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

Three patients with cirrhosis, ascites, and dilutional hyponatremia were treated with demeclocycline in an attempt to correct the abnormal water retention. Demeclocycline administration (600 to 900 mg/day for 8 to 9 days) resulted in [a] increased blood urea nitrogen and plasma creatinine concentrations; [b] reduction of the inulin clearance by between 63% to 78% and of paraaminophippurate clearance by 36% to 77%; and [c] an impairment of the renal concentrating ability. Urine osmolality decreased to hypotonic levels, but polyuria did not appear, probably because it was prevented by the reduction of the glomerular filtration rate. Renal failure was reversible on withdrawal of demeclocycline. No other causes than demeclocycline administration could be found to explain the reduction of the glomerular filtration rate and the estimated renal plasma flow.
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PMID:Renal failure associated with demeclocycline in cirrhosis. 40 25

The delayed onset of anuria/oliguria in acute tubular necrosis has been theorized to represent a complicating compartment syndrome, i.e., parenchymal swelling within an unyielding capsule. To test this proposition, 12 monkeys had suprarenal aortic cross-clamping, followed by unilateral renal decapsulation to create an experimental as well as a control kidney unit in the same animal. Histologic examination uniformly confirmed tubular necrosis at death or sacrifice. Subsequent split renal function studies (creatinine, urea, and free water clearances) indicated significantly greater maintenance of renal function by the decapsulated kidney than by its paired control. Clinical evaluation in 21 hemorrhagic shock patients, with the capsule of one kidney stripped, revealed on follow-up that 15 developed a renal failure consistent with acute tubular necrosis. Although three patients with polyuric failure died before split studies could be run and two others have been too recent for computer analysis to have been completed, nine of the remaining ten had significantly greater renal plasma flows (194 versus 121 ml/min M(2), p < .01) and significantly greater urine flows (.99 versus .18 ml/min M(2), p < .01) on the decapsulated side than on the control, as determined by differential renal scans. No significant difference in these same lateralized renal functions was noted in the tenth patient with renal failure and in the six survivors without renal failure. Renal decapsulation as prophylaxis reduced the anticipated incidence of oliguria/anuria from an expected 75% to 7% (p < .01) in these 21 shock patients. Such data suggest that delayed renal ischemia, possibly based on a compartment syndrome, may be the cause for a progression of acute tubular necrosis from polyuria to oliguria and then to anuria.
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PMID:Renal decapsulation in the prevention of post-ischemic oliguria. 40 54

A sustained loss of concentrating ability (renal dysfunction) was identified in 29% of a patient population judged to be at risk for this problem on the basis of clinical criteria. Six patients in this group fulfilled previously developed criteria for early renal failure, i.e., free water clearance CH2O between +15 and -15 ml/hr and no change after furosemide. All of these patients were maintained in the high urinary output state with furosemide. Sequential determinations of free water clearance are a sensitive means of monitoring renal function which permits early identification and therapy of patients with renal vasomotor nephropathy.
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PMID:Renal dysfunction in the surgical patient: maintenance of high output state with furosemide. 45 1

Eleven patients with different degrees of renal failure with creatinine clearances between 7 and 32 ml/min have been studied. After a standard water overload and control periods of clearances, furosemide 1 g was given/i.v. There followed significant increase of renal plasma flow and glomerular filtration rate. In one case the increase was maintained during a follow up period of 3 hours. A significant increase was evident in phosphate, uric acid, sodium, potassium, and calcium clearances, as well as an increase in the sodium delivery to the distal nephron and a decrease in tubular reabsorption of phosphate. All this may be interpreted as the result of renal vasodilation induced by furosemide and its effect upon the proximal tubule and on Henle's loop.
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PMID:Alterations induced by large doses of furosemide in chronic renal insufficiency. 46 7

