Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been postulated that hyperparathyroidism in chronic renal failure results from hypocalcemia, occurring, in part, from phosphate retention and/or deficient 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] synthesis. However, many studies have failed to demonstrate hyperphosphatemia or low 1,25-(OH)2D levels in patients with mild renal failure. We measured creatinine clearance (CCr), fractional excretion of phosphorus (FEP), and serum phosphorus, ionized calcium, and plasma N-terminal PTH, and 1,25-(OH)2D concentrations in 21 normal subjects and 51 patients with renal failure. Patients with mild renal failure (Ccr, greater than 40 mL/min.1.73 m2) had normal mean serum phosphorus and ionized calcium and decreased mean 1,25-(OH)2D levels compared with those in normal subjects. In patients with moderate renal failure (CCr, 20-40), the mean ionized calcium level was normal, plasma PTH levels and FEP were elevated, and the decrement in 1,25-(OH)2D was more pronounced. The mean ionized calcium level was decreased only in the group of patients with severe renal failure (CCr, less than 20). The 1,25-(OH)2D values correlated positively with CCr and negatively with the log of plasma PTH and serum phosphorus concentrations. Log of plasma PTH correlated negatively with CCr and positively with FEP. The ionized calcium concentration correlated very weakly with CCr and the log of the plasma PTH level. These data demonstrate the presence of hyperparathyroidism, normocalcemia, and 1,25-(OH)2D deficiency in renal failure and are consistent with a role for 1,25-(OH)2D in the suppression of parathyroid activity through as yet unidentified mechanisms.
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PMID:Hyperparathyroidism and 1,25-dihydroxyvitamin D deficiency in mild, moderate, and severe renal failure. 318 62

Fifteen patients with advanced renal failure (creatinine clearance less than 25 ml/mn) and with severe albuminuria (greater than 1.5 g/24 h) were put on a low-protein (0.3 g/kg body weight), low-phosphorus (5-7 mg/kg body weight) diet supplemented with essential amino acids and ketoanalogues. During the 6-month follow-up, urinary albumin excretion and fractional renal albumin clearance were reduced significantly while serum albumin concentration increased; no nutritional change occurred during the study.
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PMID:Effect of a low-protein diet on urinary albumin excretion in uremic patients. 323 70

The two major lesions of renal osteodystrophy are osteitis fibrosa cystica (OFC) and osteomalacia (OM). OFC is the characteristic bone lesion of uremic hyperparathyroidism. Although renal failure causes predictable parathyroid hyperplasia, the precise pathogenetic mechanism is still not defined. The "hyperphosphatemia-hypocalcemia-parathyroid hormone (PTH) hypersecretion" sequence of events is no longer an adequate model for the pathogenesis of uremic hyperparathyroidism. Other abnormalities associated with uremia include reduced 1,25-dihydroxyvitamin D (1,25D) synthesis, changes in intracellular phosphorus content or transcellular phosphate fluxes, or alteration in PTH metabolism, eg, change in set-point for PTH secretion. Each abnormality interacts with others and contributes to PTH hypersecretion, but none can completely account for the development and persistence of hyperparathyroidism in renal failure. The possibility that uremia may directly cause parathyroid hyperplasia remains open. It is also possible that factor(s) that initiate hyperparathyroidism may turn out to be quite different from that which sustains the hyperparathyroid state. Although both vitamin D-deficient and vitamin D-resistant OM may develop in patients with renal failure, the majority of uremic OM seen currently is "vitamin D-refractory." Although now there is persuasive evidence implicating aluminum (Al) accumulation as the major pathogenetic cause for the mineralization defect seen in this disorder, additional disturbances may play important contributory roles. Such factors would include extraskeletal effects of Al, differences in host-susceptibility to this element, the localization of Al within bone, uremia per se, and the participation of other metals and toxins. Finally, possible interactions between hyperparathyroidism and OM of uremia are speculated on.
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PMID:Renal osteodystrophy: some new questions on an old disorder. 328 68

Ten patients with advanced renal failure (glomerular filtration rate 25 mL/min) were treated with a low phosphorus and low protein diet supplemented with ketoacid analogues. Before starting the diet and four months afterwards, a 50 g oral glucose tolerance test with a three step euglycemic insulin clamp was carried out. A dose-response curve of total body insulin sensitivity was plotted. By the fourth month, glucose tolerance had improved with significantly lower T0, T30, and T60 insulin levels. These results are attributed to the improvement in insulin action as demonstrated by the clamp technique. The dose-response curve had a distinctly higher plateau after dietary treatment, and the tissue sensitivity index to insulin (M/l ratio) was significantly improved. It is suggested that treatment of uremic patients with a low protein diet may reduce levels of a putative insulin inhibitor.
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PMID:Low protein and low phosphorus diet in patients with chronic renal failure: influence on glucose tolerance and tissue insulin sensitivity. 331 37

Normal renal function is an essential prerequisite for normal nutrition. Renal failure results in malnutrition and growth retardation, which are particularly marked when renal failure has its onset early in life. Conversely, the careful application of nutritional therapy can ameliorate the effects of renal failure and allow improved well being and growth and possibly retard the rate of progression of renal failure. Nutritional therapy includes the provision of an adequate energy intake, appropriate intakes of water, electrolytes, vitamins and minerals and regulation of protein and phosphorus intakes. In this paper the theoretical considerations underlying these objectives are reviewed and practical ways of achieving them with least disruption to the child and his family suggested.
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PMID:Nutritional management of infants and toddlers with chronic renal failure. 332 18

