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)

A 55-year-old woman with chronic renal failure treated with hemodialysis had severe bilateral visual loss develop due to retinal ischemia. Ophthalmoscopy showed crystals in the distribution of the retinal arteries, but not veins, and this led to a diagnosis of systemic oxalosis. Factors contributing to systemic oxalosis in addition to renal failure were ascorbic acid dietary supplementation, pyridoxine deficiency, and ileal resection. Histopathologic findings showed ocular calcium oxalate deposition limited nearly entirely to the walls of retinal blood vessels.
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PMID:Retinal oxalosis. A clinicopathologic report. 281 86

Two hundred fifty eight patients had percutaneous transluminal coronary angioplasty. Of those, 48 cases underwent surgical revascularization for unsuccessful angioplasty. Sex was not a risk factor. Timely surgical revascularization reversed acute ischemia and/or myocardial infarction or limited the size of the infarction in 32 of the 48 patients or 67%. Revascularization procedures were performed in six out of forty-eight patients who had previous aortocoronary by-pass surgery and attempted PTCA, none had any complications. Death occurred in one out of forty-eight patients, or 2%. Femoral-femoral by-pass devices, in addition to intra-aortic balloon devices, should be available in the cardiac catheterization laboratory. Patients with multi-vessel disease are at greater risk of angioplasty and surgery. Sixteen out of 23 patients (70%) who had emergency revascularization procedures had multi-vessel disease. In one patient with borderline renal function, emergency surgery after PTCA with a large amount of renograffin dye injected caused renal failure and led to permanent dialysis.
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PMID:Incidence of coronary artery by-pass graft following percutaneous transluminal coronary angioplasty. 295 12

Because of its ability to increase glomerular filtration, antagonize the actions of vasoconstrictors, and produce vasodilation, alpha human atrial natriuretic peptide (alpha-hANP) was evaluated for its potentially beneficial effects in experimental ischemic renal failure induced by 45-60 min of renal artery occlusion in bilaterally or unilaterally renally intact Sprague-Dawley rats. After ischemia, a 4-h intrarenal infusion of alpha-hANP restored 14C-inulin clearances in bilaterally and unilaterally intact animals from 0.05 +/- 0.006 and 0.05 +/- 0.01 ml/min per 100 g to 0.314 +/- 0.04 and 0.25 +/- 0.01 ml/min per 100 g, respectively (P less than 0.001, n = 8), compared with normal values of 0.49 +/- 0.023 ml/min per 100 g. Histologically, there was a progressive decrease in medullary hyperemia and prevention of intratubular cell shedding and granulocyte margination as a result of the 4-h alpha-hANP infusion such that after 24 and 48 h the histological appearance of the tissue was essentially normal. The results show that a 4-h intrarenal infusion of alpha-hANP after renal ischemia can preserve glomerular filtration rate and reduce renal tissue damage.
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PMID:Atrial natriuretic peptide protects against acute ischemic renal failure in the rat. 296 Jun 93

Postischemic renal failure is a severe problem following cadaveric renal transplantation, especially if the kidney has been harvested from a non-heartbeating donor, and thereby subjected to periods of both warm and cold ischemia. It is well established that a substantial component of postischemic injury is produced by oxygen-derived free radicals generated from xanthine oxidase at reperfusion. However, the clinical potential of free radical ablative therapy is dependent upon the proportion of the total injury caused by this reperfusion mechanism, compared with the proportion resulting from ischemic injury per se. Therefore, we quantitatively evaluated these proportions in porcine kidneys subjected to various periods of warm (renal artery occlusion in situ), cold (harvest, cold preservation, and allotransplantation), and combined warm and cold ischemia. Experiments were paired, one kidney treated with either superoxide dismutase (SOD) or allopurinol for free radical ablation, the contralateral kidney serving as a control. Creatinine clearance (Ccr) was measured separately for each kidney 48 hr after reperfusion. After 1 and 2 hr of warm ischemia, Ccr dropped to 50% and 36% of normal, respectively. This was improved to 110% and 55% when SOD was given into the renal artery at reperfusion. Similarly, after 24 and 48 hr of cold ischemia, kidney function was significantly improved from 30% and 18% to 72% and 47% of normal, respectively, when allopurinol was added to the preservation solution. SOD used at harvest and again at reperfusion was particularly effective following combined warm and cold ischemia, in a situation mimicking the harvest of cadaver kidneys from a non-heartbeating donor. These findings suggest that the ablation of free radical-mediated reperfusion injury may improve posttransplant renal function sufficiently to allow expansion of the cadaveric donor pool to include non-heartbeating donors.
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PMID:Ablation of free radical-mediated reperfusion injury for the salvage of kidneys taken from non-heartbeating donors. A quantitative evaluation of the proportion of injury caused by reperfusion following periods of warm, cold, and combined warm and cold ischemia. 327 16

