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

Familial Hypomagnesemia, Hypercalciuria with Nephrocalcinosis is a rare autosomal recessive inherited disease associated with renal failure. Two girls born of consanguineous parentage aged 16 and 17 presented to us with renal failure, nephrocalcinosis and bone deformities. On evaluation they were found to have hypomagnesemia, hypercalciuria, increased fractional excretion of magnesium, hypocitraturia, renal failure and elevated PTH. Their parental screening was normal. There were no extra-renal features in them. One sibling had nephrolithiasis and the stone analysis revealed calcium phosphate stones. Both were treated with sodium bicarbonate, thiazides, calcitriol and calcium carbonate. They did not require dialysis during hospital stay. Both of them were treated conservatively. They are on regular outpatient follow up. The primary defect in this syndrome is impaired paracellular reabsorption of magnesium and calcium in the medullary thick ascending limb. Mutations in the PCLN-1gene which encodes for the tight junction protein paracellin -1 is identified as the underlying genetic defect. Ocular abnormalities and deafness are the commonly reported associations. End stage renal failure usually occurs in second to third decade. Renal transplantation is the definite treatment.
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PMID:Nephrocalcinosis in siblings--familial hypomagnesemia, hypercalciuria with nephrocalcinosis (FHHNC syndrome). 1690 3

Metformin-associated lactic acidosis (MALA) is a serious metabolic complication that occurs because of metformin accumulation in patients who become dehydrated or developed acute renal failure. Bicarbonate hemodialysis treatment should take place early in the course of management, especially in patients with severe metabolic acidosis who fail to respond to intravenous bicarbonate therapy or in whom renal failure is present. We report a case of MALA in which acute renal failure resulting from dehydration secondary to diarrhea and poor oral intake likely caused MALA. Early recognition of this condition and initiation of effective treatment can improve outcome.
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PMID:Metformin-associated lactic acidosis precipitated by diarrhea. 1766 16

Many nephrologists feel threatened by the allegation that, in patients with chronic renal failure, treatment with calcium-based phosphate binders (calcium acetate and calcium carbonate) may induce coronary artery and cardiac calcification, thereby imposing a greater risk for death compared with sevelamer, a non-calcium-based binder. Acknowledging that drug manufacturers are not unaware of the marketing advantage to their product consequent to destabilizing demand for competing drugs, the case for and against abandoning calcium-based phosphate binders in favor of sevelamer is reviewed in this study. The case for continuing prescription of calcium-based phosphate binders stands on the following: (1) flawed clinical trials that favor sevelamer as a replacement; (2) weak evidence that oral calcium intake modulates vascular and/or cardiac calcification; (3) clinical trials that reinforce the safety and efficacy of calcium-based phosphate binders; and (4) the inordinate relative cost of sevelamer. Recognizing that established as well as novel phosphate binders are currently undergoing clinical evaluation, an open mind and an awareness of developing literature are necessary when deciding how to manage hyperphosphatemia in renal failure.
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PMID:Calcium-based phosphate binders are appropriate in chronic renal failure. 1769 75

