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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

In order to evaluate the clinical usefulness of serum and urinary beta-2-microglobulin (beta 2-m) determination as a marker of renal damage following cardiopulmonary bypass surgery (CPB), 37 children, with an age range of 6 months to 13 years undergoing CPB under hypothermia and cardioplegia for congenital malformations, were studied. Renal function was monitored at baseline and on the first and third day after CPB by traditional tests such as creatinine (Cr), endogenous creatinine clearance (Ccr), and fractional sodium excretion (FeNa), as well as by serum and urinary beta 2-m measured by radioimmunosorbent assay. Data were analyzed for the group as a whole and after stratification for the presence of acute renal failure (ARF) defined by an increase in Cr greater than 0.5 mg/dl and/or FeNa greater than 2% and of renal hypoperfusion which was considered in case of hypotension resistant to volume repletion and/or dopamine infusion and of oliguria (less than 1.0 ml/kg/h). The incidence of ARF was 18.9%, mortality 21.7% and among those who developed ARF, 71.4%. Although Cr and FeNa increased significantly on the first postoperative day, values returned to baseline thereafter, probably because of the high mortality rate observed among those who developed ARF and were therefore lost to follow-up. In contrast, Ccr was significantly decreased during the whole study. Even though serum beta 2-m displayed a similar profile to Cr and FeNa returning to baseline by the third day, urinary and fractional excretion of beta 2-m were significantly increased at any time of the study.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Beta-2-microglobulin as an index of renal function after cardiopulmonary bypass surgery in children. 307 85

The etiology and clinical course of acute nontraumatic rhabdomyolysis and ensuing renal failure was surveyed in a series of 40 consecutive patients. In 28 cases the muscle damage occurred after excessive consumption of ethyl alcohol and/or other intoxications. Prolonged lying immobilized was the reason or contributing factor for rhabdomyolysis in 22 cases. The other evident etiologies were convulsions, vigorous physical exercise, arterial occlusion and hypothermia. Typical local signs of rhabdomyolysis--pain, swelling and weakness of the affected muscles--were absent in one fourth of the patients. In these cases the diagnosis was based on transient elevation of serum creatine kinase enzyme activity. Dialyses were required to manage acute renal failure in 24 subjects. All 36 survivors recovered normal renal function. Neurological defects in the extremities still persisted in 16 patients at three months' follow-up.
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PMID:Acute renal failure following nontraumatic rhabdomyolysis. 323 37

Despite the widespread use of non-steroidal anti-inflammatory drugs (NSAIDs), the current number of reported cases of poisoning is small. However, with the introduction of 'over-the-counter' preparations of NSAIDs in some countries (e.g. ibuprofen in the UK and USA) an increased incidence of acute poisoning from this group of drugs can be expected. Conventionally, NSAIDs are divided into the following groups based on their chemical structure: arylpropionic acids, indole and indene acetic acids, heteroarylacetic acids, fenamates, phenylacetic acids, pyrazolones and oxicams. Unless NSAIDs are ingested in substantial overdose, acute poisoning with these agents does not usually result in significant morbidity or mortality. In most cases the clinical features are mild and confined to the gastrointestinal and central nervous systems, though acute renal failure, hepatic dysfunction, respiratory depression, coma, convulsions, cardiovascular collapse and cardiac arrest may complicate severe poisoning. Arylpropionic acid derivatives were thought initially to have a low order of toxicity in overdose but, in addition to anticipated gastrointestinal symptoms, headache, tinnitus, hyperventilation, sinus tachycardia, hypoprothrombinaemia, haematuria, proteinuria and acute renal failure have been described. In addition, drowsiness, coma, nystagmus, diplopia, hypothermia, hypotension, respiratory depression and cardiac arrest have been reported in severe cases of poisoning. Oxyphenbutazone and phenylbutazone are considerably more toxic in overdose. Complications of severe poisoning include coma, convulsions, hepatic dysfunction, acute renal failure, sodium and water retention, haematuria, cardiovascular collapse, respiratory alkalosis, metabolic acidosis, hypoprothrombinaemia and thrombocytopenia. In contrast, indomethacin appears to be much less toxic. In addition to gastrointestinal symptoms, indomethacin taken in overdose induces headache, tinnitus, dizziness, lethargy, drowsiness, confusion, disorientation and restlessness. Only 1 case of acute sulindac poisoning has been reported in the literature. A 16-year-old boy was admitted with hypokalaemia (2.2 mmol/L), transient granulocytosis and 'scanty' haematemesis after ingesting 12 g sulindac. No case of acute tolmetin poisoning have been reported. The fenamates (flufenamic acid, meclofenamic acid, mefenamic acid, tolfenamic acid) are, with the exception of mefenamic acid, not as widely prescribed as other groups of NSAIDs. In overdose, mefenamic acid may result in nausea, vomiting, diarrhoea, muscle twitching, convulsions and coma.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute poisoning due to non-steroidal anti-inflammatory drugs. Clinical features and management. 353 13

