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

Recombinant human erythropoietin (rHuEPO) was purified from the conditioned media of Chinese hamster ovary cells with a transfected human erythropoietin gene. We investigated the effects of the rHuEPO in rats with renal anemia induced by partial nephrectomy. Five-sixth nephrectomy resulted in renal failure with anemia. Twenty-five days after the operation plasma urea nitrogen was increased about 2.5 times, and the red blood cell count, hematocrit, and hemoglobin concentration fell to 85% of normal. The reticulocyte count and plasma erythropoietin level did not change such as they do in patients with anemia due to chronic renal failure. Both total red blood cell volume and the plasma iron turnover rate were depressed in five-sixth nephrectomized rats compared with normal rats. The five-sixth nephrectomized rats were injected with rHuEPO (60 IU/kg) intravenously every second day for a total of six injections. After three injections of rHuEPO, circulation volume of total red blood cells was increased from 9.9 ml to 14.6 ml, and the plasma iron turnover rate was increased from 1.03 mg/kg/day to 2.12 mg/kg/day, and the reticulocyte count was also increased. After six injections, a marked increase of the red blood cell count, hematocrit, and hemoglobin concentration were observed. Plasma urea nitrogen and the creatinine levels as indications for renal function did not change after rHuEPO administration in both normal and five-sixth nephrectomized rats. In conclusion rHuEPO has a potent erythropoietic action and it is possible to cure the anemia caused by renal failure.
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PMID:Effect of purified recombinant human erythropoietin on anemia in rats with experimental renal failure induced by five-sixth nephrectomy. 240 Jun 29

Energy metabolism was measured by indirect calorimetry in 86 patients with various forms of renal failure and in 24 control subjects. In patients with acute renal failure with sepsis, oxygen consumption, carbon dioxide production, and resting energy expenditure were increased (P less than 0.05). In other groups with renal failure (acute renal failure without sepsis, chronic renal failure with conservative treatment or hemodialysis, and severe untreated azotemia) these indices were not different from those of control subjects. Urea nitrogen appearance was decreased in patients with chronic renal failure undergoing conservative treatment, in those with severe untreated azotemia, and in hemodialysis patients (P less than 0.05). We conclude that renal failure has no influence on energy expenditure as long as septicemia is absent. Reduced urea nitrogen appearance rates in chronic renal failure are due to a reduced energy and protein intake. Wasting is a consequence of decreased food intake but not of hypermetabolism in chronic renal failure.
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PMID:Energy metabolism in acute and chronic renal failure. 205 69

One hundred thirty blood samples from 87 patients with renal failure, but without abdominal pain, were analyzed for blood urea nitrogen (BUN), creatinine, amylase, p-isoamylase, and lipase simultaneously. We found that 74, 78, and 80% of the patients had hyperamylasemia, hyperisoamylasemia, and hyperlipasemia. None had amylase higher than five times the upper limit. A few patients (2.3%) had lipase elevated to more than 10 times the upper limit. No significant change of pancreatic enzyme level was noted as a result of hemodialysis, but a significant amount of amylase was removed from the circulation in patients receiving intermittent peritoneal dialysis. Significantly lower pancreatic enzyme levels were observed in patients with less impairment of renal function. We conclude that elevation of pancreatic enzymes in uremic patients is more frequent and more extensive than most articles indicate, and that the extent of increase is related more to renal function than to the modalities of dialysis the patients received.
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PMID:Pancreatic enzymes in uremic patients with or without dialysis. 245 11

In the acute neurosurgical setting, nonketotic hyperosmolar hyperglycemic coma (NHC) is thought to be caused by cerebral dehydration therapy and administration of steroids, glycerol, or mannitol. The mortality of this complication is reportedly very high, and is due to acute renal and/or cardiac failure. The authors evaluated the effect of low-dose dopamine (LDD; 1 to 5 micrograms/kg/min) administration in 10 patients with this syndrome. LDD was given to five patients. In these cases, hypovolemia was treated under central venous pressure monitoring with an iso-osmolar hyponatremic lactate solution given in a volume greater than the urine output. After the hypovolemia was corrected, the fluid was administered in a volume equal to the urine output until the serum osmolarity was normalized. In the five patients not given LDD, a large quantity of hypotonic solution was rapidly administered. In all patients treated with LDD, the urinary sodium increased and the urinary output stabilized. Consequently, the excess urea-nitrogen and serum sodium were quite easily washed out. The total net intake volume for the normalization of serum osmolarity was small and the duration of treatment was much shorter than that of patients not treated with LDD. The LDD regimen was not associated with complications, such as aggravation of cerebral edema, renal failure, or cardiac failure. On the other hand, three of the five patients not given LDD died of acute renal and/or cardiac failure without normalization of laboratory data. It is emphasized that this therapy, which results in beta-effect of catecholamine, sodium diuresis, and increased renal blood flow, is a practical means of managing acute neurosurgical cases complicated by NHC.
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PMID:[Low-dose dopamine treatment of patients in nonketotic hyperosmolar hyperglycemic coma]. 248 37