Hypertension can directly damage blood vessels, and leads to renal failure, intracranial bleeds, and lacunar infarctions. Of equal importance is the effect of hypertension on the development of atherosclerosis. Specific changes in both the microvasculature and macrovasculature vary depending on the degree and rapidity of blood pressure elevation. Changes in the intima and media can lead to significant narrowing of vessels and ischemia in various tissues. In addition, changes in small-resistance vessels contribute to changes in peripheral-vasculature resistance and thus affect blood pressure regulation. Treatment of moderate to severe elevation in blood pressure clearly results in a decrease in the incidence of stroke. However, evidence that treating mild hypertension reduces coronary events is less convincing. Antihypertensive therapy may result in partial regression of vascular changes, especially fibrinoid necrosis seen in malignant hypertension, but more work needs to be done to clearly define the roles of specific drugs in preventing or regressing hypertensive vascular disease.
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PMID:Vascular changes in hypertension. 330 5

There has been a serious shortage of suitable kidneys for transplantation since this procedure became the treatment of choice for many patients with end-stage renal failure. Some harvested kidneys are discarded due to complicated or injured renal vasculature and some potential living related donors are judged unsuitable because their kidneys have multiple vessels. The authors review the basic microsurgical techniques they have used in such situations to salvage kidneys for transplantation. They emphasize the ex-vivo, "bench", microsurgical method for protecting the kidney from prolonged warm ischemia time (as with multiple complicated in-situ anastomoses). Several illustrative case reports from their recent experience are presented. The authors conclude that microvascular surgery is an important adjunct to the armamentarium of the transplant surgeon.
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PMID:Microvascular surgery as an adjunctive tool in renal transplantation. 352 79

Experiments were performed on rats subjected to renal ischemia and various treatment procedures to determine the origin and functional consequences of vascular obstruction. To this end, its occurrence and severity was assessed qualitatively and quantitatively in the outer medulla, where it is particularly prominent. The incidence of medullary hyperemia was not influenced by inhibiting thrombocyte aggregation with 5 or 70 mg/kg of acetyl salicylic acid or preventing fibrin deposition with 100 IE/kg of heparin before ischemia, and these substances produced no improvement renal function. The incidence and degree of hyperemia, however, could be substantially reduced or completely eliminated by acutely raising blood pressure after ischemia or by decreasing the number of circulating erythrocytes before ischemia. These procedures were effective in raising filtration rate and tubular reabsorption from 20% to 60% of normal, in restoring renal blood flow and vascular resistance to completely normal, and in diminishing epithelial damage both three and 18 hours after ischemia. The following conclusions are drawn: first, vascular obstruction, which is not lessened by inhibiting thrombus formation but is easily reversed or prevented by raising perfusion pressure or decreasing hematocrit, is probably caused by erythrocyte aggregation during ischemia. Second, vascular obstruction, which appears to raise renal vascular resistance and lower blood flow and filtration rate, cannot be limited to the medulla but must also be present in the cortex. Finally, reversing or preventing vascular obstruction can fully restore renal perfusion, partially restore glomerular and tubular function, greatly reduce tubular necrosis and thus prevent renal failure.
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PMID:The contribution of vascular obstruction to the functional defect that follows renal ischemia. 356 Jun 46

Compromised kidney function in the perinatal period has been increasingly recognized during recent years, and acute renal failure is a frequent clinical situation in neonatal intensive care units. Renal underperfusion due to various prerenal conditions is assumed to be the most common cause of renal failure in neonates. With rapid restoration of renal blood flow, prerenal failure is completely reversible in the early course of the disease. If adequate treatment is delayed, however, structural damage to the kidneys by prolonged ischemia will ensue leading to a poor prognostic outcome. This review, therefore, mainly focuses on early diagnosis of disturbed neonatal kidney function and prophylactic therapeutical aspects which may be of particular benefit for critically ill newborns at high risk for developing acute renal failure.
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PMID:[Disorders of kidney function and acute kidney failure in newborn infants]. 356 18

Four patients with the crush syndrome due to prolonged limb compression were treated at Cook County Hospital, Chicago. Limb injury was caused when the obtunded patient fell asleep lying on the involved extremity. Prolonged limb compression may cause an acute compartment syndrome with ischemic muscle injury. Continued muscle ischemia may lead to myonecrosis resulting in shock or renal failure. A history of prolonged limb compression with a swollen limb should suggest the diagnosis of crush syndrome. Prompt therapy, including rapid correction of volume and metabolic derangements, extensive open fasciotomy, and dialysis for severe acute renal failure should provide good functional results in the majority of patients.
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PMID:Crush syndrome due to limb compression. 361 24

Prior acute renal failure (ARF) induced by either glycerol (G) or mercury provides protection against rechallenge with the same agent or the other. To ascertain whether the widely employed ischemic renal failure model also shares a similar pathogenesis, two protocols were designed. In the first protocol, unilaterally nephrectomized rats with or without a prior episode of G-induced ARF two weeks previously were subjected to an ischemic insult [60-min total left renal artery clamp (LRAC)]. At 24 or 48 h after LRAC there was no difference in renal function in the rats with or without prior ARF. In the second protocol the sequence of G and ischemia was reversed. In rats having undergone LRAC two weeks prior to G, glomerular filtration rate was virtually identical from the right (control) and left (prior ARF) kidney (right, 138 +/- 30; left, 101 +/- 22 microliter/min/100 g body weight), and not different from rats receiving G alone. We conclude that protection against ARF conferred by prior insult is not a feature of all models.
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PMID:Protection against acute renal failure by prior acute renal failure: differences between myohemoglobinuric and ischemic models. 368 91


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