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)

The disposition of the antidepressant tianeptine and its MC5 metabolite (pentanoic acid analogue of tianeptine) was studied following a single 12.5 mg oral dose of tianeptine sodium salt in 20 patients with chronic renal failure. In 12 patients (group I) having a creatinine clearance of less than 19 ml.min-1 the pharmacokinetics parameters for tianeptine and MC5 metabolite were determined and compared with those obtained in a matched control group (group II). The other 8 patients (group III) were functionally anephric and were studied during 1 dialysis to assess the haemodialysis clearances of tianeptine and MC5 metabolite. The comparison between groups I and II showed that renal failure did not appear to affect the disposition of parent tianeptine. However, the MC5 metabolite terminal half-life was found to be increased in renal patients compared to controls (14.2 +/- 9.3 h vs 4.9 +/- 1.7 h). Due to a large interindividual variability the difference did not reach a significant level (P = 0.054). According to the antidepressant activity of the MC5 metabolite in pharmacological tests, the sustained rise in its plasma level suggests that a reduced daily dose should be administered and 12.5 mg of tianeptine should be given twice daily to patients with chronic renal failure. In patients from group III elimination of the compounds by haemodialysis was found to be low. The dialysis clearances were 3.9 +/- 9.9 ml.min-1 and 19.2 +/- 8.6 ml.min-1 for tianeptine and its MC5 metabolite respectively. This low dialysability has 2 clinical implications. Firstly, patients currently undergoing haemodialysis and treated by tianeptine could be given the drug without taking dialysis into account. Secondly, haemodialysis does not appear to be an effective method for tianeptine elimination in cases of overdosage.
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PMID:Tianeptine and its main metabolite. Disposition in chronic renal failure and haemodialysis. 209 5

It has been suggested that sodium renal excretion is regulated, at least partially, by a factor with natriuretic properties called digoxin-like factor (DLF). As this substance crossreacts with digoxin antibodies, it was measured with a radioimmunoassay used to determine exogenous digoxin. Methodological conditions and quality control to determine DLF in plasma and urine have been established. Good correlation coefficients in specificity as well as dilution studies were obtained. Within--and between--assay coefficients of variations indicate good reproducibility. Moreover, changes in plasma DLF levels were detected in patients with cirrhosis or with renal failure, diseases which thrive on alterations in salt and water metabolism. In conclusion, this radioimmunoassay method for measuring DLF may be useful to investigate the role of this factor in several physiological and pathological conditions.
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PMID:[Developement and quality control of a radioimmunoassay for measurement of endogenous digoxin]. 209 36

The protective effect of acetazolamide or sodium chloride loading on cisplatin nephrotoxicity was investigated in rats. After a single dose of cisplatin (5 mg kg-1 i.p.) kidney function was studied after 5, 28 and 84 days. Acetazolamide (75 mg kg-1 i.p.) was administered as a single dose prior (30 min) to the cisplatin injection. By the time of cisplatin administration, the rats were sodium depleted except the sodium-loaded group. Five days after the cisplatin administration all rats received a regular rat chow for the rest of the experiment. Cisplatin alone caused renal failure that could be observed for up to 12 weeks (ClCr 0.32 +/- 0.13 vs. 0.62 +/- 0.06 ml min-1 x 100 g BW-1) with polyuria (UVol 41.2 +/- 4.5 vs. 18.4 +/- 4.6 ml 24 h-1). Pretreatment with acetazolamide was the most protective manoeuvre tested. Five days after cisplatin, kidney function was significantly better than in rats treated with cisplatin alone (ClCr 0.21 +/- 0.06 vs. 0.03 +/- 0.01 ml min-1 x 100 g BW-1), after 28 days the only sign of nephrotoxicity was polyuria (UVol 28.9 +/- 3.7 vs. 19.0 +/- 2.6 ml 24 h-1) after 84 days no differences could be observed at all. Sodium chloride loading was less protective on cisplatin nephrotoxicity. Impaired renal function could still be observed after 12 weeks (ClCr 0.41 +/- 0.05 vs. 0.62 +/- 0.06 ml min-1 x 100 g BW-1) with no difference in comparison with the rats treated with cisplatin alone. However, since 12 rats died in the group having received cisplatin alone and only one rat in the high-salt group, sodium chloride loading is regarded as being advantageous over sodium depletion on cisplatin nephrotoxicity.
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PMID:Long-term effects of acetazolamide and sodium chloride loading on cisplatin nephrotoxicity in the rat. 211 87

