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

Renal osteodystrophy is a metabolic bone disease resulted from chronic renal failure. The long-standing alterations in a mineral metabolism generated by renal failure have a profound effect on the skeleton and induce severe systemic metabolic bone disease. Iliac crest biopsies of 194 patients of chronic renal failure were taken and among them 10 cases were examined for Calcium(Ca), phosphorus (p), parathyroid hormone (PTH), 1,25(OH)2D3 and aluminium (Al). The histological bone changes are characterized by development of osteitis fibrosa, increase of bone resorption and the number of osteoclast, increase of osteoid volume (osteoblastic osteoid and acellular osteoid), active remodelling of bone and aluminum deposition in the bone. According to histological appearance, advanced renal bone disease could be subdivided into three groups namely: Secondary hyperparathyroid bone disease (high turnover uremic osteodystrophy), osteomalacia (low turnover uremic osteodystrophy) and mixed uremic osteodystrophy consisting of mild to moderate hyperparathyroid bone disease and defective mineralization. Aluminum-related bone changes might be obtained in various extent in all these groups. Although this classification does not fully represent all the separated entities, and there is also transformation from one form to another, it seems no less significant as a reference for clinical considerations.
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PMID:[Pathological analysis of renal osteodystrophy in 194 cases]. 181 63

Prevention of bone disease associated with impairment of the renal function is desirable. Attempts at such prevention inevitably also embrace prevention of the extraosseous consequences of autonomous hyperparathyroidism, such as the effects of hypercalcaemia, need for parathyroid surgery, and, perhaps, toxic effects of the parathyroid hormone. Strategies for prevention in early, moderate, and end-stage renal failure are reviewed and discussed with particular reference to dietary phosphorus restriction, use of gut phosphorus binders, control of acidosis, calcium supplementation, use of oral and intravenous calcitriol, and use of synthetic analogues of 1,25-dihydroxyvitamin D3. The onset of severe renal osteodystrophy can be delayed. Early attempts at prevention are logical, but we do not know whether these will reduce the need for parathyroid surgery or will make patients feel better or live longer. The costs of prophylaxis--both financial and in terms of incidence and severity of complications--remain to be defined. An individual approach to each patient with renal impairment seems at present appropriate.
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PMID:Prevention of renal osteodystrophy. 181 86

We evaluated the acute effects of varying dialysate calcium concentration on plasma concentrations and dialyzer fluxes of calcium and phosphorus in adult hemodialysis patients. Seven individuals with stable end-stage renal failure were dialyzed 4 hours, three times weekly. The effects of dialysates containing 1.75, 1.25, or 0.75 mmol/L (70.1, 50.1, or 30.1 mg/L) of calcium were compared. Each patient was studied once at each bath calcium concentration. Compared with the predialysis mean value of 2.27 mmol/L (9.1 mg/dL), plasma total calcium concentration increased, remained constant, or decreased with the 1.75-, 1.25-, or 0.75-mmol/L calcium dialysates, respectively. The 0.75-mmol/L calcium dialysate did not cause signs or symptoms of hypocalcemia (and the plasma calcium concentration did not fall below 1.80 mmol/L [7.2 mg/dL]). Plasma phosphorus concentrations decreased equally from a predialysis mean value of 2.16 mmol/L (6.7 mg/dL), regardless of the dialysate calcium concentration. After 4 hours of treatment with the three different dialysates, the cumulative calcium fluxes were significantly different. With 1.75 mmol/L calcium, mean bodily calcium accumulation was 21.9 mmol (879 mg). With 1.25 mmol/L, there was no net calcium flux. With 0.75 mmol/L, mean patient calcium loss was 5.8 mmol (231 mg). Mean phosphorus removal after 4 hours was 32.5 mmol (1,006 mg) and was unaffected by dialysate calcium concentration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcium and phosphorus fluxes during hemodialysis with low calcium dialysate. 186 78

Primary hyperparathyroidism is a common condition infrequently complicated by renal stones and overt bone disease. Most cases are asymptomatic or have vague, nonspecific symptoms. There is considerable debate as to whether mild or asymptomatic cases should be managed surgically or conservatively. Important chromosomal abnormalities have now been demonstrated in some parathyroid adenomas. Renal osteodystrophy remains a difficult condition to treat once it is fully established. The use of vitamin D metabolites in the early stages of renal failure and the maintenance of a normal serum calcium and phosphate appear to prevent the development of secondary hyperparathyroidism. Further studies are required to ascertain the optimum way of using vitamin D metabolites and how best to reduce serum phosphorus.
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PMID:Primary hyperparathyroidism and renal osteodystrophy. 188 4

