Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q92565 (GFR)
 4,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Besides rickets and osteomalacia, the X-linked hypophosphatemic male mouse (Hyp/Y) presents with low serum calcium (Ca) and increased urinary hydroxyproline (OH-Pro) excretion, suggesting a parathyroid hormone (PTH)-stimulated bone resorption despite reduced magnesium (Mg) bone content. In this study, we have investigated by histochemical methods the state of bone resorption in 50-day-old untreated Hyp/Y mice and the effects of 4 wk of Mg therapy or dietary lactose supplementation on bone formation and resorption. Mineral and skeletal changes were evaluated on serum, urinary and bone ash concentrations of Ca, phosphorus (P) and Mg, and by histomorphometric analysis of tetracycline double labeled undeclalcified caudal vertebrae. The number of acid phosphatase stained chondroclasts and osteoclasts was lower than normal in untreated Hyp/Y and was restored after Mg therapy while the osteoclastic surface was increased above normal. Accordingly, serum P and urinary Ca, P, Mg, cAMP and OH-Pro were increased while TmP/GFR was unchanged. On the other hand, dietary lactose corrected serum Ca which probably suppressed PTH secretion since the renal P conservation was improved and the osteoclast number and the osteoclastic surface were decreased. Both treatments reduced the growthplate and osteoid seam thickness and increased the bone calcification rate. The results indicate that the low skeletal Mg present in Hyp/Y partially impairs bone responsiveness to PTH since Mg therapy restored the osteoclastic bone resorption which secondarily provided new minerals for bone mineralization. The greater than normal bone resorption found in Mg treated-Hyp/Y and the decreased bone resorption observed in lactose treated animals indicate that the chronic hypocalcemia induces secondary hyperparathyroidism in Hyp/Y mice.
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PMID:Effects of magnesium and lactose supplementation on bone metabolism in the X-linked hypophosphatemic mouse. 682 87

We measured the plasma concentration of 1,25-dihydroxyvitamin D (1,25(OH)2D) in 39 children comprising three groups; eight with moderate renal insufficiency (GFR of 25 to 50 ml/min/1.73 M2, seven of whom had tubulointerstitial disease), eight with severe renal insufficiency (on chronic hemodialysis), and 23 healthy control subjects. The mean plasma concentration of 1,25-(OH)2D was reduced by some 40% (P less than 0.002) in the children with moderate renal insufficiency, and by some 80% (P less than 0.001) in the children with severe renal insufficiency. In the children with moderate renal insufficiency, the reduced concentration of 1,25-(OH)2D was associated with increased serum concentrations of immunoreactive parathyroid hormone (iPTH) and reduced serum concentrations of 1,25-(OH)2D was associated with increased serum concentrations of immunoreactive parathyroid hormone (iPTH) and reduced serum concentrations of calcium and phosphorus. When analyzed over the range of renal function from normal through severely impaired, values of iPTH correlate inversely and significantly with those of 1,25-(OH)2D. Growth was impaired in four of the eight children with moderate renal insufficiency. The results of the current study suggest that in children with moderate renal insufficiency, a reduction in the renal synthesis and in the plasma concentration of 1,25-(OH)2D may be important pathogenetic events in disordered metabolism of calcium and phosphorus, including secondary hyperparathyroidism.
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PMID:Reduced plasma concentration of 1,25-dihydroxyvitamin D in children with moderate renal insufficiency. 689 41

It is well established that the calcemic response to parathyroid hormone (PTH) is blunted in chronic uremia and is corrected partially by 1,25(OH)2D treatment. Recent evidence suggests that PTH(1-34) and not PTH(1-84) may be the actual calcemic fragment. Equivalent doses of both peptides were infused into five normal dogs (GFR = 51 ml/min) and eight dogs with a remnant kidney and chronic renal insufficiency (GFR = 15 ml/min). Both the calcemic and phosphaturic responses were studied. Remnant dogs had a blunted calcemic response to bPTH(1-84). The increase in fractional phosphate excretion was similar. In contrast, the calcemic response to bPTH(1-34) was equivalent in remnant and normal dogs. Treatment of uremic dogs with 400 ng 1,25(OH)2D daily for 3 days restored the effect of bPTH(1-84) on serum calcium and increased the control value for tubular phosphate reabsorption from 28 +/- 3 micrograms/ml GFR to 37 +/- 4 micrograms/ml GFR (P less than 0.01). These results suggest that there is an impaired conversion of PTH(1-84) to PTH(1-34) in chronic renal insufficiency and that 1,25 (OH)2D may be involved in metabolism of PTH(1-84). In addition, the effect of PTH on fractional phosphate excretion is not magnified in nonparathyroidectomized uremic dogs.
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PMID:Calcemic and phosphaturic response to parathyroid hormone in normal and chronically uremic dogs. 689 96

