Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The excretional patterns of lactate, pyruvate and alpha-ketoglutarate were investigated after renal transplantation in 36 patients. Fourteen patients had received a living-donor kidney with short ischemia time and good initial graft function, 22 had a cadaver transplant with an initial 125iothalamate clearance of more than 6 ml/min. The excretion of lactate and pyruvate did not vary significantly from that seen in normal controls or patients with uremia. In six patients with cadaver transplants, clearance values of alpha-ketoglutarate exceeded that of the glomerular filtration rate, indicating a net tubular secretion of this substance. During acute rejection episodes in 5 patients, no changes were seen in the excretional patterns of lactate, pyruvate and alpha-ketoglutarate.
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PMID:The excretional patterns of lactate, pyruvate and alpha-ketoglutarate in renal transplants. 34 53

The author presented his observations of a small group of rabbits to which he administered small doses of dopamine under conditions of warm ischemia (the time between the clamping of the renal artery till the beginning of hypothermic extracorporeal circulation). Another group of rabbits did not receive dopamine. Those rabbits that were given dopamine lived longer and were more resistant to uremia and toxemia. The effect of dopamine lived longer and were more resistant to uremia and toxemia. The effect of dopamine is thought to be due to its vasodilator action on the kidney during periods of hyoxia ad hypotension. The author explained that the kidneys withstood three hours of warm ischemia when treated with dopamine. p.s. This paper is an abstract from the authors dissertation: Protective Action of Dopamine on the Kidney Damaged During Warm Ischemia.
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PMID:[Experimental investigation of the preservation of kidneys damaged during warm ischemia]. 51 30

Clusterin is a multifunctional protein isolated from a number of tissues in several different species. In a variety of renal diseases, clusterin appears in the glomerulus and tubules in association with the membrane attack complex of complement. It is also transiently expressed after several forms of acute renal injury. In this study, we examined the expression and intrarenal distribution of clusterin following subtotal renal ablation. Male rats were subjected to either 1-1/3 nephrectomy (1-1/3 NX), uninephrectomy (UNX) or sham operation (SHAM). Two weeks after surgery, clusterin mRNA was elevated in the 1-1/3 NX group (1-1/3 NX: 1215 +/- 88; UNX: 208 +/- 11; SHAM: 207 +/- 19 OD units; P less than 0.001). Clusterin mRNA increased between 3 and 24 hours after 1-1/3 NX, plateaued, and remained elevated for at least seven weeks. The increased clusterin mRNA in 1-1/3 NX was localized to the tissue adjacent to the infarctive scar (scar 858 +/- 173 vs. non-scar 98 +/- 27 OD units; P less than 0.001). Clusterin protein followed a similar pattern of localization, being increased in most tubules and some peritubular capillaries in the peri-infarct zone. Only occasional tubules were positive for clusterin in the renal tissue distant from the scar or in the kidneys of sham operated rats. Co-localization of clusterin and C5b-9 was not detected. Evidence for apoptosis was found in the peri-infarct zone but not elsewhere in 1-1/3 NX kidney or in the normal kidney following sham operation. Infarction of 1/3 of the left kidney without contralateral nephrectomy, a maneuver which eliminates the compensatory growth, and uremia seen with 1-1/3 NX still resulted in increased clusterin mRNA in the infarcted left kidney compared to the intact right kidney (LK: 790 +/- 112 vs. RK: 128 +/- 25 OD units; P less than 0.001), although the amount of clusterin mRNA was less than that found following 1-1/3 NX. In conclusion, persistently increased clusterin mRNA and protein was seen in the peri-infarct zone following 1-1/3 NX. This increased expression of clusterin may be playing a role in the ischemia-related apoptosis present in the scar-adjacent tissue.
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PMID:Intrarenal distribution of clusterin following reduction of renal mass. 151 15

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

Transplantation of the pancreas in late stages of type I diabetes has been performed increasingly frequently during recent years. By improved surgical techniques and immunsuppressive therapy including cyclosporin A, the 1-year graft function has increased to 60-70% and the patient survival to 85-95% in the institutions with greatest experience. These results are so good, that they nearly reach those from kidney transplantation. Most of the pancreas transplantations have been performed simultaneously with kidney transplantation in patients with end stage diabetic uremia. The results should therefore be evaluated according to these circumstances. In a few institutions transplantation of the pancreas is now performed in patients with persistent proteinuria and proliferative retinopathy in an attempt to avoid development of severe diabetic complications. The first pancreas transplantation in Denmark was performed Januar 31 st 1987, and since then, 17 further transplantations have been performed. All patients had severe diabetic nephropathy and received simultaneous kidney transplantation. According to the Danish heart death criteria the organs were perfused and cooled during the donor operation to keep the warm ischemia as brief as possible. The pancreatic vessels are anastomosed to the iliac vessels. In one group of patients the exocrine pancreatic function was preserved by anastomosis to the jejunum, and in another group of patients the exocrine function was abolished by injection of latex into the pancreatic duct system. The patients receive immunosuppression therapy with methylprednisolone, azatioprine and ciclosporin A and anti-coagulation therapy.
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PMID:[Simultaneous transplantation of the pancreas and kidney in terminal diabetic nephropathies]. 264 99

