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

There have been recent reports of rhabdomyolysis associated with cocaine abuse. The pathologic findings from these cases have not been described. Pathologic abnormalities in two fatalities with cocaine-associated rhabdomyolysis, including one with hyperpyrexia, acute renal failure, and disseminated intravascular coagulation, are discussed in detail. Skeletal muscle in both cases showed necrosis without evidence of vasculitis, polarizable foreign crystals, or other specific lesions. The individual with renal failure showed acute tubular necrosis with granular myoglobin casts in tubules. The mechanism of cocaine-associated rhabdomyolysis is unclear, but potentially includes ischemia due to vasoconstriction, direct toxicity, hyperpyrexia, and increased muscle activity from agitation or seizure. Adulterants may also play a role. In unexplained cases of rhabdomyolysis, toxicologic evidence of cocaine should be sought. In those cases of rhabdomyolysis associated with acute renal failure, the presence of cocaine in blood may be prolonged because of impaired renal clearance.
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PMID:Rhabdomyolysis associated with cocaine abuse. 174 98

The present study was designed to determine whether the administration of superoxide dismutase (SOD) can alleviate ischemic kidney damage and whether there is a relationship between oxygen free radicals and thromboxane (Tx). In 17 dogs, the right kidney was removed and the vascular pedicle of the left kidney was clamped for 75 min. Prior to reperfusion, the ischemic kidney was rinsed with 5 mg SOD and an additional 20 mg SOD was infused systemically. Blood samples were drawn from the renal vein before ischemia and after reperfusion to determine serum levels of thromboxane B2 (TxB2). All eight untreated dogs died within 1 week of renal failure, and the nine treated dogs demonstrated transient renal failure, with a significant difference (P less than 0.001) being found between the two groups. A significant difference (P less than 0.001) in TxB2 levels was found in the untreated dogs before and after ischemia and between the two groups following reperfusion. Animals that are treated with SOD after the ischemic event has occurred but before reperfusion exhibit a favorable clinical course in terms of survival and renal function. Tx synthesis in the kidney can be blocked by the administration of SOD.
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PMID:The role of oxygen free radicals and prostaglandins in reperfusion injury to warm ischemic kidneys. 175 34

We investigated the role of complement activation on the resolution of acute ischemic renal failure in the rat. Acute renal failure was induced by clamping of the renal arteries of Sprague-Dawley rats for 45 minutes (Day 0). On subsequent days, groups of rats with acute renal failure were exposed to daily zymosan infusion (an activator of the complement system), or to blood incubated with cuprophane (CUP) or polyacrylonitrile (PAN) dialysis membranes. We serially measured the change in BUN daily, glomerular filtration rate and 24-hour proteinuria on Day 3 and Day 5 following ischemia. On Day 6, the animals were sacrificed and their kidneys examined histologically. Zymosan and cuprophane exposed rats had a significant delay in the recovery of renal failure, reduced glomerular filtration rate, and histologically had more neutrophil infiltration than control or PAN exposed animals. To investigate the potential pathophysiology of these observations, we assessed the response of zymosan-exposed rats to infusion of deferoxamine (DFO), a potent inhibitor of hydroxyl radical formation (OH.). Infusion of DFO prior to zymosan significantly improved recovery of renal function. We also measured urinary thromboxane B2 levels in these groups of rats. While the groups of rats exposed to zymosan had the highest levels of thromboxane B2, these levels were not different between the groups exposed to zymosan alone, or to zymosan and DFO. These observations suggest a role for hydroxyl radicals in the prolongation of renal failure in this model. Taken together, these findings may have implications for the dialytic intervention in patients with acute renal failure.
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PMID:Complement activation retards resolution of acute ischemic renal failure in the rat. 176 8