A long-term follow-up study of 27 survivors of acute renal failure in newborns was performed. A study of the evolution of renal function was possible in 20 cases, with follow-up periods ranging from 15 to 62 months (mean follow-up: 38 months). Renal function was determined by assessing glomerular filtration rate, free-water reabsorption, tubular reabsorption of phosphate and acidification ability. Results show a marked difference, according to the etiology of the acuete renal failure, between the two groups studied: 1) Most of those displaying renal failure following neonatal hipoxia, maintained persistent nephrological sequels. II) Parameters of renal function normalized between 6 and 12 months of age in those in which renal failure was related to hypovolemic shock, caused by hypertonic dehydration. Of the six patients with acute renal failure caused by neonatal hypoxia and shock (group 1), only one displayed normal renal function after 17 months. In the remaining fire patients, glomerular filtration rate continued to decrease even after three years. Three of them displayed urinary acidification disorders. An alteration in free-water reabsorption was found in the majority of the patients in both groups during the first year. This alteration persisted after three years in only four patients of group 1, although in relation to decreased glomerular filtration rate.
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PMID:[Long term renal function following acute failure in the newborn (author's transl)]. 50 74

Bone density and composition were studied in trabecular and cortical bone from control 2 and 4 year old beagles and those which had various degrees of renal failure as a result of perinatal irradiation. Changes in the two types of bone were qualitatively similar but consistently greater in trabecular bone. In a group identified as markedly uremic, the decrease (P less than 0.025) from control levels in specific gravity was about 4 times greater in trabecular than in cortical samples. The decrease (P less than 0.025) in grams of ash/ml was 9% in trabecular bone and 2% in cortical bone. These changes were associated with an increase (P less than 0.001) in water content and, on a percent by volume basis, approximately equal decreases in ash (P less than 0.025) and combustible matter (P less than 0.025). In a mildly uremic group there were similar trends in mean values but the only significant difference was an increase (P less than 0.001) in trabecular bone water.
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PMID:Density and composition of trabecular and cortical bone in perinatally irradiated beagles with chronic renal failure. 59 47

We previously have shown that chronic sodium chloride (NaCl) loading protects against HgCl2-induced acute renal failure (ARF) in dogs. To determine whether NaCl loading protects against an ischemic model of ARF, unilateral oliguric renal failure was produced by the infusion of norepinephrine (NE) into the renal artery of both saline-expanded (SE) and water-drinking (WD) dogs (n = 7). The renal renin content (30 U/g kidney) of SE dogs was suppressed (P less than 0.001) compared to that of WD dogs (132 +/- 18). Forty-eight hours after infusion of NE (1.5 microgram/kg per min X 100 min), inulin clearances from the infused kidney of SE (6 ml/min +/- 2) and WD dogs (7 +/- 2) did not differ; in both groups, respective clearances from the noninfused kidney (43 ml/min +/- 3) and (36 +/- 5) also did not differ from each other. The present fall in renal blood flow to the infused kidney 48 hours after NE in SE (44%) and WD dogs (38%) did not differ. Because of failure to demonstrate protection, a lower dose of NE (0.75 microgram/kg per min X 40 min) was infused into SE and WD animals (n = 6). Forty-eight hours after low dose NE, inulin clearances of the infused kidney of SE (17 ml/min +/- 5) and WD dogs (17 +/- 4) did not differ. Respective clearances in the noninfused kidney of SE (46 ml/min +/- 6) and WD dogs (35 +/- 4) did not differ. Therefore, despite suppression of renal renin content, NaCl loading failed to protect against this ischemic model of ARF. In conclusion, unlike HgCl2-induced ARF, it is unlikely that the renin angiotensin system contributes to the pathogenesis of this ischemic model of ARF.
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PMID:Failure of chronic sodium chloride loading to protect against norepinephrine-induced acute renal failure in dogs. 61 99

The effect of furosemide on the development of the acute ischaemic renal failure in the dog was studied. 11 canine kidneys were used as controls (group I) and 12 as a group where furosemide (6-8 mg/kg of body weight) was given (group II) immediately after releasing the clamps. Urine volume and sodium clearance were found significantly higher in the second group of kidneys during a period of 60 min after restoration of the blood flow to the kidney. Urea clearances remained low with no noted difference between the 2 groups. By the end of the first hour osmolar and potassium clearances were found to be significantly higher in the second group. The above findings suggest that furosemide given after an induction of acute ischaemic renal failure in the dog provides, up to the 1st hour after recirculation, some benefit in water and solute excretion but no benefit in urea clearance.
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PMID:Effect of furosemide on acut ischaemic renal failure in the dog. 62 97

