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

The renal response of the fetal lamb to repeated complete occlusion of the umbilical cord was studied in nine chronically instrumented animals. Five episodes of occlusion of the umbilical cord, each lasting for two minutes, produced a twofold rise in fetal urine osmolality and sodium, chloride, and potassium concentrations. Output of urine and glomerular filtration rate remained essentially unchanged while free water clearance decreased from a control of +0.10 to -0.02 ml. per kilogram per minute at the end of the fifth episode. Electrolyte concentrations in urine remained elevated for at least two hours following the occlusions. In addition to changes in urine composition, there was a 50- to 200-fold increase in the fetal plasma concentration of vasopressin. These studies indicate that complete interruption of the umbilical circulation, even though of short duration, produces disturbances in fetal renal function that can lead to loss of electrolytes in the urine. They provide an explanation for the low sodium levels reported in asphyxiated newborn infants in renal failure.
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PMID:Renal response of fetal lamb to complete occlusion of umbilical cord. 2 86

Conservative management of chronic renal failure in children is essentially based on dietary prescription including recommendations for high caloric intake and a certain limitation of protein intake according to GFR in order to avoid any extra loading with nitrogen wastes. Prescriptions for sodium potassium and water have to be adjusted on their residual output. Prevention of osteodystrophy needs supplement of calcium, chelation of phosphorus with aluminium hydroxide and the prescription of vitamin D or its active derivatives. High blood pressure when present must be carefully controlled. Drugs, when necessary, have to be given with a dosage taking into account the level of renal failure. Finally, the mode of life of the uremic child should be as close to normal as possible.
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PMID:Conservative treatment of chronic renal insufficiency in children. 4 67

In the past four years, four cases of gasoline contact burns have been treated at the Detroit General Hospital Emergency Department. Signs are erythema and blister formation within 24 hours. Treatment is removal of contaminated clothing and washing the surface with soap and water plus open exposure of the wounds. Renal failure is not caused by skin absorption but may develop following inhalation.
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PMID:Gasoline contact burns. 4 82

Patients with renal failure often have wasting syndrome, owing both to poor dietary intake and to the rigors and consequences of the uremic syndrome. Dietary therapy aims to improve nutritional status and also to minimize uremic toxicity and the metabolic imbalances associated with failing kidney function. Excessive protein intake can increase uremic toxicity, but opinion is divided as to when protein intake should be restricted. Restriction rarely is necessary until the glomerular filtration rate (GFR) is below 25 ml/min. When the GFR is between 4 and 10 ml/min, a diet containing 35 (for women and very small men) to 40 gm of high-quality protein will maintain good nutrition and relative freedom from symptoms. With a GFR below 4 to 5 ml/min, maintenance dialysis should be instituted or a supplemental diet containing essential amino acids may be used. Most patients should receive calories in the amount of at least 35 kcal/kg of body weight per day. Supplements of folic acid, pyridoxine hydrochloride, ascorbic acid, and the water-soluble vitamins should be given. Sodium and water restriction may be necessary.
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PMID:Nutritional management of chronic renal failure. 10 82

Acute oliguric renal failure due to acute interstitial nephritis developed in a patient after treatment with phenylbutazone. The histological, immuno-histological and serological features in this case are compatible with the involvement of a delayed hypersensitivity reaction in the pathogenesis of this drug-induced interstitial nephritis. Other side effects of phenylbutazone on the kidney and the water and electrolyte metabolism are discussed.
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PMID:[Acute interstitial nephritis with oliguric renal failure following phenylbutazone medication]. 14 10

As the population of nephrons diminishes, while the dietary intake and/or endogenous production of water and solutes is unchanged, there is a proportional increase in the excretion of water and solute by individual residual nephrons. This adaptive change, which preserves zero net balance in the early phase of renal insufficiency, involves a reduction in the fractional reabsorption of substances derived from the initial glomerular ultrafiltrate and an increase in the rate of secretion of solutes that are extracted by tubular epithelial cells from peritubular blood. These compensatory changes are adequate to maintain electrolyte and water homeostasis until severe renal failure ensures (GFR less than 20% of normal). After a moderate reduction in nephron population there is no evidence that the factors that modulate ion transport are qualitatively different from those that regulate renal function in the intact subject, when the excretory load of solute is varied by changes in intake or endogenous production. In severe renal insufficiency, however, it seems likely that several factors, not present in the subject with intact renal function, also play an important role in modifying the excretion of water and electrolytes. For example, an osmotic diuresis in severe renal failure apparently decreases the tubular reabsorption of sodium and divalent cations and that of water. Moreover, elaboration of a partially identified "natriuretic" substance may participate in the regulation of electrolyte excretion in severe renal insufficiency. The appearance of these factors in severe renal insufficiency probably complements mechanisms that normally regulate the transfer of water and ions across tubular epithelium, since even after a marked reduction in GFR the urinary excretion of solutes and water changes proportionally with intake, although within narrower limits than exist in normal subjects. Studies in experimental animals and in man with acquired renal disease demonstrate the important role of other factors in compensatory adaptation, in addition to changes in tubular transport. The marked increases in glomerular filtration rate and nephron blood flow, which occur at least in some conditions, increase the absolute amount of water and solute delivered to the various nephron segments in ultrafiltrate and peritubular blood. Moreover, the expansion of extracellular fluid in severe renal failure inhibits tubular reabsorption of filtered water and solute in the same qualitative way that has been demonstrated in subjects with intact renal function. Quantitatively the response to acute volume expansion is exaggerated compared with control. Concomitant changes in renal hypertrophy and hyperplasia probably play an important role in functional adaptation. The apparent marked capacity for compensatory growth in all nephron segments and even in portions of tubular segments in parenchymal renal disease increases the area for transport by tubular epithelia in residual nephrons, as the overall number of nephrons diminishes...
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PMID:Functional adaptation to reduction in renal mass. 22 Jun 46