1. In this prospective study of 613 CD and 205 one haplotype mismatched LRD transplant recipients treated with CyA, there was no influence of HLA-matching (A, B, DR or combinations) on graft survival rate at one and two years. 2. Patients who successfully received HLA-DR-matched kidneys (CD or LRD) had fewer rejection episodes during the first six months after transplantation. 3. Three factors significantly reduced the cadaveric graft survival rate: (a) presence of panel reactive T-cell antibodies in a current recipient serum, (b) cold ischemia time beyond 27 hours, and (c) recipient age above 55 years. 4. The survival rate of one haplotype mismatched LRD kidneys was excellent and is considered to be the optimal treatment for uremia also in CyA-treated patients. 5. Based on this study, exchange of well HLA-matched CD kidneys to non-sensitized patients has been terminated provisionally in Scandia-transplant. Exchange of HLA-A, B-matched kidneys will be maintained, however, for sensitized patients inasmuch as this will increase the chance of obtaining a negative cross-match and possibly improve graft survival in this high-risk patient group.
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PMID:HLA-matching in cyclosporine treated renal transplant recipients: a prospective Swedish-Norwegian multicenter study. 315 55

Up to 1 percent of renal transplant recipients have been reported to develop ischemic colitis. Immunosuppressive agents and uremia have been implicated in the development of this complication, but their exact relationship remains unclear. A rat model was developed to determine the effects of uremia alone and in combination with immunosuppression on the development of ischemic colitis. Seventy-six animals were included in the study. Uremia and ischemic colitis were induced surgically. The immunosuppressive agents azathioprine and methylprednisolone were administered for 72 hours after a colonic segment was devascularized in chronically uremic rats. One-way analysis of variance (ANOVA) showed that uremia potentiates colonic ischemia significantly (4.09 cm2 vs 1.25 cm2, P less than 0.03). The addition of parenteral steroids (methylprednisolone) or azathioprine alone and in combination did not potentiate or reduce this ischemic process in uremic animals. Each of these factors alone is commonly present in the renal transplant population and can contribute to the development of potentially fatal ischemic colitis.
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PMID:The influence of uremia and immunosuppression on an animal model for ischemic colitis. 376 86

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.
Uremia Invest
PMID:Renal morphology and function and urine electrolytes in experimental acute renal failure produced by cyclosporine and ischemia. 384 27

Cyclosporine-associated arteriopathy was the cause of graft loss in 40 percent of all allografts that failed in a series of 200 consecutive cadaveric renal transplants. Arteriopathy was diagnosed by biopsy and renal uptake of indium 111m labeled platelets in the face of acute renal deterioration. A moderate thrombocytopenia and microangiopathic picture of hemolytic uremia was also present on peripheral blood smear. Immunofluorescence and histologic characteristics of the allograft biopsy specimens failed to show evidence for acute rejection: immunoglobulin M, immunoglobulin A, immunoglobulin G, C1q, C3, and C4 were not present, and there was no evidence of an interstitial or vascular mononuclear cellular infiltrate. Two clinical presentations have been described. In Group I (seven patients), anuria occurred rapidly within the first 2 weeks after transplantation. In Group II (nine patients) renal function gradually diminished 1 to 5 months after starting cyclosporine therapy. Fifteen of the 16 recipients had progressive and irreversible loss of renal function which was pathologically associated with fibrin deposition, intimal proliferation, and thrombotic occlusion of the cortical interlobular and arcuate arteries, with subsequent focal glomerular ischemia and cortical infarction. One recipient with rapid loss of renal function received an intraarterial allograft infusion of streptokinase and subsequent systemic heparinization, which resulted in return of normal allograft function. The syndrome of cyclosporine-associated arteriopathy has been linked to a lack of or reduced amounts of prostacyclin-stimulating factor or prostacyclin.
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PMID:Cyclosporine-associated renal arteriopathy resulting in loss of allograft function. 389 78

Chronic renal failure and its sequelae, particularly secondary hyperparathyroidism, may be associated with spontaneous quadriceps tendon ruptures. This is a report of two cases of bilateral spontaneous simultaneous quadriceps tendon ruptures in uremia and a review of the literature. The level at which the tendon ruptures is inconstant. Light microscopy reveals nonspecific changes of degeneration and calcification. Under electron microscopy, the structure and maturity of collagen fibers are normal. The ruptures occur in patients younger than 40 years of age who reject medical treatment (i.e. oral phosphate binder) and have long-standing renal disease (mean = 12.3 years). The predisposing causes of rupture are unknown. An abnormality of collagen metabolism, ischemia, direct effects of parathormone, and dystrophic calcification are some of the possible contributory factors.
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PMID:Quadriceps tendon ruptures in uremia. 397 53


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