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

Chronic renal failure results in a variety of metabolic derangements that perturb glucose homeostasis. These may in part result from the fact that the kidney plays a prominent role in the metabolism of insulin as well as a number of other low-molecular-weight peptide hormones that affect carbohydrate metabolism. Specific abnormalities in glucose utilization that appear to be related to alterations in membrane receptors, resulting in increased glucagon sensitivity and decreased insulin action, are a newly recognized factor in intolerance to oral glucose. Glucose production and utilization are both abnormally increased in patients with chronic uremia, and these disturbances are only partially corrected by hemodialysis treatment. The mechanism(s) contributing to these changes is unclear, but seems to involve a combination of humoral and cellular factors. These include some degree of insulin resistance, probably inadequately modulated proteolytic responses to glucagon and parathyroid hormone, and a basic defect in energy production that alters intracellular concentrations of high-energy phosphate-containing nucleotides. It is unclear whether these changes in carbohydrate tolerance pose an increased risk for the premature development of cardiovascular disease in patients with renal failure, as they appear to do in the nonuremic population. The occasional patient with renal failure may develop clinical hypoglycemia when glucose utilization continues in a setting in which the hepatic capacity to produce glucose is reduced, probably as a consequence of altered substrate delivery and/or inhibition of one or more key gluconeogenic enzymes.
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PMID:Disorders of glucose metabolism in uremia. 11 52

Studies were carried out to evaluate whether skeletal resistance to acute increments in endogenous parathyroid hormone exists in patients with mild to moderate renal insufficiency. Hypocalcemia was induced with the infusion of ethyl-enediamine-tetra-acetate (EDTA) in 10 normal subjects and 13 patients with mild renal failure. After the induction of hypocalcemia, the concentration of serum calcium increased gradually and reached preinfusion levels by 22 h in the normal subjects; in contrast, the levels of serum calcium in patients with mild renal insufficiency were significantly lower than the preinfusion values even at the end of 26 h following the EDTA infusion. This delayed recovery occurred despite significantly higher levels of serum immunoreactive parathyroid hormone (IPTH) in the patients than in the normal subjects. The increase in the levels of IPTH reflect elevations in the concentrations of biologically active hormone since urinary cyclic AMP increased significantly. Urinary calcium excretion following the EDTA infusion was not different in both groups and, therefore, could not account for the delayed recovery of serum calcium values in the patients with renal insufficiency. These results indicate that secondary hyperparathyroidism exists early in patients with renal failure and such patients have exaggerated parathyroid hormone secretion in response to acute hypocalcemia. The data are consistent with the concept that skeletal resistance to increments in endogenous parathyroid hormone is present in such patients. This abnormality is, at least partly, responsible for the hypocalcemia and secondary hyperparathyroidism of renal insufficiency.
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PMID:Skeletal resistance to endogenous parathyroid hormone in pateints with early renal failure. A possible cause for secondary hyperparathyroidism. 16 80

The excretion of cyclic AMP in urine has been examined in normal children and in children with nephrogenic diabetes insipidus or moderate renal failure (predominantly defective concentrating ability) under basal conditions and in response to antidiuretic hormone (ADH) and parathyroid hormone (PTH). In contrast to other reported data, we could not confirm an ADH- and (PTH-unresponsiveness in hereditary, congenital nephrogenic diabetes insipidus, but our patients with structural renal disorders characterized by a defective urine concentrating ability did have reduced hormonal responses. It seems necessary to define nephrogenic diabetes insipidus very carefully, and until more data are collected, there appears to be no value in the measurement of urinary cyclic AMP level in the individual patient in the differential diagnosis of disorders due to renal concentrating defects.
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PMID:Basal and hormone-induced urinary cyclic AMP in children with renal disorders. 18 4