To assess the effects of body temperature on renal susceptibility to ischemic injury, rats were rendered acutely hypothermic (90-93 degrees F), normothermic (98-99 degrees F), or hyperthermic (101-103 degrees F) with a heat-controlled surgical board and then were subjected to 25 min of bilateral renal artery occlusion (RAO). Renal high-energy phosphates, their degradation products, and nonprotein sulfhydryl (NPSH) content were assessed at selected times during the peri-ischemic period. The severity of acute renal failure (ARF) was determined for 48 h following RAO by blood urea nitrogen (BUN) and plasma creatinine determinations and by renal histology. Ischemic ATP, ADP, AMP, GTP, GDP, UTP, and NAD levels and postischemic NPSH levels (15 min reflow) inversely correlated with temperature (P less than 0.001). BUN, creatinine concentrations (at 24 and 48 h), and histological injury (at 48 h) directly correlated with temperature (P less than 0.01). Hyperthermia in the absence of RAO had no demonstrable adverse renal effects. We conclude that hyperthermia potentiates ischemic renal injury, whereas hypothermia confers protection. These effects are associated with, and may be influenced by, temperature-induced changes in renal high-energy phosphate availability and oxidant stress during the ischemic/postischemic period.
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PMID:Body temperature: an important determinant of severity of ischemic renal injury. 372 86

An in situ flushing solution was evaluated with regard to the following: (1) its ability to protect the kidney during 60, 90, and 120 minutes of normothermic ischemia; (2) the effects of using an intracellular versus extracellular electrolyte composition in the flushing solution; and (3) the ability of the flushing solution to complement in situ hypothermia as a protective measure during long-term ischemia. Rat kidneys were briefly flushed in situ with an isotonic phosphate buffered solution (pH 7.2) containing 50 milliosmole of sucrose. The left renal pedicle was then immediately clamped to render the kidney ischemic and to hold the flushing solution in the kidney. Following removal of the pedicle clamp, a contralateral nephrectomy of the right kidney was performed and daily serum creatinine levels determined to evaluate postischemic renal function. The results indicate the following: (1) the flushing procedure is very effective in preventing postischemic acute renal failure following 60 minutes of normothermic ischemia, but is considerably less effective for ischemic times of 90 minutes or more; (2) an intracellular electrolyte composition in the flushing solution does not improve the protective effects of this solution; and (3) the flushing procedure can significantly improve on the protection otherwise provided by in situ hypothermia.
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PMID:Evaluation of a flushing solution designed to protect kidneys from in situ ischemia. 402 28

Renoprotective measures are of utmost importance for the preservation of renal function and prevention of acute renal failure of kidneys with impaired function subjected to operative procedures. Preoperatively a thorough nephrological work-up and preparation of the patient has to be performed. Potentially nephrotoxic drugs should be avoided. Examinations with radio contrast agents may lead to a deterioration of renal function, especially if risk factors are present. Hydration is an important part of preoperative renoprotection. Intraoperative renoprotective measures include atraumatic surgical techniques with preservation of renal parenchyma, the administration of diuretics and dopamine as well as a balanced substitution of blood and fluid loss. If the renal circulation has to be interrupted hypothermia should be applied. Controversy exists concerning the beneficial effect of membrane stabilisers, metabolic inhibitors and nucleotid precursors. For the prevention resp. treatment of postoperative acute renal failure balanced hydration, diuretics, dopamine and parenteral hyperalimentation have proven to be useful. The use of prophylactic dialysis leads to a reduction of the complications associated with acute renal failure.
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PMID:[Current status of renoprotective procedures in the surgery of impaired kidneys]. 653 13