The acute toxicity of hydrofluoric acid (HFA) was investigated in a 24-h lethal dose study of intravenous infusion in rats. The lethal dose lowest (LDLo) and LD50 were 13.1 and 17.4 mg/kg, respectively. Harmful systemic effects were also studied 1 h after acute sublethal exposure to HFA. The maximum dose was set at 9.6 mg/kg (LD5). Rats were injected with HFA (1.6, 3.2, 6.4 or 9.6 mg/kg), saline, sodium fluoride (NaF) or HCl solution. NaF and HCl solution concentrations corresponded to the F- and H+ concentrations of 9.6 mg/kg HFA. Blood urea nitrogen (BUN) and Cr were significantly increased in response to HFA concentrations greater than 3.2mg/kg. Acute glomerular dysfunction also occurred at HFA concentrations greater than 3.2 mg/kg. HCO3- and base excess (BE) were significantly decreased in the 6.4 and 9.6 mg/kg groups. Ca2+ was significantly decreased, and K+ was increased in the 9.6 mg/kg group. BUN was significantly increased in the NaF and HFA groups and was increased in the HFA group compared with that in the NaF group. Cr was significantly increased in the HFA group only. HCO3- and BE were significantly decreased in the NaF and HFA groups and were increased in the HFA group compared with values in the NaF group. Ca2+ was significantly decreased in the NaF and HFA groups, and K+ was significantly increased in the NaF and HFA groups. F- exposure directly affected serum electrolytes. Mortality was thought to be due to cardiac arrhythmia resulting from hypocalcemia and hyperkalemia. Metabolic acidosis and renal failure were more severe in response to HFA exposure than in response to NaF exposure because of more free F-, which has strong cytotoxicity, in the HFA group than in the NaF group. Lethal effects of HFA are promoted by exposure routes such as inhalation that cause rapid absorption into the body. Even low exposure to HFA can cause acute renal dysfunction, electrolyte abnormalities and metabolic acidosis. These complications result in a poor prognosis.
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PMID:Harmful effects and acute lethal toxicity of intravenous administration of low concentrations of hydrofluoric acid in rats. 1772 34

Accelerated atherosclerosis and vascular calcifications (VC) play a central role in the pathogenesis of cardiovascular disease in chronic kidney disease (CKD) patients. Mineral metabolism disorders and increased serum calcium-phosphate product have been recently investigated as inducing factors of cardiovascular calcification. In fact, cardiovascular disease in renal failure appears greatly associated with bone metabolism alterations. Recently, the treatment of hyperphosphatemia in CKD patients changed from either calcium- or aluminium-based phosphate-binders to new free-calcium and aluminium phosphate binders, such as sevelamer hydrochloride and lanthanum carbonate. Therefore, control of serum phosphate in CKD patients becomes crucial in preventing increases in calcium-phosphate product, secondary hyperparathyroidism and ultimately VC.
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PMID:Optimising the treatment of hyperphosphatemia and vascular calcification in chronic kidney disease. 1787 66

Vascular calcification is a very common event in patients affected by diabetes and chronic kidney disease (CKD). Recently, it has been well documented that abnormalities in mineral and bone metabolism in CKD patients associate with increased morbidity and mortality. Elevated serum phosphate and calcium-phosphate product levels play an important role in the pathogenesis of vascular mineralization in uremic patients and also appear to be associated with increased cardiovascular mortality. Together with classical passive precipitation of calcium-phosphate in soft tissues, during the last decade it has been demonstrated that inorganic phosphate may cause extraskeletal calcification directly through a real "ossification" of the tunica media in the vasculature of CKD patients. Therefore, control of phosphate retention is now an even more crucial target of treatment in patients affected by chronic kidney disease. The "classical" treatment of secondary hyperparathyroidism and hyperphosphatemia in CKD patients consists of either calcium or aluminium based phosphate-binders and calcitriol administration. Unfortunately, this "old generation" therapy is not free of complications. Patents are also reported discussing the role of derivatives of Lanthanum carbonate hydrates are also used for the treatment of hyperphosphataemia in patients with renal failure. New calcium- and aluminium-free phosphate binders, such as sevelamer hydrochloride and lanthanum carbonate, can be used to treat hyperphosphatemia and secondary hyperparathyroidism, reduce atherosclerotic process, and prevent vascular calcification in CKD patients.
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PMID:Clinical consequences and novel therapy of hyperphosphatemia: Lanthanum carbonate for dialysis patients. 1822 Nov

