Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 12 patients with chronic non-nephrotic renal failure (creatinine clearance 3.5-11 ml/min) and 8 control subjects, plasma triglyceride turnover was studied. The patients showed significantly increased fasting triglyceride concentrations and absolute plasma triglyceride turnover rates, while the fractional turnover rate was significantly decreased. The finding of an elevated triglyceride turnover rate with a near normal fractional removal rate in the patients with the highest creatinine clearance suggests the involvement of an increased triglyceride synthesis rate in these patients. However, most patients showed an impaired removal mechanism as the major cause of the hypertriglyceridemia.
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PMID:Triglyceride turnover in severe chronic non-nephrotic renal failure. 67 11

Study of case-notes and autopsy reports of patients with renal disease suggests that analgesic nephropathy is responsible for at least 12 per cent of cases of chronic renal failure, Between 1970 and 1975 eight new cases of analgesic nephropathy were seen annually in a population of three-quarters of a million. This is equivalent to an incidence of 490 new cases per year in England and Wales. Fifty-five patients with analgesic nephropathy were followed from one to 84 months for a total of 190 patient years. Changes in renal function were correlated with bacteriuria, hypertension and analgesic consumption. One-third of the cases had been misdiagnosed and analgesic abuse was only revealed by thorough examination of case-notes and autopsy records, together with careful questioning of patients and relatives. A number of cases had been classified as chronic pyelonephritis. The calculated survival rate at five years was 44 per cent. Mortality was related to the level of analgesic consumption and the degree of renal failure at the time of diagnosis. The prognosis was poor if serum creatinine at presentation was greater than 400 mumol/l. There was no significant correlation between deterioration in renal function and bacteriuria or hypertension. Forty-two per cent of the patients were taking analgesics for arthritis; 27 per cent had rheumatoid arthritis. Most had been taking large quantities of analgesic mixtures containing phenacetin. Renal papillary necrosis was present in only 26 per cent on intravenous urography but was found in all those examined at autopsy. Twenty thousand, two hundred and twenty-nine autopsy reports were examined for the presence of renal disease. Renal papillary necrosis was found in 0.41 per cent, and could be attributed to analgesic nephropathy in 24 per cent. In patients under 65 years of age analgesic nephropathy appeared to be a more frequent cause of death than chronic pyelonephritis. The report indicates the need for careful enquiry about analgesic consumption in all patients with renal disease, and emphasizes the importance of early diagnosis and cessation of analgesics in suspected cases of analgesic nephropathy.
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PMID:Analgesic nephropathy: an important cause of chronic renal failure. 67 50

The functional sequelae of 131 patients with urogenital tuberculosis were examined. At the time of diagnosis, more than half of the patients already suffered from global renal failure which was moderate in 42.7 per cent and severe in 15.5 per cent. We believe that the primary functional damage occurs at the medullary level with tubular and interstitial involvement. Indeed, the red phenol test for postglomerular blood flow was altered in a higher proportion than was the creatinine clearance (67.9 per cent). The maximum concentrating ability was altered even more frequently (84 per cent). When we compared various glomerular filtration levels with the grade of alteration of the maximum ability concentration test, we also saw clearly that the alteration of the tubular interstitial medullar function dominated the alteration of the glomerular global function. This proves at a functional level the predominantly medullary localization of the lesion in renal tuberculosis.
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PMID:Renal function damage in 131 cases of urogenital tuberculosis. 67

We have investigated serum urea, uric acid, and creatinin crealinine levels in 39 patients with craniocerebral trauma. The most impressive observation was a change in serum urea, which was found significantly increased up to 237 mg% on the seventh day (mean value) after severe injury, and turned out to be of great prognostic value. Patients with a serum urea above 100 mg% did not survive the acute stage. Uric acid and creatinine were only significantly increased in patients with lethal outcomes, the first being elevated by about 300% in the first week, the second remaining normal for four days increasing thereafter. It is concluded from these first data that a hypercatabolic state due to shock, central dysregulation, or both, is responsible for the dissociated behaviour of urea, uric acid and creatinine during the first four days, after which renal failure as a secondary change is shown by the rise in serum creatinine.
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PMID:Azotaemia in severe head injury--central dysregulation or renal failure? 68 43

A pharmacokinetic study of netilmicin was conducted in 12 healthy subjects and 24 subjects with chronic renal failure. After intramuscular administrations of 2 and 3 mg of netilmicin per kg in normal subjects, the mean peak serum concentrations were 5.46 and 8.83 mug/ml, respectively. After intravenous infusions of identical doses, the mean maximum serum levels, occurring at the end of the infusion, were 11.79 and 15.75 mug/ml, respectively. The pharmacokinetic data were very similar via the two routes of administration and for the two doses. The elimination half-life was 2.20 h, and 80 to 90% of the injected dose was recovered in urine during the first 24 h. After intramuscular administration of 2 mg/kg in subjects with chronic renal impairment, the elimination half-life increased to 29.48 h, and urinary elimination was inversely related to the degree of impairment. A study was conducted throughout hemodialysis sessions: serum concentrations decreased by 63.3%. The linear relationships between the elimination rate constant and creatinine clearance and the elimination half-life and serum creatinine allowed us to establish dosage schedules according to the degree of renal failure.
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PMID:Pharmacokinetics of netilmicin in the presence of normal or impaired renal function. 68 8

