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

Oral calcium supplementation is reported to have phosphate-binding and antihypertensive effects. Since both phosphate binders and antihypertensive agents are reported to attenuate renal injury, we studied the effect of oral calcium carbonate (CaCO3) administration on the course of renal deterioration using doxorubicin-induced renal failure in rats treated with deoxycorticosterone acetate and salt for 10 weeks. Rats were divided into four groups: the CaCO3 (6.0 g/kg/d) group (n = 12), the aluminum hydroxide (Al(OH)3; 6.0 g/kg/d) group (n = 11, as a phosphate-binder control), the hydralazine (10 mg/kg/d) group (n = 11, as an antihypertensive control), and the control group (n = 12). All agents were given as a mixed chow diet. Blood pressure and urinary protein excretion progressively increased in the control rats. CaCO3 and hydralazine lowered blood pressure, but Al(OH)3 did not (185 +/- 4 mm Hg, control; 160 +/- 5 mm Hg, CaCO3; 171 +/- 8 mm Hg, Al(OH)3; 156 +/- 5 mm Hg, hydralazine at week 10). Proteinuria was reduced in the rats treated with CaCO3 and Al(OH)3 compared with those without the treatment (986 +/- 86 mg/d, control; 551 +/- 54 mg/d, CaCO3; 527 +/- 31 mg/d, Al(OH)3; and 955 +/- 68 mg/d, hydralazine at week 10). Serum phosphate concentration and calcium phosphate products also were significantly lower in both the CaCO3 and Al(OH)3 groups than in the control group. At week 10, increased serum urea nitrogen, impaired renal function, and glomerular sclerosis present in the control group were significantly attenuated in both in the CaCO3 and Al(OH)3 groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oral calcium carbonate administration ameliorates the progression of renal failure in rats with hypertension. 777 88

Modern therapeutic concepts of chronic renal insufficiency are based on observations showing a retardation of progressive renal failure by therapeutic measures. In the context emphasis is now placed on the treatment of arterial hypertension and on the patient's adherence to a protein-restricted diet. In addition to these conservative measures it is important to avoid nephrotoxins, to hydrate the patient sufficiently and to treat advanced hyperlipidemias. Deficiencies of active vitamin D should be treated by oral vitamin D substitution after correction of hyperphosphatemia. In the treatment of the latter, preparations of calcium carbonate are now the preferred mode of treatment. In advanced renal insufficiency it is important to maintain a salt-restricted diet and to treat any attendant hyperkalemia and hyponatremia.
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PMID:[Conservative treatment in chronic kidney insufficiency]. 778 98

In 18 patients with acute myocardial infarction admitted to the Cardiological Care Department within 6 hours after the onset of chest pain, before administration of drugs and then in the 2nd, 3rd, 5th and 7th day, the levels of glucose, pyruvate, lactate in venous blood, the lactate/pyruvate ratio (L/P) and pH, actual hydrocarbons, PCO2 and PO2 in capillary arterialized were determined. Depending on the clinical status at admission the patients were classified into 2 groups: I--without complications (I class according to Killip-Kimbal; n = 10), and II--with complications (II-IV class of cardiac failure according to Killip-Kimbal and/or complex ventricular arrhythmias e.i. III-V class according to Lown and heart block of Mobitz--type II and III degree; n = 8). None of the patients had diabetes, chronic respiratory tract diseases, renal failure and liver cirrhosis. The control group consisted of 11 healthy persons. On the first day of myocardial infarction, the significant increase of blood glucose, lactate, pyruvate, as well as significant decrease of blood pH, HCO3- and PO2, and non significant increase of L/P ratio were observed in both groups as compared to the control group. Also there were non significant difference of the glucose, lactate, pyruvate L/P ratio and pH, PCO2 and HCO3- values between the I and II group on the first day of the acute myocardial infarction, with exception of the PO2, which was significantly lower in the group II. In the following days an increase of PO2 was observed. Since this effect coincided with a decrease of lactate concentration (significant only in the group II) it could be concluded, that the observed decrease of the lactate concentration resulted from the higher supply of oxygen. The obtained results have shown, that increase of glycaemia values and decrease of PO2 values may be considered as biochemical markers for hemodynamic complications of acute myocardial infarction.
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PMID:[Lactate metabolism in acute myocardial infarction]. 780 May 82