Urinary cyclic AMP (UcAMP) appropriate for the serum calcium concentration was determined in normal subjects during the base-line state and during alteration in their serum calcium concentrations by saline and calcium infusions. This was compared to the UcAMP in 76 patients with hypercalcemia and 5 patients with hypocalcemia. In 54 of 56 patients with primary hyperparathyroidism, the UcAMP was inappropriately high for their serum calcium concentration, the 2 exceptions having renal failure. In four patients with vitamin D intoxication, sarcoidosis, milkalkali syndrome, and thiazide-induced hypercalcemia and in five patients with hypocalcemia due to hypoparathyroidism, the UcAMP was appropriately low for their serum calcium concentration. In 16 patients with nonparathyroid neoplasms, 10 had UcAMP levels that were inappropriately high suggesting ectopic parathyroid hormone (PTH)-mediated hypercalcemia and 6 had UcAMP levels that were appropriately low suggesting that their hypercalcemia was due to osteolytic factors other than PTH. Correlations between UcAMP, serum calcium concentration, and carboxyl-terminal immunoreactive PTH suggest that random UcAMP is a sensitive accurate reflection of circulating biologically active PTH. If there is adequate renal function (serum creatinine concentration less than 2.0 mg/dl), a random UcAMP expressed as mumol/g creatinine and analyzed as a function of the serum calcium concentration completely separates patients with PTH and non-PTH-mediated hypercalcemia.
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PMID:Urinary cyclic AMP analyzed as a function of the serum calcium and parathyroid hormone in the idfferential diagnosis of hypercalcemia. 18 21

In 58 patients with end-stage renal failure before commencement of regular hemodialyses treatment (RTD) and 58 patients under RTD bone mineral content (BMC) was determined by the use of the photon absorptiometry. Further the effect of a treatment with bitamin D3 and 5,6-trans-25-OH-vitamin D3 on BMC was studied. There existed a negative correlation between the duration of chronic renal failure or of RDT as well as of the serum parathyroid hormone level to BMC. No correlation was found between BMC and serum calcium level. During a 14 months-course treatment with vitamin D3 or 5,6-trans-25-OH-vitamin D3 BMC increased. The method of photon absorptiometry presented itself as an easy and well reproducible technique for routine examinations.
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PMID:[The use of photon absorptiometry in renal osteodystrophy (author's transl)]. 20 Jul 91

The discovery of the vitamin D endocrine system has opened up many possibilities in our understanding of metabolic bone disease. Of particular importance is the fact that we can now manage certain genetic disorders resulting in vitamin D-resistant rickets or vitamin D-resistant hypocalcemia with the new active hormonal forms of vitamin D and with intelligent dietary management to provide for correction of the mineral difficulty. Thus, in the case of vitamin D dependency, replacement need only be with the missing hormone, 1,25-(OH)2D3. On the other hand, familial hypophosphatemia requires adjustment of the plasma phosphorus by frequent administration of oral phosphate and the adjustment of intestinal calcium absorption by 1,25-(OH)2D3. Renal failure patients require the adjustment of plasma phosphorus concentration and parathyroid hormone status, and the administration of the missing hormone 1,25-(OH)2D3. Hypoparathyroid patients require oral calcium plus 1,25-(OH)2D3, and premature infants require administration of the 1,25-(OH)2D3 because the immature kidneys and immature parathyroid glands fail to produce the required amount of this hormone. Other vitamin D-resistant rachitic conditions cannot be discussed here for lack of space and for lack of information. Undoubtedly, such patients as those having rickets secondary to renal tubular acidosis and rickets secondary to hepatic disorders will eventually come under effecti dietary and hormonal management. In this sense, the vitamin D endocrine system and vitamin D-resistant rickets can serve as a prototype of management of a genetic disorder by dietary means.
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PMID:Vitamin D-resistant rickets. A prototype of nutritional management of a genetic disorder. 23 Sep 41

Stable long-term chronic renal failure in the growing Sprague Dawley rat causes marked bone disease with impaired mineralization (i.e. rickets) and evidence of increased parathyroid hormone activity. Although significant bone disease is present, the rate of longitudinal growth is not diminished in preterminal renal failure. However, it is significantly diminished in terminal renal failure, when uremic rats are compared with sham-operated control rats at identical levels of food intake. At identical levels of food intake, weight gain is also diminished in rats with terminal uremia as compared with sham-operated control rats, suggesting increased calorie cost for growth.
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PMID:Skeletal growth in uremia. 40 7

