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

During the 1970s renal biopsies were obtained after blood pressure had been controlled in 41 black patients in Memphis who had severe hypertension plus excretory renal failure. An additional 13 binephrectomy specimens were also studied. This material yielded significant information on the state of the renal arteries--arterioles under these circumstances. Fibrinoid necrosis of the afferent glomerular arteriole and proliferative glomerulitis were not noted. Rather, the vascular lesion characterized by the accumulation of smooth muscle cells and mucopolysaccharide in the intima attended by a marked narrowing of the lumen was dominant. This lesion caused pronounced ischemia associated with obsolescence of glomeruli, atrophy, and fibrosis (end-stage kidney). This lesion has been renamed musculomucoid intimal hyperplasia as a result of changes revealed by electron microscopic and histochemical studies. Since this study the incidence of this severe vascular disease of the kidney in the same geographic area has been markedly reduced. There are a number of possible reasons for this change in incidence, but a major one appears to be improved treatment of hypertension and better compliance with antihypertensive therapy. Why such extreme changes occur in a subset of hypertensive blacks is not known. It is apparent that without improved antihypertensive treatment, this type of end-stage renal disease due to severe vascular damage will continue to be encountered.
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PMID:Histopathology of severe renal vascular damage in blacks. 262 Apr 72

Preserved organs are damaged not only by the ischemic injury due to lack of oxygen. The reperfusion injury mediated by oxygen free radicals is an important factor in the postischemic organ failure. The prevention of free radical-induced reperfusion injury with allopurinol (AP) and superoxide dismutase (SOD) is shown in a warm ischemia kidney model. Rats were treated with allopurinol (40 mg/kg i.v.) one hour, or with SOD (20,000 IU/kg i.v.) one minute before reperfusion after a period of 35 minutes of warm ischemia. Allopurinol and SOD reduced significantly the postischemic kidney failure with a less important increase of creatinine. Creatinine levels on day three in the control group: 517 +/- 87 mumol/ml, in the SOD-group: 206 +/- 105 mumol/ml, and in the AP-group: 163 +/- 81 mumol/ml (anal. of variance: p = 0.0001). AP has a wide therapeutic range. We feel, that it is important to confirm the prevention of reperfusion injury by allopurinol prophylaxis clinically.
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PMID:[Reduction of renal reperfusion damage following warm ischemia by allopurinol and superoxide dismutase]. 263 82

A previous article (Part I) described the patient population and operative management of 666 patients who had surgery for nonruptured abdominal aortic aneurysms. This article details the perioperative complications and, by chi-square and logistic regression analysis, identifies the variables that are associated with each complication. In summarizing the results (below) the incidence of each complication is listed, along with the predictive risk factors in parentheses that have significance levels less than 0.05. Vascular morbidity data are as follows: intraoperative bleeding, 4.8%; postoperative bleeding requiring transfusion, 2.3% or repeat operation, 1.4% (large volume of blood transfusion and/or use of an autotransfusion device); intraoperative limb ischemia, 3.5%; graft thrombosis, 0.9% (femoropopliteal disease and/or distal anastomosis at the femoral level); distal thromboembolism, 3.3% (male sex, femoral popliteal disease, and/or intraoperative graft thrombosis); amputation, 1.2%; graft infection, 1 case. General morbidity data are as follows: cerebrovascular event, 0.6%; paraplegia, 1 case; cardiac event, 15.1% (age, previous episode of congestive heart failure, and/or electrocardiogram [ECG] evidence of a previous myocardial infarction); myocardial infarction, 5.2% (advancing age, angina, and/or prolonged aortic cross-clamp time); congestive heart failure, 8.9% (previous history of congestive heart failure, ECG evidence of ischemia, and/or chronic obstructive lung disease); arrhythmia requiring treatment, 10.5% (preoperative ventricular premature beats and/or respiratory failure requiring ventilation for more than 48 hours); new arrhythmia, 8.4% (angina and/or chronic obstructive lung disease); respiratory failure, 8.4% (chronic obstructive lung disease, large volume of blood transfused, and/or occurrence of postoperative bleeding, cerebrovascular accident, congestive heart failure, or myocardial infarction); renal damage with rise in creatinine or blood urea nitrogen, 5.4% and/or renal failure requiring dialysis, 0.6% (elevated preoperative creatinine, suprarenal aortic cross-clamping, and/or renal vein ligation); diarrhea without evidence of ischemia colitis, 7.1% and ischemic colitis, 0.6% (pelvic flow interrupted); prolonged ileus, 11.0% (aortoiliac occlusive disease, deterioration of renal function, prolonged ventilation, and/or preoperative history of angina); superficial wound infection, 1.5% and deep infection, 0.5% (femoral anastomosis and/or female sex); coagulopathy, 1.1% (large volume of blood transfused).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Multicenter prospective study of nonruptured abdominal aortic aneurysm. Part II. Variables predicting morbidity and mortality. 264 60

