by NSAIDs that result in renal impairment, other transient effects on electrolyte and water metabolism may also occur. Reduced secretion of sodium may result in formation of edema, exacerbation of heart failure, or increased blood pressure. Hyporeninemic-hypoaldosteronism may produce hyperkalemia. Finally, reduced excretion of water has rarely caused hyponatremia. It has been suggested that NSAIDs may be renoprotective in patients with nephrotic syndrome. Others have suggested that sulindac is "renal-sparing" because of a unique metabolic pathway that supposedly limits the exposure of the kidney to the active sulfide metabolite.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Renal toxicity of the nonsteroidal anti-inflammatory drugs. 849 47

We evaluated, in renal epithelial cells with a proximal tubule phenotype, the effect of nitric oxide (NO) on ecto-5 -nucleotidase (5'-N U), the underlying mechanism and its functional consequence. Sodium nitroprusside (SNP, 1-1000 microM), a NO donor, inhibited 5'-NU activity in a time- and concentration-dependent manner. Consequently, NO blunted the inhibition by extracellular cyclic AMP (cAMP, 10-1000 microM) of sodium-phosphate cotransport, a pathway which involves degradation of adenosine monophosphate (AMP) by 5'-NU. SNP-induced inhibition of 5'-NU was not mediated by cyclic GMP, since it was not mimicked by atrial natriuretic peptide, and was reproduced by isosorbide dinitrate and sodium nitrate, two NO donors. SNP and genuine NO decreased the activity of 5'-NU in renal homogenates, and the effect of SNP was potentiated by dithiothreitol and glutathione, but not by nicotinamide adenine dinucleotide. In vivo in rats, kidney ischemia/reperfusion, which activates inducible NO-synthase, inhibited renal 5'-NU. This inhibition was prevented by Nomega-nitro-L-arginine methyl ester, a NO-synthase inhibitor. These results indicate that: (i) NO-related activity inhibited the activity of an ecto-enzyme, 5'-NU, most likely through S-nitrosylation of the enzyme; (ii) inhibition of 5'-NU activity by NOx, which can occur in vivo under pathophysiological conditions, affected the extent to which extracellular cAMP inhibited sodium-Pi cotransport.
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PMID:Inhibition of ecto-5'-nucleotidase by nitric oxide donors. Implications in renal epithelial cells. 861 29

We present a 72-year-old man who had episodes of severe, acute renal failure during severe attacks of diarrhea caused by Vibrio cholerae. Patterns of acute tubular necrosis and tubulointerstitial nephritis developed following hypotension and decrease in renal blood flow, causing secondary renal ischemia. There was severe dehydration with profound hypovolemia and infection. The clinical picture included fever, weakness, arthralgia, pedal edema, mild bilateral pleural effusions, anemia, leukocytosis, azotemia with a maximum of 330 mg/dl of urea, creatine to a maximum of 9.8 mg/dl, hypoproteinemia, severe metabolic acidosis, marked increase in lactate dehydrogenase (LDH) and creatine phosphokinase (CPK), microscopic hematuria, sterile leukocyturia, normoglycemic glucosuria and phosphaturia with diminished tubular reabsorption of phosphorus. A short oliguric phase was followed by a polyuric phase lasting about 10 days, and glomerular and tubular function became normal after about 3 weeks. Treatment was by intensive infusions of fluids, electrolytes, sodium bicarbonate, salt-free albumin and antibiotics. To the best of our knowledge, this renal complication of cholera has not yet been described in Israel.
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PMID:[Acute renal failure as a complication of cholera]. 868 55

The influence of ketanserin, a S2-serotonergic receptor blocker, on the impaired renal hemodynamics in a clamp model of renal ischemia in rats was investigated in this study. Serotonin-induced vasoconstriction of the renal vascular bed was augmented after ischemia. This constriction is blocked by ketanserin (0.05 mg/kg i.v. bolus, followed by 0.1 mg/kg per h infusion). The influence of the same ketanserin treatment on the response of RBF versus a stepwise lowering of the renal perfusion pressure was studied in post-ischemic kidneys with an established loss of autoregulation of RBF. An almost perfect restoration of the autoregulatory response was apparent after the S2-serotonergic antagonism. Despite this beneficial effect on renal hemodynamics, renal function, judged by measurement of GFR and urinary sodium excretion rate, was not influenced by an acute infusion of ketanserin in post-ischemic kidneys. It is suggested that serotonin plays a pivotal role in the suppression of autoregulation of RBF by a S2-serotonergic receptor-mediated vasoconstrictor effect in the post-ischemic kidney. It most likely masks the potential myogenic dilatory response of the smooth muscle cells in renal preglomerular microvasculature. Restoration of the renal autoregulatory capacity by S2-serotonergic receptor antagonism could be of clinical relevance in human post-ischemic acute renal failure.
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PMID:Beneficial influence of ketanserin on autoregulation of blood flow in post-ischemic kidneys. 872 97


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