The aim of this study was to evaluate the effects of a combined low-dose therapy of calcitriol and calcium carbonate on bone metabolism in the early phases of chronic renal failure. A 30-month study involving 17 patients with ECRF was made: 6 months of observation were followed by 24 months of therapy (calcitriol 0.25 microgram/day plus calcium carbonate 1 g/day). The most important results were that renal function was stable throughout the study and there was an increase in calcaemia and a decrease in plasma alkaline phosphatase, plasma osteocalcin, plasma PTH and urinary hydroxyproline. We observed a progressive slowing of the rate of loss of appendicular bone density as well as a decrease of osteoblastic and osteoclastic activity and an improvement of bone mineralization. In conclusion, low doses of calcitriol plus calcium carbonate seem to improve the biochemical and bone derangements in early renal failure.
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PMID:Calcitriol and calcium carbonate therapy in early chronic renal failure. 762 9

In normal adults eating diets with standard protein contents, urinary excretion of NH4 approximates 40 mmol/24 hours and urinary pH is variable. In patients with metabolic acidosis, a urinary pH under 5.5 suggests an extra-renal cause whereas a urinary pH above 5.5 suggests a renal disorder, although there are many exceptions to this rule of thumb. However, urinary excretion of NH4 is always above 70 mmol/24 hours in extra-renal acidosis and less than or equal to 40 mmol/24 hours in renal acidosis; the two situations can readily be differentiated by determining the urinary anion gap which is absent in the former case and present in the latter. Acidosis due to nephron loss is readily diagnosed on the basis of advanced renal failure with an elevation in nonassayed plasma anions, contrasting with the increased serum chloride level found in tubular acidosis. Oral NaHCO3 loading followed by determination of the fractional excretion of HCO3 or, preferably, of the TmHCO3 normalized for glomerular filtration rate differentiates proximal tubular acidosis (decreased TmHCO3) from distal tubular acidosis (normal or increased TmHCO3). In the latter case, decreased serum potassium levels suggest distal tubular acidosis due to defective H(+)-ATPase or H+/K(+)-ATPase pump function (no increase in urinary PCO2 after oral NaHCO3 loading) or to inability of the kidney to develop a normal H+ gradient (normal increase in urinary PCO2). Increased serum potassium levels suggest conditions involving either hypoaldosteronism or alterations in transepithelial voltage or pseudo-hypoaldosteronism. The incidence of distal tubular acidosis with increased serum potassium levels is rising, whereas tubular acidosis with low serum potassium levels remains infrequent.
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PMID:[Classification of renal tubular acidosis. Recent data]. 838 29

The milk-alkali syndrome became rare with the advent of modern ulcer therapy with nonabsorbable antacids, histamine2 blockers, and sucralfate. An increased frequency of this syndrome seems likely with the growing popularity of the use of calcium carbonate as an antacid or as calcium supplementation to prevent osteoporosis. We treated five patients who had six episodes of the milk-alkali syndrome; four of these cases were diagnosed between 1990 and 1992. All patients were ingesting massive quantities of calcium and absorbable alkali and were unaware of the toxic effects of these compounds. All patients presented with the triad of hypercalcemia, metabolic alkalosis, and renal failure. All metabolic abnormalities were corrected, and renal function improved with appropriate supportive measures and cessation of calcium and alkali ingestion. In two patients, the renal failure was so severe that dialysis was necessary. In four patients, either the serum amino-terminal parathyroid hormone or 1,25-dihydroxycholecalciferol levels were appropriately decreased in response to hypercalcemia. The serum carboxy-terminal parathyroid hormone levels were increased because of renal failure. Since both physicians and patients are often unaware of the calcium and alkali content of many nonprescription medicines, the diagnosis of the milk-alkali syndrome, a reversible cause of renal failure, can be missed if a detailed history of such intake is not elicited. Measurement of the serum amino-terminal parathyroid hormone and 1,25-dihydroxycholecalciferol levels may help differentiate milk-alkali syndrome from primary hyperparathyroidism.
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PMID:The milk-alkali syndrome. A reversible form of acute renal failure. 848 Oct 62