Cardiovascular diseases are a leading cause of death in end-stage renal disease (ESRD) largely as a result of the progressively increasing age of ESRD patients and the broad constellation of uremia-associated factors that can adversely affect cardiac function. Hypertension, one of the leading causes of renal failure, is a major culprit in this process, causing left ventricular hypertrophy, cardiac chamber dilation, increased left ventricular wall stress, redistribution of coronary blood flow, reduced coronary artery vasodilator reserve, ischemia, myocardial fibrosis, heart failure, and arrhythmias. In addition to impairing the coronary microcirculation, hypertension may contribute to the development of atherosclerotic coronary artery disease, particularly in the presence of the many lipid abnormalities observed in ESRD. These patients have reduced high-density lipoprotein cholesterol and increased plasma triglyceride concentrations, and there is a defect in cholesterol transport. Other abnormalities that may contribute to atherosclerotic coronary artery disease in ESRD are reduced high-density lipoprotein cholesterol synthesis and reduced activity of the reverse cholesterol pathway. Treatment with fibric acids, nicotinic acids, and lovastatin may be useful in lowering cholesterol and triglyceride concentrations in some of these patients. The incidence of coronary artery disease in ESRD populations is difficult to determine. About 25 to 30% of ESRD patients with angina have no evidence of significant coronary artery disease, and an undetermined number have silent coronary disease. The presence of resting electrocardiographic abnormalities caused by hypertension or conduction defects makes it difficult to accurately diagnosis coronary artery disease in ESRD populations by noninvasive methods, including exercise testing and thallium scintigraphy with or without the use of dipyridamole. Hypotension is a frequent complication of the dialytic process. Many factors have been implicated, including autonomic neuropathy. There is no consensus on the function of the efferent limb of the sympathetic nervous system. The afferent limb (arterial baroreflex function) is felt to be impaired. Further, there may be defects in the ability of the cardiovascular system to respond to sympathetic nerve activity. Most studies of autonomic function have used indirect measurements. Studies are underway that use techniques to assess sympathetic function directly. Such experiments with microneuropathy suggest greater skeletal sympathetic muscle discharge in uremic patients than in normal patients.
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PMID:Cardiovascular complications in renal failure. 177 85

The toxic metabolites of oxygen, including those which are free radicals, have been found to constitute a fundamental common pathway of tissue injury in a wide variety of disease processes, including injury in many organs resulting from post-ischemic reperfusion. Research efforts designed to prevent or ameliorate tissue injury have therefore centered on the pharmacologic inhibition of free radical-mediated mechanisms. This approach has particular application to post-ischemic renal failure seen in renal transplantation, after a well-defined period of graft ischemia, followed by reperfusion.
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PMID:Free radical ablation for the prevention of post-ischemic renal failure following renal transplantation. 179 84

Atrial natriuretic factor (ANF) ameliorates renal damage in animal models of acute ischemic renal failure. Consequently, ANF could blunt acute tubular necrosis related to ischemia that occurs frequently in cadaveric renal transplants. Ten pairs of cadaveric kidneys were transplanted into 20 recipients. Paired recipients received either alpha-human ANF (hANF) or vehicle alone in a prospective, double-blind protocol. Upon revascularization of the allograft, either hANF or vehicle was administered intravenously as a 50-micrograms bolus, followed by a 4-h infusion (0.1 microgram/kg/min). Glomerular filtration rate ([125I]iothalamate clearance) was measured between 4 and 7 days posttransplant and again between 14 and 21 days posttransplant. Serum creatinine was measured daily when patients were in the hospital, then twice weekly as patients were examined in the outpatient clinic. Between the groups, there was no significant difference in age of the recipients or donors, cold ischemia time, or histocompatibility leukocyte antigen match. Infusion of hANF had no adverse effects. When subjects receiving hANF were compared with those treated with vehicle alone, there were no significant differences in serum creatinine or glomerular filtration rate. Three hANF and four vehicle recipients required dialysis postoperatively. At 1 month posttransplant, 19 of 20 patients had functioning allografts; an allograft from one hANF recipient never functioned. It was concluded that hANF, when given by the protocol of this study, had no beneficial effect on the outcome of cadaveric renal transplantation in humans.
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PMID:Atrial natriuretic factor does not improve the outcome of cadaveric renal transplantation. 183 82