A normally functioning vascular endothelium is required for vascular tone modulation and blood fluidity. Systemic and local circulatory and coagulation alterations, even to the point of renal failure, may be observed in obstructive jaundice; bile salts are included among the potential pathogenetic factors. To assess the effects of taurocholic acid, glycocholic acid, and cholic acid on the integrity and properties of the endothelium, cultured human endothelial cells (HUVEC) were studied. Taurocholic and glycocholic acids (up to 2000 mumoles/L) did not exhibit any significant effect on 51Cr release from HUVEC after 6 h incubation. Following HUVEC exposure to 2000 mumoles/L of the unconjugated compound, cholic acid, a significant discharge of the radiolabel and LDH leakage in the supernatant were observed, to some extent prevented by the presence of human plasma or albumin (physiologic carrier). Prostacyclin spontaneous release from HUVEC was significantly depressed by both taurocholic and glycocholic acid; the action was related to bile salt concentration (200-1000 mumoles/L) and to the time of exposure (1 to 24 h); the reduced production of PGI2 was demonstrated to be reversible. Conversely, spontaneous TxA2 generation and fVIII release were not affected by the presence of bile salts in culture medium. Previous investigations showed that experimental obstructive jaundice could impair prostacyclin release from rat aortic tissue. The same effect was also demonstrated after in vitro exposure of the vessel wall to jaundiced serum and bile salts alone; furthermore, bile salts exert toxic effects on the integrity of several cells and impair the prostaglandin system of different tissues.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Bile salts and spontaneous release of PGI2, TxA2 and fVIII from cultured human endothelial cells]. 211 72

The heart atrium, as well as under certain pathophysiological conditions the ventricle, synthesize and release ANP. Exerting natriuretic, diuretic and vasorelaxant effects, this peptide plays an important role in the body's blood volume and blood pressure homeostasis. Whereas the pharmacological actions of ANP have been quite convincingly demonstrated, its physiological and pathophysiological role is less well defined. ANP plasma levels tend to be increased in diseases with salt and water retention, such as essential hypertension, congestive heart failure, renal failure or liver cirrhosis. With regard to its hemodynamic effects, ANP seems to be beneficial in patients with hypertension. ANP appears to have little therapeutic potential as a diuretic in patients with congestive heart failure and liver cirrhosis, possibly due to the decreased renal responsiveness to ANP in these diseases. However, ANP might to be a valuable therapeutic agent in acute renal failure.
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PMID:[Atrial natriuretic peptide. II. Pathophysiology and possible clinical significance. Review]. 214 57

The endocrine-metabolic disturbances of renal failure have numerous underlying mechanisms. These include abnormal secretion, transport and target cell binding and impaired synthesis or elimination by the diseased kidney. Neither hemodialysis nor CAPD removes large quantities of retained hormones. By correcting certain metabolic, fluid and electrolyte abnormalities, however, dialysis may improve some endocrine disturbances. Other factors such as malnutrition, glucose loading, protein loss, trace metal accumulation and drug ingestion may influence the endocrine-metabolic aspects of renal failure treated by dialysis. Hormonal stimulation and action can be adversely affected by hyperendorphinism due to retained opioids which may be removed by dialysis [88]. Possibly due to the more permeable membrane or because of continuous therapy, peritoneal dialysis seems to have a more salutary effect on hormonal regulation of salt and water balance, of erythrocyte mass and of female reproductive function than hemodialysis does.
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PMID:Modifications of endocrine-metabolic abnormalities of uremia by continuous ambulatory peritoneal dialysis. 218 4

Dopamine is an endogenic catecholamine which, in addition to being the direct precursor of noradrenaline, has also an effect on peripheral dopaminergic receptors. These are localized mainly in the heart, splanchnic nerves and the kidneys. Dopamine is produced in the kidneys and the renal metabolism is closely associated with the renal treatment of water and salt but the mechanism is not yet elucidated. In low doses (1-5 micrograms/kg/min), dopamine increases renal blood flow (RBF) and the glomerular filtration rate (GFR). In addition, pronounced diuretic and natriuretic effects are observed which are possible not exclusively secondary to alterations in the renal haemodynamics but may also be due to specific tubular effects. Recent investigations have revealed that dopamine does not increase RBF and GFR in patients with chronic renal failure if GFR is less than 60 ml/minute. Dopamine in low doses is frequently employed in cases of acute oliguric renal failure but the results available concerning the therapeutic effect are frequently retrospective and uncontrolled. The results suggest that early treatment with 1-3 micrograms/kg/min dopamine combined with furosemide can postpone or possibly render dialysis unnecessary in a number of patients on account of increased diuresis and natriuresis. The effect of GFR and the significance for the prognosis are not known.
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PMID:[Renal effects of dopamine]. 219 32

