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

Methoxyflurane is capable of producing high-output renal failure in some patients and animal models, probably through metabolic liberation of free fluoride. The tubular site of action of fluoride was examined in Fischer 344 rats using clearance techniques. Free water reabsorption (TCH2O) and free water excretion (CH2O) were measured during mannitol or water diuresis in control rats and in rats given methoxyflurane or pretreated with sodium fluoride. Pretreatment produced statistically significant increases in urinary flow (from 10.5 +/- 1.4 to 20.1 +/- 1.9 mul/min/100 g b. wt.), in glomerular filtration rate (from 814 +/- 31 to 1,039 +/- 53 mul/min/100 g b. wt.), in per cent sodium excretion (from 0.107 +/- 0.008 to 0.155 +/- 0.015 per cent), and in per cent water excretion (from 1.27 +/- 0.15 to 2.00 +/- 0.20 per cent). Free water excretion remained relatively unaltered in rats pretreated with fluoride, perhaps due to elevated glomerular filtration rate and/or reduced proximal tubular reabsorption combined with inhibition of reabsorption in the ascending loop. Percentage free water reabsorption, on the other hand, was markedly reduced by the pretreatment, from 2.66 +/- 0.21 to 0.66 +/- 0.09 per cent. The observations are consistent with the hypothesis that fluoride inhibits tubular reabsorption primarily in the medullary portion of the ascending limb of Henle's loop, perhaps by inhibition of an active chloride pump located in this nephron segment.
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PMID:Renal tubular site of action of fluoride in Fischer 344 rats. 84 82

The intensity of a drug's action is related to its concentration in plasma water. Since the analytical methods for determining concentrations of drugs in plasma measure this as well as the drug bound to plasma proteins, evaluation of the binding of drugs to plasma proteins is needed for proper interpretation of drug level measurements. Anionic drugs have decreased binding in plasma from patients with renal failure. With some, such as phenytoin, a reduction is required in the levels usually considered "therapeutic" for uremic patients. Basic drugs may have normal or decreased binding. Propranolol, quinidine and tricyclic antidepressants are drugs in this class that have normal binding and that do not require changes in the plasma levels usually considered "therapeutic" for these patients.
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PMID:The binding of drugs to plasma proteins and the interpretation of measurements of plasma concentrations of drugs in patients with poor renal function. 85 Nov 14

Renal failure impairs urinary excretion of drugs and may also modify drug action by alternations in protein binding, distribution, biotransformation and, possibly, by retention of active metabolites. Dialysis adds another variable by altering the blood levels of those drugs soluble in plasma water and therefore available for diffusion or ultrafiltration. Renal insufficiency clearly modifies decisions about the choice and dose of a wide variety of drugs. Although data are accumulating at a rapid rate, available information about the use of drugs in patients with kidney disease is rather limited. The following is a summary of recent information on the use of a variety of drugs frequently utilized in patients with impaired renal function. The guidelines presented here are not absolute, but they are intended to be practical and reasonable, based on current information for adult patients of average size with kidney disease.
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PMID:Drug administration in renal failure. 85 Nov 31

Nephronophthisis (previously described as familial juvenile nephronophthisis and medullary cystic disease) is characterized by insidious renal failure, its main features being increased urinary sodium loss, pitressin-resistant hypotomic polyuria, polydipsia, normal urine sediment and absence of hypertension. Renal function and histologic studies were performed in a family in which two siblings had this disorder, while the parents and two other siblings appeared clinically normal. Both parents demonstrated a moderate impairment of maximum urinary concentration. The values for tubular free water reabsorption (TcH2O) were relativley normal in the parents and the healthy siblings. One of the index patients showed only minimal sodium wasting even though he had hyposthenuria, thus suggesting an involvement of the collecting ducts in the early stage of neophronophthisis. No evidence of proximal tubular dysfunction was found. Although the light-microscopic examination of renal biopsies from the parents and the healthy siblings was unremarkable, electron microscopy revealed probable abnormalities in all four. An autosomal recessive mode of inheritance is, therefore, suggested in this family. The etiology of nephronophthisis is obscure but a likely possibility is that the renal damage results from an inborn metabolic error.
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PMID:Nephronophthisis. Renal function and histologic studies in a family. 88 91

Very fat people die earlier than people of normal weight because hypertension, diabetes and coronary disease are more frequent among the markedly obese. Most obese subjects, however, are only slightly overweight and their mortality is not elevated. Reasons for dieting are more often psychological than somatic. 2. Reducing diets are ineffective because the obese rarely follow them. Total fasting and intestinal bypass may provide better results, but are more dangerous. 3. Atkins' diet eliminates carbohydrates from food without restricting protein and fat intake. Deprived of carbohydrates, the body uses fat for fuel. A small part of metabolized fat is eliminated in the urine as ketone bodies, and this is why such diets are called "ketogenic". They have been known at least since 1863. 4. Caloric loss due to ketonuria does not exceed 100 Cal/day in the non-diabetic. It is maximal during total fasting and cannot be increased by a ketogenic diet. 5. In the short run, such diets produce rapid weight loss due to polyuria. On the other hand, refeeding carbohydrates causes water retention and weight gain. 6. The diet decreases appetite: patients eat less without feeling severe hunger and without measuring their food intake. 7. Orthostatic hypotension, fatigue, and nausea are frequent, despite what Dr. ATKINS claims. 8. The diet increases plasma cholesterol and uric acid. It may be dangerous in diabetes (anorexia, acidosis) and in heart or kidney failure (hypokalemia). 9. The diet, though far from good, is better than the book. ATKINS' theories are at best half-truths, and the results he claims lack credibility. The obese subject's disappointment with traditional reducing diets and the book's hard-sell style account for ATKINS' success.
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PMID:[Dr. Atkins' dietetic revolution: a critique]. 89 45

