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

In 42 untreated patients at various stages of chronic renal failure, plasma level of parathyroid hormone was directly proportional to the degree of renal failure and inversely proportional to the serum calcium level. Plasma parathyroid hormone levels were frequently elevated in 21 patients undergoing regular dialysis treatment, in spite of normal levels of serum total calcium and magnesium. Serum-ionized calcium levels measured in dialyzed patients were usually reduced and inversely correlated with the creatinine levels. Parathyroid hormone levels were correlated with the creatinine levels, but the inverse relationship with ionized calcium was not significant.
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PMID:Parathyroid hormone plasma level in untreated chronic renal failure and in hemodialyzed patients. 94 Jun 20

This report reviews the interrelationship between the activity of the parathyroid glands and renal function. Among the topics discussed are: effects of parathyroid hormone on various aspects of renal function such as: (1) glomerular filtration rate and renal blood flow; (2) renal handling of phosphorus, calcium, magnesium, sodium and potassium; (3) renal production of 1,25-dihydroxycholecalciferol; (4) renal handling of bicarbonate and acid-base metabolism, and (5) mechanism of action of parathyroid hormone on the renal cell. Further topics include: renal metabolism of parathyroid hormone; the kidney in hyperparathyroidism, and effects of renal failure on structure and function of the parathyroid glands.
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PMID:Relationship between the kidney and parathyroid hormone. 110 Oct 86

The presence of hypercalcemia in patients with known cancers may be due to the cancers themselves, or to co-existing primary hyperparathyroidism. The differentiation of primary hyperparathyroidism from the hypercalcemia of malignancy is important since the relief of distressing symptoms and prevention of hypercalcemic crises and renal failure can be accomplished relatively easily by parathyroid surgery in the former condition, and only with difficulty, at times, with fluids and drugs in the latter condition. The histories of three recent patients are presented, which demonstrate the difficulties inherent in the differentiation of these conditions. These patients were ultimately found at operation to have primary hyperparathyroidism in addition to malignancies of the cervix, adrenal gland and kidney. In our experience the following have been helpful in establishing a diagnosis; history of hypercalcemia prior to development of cancer, the type of cancer itself, the effect of cancer therapy on the hypercalcemia, and selective venous sampling with radioimmunoassay for parathyroid hormone.
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PMID:The differentiation of primary hyperparathyroidism from the hypercalcemia of malignancy. 111 56

Varying degrees of renal failure were produced by surgical reduction of renal mass in normal dogs and in thyroparathyroidectomized dogs (TPTX) in whom serum calcium levels were maintained in the normal range by the administration of vitamin D. Both groups of dogs maintained normal serum phosphate levels in spite of progressive decreases in glomerular filtration rates (GFR). Furthermore, both groups of dogs were able to increase the fractional excretion of phosphate as GFR decreased. Thus the same renal response to loss of GFR was maintained in the complete absence of parathyroid tissue. Finally, stable serum phosphate levels and increased fractional excretion of phosphate in response to a decrease in GFR were also demonstrated in acutely TPTX dogs who were not receiving vitamin D. These results indicate that phosphate homeostasis can be maintained in renal failure in the total absence of parathyroid hormone secretion.
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PMID:Evidence that parathyroid hormone is not required for phosphate homeostasis in renal failure. 111 83

The physiologic function of human parathyroid autografts and allografts has not been demonstrated conclusively. During the past 30 months, we have transplanted parathyroid glands in 29 patients and tested their functional status. One immunosuppressed aparathyroid patient received a parathyroid allograft from a parent who previously had been his renal transplant donor. Twenty-seven patients with renal failure and secondary hyperparathyroidism received parathyroid autografts immediately after total parathyroidectomy, and one patient received a parathyroid autograft at the time of total parathyroidectomy for primary chief cell hyperplasia. At transplantation 1 times 1 mm. parathyroid pieces were grafted into the forearm musculature. Of 11 transplanted patients (one allograft and ten autografts) followed for 1 year, ten are normocalcemic; only two (autografted patients) are on supplemental calcium. Ten of the 29 patients have had biopsies performed, and all have had intact parathyroid architecture and intracellular secretory granules demonstrated by light and electron microscopy. Parathyroid hormone content in the grafted tissue of five patients was 179 plus or minus 118.8 ng. per milligram. In 11 random patients in whom bilateral measurements have been made, the parathyroid hormone content in the antecubital vein blood draining the grafted tissue has been markedly higher than that in the simultaneously sampled antecubital vein blood of the nongrafted arm. These data demonstrate that parathyroid autografts or allografts secret hormone and maintain a normal serum calcium in the host.
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PMID:Transplantation of the parathyroid glands in man: clinical indications and results. 113 98

A case is reported of a twenty-one year old man who developed severe hypercalcemia late in the diuretic phase of acute reversible renal failure secondary to severe trauma. Hypercalcemia persisted for approximately five months. Serum immunoreactive parathyroid hormone levels were undetectable and sub-total parathyroidectomy had no appreciable effect on the serum calcium. The most likely source of this patient's hypercalcemia was resorption of calcium from metastatic deposits in soft tissue and possibly from bone. Failure to incorporate calcium into bone during the period of immobilization may explain the prolonged hypercalcemia.
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PMID:Prolonged hypercalcemia following acute renal failure. 115 48

