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

Analyses of creatinema in the cases of global respiratory failure was performed in this paper. The patients with global respiratory failure treated in General Hospital in TeSanj have been followed. For all patients laboratory analyses have been performed on the admimtion and in the time of clinical status improvement, including creatinin level, K, Na, Hb, Htc, and blood gas analyses with mesurement of pO2 pCO2 pH, BE, saturation of the blood with oxgen, BE and HCO3-. Creatinine level have been considered in coleration of body mass index, and general nutritional status. The dinamic source of creatinine level in the blood have been followed, in relation of parameters of respiratory status. The statistical significance in relation of creatinine level with the respiratory status was registrated. With the improvement of respiratory status and laboratory analyses related to respiratory status, decrease of creatinin level was registrated. Because of that the therapy given to the patients with respiratory failure could influence on potassium level, the relation of creatinnemia and potassium level in the blood wasn't considered. The high creatinin level couldn't be explained with the initial renal failure, but as the sign of metbolic adaptation to hypoxemic and hypoxyc situation on the body. The registration of high creatinine level in the situations of global respiratory failure could be the guidelines for the choice of the antibiotics for these patients, mostly for potentially nephrotoxic antibiotics, like aminoglicosides, and theirs combinations. The decision and evaluation of benefit and toxicity of antibiotics for these situations could be easier.
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PMID:[Significance of serum creatinine levels in respiratory insufficiency conditions]. 1176 41

Calcitriol deficiency and phosphorus retention are mechanisms involved in the pathogenesis of renal hyperparathyroidism. The aim of this study was to evaluate the effect of dietary phosphorus restriction versus calcium carbonate treatment for one month on PTH and calcitriol levels in patients with mild renal failure. We studied two groups of patients: Group I: 21 patients (14M/7F); mean age 61 years old; mean glomerular filtration rate 51 ml/min. Their diet contained phosphorus 700 mg/day. Group II: 30 patients (21M/9F); mean age 58; mean glomerular rate 56 ml/min. They were divided in two subgroups: 18 patients treated with calcium carbonate 2.5 g/day and 12 patients with 5 g/day. Serum PTH, calcitriol, 25(OH)D3, calcium, phosphorus and urinary excretion of calcium and phosphorus were measured before and after a 30 day period. The low phosphorus diet (Group I) resulted in a significant decrease in PTH levels (81.3 +/- 35 vs 71 +/- 39 pg/ml, p < 0.05) and significant increase in calcitriol levels (22.4 +/- 4.4 vs 33.4 +/- 7.5 pg/ml, p < 0.05). In our study calcium carbonate treatment (Group II) had no effect on PTH and calcitriol levels.
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PMID:[Early treatment of secondary hyperparathyroidism in moderate renal insufficiency: low-phosphorus diet versus calcium carbonate]. 1277 57

Phosphorus binders are used in patients with kidney failure because of the incomplete removal of phosphorus with dialysis and the inability to exclude phosphorus from the diet. Aluminium was the initial phosphorus binder used, but was replaced by calcium-containing binders because of the development of aluminium toxicity. Calcium-based binders have been the mainstay of therapy for many years, but recent investigations have pointed to increased rates of vascular calcification in patients taking calcium-containing binders. For this reason, alternative agents have been developed. Sevelamer (Renagel), GelTex Pharmaceuticals Inc.) is a polymer which has been found to effectively bind phosphorus. It has resulted in a decreased rate of vascular calcification compared to calcium-containing binders. Other agents under development include lanthanum carbonate and iron-complex preparations. Further research will likely concentrate on identifying binders that bind phosphate more efficiently, have minimal gastrointestinal side effects and provide other benefits to dialysis patients.
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PMID:Phosphate binder usage in kidney failure patients. 1278 90