Three dietary measures are useful for chronic progressive renal failure. In a hypertensive patient, salt restriction is a prerequisite for antihypertensive therapy. Protein restriction to 0.6 g/kg of body weight per day can slow down progression of renal disease with the exception of polycystic disease of the adult type. Ketosteril can be given for prevention of essential amino acid deficiency. A normalization of serum phosphorus is essential for slowing progression of disease as well as bone metabolism. Therefore, a diet reduced in phosphates, supported by phosphate binders is prescribed.
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PMID:[Nutrition in kidney diseases]. 192 35

Studies in rodents indicate that diet influences progression of renal failure. Excessive dietary intakes of protein, fat, energy and phosphorus have been implicated in promoting progression of renal failure, while restriction of some or all of these dietary constituents limits progressive renal injury. Studies confirm that renal failure is progressive in some dogs with moderate-to-advanced renal dysfunction. Recent studies also indicate that unrestricted intakes of protein promotes proteinuria in dogs and cats and glomerular injury in cats.
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PMID:Effect of modified protein diets in dogs and cats with chronic renal failure: current status. 194 Dec 9

To investigate the parathyroid function in diabetes mellitus, we performed an oral phosphate load in 6 diabetic patients and 6 nondiabetic subjects without renal failure (serum creatinine less than 1.5 mg/dl). Each subject received a total of 2.0 g of phosphate daily per os on 5 consecutive days. Blood and urine samples were obtained daily before and 2 h after the administration of phosphate in the morning. All subjects responded with a similar increase in the serum phosphorus concentration and fall in the ionized calcium concentration. Intact parathyroid hormone levels rose by 2.6-fold in the control subjects but by less than 1.5-fold in the diabetic subjects. It was concluded that hyporesponsiveness of the parathyroid hormone to phosphate administration was found in the diabetic patients without renal failure.
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PMID:Parathyroid hormone secretion in diabetes mellitus. 195 50

Signs of depression, hyperphosphatemia, azotemia, high anion gap metabolic acidosis, and renal failure developed in an adult cat following administration of an excessive dose of a phosphate-containing urinary acidifier. After extracellular fluid volume expansion, diuresis, and administration of a phosphate binder, serum phosphorus concentration returned to normal in 12 hours; the cat recovered fully. The urinary acidifier had been given as part of treatment for a urinary tract infection. Findings suggest that phosphate-containing urinary acidifiers should be administered cautiously because, like other sources of phosphate, they are capable of causing life-threatening metabolic disturbances.
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PMID:Poisoning induced by administration of a phosphate-containing urinary acidifier in a cat. 202 46

We reviewed radiographs of the hands and wrists of 33 patients with immature skeletons and chronic renal disease. Various radiographic manifestations of renal osteodystrophy were seen, including osteopenia in 23 patients (70%), subperiosteal resorption in 20 (61%), distal tuft resorption in 14 (42%), sclerosis of vertebral bodies in 2 (6%), and soft-tissue calcification in 1 (3%). We also noted that 13 patients (39%) exhibited metaphyseal sclerosis adjacent to the growth plates. Five of these 13 showed persistent sclerosis years after the growth plates had fused. None of the patients showed other radiographic changes of rickets, and there was no correlation between the serum calcium, phosphorus, or aluminum levels and the presence of metaphyseal sclerosis. Neither was there any association with the underlying cause of renal failure, method of treatment, presence of a transplant, or type of dialysis. We view this finding as another manifestation of renal osteodystrophy. The importance of distinguishing it from other sclerotic lesions is discussed.
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PMID:Metaphyseal sclerosis in patients with chronic renal failure. 205 93

We describe the clinical outcome of 13 patients with non-insulin-dependent diabetes mellitus (NIDDM), renal insufficiency, and proteinuria, treated for 12.2 +/- 12.9 months (mean +/- SD) with a low-protein, very-low-phosphorus diet (LPVLP) containing 30 g protein and 11.3 mmol (350 mg) phosphorus. After a control period of 18.2 +/- 20.4 months, LPVLP therapy was initiated and serum urea nitrogen, uric acid, and phosphate, as well as urinary excretion of protein, creatinine, urea nitrogen, uric acid, and phosphate, decreased significantly. There was no change in mean blood pressure, hemoglobin, blood pH, and HCO3-, as well as in serum creatinine, protein, albumin, calcium, magnesium, cholesterol, triglyceride, beta-lipoprotein, and high-density lipoprotein (HDL)-cholesterol. Nitrogen balances were measured over 5 weeks in nine patients. Nitrogen balance increased significantly from a negative balance of -0.795 +/- 1.367 g/d in the first week, to almost neutral in the fourth week, and later, was neutral or positive. Neither uremic symptoms nor signs of malnutrition appeared during the LPVLP period. These results suggest that negative nitrogen balance during the initial few weeks does not predict future nutritional status of patients with diabetic renal failure.
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PMID:Effect of low-protein, very-low-phosphorus diet on diabetic renal insufficiency with proteinuria. 206 52


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