5 cases of cantharidin intoxication are reported. 4 patients had used cantharidin as an aphrodisiac and one to induce abortion. All presented with urinary tract symptoms. Four patients had gross hematuria. In one case non-oliguric renal failure occurred, with increase of plasma creatinine to 5.6 mg/100 ml. renal biopsy was performed in 2 cases. On light and electron microscopy glomerula showed only minimal changes such as podocyte swelling. The tubuli were markedly altered, with luminal enlargement, intraluminal cell debris, flattening and shrinking of the epithelial cells and distortion of brush borders. Whereas all 5 patients recovered completely, some deaths due to cantharidin poisoning have been reported in the literature. Since cantharidin is markedly toxic, its use in humans should be strongly discouraged.
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PMID:[Lesions of the kidney and the efferent urinary tract due to cantharidine]. 70 10

Significant hypertriglyceridemia, the most common lipid abnormality in renal failure, first occurs when the creatinine clearance falls to 50 ml/min. The prevalence of hypertriglyceridemia continues to rise as creatinine clearance falls further with the highest rate developing at a creatinine clearance less than 10 ml/min. Hypertriglyceridemia is correlated with plasma glucagon levels but not growth hormone or insulin. Plasma cholesterol values remain normal in the face of deteriorating renal function and show no correlation with any of the hormones measured. Although all three hormones became elevated as renal function diminished, none were directly correlated with glomerular filtration rate. There was a distinct decrease in the prevalence of hyperlipidemia after 5 years of maintenance hemodialysis therapy. Plasma growth hormone and glucagon through an effect on plasma triglyceride and plasma insulin by effecting plasma cholesterol may play a role in this decline of hyperlipidemia with duration of hemodialysis.
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PMID:Relationship of plasma lipids to renal function and length of time on maintenance hemodialysis. 70 43

The amino acid content of plasma and erythrocytes in patients with severe renal failure (serum creatinine less than 8 mg/100 ml) treated with selective low-protein diets, in patients on regular hemodialysis, and in a control group of healthy subjects were studied. Most amino acids in erythrocytes of the patients showed the same changes as in plasma with the exception of histidine, serine, and alanine. In spite of low histidine plasma levels, the erythrocytes level is increased as compared with healthy controls. In uremic patients the plasma serine was constantly reduced whereas the serine content of the erythrocytes did not differ from healthy controls. Alanine concentrations in the erythrocytes of uremic patients were increased in spite of normal alanine plasma levels. This finding may be due to the increased glycolytic ratio of red cells from uremic subjects delivering more pyruvate for transmination to alanine. In the control group the cysteine content of erythrocytes was decreased with a gradient between plasma and erythrocytes of 3.5:1. The same gradient could be observed in uremic patients in spite of the elevation in their plasma cysteine levels by a factor of 2.7 compared with controls. The low cysteine levels in erythrocytes may be due to loss of cysteine for glutathione synthesis in red cells. High glutathione levels in the erythrocytes of uremic patients support this hypothesis.
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PMID:Amino acid content of erythrocytes in uremia. 70 55

Basal prolactin concentrations in 357 patients with renal disease of defined pathology have been compared with those in 210 control subjects. Elevated prolactin concentrations were found in 113 renal patients (32%) including 53 patients in whom elevated concentrations were possibly attributable to drug therapy. In the remaining 60 patients who had hyperprolactinaemia not attributable to drugs, elevated concentrations (P less than 0.005) were found exclusively in patients with impaired renal function. A significant correlation was observed between prolactin and creatinine concentrations in these patients (r = 0.45 P less than 0.005) and prolactin reverted towards normal after successful renal transplantation. A significant arteriovenous prolactin concentration difference across the kidney (mean 16% range 8-29% P less than 0.02) was found in seven patients with non-renal non-endocrine disease. It is concluded that the hyperprolactinaemia found commonly in patients with impaired renal function is only partly attributable to drug therapy. The positive correlation between prolactin and creatinine reversion of prolactin towards normal after successful transplantation and arteriovenous hormone concentration differences across the normal kidney suggests that the kidney has a important role in prolactin metabolism. Abnormal regulation of prolactin secretion in renal failure may also be involved.
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PMID:Hyperprolactinaemia in renal disease. 70 94

The spectrum of interaction between drugs and the kidney is broad. Most drugs are excreted at least partially by the kidney, and renal function affects drug bioavailability, volume of drug distribution, and drug metabolism and rate of drug elimination. Drug therapy not only is potentially hazardous in patients with renal failure but also can cause a number of renal diseases. The clinician should be familiar with the pharmacologic and potential toxic effects of any drug used in a patient with uremia and should monitor creatinine clearance or at least serum creatinine level as a gauge of renal function. The drug regimen can be modified according to these measurements, either by administering a constant dose and varying the interval or by varying the dose and keeping the interval constant.
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PMID:Drug use in renal failure. 71 30


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