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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An enhanced frequency and morbidity of urinary tract infections (UTI) have been observed in association with alcoholism and liver disease. The causes of these phenomena may relate, in part, to the defects in humoral and cellular immune mechanisms that occur in alcoholism. Urinary catheterization is the most common cause of UTI in hospitalized alcoholics. The severity of the sequelae of UTI in alcoholism is demonstrated by the unusually frequent occurrence of renal papillary necrosis (RPN) in conjunction with pyelonephritis in these patients. Indeed, in over 90% of the reported cases of RPN occurring with alcoholism or liver disease, pyelonephritis has been a contributing factor. The proclivity to medullary ischemia and RPN in this patient group may be, at least in part, a result of interstitial renal edema secondary both to infection and the effect of ethanol per se and to renal arterial vasoconstriction that occurs in cirrhosis. The frequency with which death due to sepsis or renal failure occurs in association with UTI in alcoholics obliges the physician to exercise caution in the prevention and treatment of UTI in these patients.
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PMID:Urinary tract infections and renal papillary necrosis in alcoholism. 370 22

To evaluate the combined effects of a brief ischemic insult and cyclosporine, four groups of male Munich Wistar rats were given: a) parenteral cyclosporine (60 mg/kg i.p.) for 4 days following 20 minutes of bilateral renal ischemia, b) the castor oil cyclosporine vehicle in a comparable volume and the same ischemic insult, c) saline in the same volume and ischemia, or d) saline and sham surgery. The cyclosporine animals ate and drank poorly, and therefore the other groups were pair-fed and watered with them. The cyclosporine-ischemia group developed significant renal failure. The other groups exhibited only a mild rise in blood urea nitrogen. Tubular vacuolization was a prominent feature in the cyclosporine and vehicle groups, but not in the saline groups. Vacuolization was correlated with severity of renal impairment. Lipid stains showed that many of the vacuoles contained lipid. Eosinophilic cytoplasmic inclusions were seen only in the cyclosporine or vehicle- (castor oil) treated animals. These findings emphasize the probable functional importance of tubular lesions in cyclosporine-induced acute renal failure, and suggest that the castor oil vehicle of parenteral cyclosporine may have renal effects of its own.
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PMID:Acute renal failure produced by combining cyclosporine and brief renal ischemia in the Munich Wistar rat. 370 29

Acute arterial occlusion may cause prolonged ischemia of the lower extremity. Since skeletal muscle is the major component, its reaction to the stress of ischemia best determines the final outcome for the limb. The combination of cellular damage during the period of ischemia and its exacerbation during reperfusion may result in the production of skeletal muscle necrosis. The relative resistance of skeletal muscle to normothermic ischemia is related to its low resting energy demands and large intracellular stores of available energy. If the period of ischemia is long enough, restoration of the circulation may exacerbate cellular damage, due in part to washout of adenine nucleotide precursor, free-radical-mediated injury and finally calcium-dependent necrosis. In addition to the clinical manifestation of local swelling, rhabdomyolysis can lead to systemic complications of hyperkalemia, renal failure or death. Therapeutic interventions aimed at reducing reperfusion damage may result in the salvage of functional lower limbs that might otherwise be lost.
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PMID:Pathophysiology of acute arterial occlusion. 375 55