In order to minimize interaction of sorbents with food and digestive secretions, an intestinal bypass was created for sorbent administration in normal and uremic rats (N = 18) and goats (N = 5). Two separate limbs of small intestine were fashioned, one for food absorption and one for sorbent function, which joined at a Roux-Y anastomosis before the cecum. Particulate sorbent suspensions were injected into the intestine via a cutaneous stoma, and were excreted with food wastes in the feces. In animals with normal kidneys, sorbent function was calculated from changes in fecal and urinary excretion. Nitrogen clearance by the intestinal bypass was 20 to 40% of normal renal clearance in rats and goats. Potassium clearance was 40% of normal renal clearance in rats, and over 100% in goats. Sorbent treatment in anephric animals caused serum urea nitrogen concentrations to stabilize at 210 mg/dl in rats, and 110 mg/dl in goats. Serum potassium concentrations stabilized at 4.5 mEq/liter in rats, and fell to 2 mEq/liter in goats. Water balance was maintained by producing a mild osmotic diarrhea. At least three substances which accumulate in renal failure--urea, potassium, and water--were removed in therapeutically significant amounts.
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PMID:Roux-Y intestinal bypass for administration of sorbents in uremia. 27 84

Thirty-seven of 100 consecutive patients with fulminant hepatic failure had clinical and radiological evidence of pulmonary edema. None of them had clinical evidence of left heart failure, and the pulmonary artery wedge pressure measured in 12 patients was normal. Similarly, there was no evidence to incriminate renal failure, endotoxemia, or hypoalbuminemia. However, there was a significantly higher incidence of pulmonary edema in patients with cerebral edema, suggesting either a central origin for the pulmonary edema or common factors predisposing to edema in both sites. An additional local factor may have been the presence of intrapulmonary vasodilatation. Detailed isotope studies in 11 patients showed a significantly increased pulmonary extravascular water volume in the patients with pulmonary edema which was in keeping with the severity of the radiological changes. Although the over-all mortality was higher in those patients with pulmonary edema than in those without, the difference was not significant, and early ventilation with positive and expiratory pressure achieved adequate oxygenation in all but 3 patients.
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PMID:Incidence and pathophysiology of pulmonary edema in fulminant hepatic failure. 34 31

The pathophysiology, symptoms and treatment of paraquat intoxication, primarily from oral ingestion, and the pharmacology and pharmacokinetics of paraquat are reviewed. Toxicity has occurred after topical application, oral ingestion or inhalation of paraquat. Systemic toxicity has not been reported from smoking of paraquat-contaminated marijuana but heavy abusers of contaminated marijuana may experience coughing, hemoptysis and mouth irritation. Following ingestion of 30 mg/kg or 50 ml of a 21% (w/w) solution of paraquat (as the base), hepatic, cardiac or renal failure or death may occur. Smaller doses (greater than or equal to 4 mg/kg of paraquat base) may cause respiratory distress, renal dysfunction or, occasionally, jaundice or adrenal cortical necrosis. When paraquat ingestion is suspected, the drug should be removed immediately from the gastrointestinal tract by gastric lavage or by whole-gut irrigation. Adsorbents such as Fuller's earth, bentonite or activated charcoal may be used during gastric lavage. Combined use of forced diuresis (with furosemide, mannitol and i.v. dextrose in water or normal saline), hemodialysis or hemoperfusion is recommended until the compound cannot be detected in body fluids or the dialysate. Immediate and effective treatment is necessary to prevent systemic toxicity or death from paraquat intoxication.
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PMID:Paraquat poisoning: a review. 36 Aug 33

This review of adaptive changes in renal structure and function in subjects with reduced renal mass has two primary goals. One is to provide a description of the remarkable compensatory increases in glomerular filtration rate (GFR), and renal blood flow, at the level of individual nephrons, and the alterations in water and electrolyte transport by tubular epithelium. These processes preserve fluid and electrolyte balance in subjects with progressive renal failure, until whole kidney GFR is reduced to about 20 percent of normal, and provide the basis for conservative clinical medical management. The other aim is an attempt to provide an understanding of the mechanisms involved in compensatory adaptation, since this information, in addition to amplifying our understanding of renal transport processes, helps to elucidate the functional limitations placed on subjects with renal insufficiency. An attempt has been made to analyze both clinical observations and relevant experimental models and an effort has been made to correlate renal function with different patterns of renal injury.
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PMID:Structural and functional adaptation after reduction of nephron population. 38 Jan 85


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