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

Diuretic activities of xanthine or nonxanthine adenosine antagonists and their ameliorative effects against glycerol-induced acute renal failure in rats were investigated in order to clarify the physiological and pathological function of adenosine receptors in the kidney. Diuretic and natriuretic activities of a variety of adenosine antagonists clarified systematically for the first time that the blockade of A1 receptors is more important than that of A2 receptors in sodium and water excretion and support the hypothesis that endogenous intrarenal levels of adenosine directly enhance tubular sodium readsorption. Studies of structure-activity relationships of 8-substituted xanthines in the acute renal failure demonstrated that the activation of adenosine A1 receptor was an important factor in developing such a renal failure. A series of 8-(3-noradamantyl)xanthines exhibited the extremely potent diuretic and natriuretic activities (24; 2.5 micrograms/kg, po, the ratio of urinary excretion value in treated rats to urinary excretion value in control rats = 1.69, the ratio of Na+/K+ in treated rats to Na+/K+ in control rats = 1.76) and potent ameliorative effects against glycerol-induced acute renal failure (24; 10 micrograms/kg, ip, 55% inhibition). From our detailed studies of structure-activity relationships, we can speculate that some tissue differences of the adenosine A1 receptor might exist between kidney and brain and sites of action for adenosine antagonists could be different between two renal pharmacological assays. 1,3-Dipropyl-8-(3-noradamantyl)xanthine, KW-3902 (24), was chosen for further studies and is under development as a drug for treating the acute renal failure.
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PMID:Adenosine A1 antagonists. 2. Structure-activity relationships on diuretic activities and protective effects against acute renal failure. 150 Dec 34

Benign intracranial hypertension (also called pseudotumor cerebri, otitic hydrocephalus, or meningeal hydrops) is a syndrome of markedly elevated intracranial pressure in the absence of intracranial mass, inflammation, or obstruction. Numerous disease processes and medications have been associated with it. However, renal failure has not been documented as an associated condition. In this report, the case of a 27-year-old Native American man with chronic renal failure of unknown etiology is described, with new-onset headache, papilledema, and elevated intracranial pressure. After normal cerebrospinal fluid, computed tomography, and magnetic resonance imaging studies, a diagnosis of benign intracranial hypertension was made. Despite repeated lumbar punctures with cerebrospinal fluid removal, the patient's headaches persisted, and intracranial pressures remained in the 200 to 400 mm H2O range. After initiation of hemodialysis due to progressive deterioration of renal function, the patient's headaches became less severe and eventually disappeared. This case represents a unique association of chronic renal failure with benign intracranial hypertension.
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PMID:Benign intracranial hypertension and chronic renal failure. 152 75

Effective constituents for renal disease were partially purified from a herbal prescription. The efficacy on renal diseases was examined using an experimental model system of glomerular lesion in mice induced by Agkistrodon acutus venom (Ac1-P). The extract of boiling water of the herbal prescription (P-3) was first fractionated by ether into an acidic fraction and a mixture of basic and neutral fractions. The acidic fraction was proved to be more effective and then further examined by thin layer chromatography and spectrophotometry. One of the main components was confirmed to be caffeic acid which had inhibitory effect on renal failure in mice by Ac1-P. This effect was considered to be caused by caffeic acid inhibiting the proteolytic enzyme activity of Ac1-P. Caffeic acid should thus have prophylactic or inhibitory effect on glomerular disease in which proteolytic enzymes may have pathogenic roles.
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PMID:Identification of effective component from a traditional herbal medicine and the inhibitory effects on experimental glomerular lesion in mice. 155 73

Clofibrate affects lipid and alcohol as well as drug and eicosanoid metabolism. Spontaneous hypertensive rats (SHR) further increase their high voluntary alcohol consumption during clofibrate feeding. The interaction of alcohol and clofibrate was studied in two long-term trials. Seventy-nine male SHR (aged 27 weeks) were offered increasing concentrations of ethanol, up to 30% (tap water ad lib), and 3 months later 0.5% clofibrate-food. Four groups were established: N, normal controls; NA, standard diet+alcohol; C, clofibrate feeding; and CA, clofibrate feeding + alcohol. Food intake, alcohol consumption, body weight, and laboratory values were recorded continuously. Life duration (weeks) after the start of the trial was 63.3 +/- 3.3 in N, 73 +/- 2.6 in NA, 77.7 +/- 4.3 in C, and 90.3 +/- 2.8 in CA. There were no alcohol-related liver findings in NA and CA. Most of the animals died of cardiac and renal failure. An increase of tumors in clofibrate-treated rats was not observed. Voluntary alcohol consumption or clofibrate feeding significantly lengthens lifetime, which is prolonged by 42% if ethanol is combined with clofibrate. This is obviously not mediated by the lipid lowering effect or an influence on body weight and blood pressure of either clofibrate or alcohol.
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PMID:Lifetime prolongation in voluntary alcohol-consuming rats (SHR) treated with clofibrate. 159 25