Several lines of evidence suggest that tyrosine formation is impaired in renal failure. The concentration of tyrosine is decreased and the phenylalanine/tyrosine ratio is increased in plasma and in skeletal muscle cells. After an oral or intravenous load, the rise of plasma phenylalanine is augmented, the clearance is decreased, oxidation is diminished and the corresponding rise of plasma tyrosine level is blunted. Tyrosine elimination and oxidation are not altered in uremia. The defect in tyrosine formation may be especially important in uremic patients on a low protein diet supplemented with tyrosine-free essential amino acid preparations and in subjects on artificial nutritional support. Thus, tyrosine should be regarded as a conditionally essential amino acid in renal failure and should be supplied exogenously, at least in these patient groups. Oral tyrosine supplementation was shown to replete plasma and intracellular pools and improve nitrogen balance in chronic renal failure patients on a low protein diet. However, because of poor solubility in aqueous solutions, tyrosine cannot be included in the free form in amino acid solutions for parenteral nutrition. To circumvent stability or solubility problems, tyrosine containing dipeptides and/or N-acetyl-tyrosine may serve as tyrosine sources for parenteral supply. Renal failure does not affect alanyl-tyrosine hydrolysis, and there is an immediate increase of plasma tyrosine concentration after peptide infusion. Elimination and hydrolysis of glycine-tyrosine is retarded in renal failure, but the clearance exceeds clinically relevant infusion rates. After infusion of N-acetyl-tyrosine, no increase in plasma tyrosine is seen, and the half-life N-acetyl-tyrosine is grossly prolonged in uremia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Phenylalanine and tyrosine metabolism in renal failure: dipeptides as tyrosine source. 251 76

To determine whether pharmacological control of blood pressure could affect the renal function and levels of atrial natriuretic polypeptide (ANP) in spontaneously hypertensive rats (SHR) with renal ablation, and to ascertain the benefits of antihypertensive drugs, we studied effects of oral administration of captopril (50 mg/kg/day), an inhibitor of angiotensin converting enzyme, benidipine (3 mg/kg/day) and nilvadipine (10 mg/kg/day), newly developed blockers of calcium channel, and indapamide (10 mg/kg/day) for 14 days on systolic blood pressure, serum creatinine, blood urea nitrogen, and plasma ANP concentration in SHR subjected to surgical removal of the left kidney and infarction of two-thirds of the right kidney (5/6 nephrectomy) a week before. Three weeks after the surgery, systolic blood pressure (mmHg) in the untreated group was 253 +/- 9 (n = 10), in the captopril group 156 +/- 9 (n = 7, p less than 0.05), in the benidipine group 197 +/- 9 (n = 7, p less than 0.05), in the nilvadipine group 146 +/- 9 (n = 7, p less than 0.05) and in the indapamide group 206 +/- 5 (n = 7, p less than 0.05). Serum creatinine (mg/100 ml) was lower in the captopril group (0.58 +/- 0.02, n = 7, p less than 0.05) and in the benidipine group (0.50 +/- 0.03, n = 7, p less than 0.05) but not in the nilvadipine group and in the indapamide group 3 weeks after 5/6 nephrectomy compared to the untreated group. Blood urea nitrogen was also lower in the captopril group and in the benidipine group but not in the nilvadipine group and in the indapamide group. Plasma ANP concentration was significantly reduced by the treatment with captopril and benidipine but not with nilvadipine and indapamide. These results suggest that the reduction of blood pressure by the inhibition of angiotensin converting enzyme with captopril has the potential to ameliorate renal function of the SHR with remnant kidney, a model of chronic renal failure with hypertension, associated with the decreased concentration of plasma ANP. However, it remains to be determined whether the reduction of blood pressure by calcium channel blockers may be involved in the delayed progression of renal failure in this model since there were disparate effects on renal function and plasma ANP concentration with these two calcium channel blockers.
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PMID:Effects of antihypertensive drugs on renal function and atrial natriuretic polypeptide in spontaneously hypertensive rats with renal ablation. 252 46