Endoaortic calcified proliferation, also known as coral reef atherosclerosis represents a rare form of atherosclerosis characterized by a gross appearance and location in the thoracic and celiac aorta. We report two new cases of calcified obstruction of the aorta. In the first case, clinical examination revealed hypertension, abdominal angina associated with abdominal bruit, and diminished femoral pulses. The second case was diagnosed postoperatively when intractable hypertension and renal failure ensued following reconstruction of an abdominal aortic aneurysm. Accurate evaluation of lesions was possible through Doppler sonography, CT scan, and aortography. Because of hypertension and visceral ischemia, surgical treatment was required. Hypertension and intestinal angina were completely relieved in the first case, while hypertension and renal failure improved greatly in the second.
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PMID:Endoaortic calcific proliferation of the upper abdominal aorta. 266 16

Phosphorus-31 (31P) magnetic resonance spectroscopy of the kidneys promises to provide metabolic information leading to better assessment of renal physiology. However, the problems of studying the metabolism of the heterogeneous renal architecture by precisely localizing the origin of the signal obtained from small voxels and eliminating motion artifacts have not been solved as yet. The normal 31P MRS spectra show a characteristic fingerprint of six peaks including phosphomonoesters, phosphodiesters, inorganic phosphorus, and gamma, alpha, beta adenosine triphosphate (ATP). Renal failure, regardless of its etiology and mechanism of inducement (hypoxia, ischemia, acidosis, or obstruction) produces a loss of ATP with a progressive increase of inorganic phosphorus and a decline in intracellular pH. The severity of renal failure correlates with the severity of the metabolic disturbance. The potential use of 31P MRS in the assessment of renal viability has been applied to the study of renal preservation methods and prediction of renal function following transplantation.
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PMID:Phosphorus-31 MRS of the kidney. 269 45

When major vascular occlusion is carried out in the presence of systemic shock and there has been obstruction to blood supply of an extremity, restoration of circulation is not without risk. Morbidity and mortality relate directly to the duration and the degree of ischemia and the mass of tissue involved. The initial problem following the onset of ischemia relates to acidosis and hyperkalemia when limbs are reperfused after several hours of ischemia. When ischemia has been present for more than six to eight hours, there will be death of tissue and reperfusion at this point results in the products of dead and devitalized tissue being washed into the systemic circulation. This produces intravascular coagulation and a diffuse inflammatory response with systemic vascular permeability. Respiratory distress syndrome will develop if the ischemic injury is severe. If patients are not adequately monitored and blood volume maintained, renal failure and multiple organ failure will develop in parallel.
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PMID:The reperfusion syndrome. 270 Mar 72

Three healthy adult males developed acute renal failure following cocaine abuse. Muscle pain, tenderness, elevated levels of serum muscle enzymes, heme-positive urine and the presence of pigmented granular casts in urine all indicated occurrence of rhabdomyolysis. One of them developed acute compartmental syndrome of the left leg and required emergency fasciotomy. The course of renal failure and fast recovery were suggestive of acute tubular necrosis in all 3 patients. A possible role of cocaine in the aggravation of renal and/or muscle ischemia has been speculated.
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PMID:Acute renal failure following cocaine abuse. 231 44

Renal atherosclerosis and fibromuscular dysplasia are the most common causes of curable human renovascular hypertension and renal failure. Vascular reconstruction often preserves renal function, but renal failure is rarely reversed, especially after days of anuria. We report a case of a 23-year-old woman who as a child underwent a nephrectomy for congenital hydroureter and renal hypoplasia. She later experienced fibromuscular dysplasia of the remaining renal artery, which ultimately progressed to a complete occlusion and 31 days of total anuria. The patient was revascularized, and within 2 months renal function returned with a blood urea nitrogen and creatinine of 9.0 and 1.0 mg/dl, respectively. After a follow-up of 6 months the patient's blood pressure remained 120/80 to 130/80 mm Hg without administration of hypertension medication. In this report we emphasize that under selected circumstances a kidney can survive prolonged ischemia and that delayed revascularization may reestablish renal function.
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PMID:Successful revascularization of an occluded renal artery after prolonged anuria. 272 67

Fructose 1,6-diphosphate (FDP) has been shown to attenuate tissue injury associated with ischemia and shock by enhancing the anaerobic carbohydrate utilization and by inhibiting oxygen-free-radical generation by the neutrophils. Previously, we have reported that FDP prevents ischemic renal failure if administered prior to the ischemic insult. The present study was designed to determine whether this agent could prevent renal damage when administered during the postischemic reperfusion period. Rats were subjected to 30 min of bilateral renal artery occlusion and infused with FDP (350 mg/kg body wt) beginning 10 min after release of the renal artery clamps. Control rats received an equal volume of glucose/saline solution. A third group of rats were sham operated. Twenty-four hours after injury, BUN, creatinine, and fractional sodium excretion values were less in FDP-treated rats than in control rats (P less than 0.001, P less than 0.005, and P less than 0.001, respectively) and not different from values observed in sham-operated rats. Inulin clearance was greater (P less than 0.001) in FDP-treated rats than in control rats (665 +/- 38 microliters/min/g kidney wt). Renal histology was also better preserved in the FDP-treated group. These data suggest that FDP infused after the initiation of an acute ischemic insult provides significant, but not complete, functional and histologic protection from renal damage.
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PMID:Attenuation of ischemic renal injury with fructose 1,6-diphosphate. 277 Feb 78

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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