We have found that nanobacteria, recently discovered Gram-negative atypical bacteria, can cause local calciphylaxis on the mitral valve in a setting of high-calcium X phosphorous product in the blood. We present the case of a 33-year-old man with diabetic renal failure on continuous ambulatory peritoneal dialysis who died as a result of multiple brain infarcts due to embolizations from mitral valve vegetations. Systemic calciphylaxis was not present. Spectrometric analysis of the mitral valve vegetations showed that they were composed of calcium phosphate, carbonate apatite form, and fibrin. The electron microscopy of the thrombotic vegetation demonstrated nanobacterium as a nidus for carbonate apatite formation. Investigation for the presence of nanobacteria in the multiple organs involved in systemic calciphylaxis may be of help in elucidating the pathogenesis of this frequently fatal disorder.
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PMID:Nanobacteria-caused mitral valve calciphylaxis in a man with diabetic renal failure. 1498 74

A comparison of clinically useful phosphorus binders for patients with chronic kidney failure. Over the past 30 years it has become apparent that hyperphosphatemia plays a major causative role across the entire spectrum of morbidity associated with advancing kidney dysfunction and failure. A large fraction (60% to 70%) of dietary phosphorus is absorbed and normally excreted by the kidneys. Ideally, as kidney function deteriorates, the net quantity of phosphorus absorbed from the GI tract should be proportionally reduced to match the decrease in kidney function. After initiation of chronic dialysis therapy, the absorbed phosphorus load should match the amount of phosphorus removed via dialysis plus any excreted by residual kidney function. Because it is very difficult to reduce dietary phosphorus to these levels, a variety of oral phosphorus binders have been employed. Currently available binders include alkaline aluminum, magnesium, and calcium salts (primarily calcium carbonate and calcium acetate), various iron salts, and the binding resin sevelamer hydrochloride. Lanthanum carbonate is the newest agent and will probably be released shortly. This review compares the theoretic and in vitro chemistry of these drugs with in vivo data obtained in both normal patients, and in patients with kidney failure. The clinical potency and potential toxicity of the binding agents are compared, and optimal drug administration strategies are also reviewed.
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PMID:A comparison of clinically useful phosphorus binders for patients with chronic kidney failure. 1529 4

The recent recognition that hyperphosphatemia is a strong predictor of survival on dialysis has rekindled interest in the regulation and control of serum phosphate. In incipient renal failure hyperphosphatemia is prevented by increased fractional renal phosphate excretion mediated via an increase in parathyroid hormone and the novel phosphaturic hormone FGF-23 (and possibly others). At a glomerular filtration rate of approximately 30 ml/min this compensatory mechanism fails and hyperphosphatemia ensues. Pre-dialytic serum phosphate concentrations of >6 mg/dl increase cardiac mortality presumably to a large extent, but not exclusively, via promoting vascular calcification. It has recently been recognized that vascular calcification is not only a passive precipitation process following transgression of the critical Ca-x-P product, but is an active process accompanied by expression of osteoblastic bone markers in the vessel wall. Because of the recent recognition of the relation between vascular calcification and serum phosphate as well as serum calcium, there is a need for novel calcium-free phosphate binders. Currently sevelamer and lanthanum carbonate have been introduced and trivalent iron preparations are under development.
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PMID:Hyperphosphatemia in renal failure. 1562 30

Our knowledge of the mineral metabolism disturbances and skeletal disorders in patients with chronic renal insufficiency has advanced significantly in the last years. Probably the most important what we have learned is, that apart of bone disease, hyperparathyroidism and its treatment can also lead to severe extra-skeletal complications, contributing to the progression of cardiovascular disease in this population. This fact has fundamentally changed our approach to the treatment, and - as a result - the new clinical practice guidelines on the management of mineral metabolism and bone disease in chronic renal failure have been developed. Mainstays of the new approach are lower recommended serum calcium and calcium-phosphate product. However, these targets are very difficult to achieve in clinical practice. During the last decade, some additional therapeutic agents have been welcomed. There are two effective calcium-free, aluminium-free phosphate binders, sevelamer hydrochloride, and lanthanum carbonate, four vitamin D analogues of newer generation, and--last but not least--modulators of calcium-sensing receptor, calcimimetics. Future studies will be needed to determine how these recent developments will be helpful. The optimal therapy for all end-stage renal failure complications is definitely renal transplantation.
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PMID:[New aspects in the management of renal osteodystrophy]. 1566 6

