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)

1. We investigated the effects of the selective endothelin (ET)A receptor antagonist BQ-485 and the selective ETB receptor antagonist BQ-788 on circulatory failure, multiple organ dysfunction syndrome (MODS) and the alterations in acid base balance caused by endotoxaemia in the anaesthetized rat. 2. Male Wistar rats were anaesthetized (thiopentone sodium; 120 mg kg-1, i.p.) and received a continuous infusion of vehicle (saline, 0.6 ml kg-1h-1, i.v.), BQ-485 (10 nmol kg-1 min-1, i.v.) or BQ-788 (10 nmol kg-1 min-1, i.v.). Fifteen min later, animals received a bolus injection of either saline (0.9% NaCl, 1 ml kg-1, i.v.) or E. coli lipopolysaccharide (LPS, 10 mg kg-1, i.v.). 3. Injection of LPS resulted in a fall in blood pressure from 115 +/- 4 mmHg (time 0) to 82 +/- 4 mmHg at 360 min (n = 15) as well as a hyporeactivity to the pressor responses to noradrenaline (NA, 1 microgram kg-1, i.v.). Infusion of BQ-788 attenuated the delayed hypotension (at 360 min: 100 +/- 4 mmHg, n = 7; P < 0.05) and significantly enhanced the pressor responses elicited by NA (at 60 to 240 min). In contrast, treatment of LPS-rats with BQ-485 augmented the hypotension (at 360 min), but did not affect the vascular hyporeactivity elicited by endotoxaemia. 4. Endotoxaemia for 360 min resulted in rises in the serum levels of urea and creatinine (indicators of renal failure), glutamate-oxalate-transferase (GOT) and glutamate-pyruvate-transferase (GPT) (indicators of hepatocellular injury), and bilirubin and gamma-glutamyl transferase (gamma GT) (indicators of liver failure) as well as nitrite (indicator of the induction of nitric oxide synthase; iNOS). Treatment of LPS-rats with BQ-788, but not with BQ-485, attenuated the degree of liver injury and failure, while neither BQ-788 nor BQ-485 affected the acute renal failure or the induction of iNOS caused by endotoxin. 5. Endotoxaemia also caused (within 15 min) an acute metabolic acidosis (falls in pH, HCO3-and base excess) which was compensated by hyperventilation (fall in PaCO2). Treatment of LPS-rats with BQ-788 or BQ-485 did not affect the metabolic acidosis caused by LPS. 6. Thus, the selective ETB receptor antagonist BQ-788 attenuated (i) the delayed hypotension, (ii) the vascular hyporeactivity to NA as well as (iii) the degree of hepatocellular injury and dysfunction caused by endotoxin in the anaesthetized rat. In contrast, the selective ETA receptor antagonist did neither attenuate the circulatory failure nor the liver or renal dysfunction associated with endotoxaemia. We propose that the prevention of the hepatocellular dysfunction and injury caused BQ-788 in endotoxaemia is due to an improvement in oxygen delivery to the liver secondary to (i) inhibition of pre-sinusoidal constriction, (ii) inhibition of sinusoidal constriction, and (iii) improvement in perfusion pressure.
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PMID:Effect of selective blockade of endothelin ETB receptors on the liver dysfunction and injury caused by endotoxaemia in the rat. 889 67