It has been difficult to produce a good animal model for cyclosporine nephrotoxicity. It has been suggested that by following 20 minutes of renal ischemia with four daily doses of cyclosporine 60 mg/kg intraperitoneally, one can create a model of reproducible renal failure. We observed excessive mortality (65%), due in part to cyclosporine's CNS effects, with these combined insults in the Munich Wistar rat. In contrast, cyclosporine alone in this dosage produced only 17% mortality and resulted in a similar degree of renal failure. Pair-fed and pair-watered vehicle and saline controls were used. The morphologic changes brought about by the castor oil vehicle of the parenteral cyclosporine solution were qualitatively similar to those brought about by cyclosporine by light microscopy, although the severity of the changes was considerably less in the vehicle-treated groups. However, by electron microscopy, pale lipid vacuoles were seen only in the cyclosporine-treated groups, whereas dense alterations in lysosomes and dilated endoplasmic reticulum also were seen in other groups. Urine sodium determined by flame photometry and urine chloride determined by Saltex reagent strips tended to be high in the initiation phase of cyclosporine-induced acute renal failure and low in the maintenance phase. In animals that developed acute renal failure following the combination of ischemia and cyclosporine, the initial urine sodium and chloride were significantly correlated with the eventual degree of renal failure. The use of Saltex urine chloride sticks in clinical urine samples showed that the readings correlated well with urine sodium and chloride determined by conventional methods, suggesting that these strips may be useful in making a quick diagnosis in the setting of acute renal failure.
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PMID:Renal morphology and function and urine electrolytes in experimental acute renal failure produced by cyclosporine and ischemia. 384 27

We evaluated the hypothesis that postischemic renal failure is caused primarily at reperfusion by oxygen-derived free radicals in a swine model designed to realistically mimick human cadaveric renal transplantation. Both kidneys were removed, flushed with Euro-Collins solution, stored 24 hr at 4 degrees C, and then transplanted to a second pig. Experiments were paired, each pig receiving one treated and one control kidney. All pigs received the optimal conventional regimen of hydration, phenoxybenzamine, furosemide, and mannitol to allow assessment of free radical treatment superimposed thereupon. Two days later creatinine clearance (CCR) was measured from each kidney via separate ureterostomies. Untreated kidneys developed severe functional impairment, CCR falling from a normal level of 25.5 +/- 6.3 ml/min (n = 8) to 7.7 +/- 0.9 ml/min (n = 14, P less than .05 vs. control). The infusion of 20 mg of the free radical scavenger superoxide dismutase (SOD) into the renal artery at reperfusion substantially ameliorated this injury (CCR = 15.9 +/- 1.7 ml/min, n = 18, P less than 0.05 vs. control). A dose-response curve to SOD showed no effect of doses of 0.2 mg (CCR = 8.0 +/- 1.1 ml/min, n = 4) or 2 mg (CCR = 7.7 +/- 0.9, n = 5), and no greater benefit from 100 mg (CCR = 16.1 +/- 2.1 ml/min, n = 3, P less than 0.05 vs. control). Blocking the generation of superoxide radicals from xanthine oxidase with allopurinol (50 mg/kg) afforded similar protection (CCR = 18.2 +/- 1.8; n = 11, P less than 0.01 vs. control). On the other hand, following an 18-hr period of cold ischemia, little damage was sustained by the untreated (control) kidneys (CCR = 22.1 +/- 0.6 ml/min). Consequently, under these conditions the ablation of free radical generation with allopurinol provided no significant benefit. These findings suggest that after a critical period of cold ischemic preservation, metabolic changes take place within the kidney that lead to free radical generation and consequent tissue injury upon reperfusion, despite optimal preservation by conventional methods. This damage can be prevented by simple nontoxic measures--which, therefore, show great promise for use in the prevention of early renal failure following cadaveric renal transplantation.
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PMID:The role of oxygen free radicals in mediating the reperfusion injury of cold-preserved ischemic kidneys. 390 28

To estimate the renal ischemia-protective effect of saralasin, model studies were performed on rats and dogs. Acute ischemic renal failure was induced in rats by clamping off the vascular pedicle for 90 minutes. When the drug was prophylactically administered before the ischemia episode, a premature increase in post-ischemic plasma urea level and a shortening of survival time of the animals were observed compared with the untreated control. Following auto-transplantation of 24-hour cold-stored dog kidneys, the infusion of saralasin failed to improve renal blood flow (MRBF), glomerular filtration rate (KrCl) and fractional sodium excretion (FENa). On the other hand, the angiotensin blockade with captopril led to an increase in MRBF which was associated, however, with significant decreases in KrCl and FENa. This discrepancy was suggested to be due to a predominant postglomerular vasodilation. The results show that the application of saralasin before renal ischemia may aggravate the loss of renal function whilst the post-ischemic administration of the drug has no substantial effect on the acute failure of transplanted kidneys.
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PMID:[Experimental studies on the modifiability of ischemic acute renal failure by saralasin]. 391 17

