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

To determine whether green tea polyphenol ameliorates the pathological conditions induced by excessive dietary arginine, green tea polyphenol was administered to rats at a daily dose of 50 or 100 mg/kg body weight for 30 days with a 2% w/w arginine diet. In arginine-fed control rats, urinary and/or serum levels of guanidino compounds, nitric oxide (NO), urea, protein, and glucose increased significantly, while the renal activities of the oxygen species-scavenging enzymes superoxide dismutase (SOD) and catalase decreased, compared with casein-fed rats. However, rats given green tea polyphenol showed significant and dose-dependent decreases in serum levels of creatinine (Cr) and urea nitrogen and urinary excretion of Cr, and they exerted a slight reduction of nitrite plus nitrate, indicating that green tea polyphenol reduced the production of uremic toxins and NO. In addition, in arginine-fed rats the urinary urea, protein, and glucose level increases were reversed by the administration of green tea polyphenol. Moreover, in rats given green tea polyphenol the SOD and catalase activities suppressed by excessive arginine administration increased dose-dependently, implying the biological defense system was augmented as a result of free radical scavenging. These results suggest that green tea polyphenol would ameliorate renal failure induced by excessive dietary arginine by decreasing uremic toxin, and NO production and increasing radical-scavenging enzyme activity.
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PMID:Influence of green tea polyphenol in rats with arginine-induced renal failure. 1267 Jan 91

Hypercalcemia is a common, life-threatening metabolic disorder that can be associated with cancer. Its pathophysiology includes enhanced osteoclastic bone resorption and decreased renal excretion of extracellular calcium. Symptoms of hypercalcemia include nausea, vomiting, bone pain, polyuria, renal insufficiency, bradycardia, and arrhythmia. The goals of medical therapy are to inhibit bone resorption and promote renal calcium excretion. Hydration is the first step in management. Treatments for hypercalcemia include phosphates, calcitonin, bisphosphonates, and gallium nitrate. Although intravenous phosphates prevent intestinal calcium absorption and inhibit mineral and bone matrix resorption, serious adverse events include renal failure, hypotension, extraskeletal calcification, and severe hypocalcemia. Calcitonin has a rapid onset of action and can lower serum calcium concentrations within hours, but its usefulness is limited by its short duration of effect and the development of tachyphylaxis. Bisphosphonates are effective inhibitors of bone resorption but appear to have decreased response rates in hypercalcemic patients with high levels of parathyroid-related protein. Gallium nitrate, an antitumor agent noncytotoxic to osteoclasts and bone cells, appears to be more effective than pamidronate, etidronate, and calcitonin in the treatment of cancer-related hypercalcemia. Importantly, unlike bisphosphonates, gallium nitrate is effective in both parathyroid-related protein-mediated and non-parathyroid-related protein-mediated hypercalcemia.
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PMID:Treatment of cancer-related hypercalcemia: the role of gallium nitrate. 1277 55

The study of salt-sensitive hypertension has been facilitated by development of genetic models, especially the Dahl/Rapp salt-sensitive (S) rat. S rats rapidly become hypertensive after initiation of a diet containing 8.0% NaCl and subsequently develop arteriolonephrosclerosis and renal failure, whereas the salt-resistant (R) strain remains normotensive on the same diet. The purpose of the present study was to use these strains to demonstrate the interactions between transforming growth factor-beta1 (TGF-beta1) and nitric oxide (NO). Young, male S and R rats were fed for 4 days diets that contained either 0.3 or 8.0% NaCl. An increase in dietary salt increased kinase activities of both p38 MAPK and p42/44 MAPK in cytoplasmic extracts from aortic rings and isolated glomeruli from both strains. Inhibition of either pathway with PD-098059 or SB-203580 decreased production of TGF-beta1 and nitrate plus nitrite (NOx). In both strains, production of active TGF-beta1 and NOx linearly correlated. Incubation of aortic rings and isolated glomeruli with the NO donor NOR3 decreased TGF-beta1 levels, whereas the NO synthase inhibitor Nomega-nitro-l-arginine methyl ester increased production. The inhibitory effect of NO on production of TGF-beta1 was reduced in preparations from S rats. Although a close interrelationship existed between TGF-beta1 and NO in both strains, production of TGF-beta1 was increased in prehypertensive S rats and was further exaggerated with the increase in dietary salt intake. Augmented vascular and glomerular production of TGF-beta1 and diminished NO may contribute to the development of hypertensive nephrosclerosis in S rats.
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PMID:The interrelationship between TGF-beta1 and nitric oxide is altered in salt-sensitive hypertension. 1286 56