Over a six-week period a 60-year-old patient had several unexplained intoxication-like episodes. He finally had severe abdominal cramps with changes in the level of consciousness and oligoanuric renal failure (creatinine 4.7 mg/dl). The history, marked metabolic acidosis (pH 7.15, HCO3- 2.2 mmol/l, pCO2 6.6 mmHg) as well as raised anion residue (43 mmol/l) and the presence of oxalates in urine suggested poisoning by ethylene glycol contained in antifreeze liquid. Intensive haemodialysis adequately eliminated ethylene glycol and its toxic metabolites (glycol aldehyde, glycolic acid). Renal function returned within 10 days, although the concentrating power of the kidney remained impaired for several weeks because of interstitial nephritis. The intoxication had been caused by a defective heating-pipe system from which the antifreeze had leaked into the hot-water boiler (the patient had habitually prepared hot drinks by using water from the hot-water tap). Gas chromatography demonstrated an ethylene glycol concentration of 21 g per litre of water.
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PMID:[Chronic ethylene glycol poisoning]. 848 40

We describe a case of a 26 year old patient affected by a rare syndrome characterized by hyperkalemia, arterial hypertension and normal glomerular filtration rate (Gordon's syndrome), probably due to a renal tubular defect in the reabsorption of sodium or chloride. The patient, who had hyperkalemia since the age of 4 years, was referred to our Centre because of hypertension not well controlled with antihypertensive treatment. After drug therapy wash-out, we confirmed the existence of hypertension (180/100 mm Hg; ambulatory BP monitoring: 24-h mean BP = 151/91 mm Hg; 7 am-11 pm = 157/95; 11 pm-7 am: 133/82) and blood and urine tests showed hyperkalemia (6.6 mEq/L), hyperchloremia (115 mEq/L), mild metabolic acidosis (pH = 7.35, HCO3 = 19 mEq/L), low levels of plasma renin activity ( < 0.2 ng/ml/h), slight increase of plasma (1.08 nM/L) and daily urine aldosterone (129 nM) and normal serum creatinine (1.1 mg/dl) and glomerular filtration rate (91 ml/min). These data allowed to exclude the presence of renal failure and hyporeninemic hypoaldosteronism, which are the most common diseases with hypertension and hyperkalemia, and suggested the diagnosis of Gordon's syndrome. After 1 month of treatment with chlorthalidone (12.5 mg o.i.d) we observed the normalization of BP (130/80 mm Hg; ambulatory BP monitoring: 24-h BP: 132/76 mm), serum potassium (5,1 mEq/L) and the other blood and urine tests. These results were confirmed 6 months later and at present the patient has good clinical conditions.
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PMID:[Hypertension, hyperpotassemia and normal glomerular filtration (Gordon's syndrome): a case report]. 868 60