27 cases of uremia with abnormal appearances on the chest films were analysed. The results showed that the clinical features were cough, expectoration dyspnea and hemoptysis. However, the degree of these symptoms was relatively mild as judged from the amount of pulmonary edema found on the chest films. The chest X-ray finding in these group of patients were characterized by pulmonary blood stasis, interstitial edema of the lung and edematous alveoli. The pathogenesis of uremic lung was said to be related to blood urea nitrogen and creatinine retention and the concurrent presence of left side heart failure may also play a role. Hemodialysis and other comprehensive treatments could help the patients with uremic lung for relief the symptoms. But the fundamental managements to improve the prognosis for this disease are early treatment of the primary renal diseases, in order to prevent the occurrence of renal failure. Kidney transplantation should be advised.
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PMID:[The uremic lung]. 263 29

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

A persisting incidence of acute renal failure has been observed after operative treatment of thoracoabdominal aortic aneurysm, ruptured abdominal aortic aneurysm and renal artery occlusive disease in patients with preoperative impairment of renal function. Because preservation of kidney function can play an important role in the outcome of these patients, the effects of prostaglandin E1 (PGE1) to prevent ischaemic renal failure were studied in an experimental model. Twenty dogs were exposed to 3 h warm ischaemia by clamping of the supra- and infrarenal aorta and both renal arteries. In 10 dogs PGE1 was given intravenously (100 ng/kg/min) for 15 min before clamping. Ten dogs treated with normal saline served as controls. Glomerular filtration rate, renal plasma flow, plasma creatinine, blood urea nitrogen, urine volume, free water clearance and renovascular resistance were calculated before and after renal ischaemia for both groups. The dogs were followed-up for 2 weeks and radionuclide studies with Tc-99m-MAG3, I-131-OIH and In-113m-DTPA were performed on the third postoperative day to calculate global and split renal clearance, tracer extraction fraction and mean transport time. After renal ischemia 9 dogs of the control group and 3 dogs of the PGE1-group developed acute renal failure (P less than 0.05 due to Fisher's exact text). PGE1 infusion significantly attenuated the postischaemic fall in glomerular filtration rate and renal concentrating ability as well as the postischaemic increase of plasma creatinine and blood urea nitrogen induced by 3 h warm renal ischaemia (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Winner of the ESVS Prize 1988. Effects of prostaglandin E1 (PGE1) on experimental renal ischaemia. 265 70

The uremic syndrome is multifactorial, and affects most tissues and organs. Disturbances in protein and amino acid metabolism may play important roles, especially in chronic uremia, either directly or by production of toxic metabolites, with resultant negative nitrogen (N) balance, muscle wasting, reduced protein synthesis, and characteristically abnormal intracellular free amino acid concentrations. There are also grossly abnormal amino acid levels in the plasma of uremic patients, e.g., increases in conjugated amino acids, high levels of several nonessential and low levels of essential amino acids. The ratios of tyrosine/phenylalanine and of valine/glycine are decreased. The low tryptophan levels may contribute to encephalopathy as a result of an imbalance in neurotransmitter synthesis. Citrulline is found in excess; the explanation is unresolved. There are elevated concentrations of the sulfur-containing amino acids: cystine, taurine, cystathionine, and homocysteine. Excess of the latter is implicated in the atherogenesis of renal failure. Disturbed metabolism and interorgan exchange of amino acids in the uremic state explains some of the abnormalities in tissue and plasma concentrations of individual amino acids. Enzymatic defects are involved in the disturbed metabolism of branched chain amino acids (BCAA), with possible antagonism among them, which impairs growth and amino acid utilization. Carbohydrate intolerance, associated with insensitivity of peripheral tissues to insulin and hyperinsulinemia, elicits decreased plasma BCAA. Protein synthesis rates in normal and pathological conditions are more closely related to the intracellular amino acid pool than to plasma amino acid levels. Concentrations of individual amino acids in the plasma pool are poor indicators of their intracellular concentrations. Muscle contains the largest pool of protein and free amino acids in the body. In chronic renal failure patients, the intracellular concentrations of valine, threonine, lysine, and carnosine are low. With low protein diets and in hemodialysis, serine, tyrosine, and taurine often are also low. The low taurine may be related to fatigue and to uremic cardiomyopathies. The commonly used amino acid supplements generally fail to correct the intracellular amino acid deficits. A "New Formula" has been developed to correct these intracellular amino acid abnormalities, and to supplement a low protein diet. It provides more valine than leucine, increased tyrosine and threonine, and less histidine, leucine, isoleucine, lysine, methionine, and phenylalanine than in formulas customarily used for patients with chronic renal failure. It is uncertain whether other ap
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PMID:Amino acid metabolism in uremia. 267 58


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