The effect of 1,25(OH)2 vitamin D3-induced hypercalcemia on the course of aminoglycoside nephrotoxicity in the rat was studied. Daily gentamicin, 100 mg/kg body weight, was administered subcutaneously concomitant with 1,25(OH)2 vitamin D3, 50 ng s.c. to male Sprague-Dawley rats. This group was compared to rats injected with gentamicin alone, 1,25(OH)2 vitamin D3 alone, and an ethanol vehicle as a control. Structural and functional parameters of acute renal failure were assessed following 4, 6 and 7 days of treatment. Severe morphologic evidence of tubular injury was documented on day 6 in the group injected with gentamicin and 1,25(OH)2 vitamin D3. Correlative functional and metabolic evidence of tubular cell deterioration occurred in this group on day 7 as represented by an elevated blood urea nitrogen (BUN), 198 +/- 14 mg/dl (p less than 0.001 compared to all other groups), a heightened mean renal cortical homogenate calcium, 1,028.3 +/- 304.8 nmol/mg protein (p less than 0.05 or better compared to all other groups), and significantly increased mean cortical mitochondrial calcium content, 796.3 +/- 116.5 nmol/mg protein (p less than 0.01 in relation to all other groups). Elevated total serum calcium to a level of 11.9 +/- 0.2 mg/dl (p less than 0.001 compared to control group) developed in the gentamicin/1,25(OH)2 vitamin D3 group on day 4, 2 days prior to pronounced structural damage, and continued to be elevated through day 7. No difference in serum phosphorus levels, however, developed between control and gentamicin-plus-vitamin-D-treated animals except on day 7 when severe renal failure developed in this group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Potentiation of aminoglycoside nephrotoxicity by vitamin-D-induced hypercalcemia. 338 67

In a historical cohort study, acute renal failure developed in 16.5% of 157 patients with rhabdomyolysis over a two-year study period. Underlying clinical, laboratory, and causative factors associated with the development of acute renal failure were examined. Factors predictive of renal failure in this setting, determined by multiple logistic regression analysis, included the degree of serum creatine kinase, serum potassium, and serum phosphorus level elevation; the degree of depression of serum albumin level; and the presence of dehydration at presentation or sepsis as the underlying cause. The predictive model that was developed correctly classified 93% of subjects and was statistically validated.
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PMID:Factors predictive of acute renal failure in rhabdomyolysis. 338 1

This study reports the effects of a low-protein, low-phosphorus, supplemented diet in 8 type 1 diabetics with renal failure. The rate of decline of creatinine clearance, the changes of the urinary protein loss, of total serum protein, of the daily insulin requirement, of the nutritional status and of some hormonal derangements were examined. The rate of decline of creatinine clearance decreased from 1.38 +/- 0.27 ml/min/month during a previous 15.9-month period of unrestricted protein diet, to 0.03 +/- 0.37 ml/min/month during the 17.4 months on supplemented diet. Urinary protein loss significantly decreased, and total serum protein increased. The daily insulin requirement decreased and no deterioration of the nutritional status occurred. Secondary hyperparathyroidism was partially reversed and the mild hypothyroidism corrected. A restricted protein and phosphorus diet supplemented with essential amino acids and ketoanalogs seems to exert several beneficial and no unwanted side effects in type 1 diabetics with renal failure.
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PMID:Nutritional treatment of renal failure in type 1 diabetic nephropathy. 339 30

A low-protein, low-phosphorus diet supplemented with essential amino acids and keto analogues was given to 12 rats, starting from the 90th day after subtotal nephrectomy. The purpose was to assess its effect on the residual renal function and on the nutritional status in rats with already established severe renal failure. Ten control rats in the same conditions, following a standard diet supplying normal amounts of protein and phosphorus were also studied. The supplemented diet exerted a well-evident protection of residual renal function and structure: lower rate of decline of creatinine clearance, lower mortality, significant decrease of proteinuria and almost total absence of histological signs of activity. The nutritional status was also well protected by the dietary therapy: increase of body weight, normal values of total serum protein, and low-constant values of urea appearance. In the control rats body weight decreased, total serum protein was lower than normal and the values of urea appearance were increasing simultaneously with a decreasing food intake and body weight.
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PMID:Protection of renal function and of nutritional status in uremic rats by means of a low-protein, low-phosphorus supplemented diet. 339 80

In this paper we studied the effects of a low-protein, low-phosphorus supplemented diet in 8 type I diabetics with 'overt' diabetic nephropathy and mild or severe renal insufficiency. We examined the following parameters: the rate of decline of creatinine clearance, the urinary protein loss, the total serum protein, the daily insulin requirement, the serum fasting glucose, the pattern of serum lipids (serum total cholesterol, HDL cholesterol and serum triglycerides), the mean blood pressure and body weight. The rate of decline of creatinine clearance decreased monthly from 1.48 +/- 0.20 ml/min during a previous 15.6-month period of unrestricted protein diet (UPD), to 0.13 +/- 0.3 ml/min during the 11.4 months on the supplemented diet (SD). The mean blood pressure did not differ during UPD (130.9 +/- 7.0 mmHg) and during SD (128.1 +/- 1.6 mmHg). Urinary protein loss significantly decreased on SD, and total serum protein increased. The daily insulin requirement and the serum fasting glucose levels significantly decreased on SD. Serum cholesterol was lower during SD than during UPD, while serum HDL cholesterol and serum triglycerides were not significantly modified. In some patients the body weight decreased on SD as a consequence of the disappearance of edema. In conclusion, on the basis of these preliminary observations, the SD slows the progression of renal failure and seems to exert several beneficial and no unwanted side-effects in renal failure of type I diabetics.
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PMID:Effects of a low-phosphorus, low-protein diet supplemented with essential amino acids and keto analogues on 'overt' diabetic nephropathy. 343 63


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