1. This study investigates the effects of the non-selective ETA/ETB receptor antagonist, SB 209670, on systemic haemodynamics, renal function, liver function, acid-base balance and survival in a rat model of endotoxic shock. 2. Injection of E. coli lipopolysaccharide (LPS, 10 mg kg-1, i.v.) resulted in increases in the serum levels of tumour necrosis factor-alpha (TNF-alpha, maximum 60 min after LPS), endothelin-1, (ET-1; maximum 120 min after LPS), and interferon-gamma (IFN-gamma, maximum 180 min after LPS). 3. Injection of LPS also resulted in a fall in blood pressure from 113 +/- 3 mmHg (time = 0) to 84 +/- 4 mmHg at 360 min (n = 15) as well as a hyporeactivity to the vasoconstrictor responses elicited by noradrenaline (NA, 1 microgram kg-1, i.v.). Pretreatment of rats with a continuous infusion of SB 209670 (3 mg kg-1, i.v. bolus + 100 micrograms kg-1, i.v. infusion commencing 15 min prior to LPS) significantly augmented the hypotension as well as the vascular hyporeactivity to NA caused by endotoxaemia. 4. Pretreatment of LPS-rats with SB 209670 (3 mg kg-1, i.v. bolus given 15 min prior to LPS) or infusion of SB 209670 (bolus dose and infusion as above) resulted in a reduction in 6 h-survival from 71% (control) to 30% and 13%, respectively. 5. Endotoxaemia for 4 h resulted in rises in the serum levels of urea and creatinine (indicators of renal failure), but not in the serum levels of bilirubin, GPT and GOT (indicators of liver dysfunction and/or hepatocellular injury). Pretreatment of LPS-rats with SB 209670 (3 mg kg-1, i.v. bolus 15 min prior to LPS) significantly augmented the serum levels of creatinine, bilirubin, GPT and GOT caused by endotoxin. In addition, endotoxaemia caused, within 15 min, an acute metabolic acidosis (falls in pH, HCO3- and base excess) which was compensated by hyperventilation (fall in PaCO2). Pretreatment of LPS-rats with SB 209670 (3 mg kg-1, i.v. bolus) significantly augmented the metabolic acidosis caused by LPS. 6. Thus, the non-selective ETA/ETB receptor antagonist, SB 209670, augments the degree of (i) hypotension, (ii) vascular hyporeactivity to noradrenaline, (iii) renal dysfunction and (iv) metabolic acidosis caused by endotoxin in the anaesthetized rat. In contrast to rats treated with LPS alone, LPS-rats treated with SB 209670 exhibited liver dysfunction and hepatocellular injury. We propose that the release of endogenous ET-1 serves to maintain blood pressure and subsequently organ perfusion in septic shock.
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PMID:Effects of the endothelin receptor antagonist, SB 209670, on circulatory failure and organ injury in endotoxic shock in the anaesthetized rat. 873 96

We systematically compared the individual effects of infusion rate, solution osmolality, and temperature on plasma solute secretion during luminal perfusion of an isolated 90-cm jejunal segment in the conscious and otherwise normal dog. The control state was perfusion at a rate of 3 ml/min of a 25 degrees C temperature solution containing (mM): NaCl, 40; NaHCO3, 10; and mannitol, 220 (320 mosm/kg). Increasing infusion rate from 3 to 9 ml/min increased secretion of Na-, K+, and urea (P < 0.05); further elevation of infusion rate to 18 ml/min increased only Cl- and urea secretion (P < 0.05). Thus, increasing infusion rate of the control solution had only a limited role in promoting solute secretion. In contrast, perfusion solutions elevated in osmolality to 600 and 1200 mosm/kg by mannitol progressively augmented the secretions of water, Na-, K+, Cl-, HCO3(-), Ca2+, and urea (P < 0.05). Perfusion of the 1200 mosm/kg solution produced solute secretions either equivalent to or greater than secretions obtained during 18-ml/min perfusion with the control solution, despite the fact that 1200 mosm/kg perfusion yielded about one-third the effluent volume. Warming of the control solution to progressively increase infusion temperatures from 29 to 41.9 degrees C increased (P < 0.05) water, Na+, K+, and Cl- secretion and HCO3 absorption linearly. Urea secretion increased (P < 0.05) above a temperature threshold of 38-38.9 degrees C. In conclusion, perfusion solution infusion rate, osmolality, and temperature are unique independent determinants of plasma solute secretion by jejunum. These data are the basis for optimizing the physical determinants of jejunal clearance for applying jejunal perfusion to treatment of renal failure.
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PMID:Physical determinants of solute and water clearance by the perfused dog jejunum. 876 69


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