A series of experiments was designed to investigate the influence of acute renal failure on selected gastrointestinal bacteria. Sprague-Dawley male rats were bilaterally nephrectomized to induce acute renal failure, with sham-operated animals serving as controls. After 48 h animals were sacrificed and the stomachs, upper and lower small intestines, ceca, and colons were excised and subjected to microbial analyses. Lactobacilli and streptococci including enterococci, were 1-2 log counts higher in the stomachs of anephric rats than those of sham-operated controls; lactobacilli were increased similarly in the upper small intestines of these animals. Coliforms including Escherichia coli, and Proteus were 1-2 log counts higher in the lower small intestine of anephric rats than those of sham-operated rats. The decreased gastric pH, increased cecal pH, hypothermia, and delayed gastric emptying observed in nephrectomized rats could partly explain the different microfloras in these animals.
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PMID:Influence of bilateral nephrectomy on selected gastrointestinal bacteria in the rat. 710 54

Cimadronate (YM175) is a novel bisphosphonate with potent inhibitory activity on bone resorption under development for the treatment of tumor-induced hypercalcemia, metastatic bone disease and osteoporosis. We conducted intravenous single and repeated dose toxicity studies of cimadronate in beagle dogs. In the single dose study, animals received a single dose of 0.3, 1, 3 or 10 mg/kg of cimadronate and the animals were observed for at least 14 days. At 10 mg/kg, both the male and female dog showed toxic signs such as vomiting, decreased locomotor activities and hypothermia and were killed in extremis within a week after dosing. In the 30-day study, animals received cimadronate at a dosage of 0 (vehicle), 0.03, 0.1, 0.3 or 1 mg/kg/day. At 0.03 mg/kg/day or more, histological findings indicated an increased amount of primary spongiosa in the rib and ilium. At 1 mg/kg/day, degenerative nephropathy, aggregation of spermatozoa and glandular hypoplasia of the prostate gland were observed. On day 16 of dosing one male animal died of acute renal failure. In the 26-week study, animals received cimadronate once weekly at a dosage of 0 (vehicle), 0.31, 0.62, or 1.25 mg/kg. Histopathological examination showed an increased amount of primary spongiosa in the rib at all dosage levels. In addition, similar findings were observed in the lumbar vertebrae at 1.25 mg/kg/week. Histopathological changes in the kidney and male reproductive organs were not observed.
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PMID:Intravenous single and repeated dose toxicity studies of cimadronate (YM175), a novel bisphosphonate, in beagle dogs. 749 Jul 87

Thirty-one infants and children with acute failure were treated with peritoneal dialysis using a surgically placed Tenckhoff catheter. In 10 patients a peritoneal dialysis cycler was used, and 21 were dialyzed by the manual method. Initially, hourly exchanges were given for 24 to 48 h and, as the patients stabilized, 10 exchanges per day at 1-h intervals were given. The mean stabilization period was 36 +/- 8 h. The predialysis mean serum creatinine was 5.8 +/- 1.8 mg% and the serum creatinine while on daily dialysis was 2.8 +/- 1.1 mg%. Peritoneal dialysis succeeded in controlling metabolic abnormalities and improving fluid balance. All the catheters except one functioned immediately following insertion. Median duration of catheter placement for dialysis was 18 days (range 2 to 90). The incidence of peritonitis was 12.8%, and exit site infection was 6.4%. The infection rate was decreased when a cycler was used compared with the manual method (23.8% vs. 10.0%), though not statistically significant. Two patients developed hypothermia while being dialyzed via the manual method. To conclude, 10 daily peritoneal dialysis exchanges performed at 1-h intervals after initial stabilization using a surgically placed Tenckhoff catheter is an effective and safe mode of dialytic therapy for children with acute renal failure. Complications (infection and hypothermia) are reduced with the use of a cycler.
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PMID:Daily peritoneal dialysis using a surgically placed Tenckhoff catheter for acute renal failure in children. 777 Jun 44


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