Serum immunoreactive parathyroid hormone (iPTH) was estimated in 30 patients with renal failure before and after haemodialysis. All patients were anuric or oliguric at the time of the investigation. Pre-dialysis iPTH values were significantly elevated (3.4 ng/ml) as compared with normal subjects (less than 0.5 ng/ml). Simultaneously, a significant hypocalcaemia (4.15 mEq/litre) was confirmed which was negatively correlated with iPTH levels. After 7-8 h of haemodialysis using a calcium concentration of 4.0 mEq/litre in the dialysate, a significant drop of iPTH level to 1.8 ng/ml was noted.
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PMID:Influence of extracorporeal dialysis on parathyroid hormone secretion in patients with acute renal failure. 125 Apr 96

Hypocalcemia is a well known finding in critically ill patients. Subsequent occurrence of mild hypercalcemia has also been reported. In order to investigate the incidence and nature of critical care hypercalcemia serum calcium was measured in 83 critically ill ICU patients (TISS score > or = 40) and related to the occurrence of acute renal failure (ARF) and severity of illness, evaluated by the APACHE-II and the multiple organ failure scoring systems. Thirty-two percent of the patients developed hypercalcemia (serum calcium > or = 2.60 mmol/l) during their ICU stay. These hypercalcemic episodes (mean maximal value 2.71 +/- 0.12 mmol/l) were more common and occurred earlier in patients with co-existing ARF. However, multiple regression analysis showed the number of failing organ systems in the first days to be the best predictors for later occurrence of hypercalcemia (p < 0.0001). When serum parathyroid hormone (PTH) was measured in 6 of the patients without ARF during their hypercalcemic episodes, PTH was not suppressed but slightly elevated, to a similar extent as in patients with mild primary hyperparathyroidism. In conclusion, a high incidence of hypercalcemia was found in critically ill ICU patients. The hypercalcemia was mild and was more frequently found in patients with co-existing renal failure. The most powerful predictor to later occurrence of hypercalcemia was however the severity of the illness in itself. The raised levels of PTH found during the hypercalcemic episodes suggest ICU hypercalcemia to be caused by parathyroid overactivity.
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PMID:Critical care hypercalcemia--a hyperparathyroid state. 130 66

It has been suggested that frusemide affects plasma parathyroid hormone (PTH) concentrations. To further investigate this issue we analysed plasma intact PTH in 77 patients with chronic renal failure (CCr 8.0-89.8 ml/min per 1.73 m2) as a function of frusemide therapy. The rate of increase of plasma PTH observed with progression of renal failure was faster in patients who received frusemide as compared to patients who did not receive the drug. The slope of the regression line of PTH on CCr was steeper (P less than 0.02) for patients with frusemide (n = 40, slope -0.34) than without frusemide (n = 37, slope -0.20). This effect was specific for frusemide therapy since therapy with other antihypertensive drugs (including thiazides and beta-blockers) was not correlated with PTH plasma concentrations. Frusemide therapy was also associated with a significantly greater urinary calcium excretion in uraemic patients but did not influence other parameters of calcium metabolism. To clarify mechanisms involved in the effect of frusemide on plasma PTH values, seven normal subjects were studied for 24 h before and for 24 h after oral administration of 80 mg frusemide. The main findings were: (1) Median PTH values were higher than on a control day (P less than 0.05) 3 h after frusemide (3.9 pmol/l vs 1.8) and 6 h after frusemide (4.0 vs 2.6); (2) ionised plasma calcium did not change significantly, whereas mean calcium/creatinine ratio increased from 0.20 to 0.46 after frusemide treatment through an increase in absolute calcium excretion; (3) plasma 1 alpha,25-dihydroxyvitamin D3, catecholamines, and magnesium concentrations did not change significantly after frusemide.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Frusemide therapy and intact parathyroid hormone plasma concentrations in chronic renal insufficiency. 131 86

1. Twelve patients receiving haemodialysis for end-stage renal failure were studied at a single dialysis session. Platelet cytosolic calcium concentration, plasma ionized calcium concentration and serum parathyroid hormone concentration were measured before dialysis, mid-dialysis and 30 min after dialysis. 2. Plasma ionized calcium concentration increased towards dialysate calcium concentrations, falling insignificantly after cessation of dialysis. Serum parathyroid hormone concentration fell by 39% during dialysis, with incomplete recovery afterwards. There was no overall change in platelet cytosolic calcium concentration. 3. Patients were divided into two subgroups: low parathyroid hormone (serum parathyroid hormone concentration less than 10 pmol/l) and high parathyroid hormone (serum parathyroid hormone concentration greater than 10 pmol/l). Before dialysis, values of platelet cytosolic calcium concentration or plasma ionized calcium concentration were not statistically different between the subgroups, but the platelet cytosolic calcium concentration was higher in the high-parathyroid hormone subgroup during and after dialysis. 4. Before haemodialysis there was a linear correlation between plasma ionized calcium concentration and platelet cytosolic calcium concentration, which disappeared during dialysis. In contrast, there was no relationship between serum parathyroid hormone concentration and platelet cytosolic calcium concentration before dialysis, but after dialysis a hyperbolic relationship was evident. 5. These results suggest that uraemic toxins may interfere with cytosolic calcium homoeostasis, allowing passive diffusion of extracellular calcium to influence the resting concentration, and that this effect is reversible by haemodialysis.
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PMID:Platelet cytosolic free calcium concentration and parathyroid hormone: changing relationships with haemodialysis in end-stage renal disease. 132 May 45


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