Sevelamer hydrochloride (SH) is widely used for the treatment of hyperphosphatemia in patients with renal failure who are on maintenance hemodialysis. In this study, we investigated the clinical effects of SH, administered as either monotherapy or combined with a calcium carbonate formulation, on the metabolism of calcium (Ca) and phosphorus (P) in patients who had been taking a Ca-based binder. Patients were divided into three groups (i): switched completely from a Ca-based binder to SH (complete switch); (ii) dosage of the Ca-based binder was reduced, and SH introduced (partial switch); and (iii) dosage of the Ca-based binder was not reduced and SH introduced (combination therapy). We also examined the effects of the introduction of SH on the lipid profile and parathyroid hormone (PTH) concentration. Comparison between groups of the numbers of successfully treated cases (reaching target concentrations of serum P=5.5 mg/dL and Ca x P product=55 mg2/dL2 within 6 months of treatment) showed that the likelihood of reaching target levels was higher if Ca-based binder was maintained as much as possible (combination therapy>partial changeover>complete changeover). Furthermore, treatment with SH decreased total cholesterol and non-HDL cholesterol concentrations significantly, and also increased HDL cholesterol and PTH concentrations compared to pre-treatment. These results suggest that when a calcium carbonate formulation is already in use, as far as compliance allows, the dosage should not be reduced when SH is added. Despite its beneficial effects on the lipid and PTH concentrations, preventing an excessive increase in the PTH concentration is essential when using SH.
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PMID:Introduction to sevelamer hydrochloride and its clinical effects. 1610 37

Accumulation of inorganic phosphate due to renal functional impairment contributes to the increased cardiovascular mortality observed in dialysis patients. Phosphate plays a causative role in the development of vascular calcification in renal failure; treatment with calcium-based phosphate binders and vitamin D can further increase the Ca x PO(4) product and add to the risk of ectopic mineralization. The new generation of calcium-free phosphate binders, sevelamer and lanthanum, can control hyperphosphatemia without adding to the patients calcium load. In this article, the metabolism of lanthanum carbonate and its effects in bone, liver and brain are discussed. Although lanthanum is a metal cation its effects are not comparable to those of aluminum. Indeed, in clinical studies no toxic effects of lanthanum have been reported after up to four years of follow-up. The bioavailability of lanthanum is extremely low. The effects observed in bone are due to phosphate depletion, with no signs of direct bone toxicity yet observed in rats or humans. The liver is the main route of excretion for lanthanum carbonate, which can be localized in the lysosomes of hepatocytes. No lanthanum could be detected in brain tissue.
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PMID:Lanthanum: a safe phosphate binder. 1668 67

A 42-year-old man was transferred to the Emergency Department after his friends had found him unresponsive and confused in his room. He had been experiencing upper abdominal complaints for a period of several months. He had taken large amounts of a calcium carbonate/magnesium subcarbonate preparation (Rennie) and had consumed at least 3 litres of dairy products per day. His behaviour was reported as being more and more abnormal during the previous few weeks. On admission he was confused and agitated and had involuntary movements of his limbs. Laboratory investigation indicated a triple acid base disorder, i.e. metabolic alkalosis, respiratory alkalosis and high anion gap metabolic acidosis, with severe dehydration. The metabolic alkalosis was caused by the intake of large amounts of dairy and antacids: milk-alkali syndrome. The metabolic acidosis was the result of hypovolaemia and pre-renal renal failure and the respiratory alkalosis was caused by hyperventilation due to the organic psychosyndrome. The patient was treated with volume expansion by isotonic saline and the administration of potassium and he was sedated with low-dose midazolam, which led to a full respiratory compensation of the metabolic alkalosis. A few days following admission, both the plasma calcium concentration and renal function returned to normal; the acid-base disorder completely normalized and the organic psychosyndrome disappeared. On gastroduodenoscopy a gastric ulcer was found; biopsies revealed a signet ring cell adenocarcinoma of the stomach.
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PMID:[A man with a classic serious milk-alkali syndrome and a carcinoma of the stomach]. 1690 Oct 67


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