1. The pathological features of Gram-positive shock can be mimicked by the co-administration of two cell wall components of Staphylococcus aureus, namely lipoteichoic acid (LTA) and peptidoglycan (PepG). This is associated with the expression of the inducible isoform of nitric oxide synthase (iNOS) in various organs. We have investigated the effects of dexamethasone (which prevents the expression of iNOS protein) or aminoguanidine (an inhibitor of iNOS activity) on haemodynamics, multiple organ dysfunction syndrome (MODS) as well as iNOS activity elicited by LTA + PepG in anaesthetized rats. 2. Co-administration of LTA (3 mg kg-1, i.v.) and PepG (10 mg kg-1, i.v.) resulted in a significant increase in the plasma levels of tumour necrosis factor-alpha (TNF alpha, maximum at 90 min) as well as a biphasic fall in mean arterial blood pressure (MAP) from 120 +/- 3 mmHg (time 0) to 77 +/- 5 mmHg (at 6 h, n = 8; P < 0.05). This hypotension was associated with a significant tachycardia (4-6 h, P < 0.05) and a reduction of the pressor response elicited by noradrenaline (NA, 1 microgram kg-1, i.v., at 1-6 h; n = 8, P < 0.05). Furthermore, LTA + PepG caused time-dependent increases in the serum levels of markers of hepatocellular injury, glutamate-pyruvate-transminase (GPT) and glutamate-oxalacetate-transaminase (GOT). In addition, urea and creatinine (indicators of renal dysfunction) were increased. There was also a fall in arterial oxygen tension (PaO2), indicating respiratory dysfunction, and metabolic acidosis as shown by the significant drop in pH, PaCO2 and HCO3-. These effects caused by LTA + PepG were associated with the induction of iNOS activity in aorta, liver, kidney and lungs as well as increases in serum levels of nitrite+nitrate (total nitrite). 3. Pretreatment of rats with dexamethasone (3 mg kg-1, i.p.) at 120 min before LTA + PepG administration significantly attenuated these adverse effects as well as the increases in the plasma levels of TNF alpha caused by LTA + PepG. The protective effects of dexamethasone were associated with a prevention of the increase in iNOS activity (in aorta, liver, lung, kidney), the expression of iNOS protein (in lungs), as well as in the increase in the plasma levels of total nitrite. 4. Treatment of rats with aminoguanidine (5 mg kg-1 + 10 mg kg-1 h-1) starting at 120 min after LTA + PepG attenuated most of the adverse effects and gave a significant inhibition of iNOS activity (in various organs) as well as an inhibition of the increase in total plasma nitrite. However, aminoguanidine did not improve renal function although this agent caused a substantial inhibition of NOS activity in the kidney. 5. Thus, an enhanced formation of NO by iNOS importantly contributes to the circulatory failure, hepatocellular injury, respiratory dysfunction and the metabolic acidosis, but not the renal failure, caused by LTA + PepG in the anaesthetized rat.
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PMID:Role of nitric oxide in the circulatory failure and organ injury in a rodent model of gram-positive shock. 896 50

The authors present a case of disseminated tuberculosis in a patient under dialysis with endstage renal disease. Fever, nocturnal sweating, anorexia, asthenia, ascites, lymph node involvement and granulomatous involvement of the bone marrow were observed. In the twenty nine months of renal failure which preceded the beginning of the tuberculosis, serum calcium levels were normal or low-normal and there was a secondary hyperparathyroidism. During that period the patient was treated with calcium carbonate and calcitriol. At the onset of tuberculosis, serum calcium levels rose above normal. Treatment with calcium and calcitriol was withdrawn but hypercalcemia remained unchanged. Serum concentration of parathormone fell significantly. Antituberculosis drugs were started. The resolution of active tuberculosis was accompanied by normalization of serum calcium levels and by elevation above normal of serum concentration of parathormone.
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PMID:[Tuberculosis and hypercalcemia]. 900 10

Ischemic renal injury is associated with changes in the expression of a number of genes. Although pH regulation is undoubtedly important during the recovery from ischemia, the expression of acid-base transporters during acute ischemic renal failure has not been studied. In the present study, levels of mRNA encoding the colonic H+-K+-ATPase and four isoforms of the Na+/H+ exchanger (NHE-1, NHE-2, NHE-3 and NHE-4) were measured by quantitative Northern analysis in rat renal cortex and medulla following ischemia-reperfusion injury. Rats were subjected to 30 minutes of renal artery occlusion and then sacrificed either 12 or 24 hours after the occlusion was released. The most striking changes followed 30 minutes of occlusion and 12 hours of reperfusion and involved the mRNA for NHE-3 (involved in HCO3- reabsorption in proximal tubule and thick limb) and colonic H+-K+-ATPase (involved in HCO3- reabsorption in collecting duct). These changes were: (1) a approximately 75% decrease in NHE-3 mRNA in both cortex and medulla; and (2) an approximately 8-fold increase in colonic H+-K+-ATPase mRNA in the cortex. At 12 hours of reperfusion, there was a 66% reduction in the Na+/H+ exchanger (NHE-3) activity as assayed by acid-stimulated 22Na+ influx into brush border membrane vesicles (P < 0.01). After 24 hours of reperfusion, NHE-3 mRNA remained suppressed while cortical colonic H+-K+-ATPase mRNA declined to only twice the control level. Medullary colonic H+-K+-ATPase mRNA did not change significantly. Gastric H+-K+-ATPase mRNA in cortex or medulla remained the same at 0, 12, and 24 hours after reperfusion. Cortical NHE-1 increased mildly at 12 and 24 hours of reperfusion whereas a moderate decrease in NHE-2 and NHE-4 mRNAs was observed in cortex and medulla after both 12 and 24 hours of reperfusion. We suggest that overexpression of colonic H+-K+-ATPase in the early phase of renal reperfusion injury may be responsible for compensatory reabsorption of increased HCO3- load resulting from suppression of NHE-3. This was supported by a fourfold increase in colonic H+-K+-ATPase mRNA in rats treated with acetazolamide, which causes renal HCO3-wasting. Rapid decline in colonic H+-K+-ATPase expression at 24 hours after reperfusion is likely due to reduced HCO3- delivery to distal tubules resulting from decreased GFR. Overexpression of H+-K+-ATPase may be vital to acid-base homeostasis in the early phase of acute ischemic renal failure.
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PMID:Ischemic-reperfusion injury in the kidney: overexpression of colonic H+-K+-ATPase and suppression of NHE-3. 908 76