Cardiovascular mortality and morbidity are high in chronic renal failure (CRF) patients. Previous studies on non-uraemic patients with heart failure (HF), hypertension or diabetes mellitus (DM) showed that QT and QTc prolongation and dispersion represent cardiovascular risk factors. The patients with long QT interval have more often ventricular premature beats and sudden death than those with normal QT interval. The aim of our study was to evaluate the frequency and predictive value of QT and QTc prolongation in CRF patients, included or not in a chronic dialysis programme. On 68 patients (M/F = 36/32, mean age = 47.6 years), with CRF we analyzed QT and QTc interval with a digital 12 lead electrocardiogram-CARDIAX. 8/68 patients (11.8%) had long QT interval (>0.45"). After having calculated QT corrected (QTc) interval according to the heart rate, 28/68 patients (41.2%) had QT prolongation (>0.45"). Multivariate statistical analysis of clinical factors, but also of biological, electrocardiographic, echocardiographic data and 24 hours of ECG and blood pressure monitoring showed that QT prolongation is statistically significant (p < 0.05) correlated with: number of years of renal failure (p = 0.0001), serum concentrations of potassium and calcium (p = 0.0001) and diastolic BP (p = 0.05). QT prolongation in CRF patients is not dependent on the level of uremia or the type of chronic renal substitution (hemodialysis or continuous ambulatory peritoneal dialysis). There were no statistically significant correlations between QT prolongation and serum concentrations of Mg, PO4, HCO3 and Hb. Long QT interval was not dependent either on the dipper/nondipper profile of mean BP values or ejection fraction of left ventricle. In our study long QT interval was not statistically significant correlated with arrhythmias or sudden death. Despite the high incidence of QT prolongation in CRF patients (41.2%), short-term consequences are not as severe as those in cardiac patients. This is possibly explained by the different pathogenic mechanisms of arrhythmia in CRF when electrolytic disorders are the main cause for the development of arrhythmia. During a mean follow-up of 3.8 months (3-5.5) there were no cases of sudden death on patients with QT prolongation, and arrhythmia incidence was not statistically significant higher than in subjects with normal QT interval.
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PMID:Frequency and prognostic significance of QT prolongation in chronic renal failure patients. 1838 17

Milk alkali syndrome is a cause of hypercalcaemia, renal failure and alkalosis, and is potentially reversible if detected early and the calcium and alkali source withdrawn. It was originally described in patients ingesting large amounts of calcium containing milk for the treatment of peptic ulcer disease. We present a modern day version of the syndrome in three cases which were associated with excessive intake of Rennie, a calcium carbonate containing antacid.
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PMID:Milk alkali syndrome associated with excessive ingestion of Rennie: case reports. 1849 70

The present report describes different aspects of Fosrenol (lantahnum carbonate) which can be summarized as follows: Lanthanum shows a great binding affinity for phosphate. It is minimally absorbed by intestine and is eliminated by biliary route thus renal failure does not favour body accumulation of lanthanum. The effectiveness and safety of Fosrenol has been proven in clinical trials which have include more of 5,500 patients. Fosrenol has shown to be effective in controlling serum phosphate in short and long term studies (6 years). Lanthanum does not accumulate in the bone mineralization front and does not produce low bone turnover. Lanthanum is not found in the central nervous system. The presence of lanthanum in liver is explained by the fact that the minimal amount of lanthanum absorbed has to be disposed through liver.
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PMID:[Introduction to lanthanum carbonate: pharmacology, safety and tolerability]. 1884 13

Calciphylaxis is a rare and debilitating vasculopathy predominantly seen in patients with renal failure. The proposed mechanism of injury is active vascular calcification with associated elevated parathyroid hormone, hypercalcemia, or hyperphosphatemia. With improved pharmacologic agents including non-calcium containing phosphate binders, vitamin D analogues, calcimimetics, and bisphosphonates, targeted therapy on the mineralization process has been tried with varied success. We report a case of biopsy-proven calciphylaxis in a patient with acute kidney injury requiring dialysis that had persistently elevated calcium-phosphorus product refractory to treatment. The patient, however, responded rapidly to the initiation of lanthanum carbonate therapy and modified dialysis. This is the first known case reported in the literature utilizing this new non-calcium-based phosphate binder in the setting of calciphylaxis.
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PMID:Calciphylaxis responsive to lanthanum carbonate (FOSRENOL) therapy. 1918 Aug 73


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