Endocrine-metabolic disturbances of renal failure have many underlying mechanisms, including abnormal secretion, transport, and target cell binding, impaired synthesis and elimination by the diseased kidney, and responses to stimuli resulting from altered homeostasis. Neither hemodialysis nor continuous ambulatory peritoneal dialysis (CAPD) removes large amounts of hormones. By correcting metabolic, fluid and electrolyte disturbances, dialysis may improve some endocrine abnormalities. Possibly because of more permeable membranes, or continuous treatment including ultrafiltration, CAPD has a somewhat more salutary effect on uremic endocrinopathy than hemodialysis. In particular, hormonal regulation of salt and water balance, erythropoietic function, female reproductive function, and some aspects of renal osteodystrophy respond more favorably to CAPD. The endocrine response suggests that there is no inferiority of CAPD as a treatment for renal failure.
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PMID:Endocrine abnormalities in patients treated by continuous ambulatory peritoneal dialysis. 219 16

Horses suffering from trauma, sepsis, and severe burns need 12% to 16% of protein (dry matter basis) in their diet. Since reduced appetite may be a problem, relatively energy dense (greater than 2 Mcal DE/kg) feeds should be offered. In hepatic failure, maintenance protein requirements (8% on a dry matter basis for adult horses) should be met with feeds that are high in short branched-chain amino acids and arginine but low in aromatic amino acids and tryptophan (for example, milo, corn, soybean, or linseed meal) in addition to grass hay. Vitamins A, C, and E should also be supplemented. In cases with renal failure, protein, calcium, and phosphorus should be restricted to maintenance or lower levels. Grass hay and corn are the best feeds for horses with reduced renal function. Do not offer free-choice salt to horses with dependent edema from uncompensated chronic heart failure. Following gastrointestinal resection, legume hay and grain mixtures are the feeds of choice. Horses with diarrhea should not be deprived or oral or enteral alimentation for prolonged periods of time. Liquid formulas may be used if bulk or gastrointestinal motility are a problem. Apple cider vinegar and a high grain diet may reduce the incidence of enteroliths in horses prone to this problem. Pelleted feeds will reduce fecal volume and produce softer feces for horses that have had rectovaginal lacerations or surgery. Horses with small intestinal dysfunction or resection should be offered low residue diets initially, but long-term maintenance requires diets that promote large intestinal digestion (alfalfa hay, vegetable oil, restricted grain). Geriatric horses (greater than 20 years old need diets similar to those recommended for horses 6 to 18 months old.
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PMID:Clinical nutrition of adult horses. 220 96

Cyclosporine CsA nephrotoxicity was examined in male Sprague-Dawley rats with or without prior uninephrectomy, injected daily with 12.5 mg/kg CsA, and fed a salt-depleted or normal diet for 3-10 weeks. Control rats received the CsA vehicle. CsA induced a fall in creatinine clearance in salt-depleted rats, from 1.3 +/- 0.1 to 0.8 +/- 0.1 ml/min (P less than 0.001), and in normally fed rats from 1.8 +/- 0.2 to 1.0 +/- 0.2 ml/min (P less than 0.02). Vehicle treatment had no effect. The most striking morphologic changes were those of thick ascending limb cell atrophy with concomitant fibroblastic proliferation and collagen formation; these alterations were present in the inner stripe of the outer medulla and the medullary ray. The medullary-ray findings included S2-S3 degenerative changes as well and apparently correspond to the striped fibrosis described in human CsA nephropathy. The alterations were specific to the CsA group, progressive, and most severe in the salt-depleted, CsA-injected rats (on a scale of 0-4: 1.7 +/- 0.2 for medullary rays, and 2.0 +/- 0.2 for inner stripe, P less than 0.001). Morphologic changes predicted renal failure (r = 0.3, P less than 0.01 for cortical alterations, and r = 0.5, P less than 0.001 for medullary alterations). Prior uninephrectomy did not enhance these changes. Thus, chronic CsA administration impaired kidney function and induced morphologic alterations found in regions characterized by, and in nephron segments particularly vulnerable to, limited O2 availability. Salt depletion appears to accelerate the development of chronic CsA renal injury in the rat.
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PMID:Chronic cyclosporine-induced nephropathy in the rat. A medullary ray and inner stripe injury. 230 70


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