The renoprotective effect of losartan and quinaprilat was tested in two different animal models of renal failure [female Wistar rats, single administration of 0.5 mg uranyl nitrate (UN)/100 g body wt. or 5/6 nephrectomy (5/6NX)]. Losartan (1 mg/100 g body weight [wt.]) and quinaprilat (1 mg/100 g body wt.) were administered intraperitoneally, once daily, starting 10 days after UN and one week after 5/6NX till the end of 10 weeks experimental period. Parameters characterizing the therapeutic effect were blood pressure, urinary protein excretion 4 and 10 weeks after the injury, and p-aminohippurate accumulation in renal cortical slices in vitro, hydroxy-proline concentration in renal tissue and morphology at the end of the experiment. Summarizing our results we state: (1) the angiotensin 1 receptor blocker losartan is more effective in UN-treated than in 5/6 NX rats, and (2) the angiotensin converting enzyme inhibitor quinaprilat is more effective than losartan because of the amelioration of blood pressure and OH-proline concentration in renal tissue of UN-treated rats.
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PMID:Effects of a therapy with losartan and quinaprilat on the progression of chronic renal failure in rats after a single dose of uranyl nitrate or 5/6 nephrectomy. 1287 46

Since hepatorenal syndrome is a functional renal failure due to renal ischemia in cirrhotics with refractory ascites, we investigated whether increased intra-abdominal pressure (IAP) impairs the renal function and perfusion in cirrhotic portal hypertensive rats. Eight groups of 32 rats each were studied, including 4 control and 4 CCl(4) cirrhotic groups. These were subdivided into two groups each, with and without an increased IAP, and further subdivided into groups of rats with and without NO inhibition. IAP was increased to 20 mm Hg for 7 consecutive days by means of an intraperitoneally placed balloon filled with water. The animals were studied in normal conditions and after inhibition of NO synthesis. Changes in mean arterial pressure and renal microcirculation by means of femoral artery catheterization and laser-Doppler technique, respectively, were recorded. Venous samples for determination of plasma renin-aldosterone activity, biochemical parameters of liver and renal function, and plasma nitrite/nitrate levels as an index of NO synthesis were drawn. Cirrhotic rats showed decreased renal microcirculation (P = 0.05), while elevated IAP produced a further decrease (P = 0.01). Renin-aldosterone levels found increased (P = 0.001) in cirrhotics, and elevated IAP produced a further increase (P = 0.01] in both groups. Inhibition of NO synthesis resulted in a nonsignificant decrease in both renal microcirculation and renin-aldosterone levels in all experimental groups. Liver and renal function was found to be impaired in cirrhotics, but increased IAP had a nonsignificant further functional impairment in both organs. In conclusion, chronically elevated IAP in cirrhotic rats is associated with an increase in renin-aldosterone levels and significant impairment of renal perfusion.
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PMID:The influence of continuous seven-day elevated intra-abdominal pressure in the renal perfusion in cirrhotic rats. 1457 84

Human envenoming by caterpillars of the saturniid moth Lonomia obliqua in southern Brazil produces a mild local response (erythema, some edema, and pain) and systemic effects that include incoagulable blood, renal failure and in severe accidents intracerebral hemorrhage. In this work, we used light and electron microscopy to investigate the morphological alterations in the brain and blood-brain barrier of rats injected intravenously with venom from L. obliqua spicules (200 microg/kg). Five semi-purified fractions of venom (200 microg/kg each) were also assayed. Quantitative morphological and ultrastructural analyses were done 6, 18, 24 and 72 h after the i.v. injection of venom and its fractions. Light microscopy showed that 6h after envenoming there was cerebellar edema, which decreased by 72 h. Intracerebral hemorrhage occurred in only one rat 24h after the injection of venom. Blood-brain barrier (BBB) breakdown, assessed by transmission electron microscopy based on the passage of an extracellular tracer (lanthanum nitrate) between brain capillary endothelial cells, was observed in the cerebellum and hippocampus 18 h after venom injection. At this time, the cerebellum was more sensitive to the venom than the hippocampus, as shown by the greater number of leaky vessels. The number of capillaries showing breakdown was lower after 72 h than after 18 h. None of the semi-purified fractions significantly increased the number of leaky vessels. These results indicate that L. obliqua caterpillar venom has a deleterious action on the rat BBB. The lack of effect of the venom fractions when administered alone suggested that a synergistic action of venom components may be responsible for the damage seen in the central nervous system, but this was not confirmed when three combinations of the fractions were tested.
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PMID:Lonomia obliqua caterpillar venom increases permeability of the blood-brain barrier in rats. 1550 Dec 88

Renal failure was experimentally induced in 36 hamsters by intraperitoneal injection with uranyl nitrate (5 mg/kg). Twenty-four h later [during acute renal failure (ARF), as indicated by the serum concentrations of creatinine and urea nitrogen] or 72 h later [during chronic renal failure (CRF)] these hamsters plus 18, uninjected, control hamsters were each given a single, intramuscular dose of sodium stibogluconate (120 mg pentavalent antimony/kg). The pharmacokinetic parameters for the antimonial drug were calculated using a non-compartmental model. Urine was collected for 72 h after similar treatment with the antimonial drug, from another 30 hamsters (10 controls, 10 with ARF, and 10 with CRF), so that the fraction of the antimony administered that was subsequently excreted in the urine could be estimated. Compared with the controls, both the hamsters with ARF and those with CRF had significantly higher maximum concentrations of antimony (C(max)), significantly larger 'areas under the curve' for the plots of blood concentration v. time, and significantly longer plasma half-lives (P < 0.001 for each). The mean (S.D.) values of C(max), for example, were more than three-fold higher in the hamsters with ARF [467.5 (59.04) microg/ml] or CRF [461.1 (68.9) microg/ml] than in the controls [154.01 (17.3) microg/ml]. The systemic clearance of antimony was also significantly lower in the hamsters with CRF than in the control animals [0.051 (0.002) v. 0.296 (0.047) litres/h/kg; P < 0.01]. In addition, the fraction of the antimony administered that was excreted in urine was significantly lower in the animals with ARF (0.25) or CRF (0.08) than in the controls (0.37), indicating significant dysfunction of the kidneys in the hamsters injected with uranyl nitrate. It seems clear that, if severe toxicity is to be avoided, patients with renal dysfunction requiring treatment (for leishmaniasis) with sodium stibogluconate should be given lower doses than similar cases with normal kidney function.
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PMID:Effect of renal impairment on the pharmacokinetics of antimony in hamsters. 1566 12