Hypovolemic hyponatremia attributable to severe fluid and electrolyte alterations was diagnosed in a foal with diarrhea. Subsequent consumption of water resulted in rapid reduction of serum sodium concentration and serum osmolar depression. Clinical signs of neurologic disease developed including blindness, loss of menace response, and seizures. Treatment of this condition with IV administered fluids included hypertonic saline solution (7.2%; 2 ml/kg of body weight), and frequent monitoring of serum electrolyte concentrations and osmolality resulted in gradual correction of the fluid and electrolyte imbalance and resolution of the neurologic signs. Hyponatremia has been recognized in foals with renal failure, ruptured urinary bladder, and iatrogenic water overload. The key to diagnosis and management of profound hyponatremia is accurate diagnosis of the status of plasma volume and association of the electrolyte imbalance with clinical signs of neurologic disease. This report describes an unusual complication of a commonly encountered problem in equine practice and documents that the severe metabolic and electrolyte abnormalities associated with diarrhea can result in clinical neurologic disease. The differential diagnosis also should include bacterial sepsis, parasitism, thoracic mass, acute renal failure, congenital neurologic deficit, or seizure syndrome. Serum electrolyte disorders should be considered as a potential cause of signs of neurologic disease in foals with diarrhea.
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PMID:Hypovolemic hyponatremia and signs of neurologic disease associated with diarrhea in a foal. 160 18

Aluminum (Al) accumulation in renal failure is an etiological factor in the pathogenesis of low turnover bone disease. Aluminum-induced impairment of mineralization has been related to a reduced extent of active bone-forming surface. The present study investigated the effect of fluoride, a potent stimulator of osteoblast number, on the toxicity of aluminum in rats with renal failure (Nx). Following a large parenteral aluminum load (3.2 mg/kg x day) over a period of nine weeks, bone histomorphometry of vertebral cancellous bone revealed a severe low-turnover osteodystrophy as evidenced by a fall in osteoblastic osteoid surfaces and mineral apposition rates. Concurrent administration of fluoride [20 mg/liter (F20) or 40 mg/liter (F40) supplied with the drinking water] resulted in a significant increase in the number of osteoblasts (Nx+Al+F40 vs. Nx+Al, 33.75 +/- 2.83 vs. 1.81 +/- 0.43 mm-1, P less than 0.001) together with an overall reduced deposition of aluminum in bone (469.3 +/- 24.6 vs. 592.2 +/- 28.3 micrograms/g, P less than 0.01). However, there was an increase in the fraction of osteoid surface exhibiting stainable aluminum at the bone-osteoid interface (70.7 +/- 7.1 vs. 44.3 +/- 6.0%, P less than 0.005). Fluoride-exposed rats accumulated a significantly larger osteoid volume, suggesting an exacerbation of the osteomalacic lesion, and furthermore, dynamic histomorphometric parameters remained depressed. These results indicate that fluoride has a distinct effect on the pattern of aluminum deposition in bone. In addition, fluoride antagonizes the aluminum-induced reduction in osteoblast number but provides no amelioration of the impaired mineralization in aluminum-intoxicated rats. Thus, in this model a decrease in the extent of osteoblast surface does not account for the development of aluminum-related bone disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of fluoride on aluminum-induced bone disease in rats with renal failure. 161 48

Previous studies in experimental models of progressive renal failure have shown that the capacity of antihypertensive drugs to protect glomeruli from sclerosis is often unpredictable from their effect on systemic blood pressure. The present study was undertaken to ascertain whether this systemic blood pressure-independent structure-preserving effect of antihypertensives, particularly angiotensin II converting enzyme inhibitors (ACEI), is confined to the glomerulus or not, as well as whether this effect is mediated via angiotensin II (Ang II). The following experimental drug regimens were used in the rat model of subtotal nephrectomy (sNPX): so-called triple therapy [TRX; a combination of reserpine 5 mg/liter drinking water (DW), hydralazine 80 mg/liter DW and hydrochlorothiazide 25 mg/liter DW], or ACEI (either captopril, CPL, 600 mg/liter DW, enalapril, ENL, 400 mg/liter DW or lisinopril, LSL, 200 mg/liter DW), or a novel Ang II receptor antagonist (Ang IIR, L-158,809, 20 mg/liter DW). These dosages were identified in pilot studies to be the minimum required to control systemic blood pressure in the early phase up to 12 weeks. In addition, a separate group was treated with a higher dose of L-158,809 (80 mg/liter DW) with equipotent systemic pressor effect. Treatment was initiated eight weeks after subtotal nephrectomy following renal biopsy, and animals were sacrificed at 16 weeks. In ACEI treated rats, carotid arterial wall thickening (WT), defined as ratio of media thickening to radius of outer vessel wall, was similar to normal age-matched control (0.073 in all ACEI treated rats, vs. 0.074 in normal control) and significantly less than with TRX (ratio 0.118) or untreated sNPX (0.130). Even more remarkably, coronary arteriole WT in ACEI-treated rats averaged 0.139, a value less than one half and one third of TRX (0.298) and untreated sNPX control (0.388), respectively. Similar results were obtained for mesenteric artery WT. These findings were closely paralleled by changes of glomerular sclerosis. In untreated sNPX control rats, glomerular sclerosis increased from biopsy to autopsy specimens by an average of 458%. Although TRX dampened the degree of increase in sclerosis to on average 212%, this protective effect was far less than that achieved by ACEI. In the latter, sclerosis increased on average only 65% from biopsy to autopsy. Although all ACEIs were more effective than TRX, captopril and lisinopril groups showed greatest benefit at these doses. Ang IIR also protected renal and extrarenal structures with 34% increase of sclerosis index in low dose and WT 0.088, 0.117 and 0.112, respectively in carotid, mesenteric and coronary arteries.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Blood pressure-independent effect of angiotensin inhibition on vascular lesions of chronic renal failure. 163 54