Patients with nephrotic syndrome have low blood levels of 25 hydroxyvitamin D (25-OH-D) most probably because of losses in urine, and a vitamin D-deficient state may ensue. The biological consequences of this phenomenon on target organs of vitamin D are not known. This study evaluates one of these target organs, the bone. Because renal failure is associated with bone disease, we studied six patients with nephrotic syndrome and normal renal function. The glomerular filtration rate was 113+/-2.1 (SE) ml/min; serum albumin, 2.3+/-27 g/dl; and proteinuria ranged between 3.5 and 14.7 g/24 h. Blood levels of 25-OH-D, total and ionized calcium and carboxy-terminal fragment of immunoreactive parathyroid hormone were measured, and morphometric analysis of bone histology was made in iliac crest biopsies obtained after double tetracycline labeling. Blood 25-OH-D was low in all patients (3.2-5.1 ng/ml; normal, 21.8+/-2.3 ng/ml). Blood levels of both total (8.1+/-0.12 mg/dl) and ionized (3.8+/-0.21 mg/dl) calcium were lower than normal and three patients had true hypocalcemia. Blood immuno-reactive parathyroid hormone levels were elevated in all. Volumetric density of osteoid was significantly increased in three out of six patients and the fraction of mineralizing osteoid seams was decreased in all. Evidence for an increase in active lacunae (bone-osteoclast interface) occurred in three out of six patients and in inactive (Howship's lacunae) bone resorption in six out of six. The data indicate that the loss of 25-OH-D in urine of patients with nephrotic syndrome and normal renal function may result in a decrease of blood levels of ionized calcium, secondary hyperparathyroidism and enhanced bone resorption. In addition, the vitamin D-deficient state causes osteomalacia as evidenced by defective mineralization and increased osteoid volume.
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PMID:Osteomalacia and hyperparathyroid bone disease in patients with nephrotic syndrome. 42 68

During the period 1971-1976, subtotal parathyroidectomy was performed on 34 patients with chronic renal failure, representing 8% of all uraemic patients treated on the Renal Ward. Preoperative treatment of renal failure was conservative therapy in 6, haemodialysis in 20 and renal transplantation in 8 patients. The operation was indicated by grave clinical symptoms (pruritus, bone pains and mental disturbances), gastric ulcer and radiological abnormalities (osteoporosis, fractures, subperiosteal resorption and metastatic calcifications). The serum immunoreactive parathyroid hormone was determined in 13 cases, and the value was elevated in all. The serum calcium level was elevated in 8 out of 34 cases. Less than 500 mg of parathyroid tissue was removed in 12 cases, between 500 and 6000 mg in 19 and over 6000 mg in 3. Nodular hyperplasia was present in 11 patients, diffuse hyperplasia in 23. Postoperatively marked falls in serum parathyroid hormone and serum calcium values were observed. The bone pains, pruritus and mental disturbances were alleviated, and the general condition was favourably influenced. The operation had a lesser and more retarded effect on the radiological changes. Complete recovery was only achieved with successful renal transplant. Parathyroidectomy often had a favourable effect on the grave symptoms and may, therefore, be considered in some cases of severe hyperparathyroidism secondary to chronic renal failure.
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PMID:Parathyroidectomy in chronic renal failure. 43 13

Fourteen patients with chronic renal failure underwent parathyroidectomy. Postoperatively, seven patients exhibited a rise in hematocrit reading, but seven others did not. Responders had more severe bone disease and lower initial hematocrit values than did nonresponders. Marrow fibrosis was slightly more prominent in responders. Current concepts of marrow erythropoietic inhibition in renal failure suggest a toxic serum factor as the cause. This report fails to support parathyroid hormone as the toxic agent directly responsible for marrow inhibition. Rather, parathyroid hormone may contribute to anemia in renal failure by causing marrow fibrosis, a process sometimes reversible by successful therapy of hyperparathyroidism.
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PMID:Effect of parathyroidectomy on anemia in chronic renal failure. 46 2


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