Secondary hyperparathyroidism and renal osteodystrophy are the consequences of abnormal calcium, phosphate, and calcitriol metabolism ensuing from renal failure. Evidence suggests that calcium balance tends to become negative as we grow older than 35 years of age; however, the current dialysis modalities provide patients regardless of age with excessive calcium during dialysis. Administration of calcitriol in the management of hyperparathyroidism further increases the calcium and phosphate absorption. Furthermore, the current thrice-weekly renal replacement therapies fail to remove the daily absorbed phosphate, and we have to use calcium carbonate as a primary phosphate-binding agent to reduce intestinal phosphate absorption. The large calcium mass transfer and phosphate retention could lead to soft tissue calcification, especially in older end-stage renal disease (ESRD) patients. Consequently, only by maintaining a negative calcium balance during renal replacement therapy can we safely use calcitriol and calcium carbonate for the management of secondary hyperparathyroidism. Recent studies have indicated that phosphate restriction alone independent of plasma calcitriol or calcium can lower plasma parathyroid hormone (PTH) in renal failure and prevent hyperplasia of parathyroid glands. Therefore, phosphate control perhaps is the most important means to prevent secondary hyperparathyroidism. Previous studies have shown that ferric compounds are potent phosphate-binding agents; hence, these compounds warrant further trial in the management of phosphate metabolism in renal failure.
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PMID:Are we mismanaging calcium and phosphate metabolism in renal failure? 910 59

Calcium is necessary for the prevention and treatment of diseases such as osteoporosis, hypertension, and, possibly, colon cancer. Supplementation is useful when dietary calcium intake is low, as is the current situation in North America. There are many factors to consider before recommending any one form of supplement. A consideration for calcium carbonate tablets is whether the tablet disintegrates and whether or not a lack of food or acid in the stomach will hinder utilization. Other forms of calcium, particularly the chelated calcium salts, are better absorbed in fasting achlorhydric subjects but have less calcium per gram of supplement. Interaction of calcium with other mineral nutrients and the presence of contaminating metals has focused attention on safety. Based on present evidence, chelated calcium and refined calcium carbonate tablets (including those labeled as antacids) may be safely and effectively ingested by most people at doses generally recommended for treatment or prevention of osteoporosis. One should not exceed 2,000 mg of calcium, except at the advice of their health care provider, as inadvertent mineral deficiencies may arise. Persons at risk for developing milk-alkali syndrome, such as thiazide users and persons with renal failure, should be identified and monitored for alkalosis and hypercalcemia when using calcium supplements.
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PMID:Calcium supplementation. 927 39

Muscle potassium content and supplementation with potassium gluconate were evaluated in normokalemic cats with chronic renal failure (CRF). Affected cats received standard medical therapy for renal failure and either placebo (sodium gluconate) or potassium gluconate. At the beginning of the study and after 6 months of supplementation, glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) were estimated using 3H-inulin and 14C-tetraethylammonium bromide (TEA) clearances. Muscle potassium content was determined in biopsy specimens using atomic absorption spectroscopy. Muscle biopsy samples obtained from cats with CRF before treatment had significantly lower muscle potassium content than did those from normal control cats. Over the 6-month period of supplementation, muscle potassium content increased both in cats with CRF that received potassium gluconate and in those that received placebo (sodium gluconate). Serum potassium concentration and fractional excretion of potassium remained relatively unchanged in both groups of cats throughout the treatment period. There were no significant differences in the percentage change in GFR and ERPF between treatment groups over the 6-month time period. Median values for pH, HCO3-, and total CO2 at 6 months were higher than baseline in the potassium gluconate group but lower than baseline in the sodium gluconate group.
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PMID:Muscle potassium content and potassium gluconate supplementation in normokalemic cats with naturally occurring chronic renal failure. 929 75