The glomerular and tubular basement membranes are the principal barriers to filtration and re-absorption of water and molecules in the nephron. They are composed primarily of type IV collagen, laminin, fibronectin, sulphated proteoglycans and collagen type I. Three common inherited diseases are associated with abnormalities of basement membrane proteins: Alport's syndrome, thin basement membrane disease (TBMD) and adult polycystic kidney disease. In this review we describe the application of molecular biological techniques to the study of these conditions. Classic Alport's syndrome is an X-linked disorder with a lamellated glomerular basement membrane (GBM) which typically results in renal failure in males. Studies with sera from patients with Goodpasture's syndrome, or monoclonal antibodies specific for the Goodpasture antigen, show that the Goodpasture antigen is absent or masked in the kidneys of individuals with Alport's syndrome. There is some evidence to suggest that the Goodpasture antigen is best represented by the non-collagenous domain of the alpha 3 chain of type IV collagen, but that other non-collagenous regions may also contribute to the antigen. It is through these non-collagenous regions that the type IV collagen chains form the typical network, and the abnormality in Alport's syndrome interferes with this network formation. However, we have recently demonstrated that the gene for the non-collagenous domain of the alpha 3 collagen chain is present in individuals with Alport's syndrome. Furthermore, other groups have shown a defect in a novel type IV collagen chain, the alpha 5 chain, in 3 unrelated cases of Alport's syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hereditary abnormalities of renal basement membranes. 168 82

Rat experiments indicate that oral ingestion of cadmium through drinking water leads to an accumulation of cadmium in bone, in addition to liver and kidney. After five weeks of cadmium intake in drinking water (50 to 100 mg/L), the bone cadmium levels increased in proportion to the intake concentration. Bone and kidney histology showed no signs of bone or kidney damage up to 5 wk of cadmium ingestion. Cadmium accumulation in bone was a primary phenomenon and not secondary to renal failure. In addition, cadmium levels have been estimated in a variety of sources, e.g., foodstuff, fertilizer, and sewage sludge, using neutron and proton activation analyses and atomic absorption spectrophotometry. Cadmium levels of Canadian foods are in the range of 0.002-0.07 mg/kg, and soils are in the range of 0.55 to 1.72 mg/kg. Fertilizers contain cadmium from 0.3 to 1.25 mg/kg, whereas sewage sludge contains up to 122 mg/kg.
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PMID:Studies of cadmium uptake in bone and its environmental distribution. 170 26

Renal failure in itself generates a state of malnutrition, due to three main causes: inadequate ingestion (anorexia, vomiting or diet insufficiencies), the existence of catabolic factors (proteins, acidosis, PTH) and extrarenal depuration (which provokes a lack of amino acids and vitamins). Artificial nutrition constitutes a series of measures that can be adopted to act upon each of the above causes. Adequate ingestion compared to inadequate ingestion can be performed orally (especially in chronic renal failure) by parenteral administration (preferable in acute renal failure) and enteral administration (complementary in both cases). The quantity and quality of adequate nutrients is non-dependent on the method of administration; 500 ml, of water should be administered plus diuresis, plus loss from other tracts; the mineral intake of sodium, potassium and phosphorus should be restricted; in the case of vitamins, these should be administered, especially the B and D complexes; there should be sufficient calories to constitute a hypercaloric diet (from 30-50 kg/day), at least 50% in the form of carbohydrates (hypertonic glucose, if administered intravenously, and dextrinolmaltose or starch if administered through the digestive tract) and at least 40% in the form of lipids (preferably of vegetable origin, rich in non-saturated fatty acids); proteins are the mainstay of nutrition in renal failure; thus, with a normal renal function or in dialysis, a dose of 1 g/kg/day is recommended; in chronic renal failure, 0.5 g/kg/day; in cases of renal failure not on dialysis, 0.3 g/kg/day, supplemented by essential amino acids or cetoacids (the effectiveness of the latter is still in dispute).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Artificial nutrition in kidney failure]. 176 Apr 78


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