Amongst the principal metabolic situations that can require emergency attention in the oncology patient we find: hypercalcaemia, hyponatraemia, tumoural lysis syndrome, lactic acidosis, hyperuricaemia, renal failure, hyperammonaemia, hypermpotasaemia, etc. Hypercalcaemia is the most frequent metabolic complication in oncology, appearing in 10-30% of these patients. It has two main mechanisms, tumoural lysis and humoural hypercalcaemia mediated by PTHrP (a protein related to parathormone). The principal factor for its diagnosis is suspicion, since some symptoms are non-specific and can be attributed to other causes such as somnolence, constipation, etc. Treatment will be based on intensity and is started with calciuretic measures with an intense hydration with physiological serum and on some occasions with furosemide. Anti-reabsorptive measures include calcitonin, bisphosphonates, mithramycin, gallium nitrate and on occasions corticoids. Bisphosphonates such as pamidronate and zoledronate seem to be highly useful in these cases. Hyponatraemia is classified depending on plasmatic osmorality; when this is low we find ourselves facing an authentic hyponatraemia that can develop with an extra-cellular volume that is high (cardiac insufficiency, cirrhosis, nephrotic syndrome and renal insufficiency), low (renal and extra-renal sodium losses) and normal (principally SIADH, related to a high elimination of sodium in the urine with high urinary osmolarity in spite of this being low in blood). Several types of tumour and different chemotherapy drugs can produce this SIADH. Treatment will vary according to the type and intensity, but in general this is based on hydric restriction and the replacement of the sodium deficit, either through physiological serum or through hypertonic saline serums depending on the case, and on occasions furosemide for the elimination of excess water.
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PMID:[Metabolic emergencies in the oncology patient]. 1572 5

Lysinuric protein intolerance (LPI) is a disorder of dibasic amino acid transport secondary to mutation of the SLC7A7 gene characterized by renal failure, pulmonary alveolar proteinosis, lupus-like autoimmune symptoms and usually increased plasma citrulline. In order to better understand the underlying mechanism, we studied the plasma and urinary nitrite/nitrate (NO2-/NO3-) concentrations in three LPI patients and the in vitro NO2- production in cultured fibroblasts. Our data show that NO3- levels are increased in the plasma of patients with LPI. Similarly, NO2- release in the medium of cultured fibroblasts was increased. On this basis, we hypothesize that some of the poorly understood clinical signs of LPI could be related to the activation of the NO-citrulline pathway.
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PMID:Increased NO production in lysinuric protein intolerance. 1587

Chronic inhibition of nitric oxide (NO) synthesis is characterized by increased blood pressure accompanied with both cardiac hypertrophy as well as renal damage. We investigated whether the angiotensin-converting enzyme (ACE) inhibitor captopril can inhibit the cardiac hypertrophy and reverse the renal failure. We tested the influence of captopril on the nitrate-nitrite (NO(x)) in plasma and heart and kidney tissues. Oxidative stress, in terms of glutathione and thiobarbituric acid-reactive substances measured as malondialdehyde, was monitored examining their involvement in the cardioprotective and renoproptective actions. Three groups of Wistar rats were used: untreated group, and rats treated with the NO synthase inhibitor N(w)-nitro-L-arginine methyl ester (L-NAME) and L-NAME plus captopril (10 mg/kg/day). Systolic, diastolic and mean blood pressure (BPs, BPd and BPm respectively) was measured weekly in addition to the heart rate using rat-tail plethysmography. After 3 weeks, L-NAME significantly increased BPs, BPd and BPm. Captopril treatment reversed the increments in pressure back to normal values by the fourth week. ACE inhibition by captopril reverted the L-NAME-induced hypertrophy and inhibited the enzymatic indices of cardiac damage (glutamate oxaloacetate transaminase and lactate dehydrogenase) back to normal values. Furthermore, the NO synthesis inhibition produced renal damage as indicated by significant increase in creatinine. Captopril ameliorated the raised creatinine to normal. Chronic L-NAME treatment increased serum NO(x) levels but concomitant treatment with captopril was without effect.
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PMID:Effects of captopril on cardiac and renal damage, and metabolic alterations in the nitric oxide-deficient hypertensive rat. 1622 7


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