At one time, when antacids were the primary medical means of treating peptic ulcer disease, the milk-alkali syndrome was not an uncommon cause of hypercalcemia. The simultaneous occurrence of hypercalcemia, alkalosis, and renal failure, in conjunction with the appropriate history of ingestion fof antacids, was suggestive of the syndrome. With the advent of antisecretory therapy, however, the milk-alkali syndrome has become an uncommon diagnosis. I report a case of milk-alkali syndrome and review the history of this syndrome as reported in the medical literature. Contemporary reports have focused on understanding the pathophysiology of the syndrome. Recent series have identified a shifting demographic profile, as increasing numbers of elderly women consume calcium carbonate as an anti-osteoporosis measure.
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PMID:Hypercalcemia and alkalosis due to the milk-alkali syndrome: a case report and review. 943 95

Hemodialysis (HD) has been used in the management of renal failure in dogs, but its feasibility has not been reported for uremic cats. Therefore, we investigated the technical possibility, efficacy, and complications of intermittent HD in cats with severe uremia. A total of 160 HD treatments were performed on 29 cats with acute renal failure (ARF) (n = 15), chronic renal failure (CRF) (n = 6), or acute on CRF (n = 8) between November 1993 and June 1996. Hemodialysis treatments were performed with transcutaneous dialysis catheters using a bicarbonate-based delivery system, sodium modeling, and volumetric-controlled ultrafiltration. Presenting serum chemistries (mean +/- SD) for all cats were creatinine, 16.4 +/- 7.5 mg/dL; blood urea nitrogen (BUN), 229 +/- 87 mg/dL; phosphate, 15.4 +/- 5.4 mg/dL; potassium, 6.0 +/- 1.6 mEq/L; and HCO3-, 16.0 +/- 4.4 mEq/L. For intensive HD treatments, pre-HD versus post-HD creatinine changed from 10.3 +/- 4.4 to 1.6 +/- 0.9 mg/dL and BUN from 105 +/- 33 to 8 +/- 10 mg/dL. One or more adverse events occurred during 111 (69%) treatments. Dialysis-related events included hypotension, dialysis dysequilibrium, clotting, and bleeding. Nine of 15 (60%) cats with ARF and 1 cat with CRF recovered sufficiently to survive without ongoing need for HD. For the remaining cats, the proximate causes of death were dialysis related in 9 cats, uremia related in 6 cats, and iatrogenic or unknown in 4 cats. Hemodialysis is technically feasible and effectively controls the biochemical disturbances of uremic cats. It is especially valuable for the management of severe ARF, permitting recovery in a large number of cats refractory to conventional therapy. Technical complications and chronic debility, however, may limit its usefulness for cats with advanced CRF.
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PMID:Applications and outcome of hemodialysis in cats: a review of 29 cases. 947 Jan 60

Dialysis-induced hypoxemia can occur in spontaneously breathing renal failure patients but whether it occurs during bicarbonate hemodialysis in critically ill patients receiving mechanical ventilation in assist-control mode is not clear. Twenty-one patients admitted to the medical intensive care unit who required mechanical ventilation and hemodialysis with the use of a cuprammonium dialyzer were enrolled and 25 sessions of hemodialysis were performed. Arterial blood gas, white blood cell count, minute ventilation, respiratory rate, and blood pressure were measured before dialysis (time 0) and at 15, 30, 60, 120, 180, and 240 minutes thereafter. The white blood cell count dropped immediately and reached the nadir 15 minutes after hemodialysis began. Thereafter, it recovered and overshot the predialysis value at the end of dialysis. The serum HCO3- concentration increased progressively after dialysis began and resulted in significant metabolic alkalosis. The P (A-a)O2 was not aggravated and minute ventilation was not depressed by rapid metabolic alkalosis under mechanical ventilatory support. The PaO2 remained stable throughout hemodialysis. No significant hypoxemia occurred in groups of varying predialysis cardiopulmonary dysfunction. These findings suggest that in renal failure patients ventilated in assist-control mode, l) hypoventilation and accompanying hypoxemia did not occur during bicarbonate (35 mEq/L) dialysis, despite significant metabolic alkalosis; and 2) patients with higher Acute Physiologic and Chronic Health Evaluation (APACHE) III scores and P(A-a)O2 levels were not more prone to dialysis-induced hypoxemia.
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PMID:Arterial oxygenation is unchanged during hemodialysis in patients mechanically ventilated in assist-control mode. 950 42


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