Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of catecholamine in vivo was studied on purine catabolism in rats and chickens. Catecholamine, administered intraperitoneally in a high dose, markedly increased plasma uric acid and allantoin in rats, and an increase was also observed with intravenous infusion of a lower dose of catecholamine. The effects of catecholamine were characterized by inhibition with alpha and beta adrenoceptor antagonists. Regarding the mechanism of this catecholamine action on purine catabolism, it was shown that catecholamine stimulated degradation of tissue ATP into the end-product. Plasma allantoin, the final purine catabolite in rats, elicited by catecholamine could be maintained under conditions of renal failure, although the action of catecholamine in intact rat was short lasting. The effect of catecholamine was potentiated and/or prolonged by angiotensin-II and aminophylline, and a hyperuricemic state could be induced by catecholamine treatment in chickens. In addition, increase of plasma purine catabolite by immobilization stress in rats suggested the involvement of endogenous catecholamine. From these experimental results, it is considered that catecholamines probably play a important role in the pathogenesis of hyperuricemia.
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PMID:Stimulation by catecholamine of purine catabolism in rats and chickens. 4 10

Two brothers, 29 and 33 years of age, had recurrent myoglobinuria, renal failure and azotemia, but were otherwise normal, without apparent muscle weakness or exercise intolerance. Ischemic exercise resulted in normal lactate production. Muscle glycogen content and activities of phosphorylase and phosphofructokinase were normal. Plasma triglycerides were elevated (500 mg per deciliter) on a regular diet and rose during fasting. During a 72-hour fast, serum creatine phosphokinase rose more than 10 times, and myoglobin was detected in urine. Plasma ketone production was minimal during fasting, but prompt ketonemia ( a normal response) occurred after ingestion of medium-chain triglycerides. Carnitine palmityl transferase activity was virtually absent in crude muscle extracts and mitochondrial fractions. Lack of this enzyme impairs long-chain fatty acid utilization, reflected in increased content of plasma free fatty acids and plasma triglycerides. Depletion of ATP because of this metabolic block in muscle may account for the attacks of myoglobinuria.
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PMID:A disorder of muscle lipid metabolism and myoglobinuria. Absence of carnitine palmityl transferase. 12 38

Biochemical changes in the blood following induction of renal failure by glycerol or mercuric chloride have been studied in 16 rats. Plasma creatinine, urea and Pi levels indicated that renal impairment followed the same time course in both renal failure models, with the severest effects on day 3 and returning to normal by day 7. Erythrocyte ATP and guanine triphosphate (GTP) levels were significantly elevated above contorl values on day 1 and remained elevated in both models. ATP/ADP and GTP/GDP ratios also increased in both models. In renal failure the increased purine 'salvage' in the erythrocyte may be attributed to accumulation of purine metabolites in the serum associated with increased P-ribose-PP levels due to elevated cellular Pi. Nucleotide changes in both these models are analogous to those found in chronic renal failure in man.
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PMID:Elevation of rat erythrocyte nucleotide levels following acute renal failure induced by glycerol or mercuric chloride. 74 Jan 15

The purpose of this study was to examine if ATP-MgCl2, an agent that protects against acute cisplatin toxicity in vitro, protected against cisplatin toxicity in vivo. Baseline renal function measurements were obtained on dogs (n = 12) and rats (n = 20) on day -1. Dogs were given 90 mg m-2 cisplatin (n = 5), 90 mg m-2 cisplatin and 50 mumol kg-1 ATP-MgCl2 (n = 5), or 90 mg m-2 cisplatin and 150 mumol kg-1 ATP-MgCl2 (n = 2), in a slow bolus i.v. injection on day 0. Rats were given 4 mg kg-1 cisplatin i.p. (n = 6) and 25 mumol kg ATP-MgCl2 (n = 8) i.v. or 4 mg kg-1 cisplatin i.p. and 25 mumol kg-1 ATP-MgCl2 (n = 6) i.v. on day 0. Renal function was assessed on a routine basis for 14 days. All dogs had significantly decreased creatinine clearance following cisplatin administration. There were no significant differences in renal function tests between groups of dogs. One dog given 50 mumol kg-1 ATP-MgCl2 and both dogs given 150 mumol kg-1 ATP-MgCl2 in addition to cisplatin developed acute anuric renal failure and were euthanatized prior to completion of the study. Rats given 4 mg kg-1 cisplatin and 25 mumol kg-1 ATP-MgCl2 had significantly increased blood urea nitrogen and serum creatinine after drug administration, compared to rats given cisplatin alone. The results indicated that ATP-MgCl2 worsened in vivo cisplatin renal toxicity in the dog and rat.
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PMID:ATP-MgCl2 increases cisplatin toxicity in the dog and rat. 144 84