The outcome of patients with acute renal failure following cadaveric renal transplant has been evaluated in a prospective, controlled trial, comparing treatment with cyclosporine (CSA) to prednisone, azathioprine, and antilymphocyte globulin (AZA). There was a high incidence of acute post-transplant renal failure in both groups: 37 of 51 CSA and 31 of 45 AZA patients, due to the long exposure of kidneys to warm and cold ischemia. Onset of adequate renal function was delayed for three or more weeks in 27 (53%) CSA and only nine (20%) AZA patients, and the only predisposing factor found was donor hypotension. All nine AZA and 18 of the 27 CSA patients with prolonged oliguria subsequently had a spontaneous diuresis. Nine of the CSA patients were changed to azathioprine and prednisone because of suspected CSA toxicity, and eight of these kidneys began functioning within days, even though they had been oliguric for 21 to 83 days. Of these nine patients, five had adequate long-term function on AZA, three developed CMV infections that were fatal to two individuals, and two rejected their grafts. Plasma CSA levels fluctuated widely in all patients, but were not higher in any group, including those with prolonged oliguria. During the oliguric period, biopsy specimens proved rejection was more common in the nine patients who had their CSA stopped than in the other CSA patients, and seven of these nine developed a diffuse interstitial fibrosis that was thought to be a manifestation of CSA toxicity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Post-transplant acute renal failure in cadaver renal recipients treated with cyclosporine. 391 72

31 patients underwent embolectomy for acute embolism of the aortic bifurcation. In most instances paralysis of the extremity (84%) was present, sudden onset of pain (16%) was less common. Neurological disease had been considered in 55%. The heart was source of emboli in 92%. Postoperative complications were mainly due to renal failure (23%) and irreversible limb ischemia (10%) requiring amputation. Mortality after embolism of the bifurcation was 39%. The major cause of death was cardiac failure (58%) followed by renal failure and pulmonary embolism. Even after long delay (4 weeks) successful operation is possible due to adequate collateral circulation supplying the extremity until the blockade is removed.
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PMID:[Symptoms and therapy of aortic bifurcation embolism]. 398 34

A 23-year-old male was admitted to hospital with severe dehydration and hypokalemic myopathy due to secondary aldosteronism. On admission serum sodium and chloride were markedly elevated to 198 mEq/l and 169 mEq/l, respectively, and serum potassium was down to 2.3 mEq/l. Serum electrolytes were normalized by transfusion therapy, but subsequently rhabdomyolysis grew worse due to metabolic abnormalities such as dehydration, hypothermia, oppressive ischemia and metabolic acidosis, at the same time transient polyuria and the elevation of serum myoglobin and enzymes originating in muscle tissue were observed. Serum CPK went up to 26,532 IU/l on the sixth day and other enzymes reached a peak following CPK. Dexamethasone was administered when the increase in enzyme levels caused the patient to fall into a stupor. He rapidly regained consciousness from the 15th day after admission, and he was able to stand up on the 29th day. Serum enzymes originating in muscle tissue decreased gradually to the normal range by the 30th day and no renal failure occurred.
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PMID:A case of severe dehydration with marked rhabdomyolysis. 402 Dec 12

Necrosis of the cecum occurs in various settings, including low-flow states. Cecal necrosis in two dialysis patients with documented, sustained hypotension is presented. Spontaneous left colon perforations, which have been previously reported in renal failure patients, were considered secondary to distention from constipation. The cecum may be more susceptible to ischemia than the remainder of the colon. Maximal distention develops at this point. With an associated low-flow state, in a possible watershed area, necrosis can occur. The diagnosis of cecal necrosis and perforation should be entertained in any dialysis patient with an acute abdomen. Early exploration may be necessary.
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PMID:Cecal necrosis in the dialysis-dependent patient. 406 55


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