Neurological abnormalities are a major cause of morbidity in patients with renal failure. The pathophysiology of these neurological changes is unclear, and the effects on them of dialysis and return of renal function have not been well studied. Studies were done in 31 patients who had acute renal failure (ARF), all of whom were either treated with dialysis within 5 days or did not survive. Studies on these patients included the electroencephalogram (EEG), motor nerve conduction velocity, and plasma Ca(++) and parathyroid hormone (PTH) levels. Studies were done at the time ARF was diagnosed, after stabilization on dialysis, during the diuretic phase of ARF, and 3 mo after recovery from ARF. In 16 patients with acute or chronic renal failure who did not survive and in nine patients without renal disease who died, measurements were made in brain of content of Na(+), K(+), Cl(-), Ca(++), Mg(++), and water. In patients with ARF for less than 48 h, despite the fact that there were only modest increases in plasma urea and creatinine, there were striking abnormalities in the EEG. The percent EEG power < 5 Hz+/-SE was 41+/-8% (normal = 2+/-1%), whereas the percent of frequencies > 9 Hz was only 22+/-6% (normal = 62+/-3%). These changes were unaffected by dialysis, but became normal with return of renal function and remained normal at 3 mo follow-up. The motor nerve conduction velocity was unaffected by either ARF or dialysis. In patients with ARF, the brain Ca(++) was 46.5+/-3.2 meq/kg dry wt, almost twice the normal value of 26.9+/-1.0 meq/kg dry wt (P < 0.001). The plasma PTH level was 3.2+/-0.6 ng/ml (normal < 1.5 ng/ml, P < 0.01). The increased brain Ca(++) was not related to an increased plasma (Ca(++)) (PO(4) (---)) product (r(2) = 0.14, P > 0.05). There was a small but significant decrement in brain Na(+) (P < 0.05), but brain water, K(+), and Mg(++) were unaffected by ARF.Thus, in patients with ARF for less than 48 h, the EEG is grossly abnormal and there are elevated levels of PTH in plasma. The PTH appears to have a direct effect on the brain, resulting in an increased brain Ca(++) content. The EEG abnormalities are unaffected by dialysis, but they become normal with return of renal function and remain normal after 3 mo follow-up. Thus, PTH may be a major uremic toxin, demonstrating evidence for central nervous system toxicity when there are only minimal abnormalities of other biochemical markers of ARF.
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PMID:Neurodiagnostic abnormalities in patients with acute renal failure. 65 7

A case of chlorpropamide-induced, symptomatic hyponatremia in a diabetic patient is reported. The hyponatremia was associated with loss of appetite, nausea, and vomiting. These symptoms caused reduced food intake which provoked severe hypoglycemia with disturbed consciousness. The hyponatremia developed when the chlorpropamide doses were increased from 400 to 600 mg/day. Withdrawal of chlorpropamide was followed by remission of hyponatremia. Chlorpropamide-induced hyponatremia is a rare complication and is due to an antidiuretic effect of chlorpropamide caused by increased secretion of adiuretin and potentiation of the effect of chlorpropamide caused by increased secretion of adiuretin and potentiation of the effect of adiuretin in the tubuli of the kidney. This case report and the analysis of 18 published cases in the literature show the following characteristics for chlorpropamide-induced hyponatremia: (1) Hyponatremia is a rare complication in the treatment of diabetics with chlorpropamide. The patients typically are female and over sixty. The dosage of chlorpropamide usually was 500 mg daily or even more. (2) Hyponatremia is often unrecognized for a long time because the symptoms are not specific. The characteristic symptoms include loss of appetite, nausea, vomiting, abdominal pain, confusional state and, rarely, convulsions and coma. Recovery occurs spontaneously after withdrawal of the drug. (3) The incidence of this type of hyponatremia is increased in cases of preexisting tendency to water retention such as heart failure and renal failure, and in cases of diuretic therapy. In the light of these findings, the authors believe that chlorpropamide is no longer a drug of choice in the treatment of diabetic women, especially in cases of preexisting tendency to water retention and in diuretic therapy. In such cases, a sulfonylurea without antidiuretic effect is to be preferred.
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PMID:[Hyponatremia and hypoglycemia after treatment with chlorpropamide. Case histories with review of the literature on 18 cases of chlorpropamide induced hyponatremia]. 66 98


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