We describe a new enzymatic determination of urinary guanidinoacetic acid (GAA) with guanidinoacetate kinase (ATP: guanidinoacetate N-phosphotransferase, EC 2.7.3.1), which does not require a blank to correct for endogenous constituents (ADP and pyruvate). In the first step, pyruvate kinase (ATP: pyruvate 2-O-phosphotransferase, EC 2.7.1.40) and lactate dehydrogenase (L-lactate: NAD+ oxidoreductase, EC 1.1.1.27) were used to eliminate endogenous constituents (ADP and pyruvate) in the presence of phosphoenolpyruvate and NADH. In the second step, urinary GAA was phosphorylated in the presence of ATP by guanidinoacetate kinase to form phosphoguanidinoacetate and ADP. The resultant ADP was sequentially measured at 340 nm in a coupled reaction catalyzed by pyruvate kinase and lactate dehydrogenase. The standard curve was linear up to 20 mg/dl for standard solutions of GAA. Analytical recovery of GAA added to normal urines ranged from 97.0 to 103.2% (mean 100.7%). The within-run and between-run studies gave CV values of less than or equal to 3.6% and less than or equal to 4.8%, respectively. No significant interference by endogenous urinary compounds were observed with the proposed method under this study. The results obtained by the present method correlated well with those obtained by a high-performance liquid chromatographic method. This method is accurate and simple, and less time-consuming than those previously reported. We determined the concentrations of GAA in 24-h urine samples by the proposed method, and observed that the urinary excretion of GAA decreased markedly in patients with renal failure.
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PMID:A new enzymatic assay of urinary guanidinoacetic acid. 166 26

Renal failure often complicates endotoxin shock. This might be due to renal hypoperfusion, but endotoxemia could also have additional effects. We studied in anesthetized rats renal plasma flow (RPF), glomerular filtration rate (GFR), and metabolism (ATP, CrP = creatine phosphate, energy charge = [ATP + 0.5 ADP]/[ATP + ADP + AMP], lactate, glucose) during endotoxin shock (Escherichia coli endotoxin, 10 mg/kg for 60 min; n = 10) and "balloon shock" (balloon inflated in vena cava below renal vein to cause comparable decreases in cardiac output and RPF as in endotoxin-treated rats; n = 10). A third group of rats served as controls (n = 10). At t = 0 infusion of endotoxin was started. At t = 90 min, when cardiac output was low and serum lactate was high (indicating shock), GFR and RPF were obtained from plasma disappearance rates (from t = 90 to t = 135 min) of 125I-thalamate and 131I-hippurate, respectively. Experiments ended at t = 135 min. In both shock groups RPF decreased (by ca. - 75% compared with control rats), but filtration fraction only increased (by 72%) in the "balloon shock" rats. In renal biopsies lactate concentration increased more (by 407 vs. 167%) and ATP decreased more (by -63 vs. - 35%) during endotoxin shock than during "balloon shock"; the endotoxin-treated rats also showed a significant decrease in CrP (by - 58%), energy charge (by - 31%), and glucose concentration (by - 34%), and an increase in the number of leukocytes in the glomeruli (by 730%). Renal function and metabolism thus was more affected in this hypodynamic form of endotoxin shock than in "balloon shock." This may be caused by the effects of endotoxin on sticking of leukocytes and renal metabolism.
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PMID:Renal function and metabolism during endotoxemia in rats: role of hypoperfusion. 177 55