Diltiazem--a calcium entry blocker--was tested in a porcine model under continuous chlormethiazole-pancuronium anaesthesia as protection against renal failure following 60 min of renal ischaemia. Fourteen pigs were randomly allocated to one experimental (diltiazem and ischaemia) and one control group (only ischaemia) (n = 7 in each). Diltiazem was administered as a continuous intravenous infusion started before the ischaemic insult. In two additional animals diltiazem was given but ischemia was not induced. The postischaemic renal cortical microcirculation was simultaneously investigated in four different regions in the left kidney during the first 4 h of reperfusion. Laser Doppler flowmetry (LDF) was performed in two different regions and measurement of tissue oxygenation was done in two other regions. In the two animals treated with diltiazem without ischaemia, only minor variations in central haemodynamic and renal microcirculatory parameters were evident. In the control group (ischaemia), superficial renal cortical blood flow (Qsrc) decreased from 49 +/- 11 (s.d.) arbitrary units at baseline to 24 +/- 4 arb. units 4 h after start of reperfusion (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of diltiazem on postischaemic renal cortical microcirculation in the pig. 188 44

Since 1980, 498 patients with 627 critically ischemic legs (rest pain, gangrene, ischemic ulcer, and ankle-brachial pressure index less than 0.40) were treated with revascularization regardless of operative risk or anticipated operative difficulty. Primary amputation was performed only when no graftable distal vessels were present (14 primary amputations [2.8%]) or in neurologically impaired, hopelessly nonambulatory patients. The mortality for revascularization was 2.3%, and the median hospital stay was 11 days. During follow-up, 41 limbs (7%) required amputation, 31 after failure of revascularization and 10 despite patent revascularizations. Renal failure had an adverse influence on limb salvage (67%) because of a significantly increased requirement for amputation despite patent revascularizations. We conclude aggressive limb revascularization in patients with critical lower-extremity ischemia results in low operative morbidity and mortality and excellent long-term limb salvage. Patients with critical leg ischemia and renal failure are at higher risk for limb loss than patients without renal failure.
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PMID:Limb salvage vs amputation for critical ischemia. The role of vascular surgery. 192 26

In order to investigate the role of the outer medulla in acute ischemic renal failure (Epstein FH, Balaban RS, Ross BD: Redox state of cytochrome aa3 in isolated perfused rat kidney. Am J Physiol 1982;243: F356-F363), the distribution of ATP in the in vivo porcine kidney and its relationship to Na transport and to ischemia was examined by using localized 31P magnetic resonance spectroscopy. Renal cortex (ATP) was higher than medulla. Reduction in Na transport produced by partial renal arterial occlusion ("hypofiltration"), resulted in a 13% increase in the ATP/Pi ratio of the whole kidney (from 2.61 +/- 0.26 to 2.96 +/- 0.27; P less than 0.03). This increase was accounted for by a statistically significant increase in (ATP) in the cortex, with medulla contributing to an insignificant extent. Further occlusion of the renal artery to reduce GFR to zero ("hypoperfusion") resulted in a 70% fall in ATP/Pi ratio. (ATP) was reduced most in the cortex, but pH fell equally in cortex and medulla. After release of arterial occlusion, cortical ATP recovered less completely than medulla ATP. Intracellular pH and Pi were restored in both cortex and medulla. It was concluded that cortex and medulla contribute equally to the pattern of disordered energy metabolism in acute renal failure. Sparing of ATP during hypofiltration may reflect the reduced energy requirements of active Na transport.
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PMID:Renal corticomedullary metabolite gradients during graded arterial occlusion: a localized 31P magnetic resonance spectroscopy study. 195 32

A forty-two years old male underwent an aortic arch replacement for an emergency treatment of dissecting aortic aneurysm (DeBakey type I). Separate cardiopulmonary bypass was used with main arterial inflow cannula inserted to right femoral artery. After the operation, ischemia of the right lower extremity led to acute renal failure due to myonephropathic-metabolic syndrome. Peritoneal dialysis, hemodialysis, and continuous arterio-venous hemofiltration were performed. Renal failure improved gradually. At the diuretic phase serum calcium concentration began to rise. Inspite of large amount of fluid and furosemide injection it became higher and finally reached to 20 mg/dl level. Calcitonin injection (320 mu/day) was very effective. In 2 months after surgery serum creatinine and calcium concentrations went down to normal range. Abnormalities in calcium metabolism are frequent in rhabdomyolysis-induced acute renal failure. However, it is rare to encounter such a remarkable hypercalcemia as seen in this patient. When treating MNMS we should pay attention to the changes of serum calcium concentration.
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PMID:[Dissecting aortic aneurysm associated with myonephropathic-metabolic syndrome and hypercalcemia]. 202 21


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