One to four weeks after the left renal artery was clipped and the contralateral kidney was left untouched in Sprague-Dawley rats (two-kidney Goldblatt preparation), the clips were removed under ether anesthesia and 10 ml/kg body wt of either 150 mM NaCl (control) or 50% glycerol in water (experimental) were injected intramuscularly. The next day the rats were anesthetized (sodium pentobarbital) and the renal function of both kidneys was measured, after which the renal cortical renin content was measured by incubation of tissue homogenate with angiotensinase-free rat renin substrate. Radioimmunoassay was used to determine the rate of angiotensin I production. Compared with controls, both kidneys of glycerol-injected rats had reduced GFR (left 28, right 18% of controls), increased percentage of fractional water excretion (left 5, right 6 times controls), and increased percentage of fractional Na excretion (left 3, right 4 times controls). Despite large differences in renal renin (left 28, 676, right 1,329 ng angiotensin I/h per mg protein), the extent of renal failure produced by glycerol was equal in the left and right kidneys. These results are inconsistent with the hypothesis that renal renin content is directly related to the severity of glycerol-induced renal failure in rats.
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PMID:Glycerol-induced acute renal failure in the two kidney Goldblatt rat. 91 Sep 21

Forty consecutive patients who underwent open-heart procedures using a hyperosmolar perfusion prime were studied to determine the significance of free-water clearance and urinary osmolality early after bypass in predicting the likelihood of postoperative renal dysfunction, defined as a blood urea nitrogen (BUN) level over 50 mg/100 ml. Urinary osmolality increased in all patients during the first 18 hours after bypass, but the increase was substantially less for those who subsequently developed renal dysfunction. Free-water clearance, which was significantly less negative in the patients with renal dysfunction by 2 hours after bypass and remained so throughout the 18 hours of this study, served as an early postoperative indicator of impaired renal function in the patients who eventually developed BUN elevation. Moreover, it was more sensitive as an index of renal dysfunction than was osmolality alone. Early recognition of renal impairment is important, as it may prevent dangerous fluid overloading and allow for corrective measures to be undertaken before frank renal failure develops.
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PMID:Urinary osmolal changes in renal dysfunction following open-heart operations. 93 37

Failing kidneys can play havoc with other parts of the body. Specific treatment of these associated problems may help ward off uremia and preserve whatever renal function remains. Sodium levels may drop if too much water is mistakenly given to counteract kidney failure. Hyperkalemia can lead to cardiac arrest if potassium levels aren't reduced without delay. Acidosis also may reach life-threatening proportions, especially if diarrhea occurs. Almost all patients with chronic renal failure have a bleeding tendency and anemia, with the hematocrit dipping as low as 20 percent. Over half have decreased tolerance to carbohydrares, although severe hyperglycemia is rare. Disorders of calcium metabolism also are common, ranging from asymptomatic hypocalcemia to osteomalacia. The kidneys' impaired filtration ability should be kept in mind when drugs are prescribed. Dosages may need to be cut to avoid an adverse reaction.
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PMID:Conservative management of chronic renal failure. 95 17

A case of cerebral arterial aneurysm associated with renal failure is reported which was treated by surgery. The anaesthesiological and post-operative problems are discussed. Surgery of the aneurysm is urgently indicated in these cases on account of the increased risk of subarachnoid haemorrhage due to heparinization during haemodialysis. Pre-operative replacement of haemodialysis by peritoneal dialysis is advisable to facilitate the treatment of cerebral oedema, maintain the electrolyte and water balance and ensure adequate post-operative enteral and parenteral feeding. The choice of anaesthetic technique, the use of controlled hypotension, the treatment of hypertensive crises, laboratory tests and the post-operative care of these cases are discussed. Experience has shown that from the anaesthesiological point of view there is no contra-indication to neurosurgery or vascular surgery in cases of renal failure provided adequate precautions are taken.
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PMID:[Surgical removal of a cerebral arterial aneurysm complicating renal failure; anaesthesiological and post-operative problems (author's transl)]. 95 38

Renal function was evaluated in 40 patients with fulminant hepatic failure, They were divided into two groups on the basis of glomerular filtration rates greater than 40 ml/min or less than 25 ml/min. A number of patients in group 1 had markedly abnormal renal retention of sodium together with a reduced free water clearance and low potassium excretion which could be explained by increased proximal tubular reabsorption of sodium. The patients in group 2 had evidence that renal tubular integrity was maintained when the glomerular filtration rate was greater than or equal ml/min (functional renal failure), but evidence of tubular damage was present when this was less than 3 ml/min (acute tubular necrosis).
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PMID:Abnormalities of sodium excretion and other disorders of renal function in fulminant hepatic failure. 96 82


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