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

Renal effects of 1,4-dihydropyridine (DHP)-type calcium antagonists (nitrendipine and nisoldipine) were analyzed in diverse conditions, such as long-term antihypertensive treatment, acute saline-loading, and acute renal failure in rats. In spontaneously hypertensive rats (SHR), 60-week treatment with nitrendipine resulted in normotensive blood pressure values without increasing body weight, an indicator of salt-water retention, or increasing plasma renin activity and plasma aldosterone concentration compared with the untreated rats. After acute saline-loading of normotensive or hypertensive rats, administration of calcium antagonists nitrendipine and nisoldipine increased urinary volume and sodium excretion. This was in contrast to the effects observed with the vasodilator minoxidil, with which salt-water retention was shown. In acute renal failure induced by 60-min renal ischemia in uninephrectomized rats, administration of nisoldipine decreased mortality rate and improved kidney function. The increase in renal tissue calcium content and the decrease in ATP content associated with the renal failure was abolished by nisoldipine treatment. In conclusion, renal protective effects are present with DHP-type calcium antagonists; however, mechanisms in situations such as hypertension or acute renal failure might be different and deserve further analysis.
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PMID:Renal effects of 1,4-dihydropyridines in animal models of hypertension and renal failure. 244 Nov 91

In dialysis and non-dialysis patients with terminal renal failure the red cell ATP and 2,3 DPG concentrations are increased. Inorganic phosphate level in red cells is nearly normal in both groups of patients. The red cell potassium concentration is decreased in both groups. Sodium concentration in red cells is significantly lower in dialysis than in non-dialysis patients, the former being lower and the latter being higher, than the average normal value.
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PMID:The red cell sodium, potassium, inorganic phosphate, ATP and 2,3DPG concentrations in chronic renal failure. 244 86

The purpose of this study was to assess the degree, time sequence, and biochemical correlates of hypothermic protection against ischemic acute renal failure. Rats subjected to 40 minutes of bilateral renal artery occlusion (RAO) were made mildly hypothermic (32 degrees-33 degrees C, by cold saline peritoneal lavage) during the following time periods: 1) RAO only, 2) reperfusion only (beginning at 0, 15, 30, or 60 minutes after RAO and maintained for 45 minutes), or 3) during and after (0-45 minutes) RAO. Continuously normothermic (37 degrees C) RAO rats served as controls. The control rats developed severe acute renal failure (blood urea nitrogen [BUN], 95 +/- 4 mg/dl; creatinine, 2.2 +/- 0.1 mg/dl; and extensive tubular necrosis at 24 hours). Hypothermia confined to RAO was highly protective (BUN, 33 +/- 5 mg/dl; creatinine, 0.62 +/- 0.07 mg/dl; and minimal necrosis). Hypothermia partially preserved ischemic renal adenylate high-energy phosphate (ATP and ADP), increased AMP and inosine monophosphate concentrations, and lessened hypoxanthine/xanthine buildup (assessed at end of RAO). Hypothermia confined to the reflow period (beginning at 0, 15, and 30 minutes) was only mildly protective (e.g., BUN, 58-63 mg/dl); the degree of protection did not differ according to the time of hypothermic onset. Lowering reflow temperature to 26 degrees C had no added benefit. Hypothermia that started at 60 minutes after RAO conferred no protection. Combining ischemic and postischemic hypothermia abolished all renal failure (assessed at 24 hours). This study offers the following conclusions: Mild hypothermia can totally prevent experimental ischemic acute renal failure. Hypothermia is highly effective during ischemia, and it is mildly protective during early reflow; these benefits are additive. During early reflow, hypothermic protection is not critically time dependent. By 60 minutes of reflow, no effect is elicited; this absence of effect possibly signals completion of the reperfusion injury process. Hypothermia's protective effects may be mediated, in part, by improvements in renal adenine nucleotide content and, possibly, by decreasing postischemic oxidant stress.
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PMID:Degree and time sequence of hypothermic protection against experimental ischemic acute renal failure. 280 43


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