1,25-diOH vitamin D, 25-OH vitamin D, parathyroid hormone, calcium and phosphorus were measured in the blood of 34 children and correlated. These children, 3 months to 17 years old, had chronic renal insufficiency of varying intensity. 15 of them were treated with vitamin D. We found a negative correlation between the 1,25-diOHD levels and the reduction of the clearance of inuline, serum creatinine and uremia. This suggests a defect in 1,25-diOHD synthesis appearing when the glomerular filtration rate is decreased by about 50%, except in the case of tubulopathies, where it appears earlier. In these children, the 1,25-diOHD levels correlated with calcemia, but not with phosphoremia. The high levels of PTH were related with the lowest levels of 1,25-diOHD. The regulation of calcemia is thus basically controlled by the renal possibilities. There was a positive correlation between 1,25-diOHD and 25OHD levels when GFR was lower than 0.6 ml/sec./1,73 m2, indicating a dependence of 1,25-diOHD levels or its substrate in severe chronic renal failure.
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PMID:[Levels of plasma 1,25-dihydroxyvitamin D and parameters of phospho-calcium metabolism in children with non-dialyzed chronic renal failure]. 689 3

Patients after kidney transplantation were investigated for parameters for kidney function and calcium metabolism including a definitively characterized parathyroid hormone (PTH) radioimmunoassay, of which quality criteria have been documented. In 72 transplanted patients 3 months to 7 years after operation a close correlation between graft function and plasma PTH concentrations was found. Patients with clearly elevated PTH revealed definitively decreased graft function. Three patients with normal GFR and clearly elevated PTH showed - at least transiently - all criteria of an autonomous hyperparathyroidism including hypercalcaemia and hypophosphataemia. Borderline PTH elevations associated with normal GFR can be explained by corticosteroid treatment. In 100 patients, which were investigated before and during the first 10 days after transplantation, again a close correlation was documented between the development of PTH concentrations and the function of the transplanted kidney. PTH concentrations are not only a very sensitive parameter of graft function; in various situations plasma PTH concentrations additionally allow an estimate of graft prognosis. This is particularly true in primary graft failure and in early rejection episodes.
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PMID:[Plasma parathyroid hormone after kidney transplantation. A sensitive parameter for the estimation of graft function (author's transl)]. 699 7

The purpose of this investigation is to analyze changes in plasma 1,25-(OH)2D and 24,25-(OH)2D after successful renal transplantation in 20 children and young adults. Studies were performed on 8 subjects between the 1st and 10th month and on 12 others between the 20th and 30th to 36th month. Samples were assayed for plasma and urinary calcium, inorganic phosphate, creatinine, plasma bicarbonate, immunoreactive parathyroid hormone, 25-(OH)D, 24,25-(OH)2D, and 1,25-(OH)2D concentrations. Results showed the following: (1) All subjects had normal or high plasma levels of dihydroxyvitamin D metabolites. (2) In subjects with normal GFR's there was a significant inverse correlation between plasma 1,25-(OH)2D concentrations and tubular reabsorption of phosphorus. (3) These correlations were not found in subjects with subnormal creatinine clearances (50 to 100 ml/min/1.73 m2) even though plasma 1,25-(OH)2D concentrations in these subjects were similar to those with normal creatinine clearances. (4) In subjects with subnormal creatinine clearances, an increase in plasma 1,25-(OH)2D concentrations to very high levels was observed during the first months following renal transplantation.
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PMID:Changes in plasma 1,25 and 24,25-dihydroxyvitamin D after renal transplantation in children. 702 20

Renal handling of phosphate and calcium was studied in 17 hypercalciuric stone-formers, 6 normocalciuric stone-formers and 10 normal subjects before (fasting state) and 45 and 75 min after the ingestion of 100 g glucose. The ratio of fasting urinary calcium to creatinine (UCa/creat) was higher in hypercalciuric than in normocalciuric stone-formers or controls. A positive correlation was found between weight index and fasting UCa/creat for all subjects studied (r = 0.36; P less than 0.05). A negative correlation was apparent between the weight index and the fasting renal threshold phosphate concentration (TmP/GFR) (r = 0.40; P less than 0.02), the latter parameter being slightly but insignificantly lower in hypercalciuric stone-formers than in controls. After glucose ingestion. UCa/creat rose significantly in all groups. The maximal rise in UCa/creat was also positively correlated with the weight index for all patients ( r = 0.42; P less than 0.02), and 75 min after glucose ingestion, TmP/GFR decreased in all groups, dropping to a significantly lower level in the hypercalciuric patients than in the controls. No correlation was apparent between the weight index and the magnitude of the reduction in TmP/GFR. Plasma 1, 25-dihydroxyvitamin D3 and immunoreactive parathyroid hormone were measured before glucose ingestion and were not correlated either with each other or with plasma phosphorus, TmP/GFR, or UCa/creat before or after glucose ingestion. These results imply that weight is a determining factor in the renal handling of calcium and phosphorus. Such findings might be of importance to the clinical investigation and management of calcium stone-formers.
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PMID:Effects of weight and glucose ingestion on urinary calcium and phosphate excretion: implications for calcium urolithiasis. 706 97

The tubular transport of inorganic phosphate (Pi) is controlled by a parathyroid hormone-independent mechanism that responds to variations in the Pi intake. This adaptation mechanism could also respond to growth-mediated variation in the utilization of Pi by the organism. In the present work we have determined the maximal net Pi reabsorption per volume of glomerular filtrate (max TRPi/ml GF) in the young growing (2-mo) and adult 8- to 9-mo) rats. Max TRP[i/ml GF was significantly lower in intact adult (1.44 +/- 0.06 mumol/ml) compared with intact young growing animals (2.22 +/- 0.12 mumol/ml GF). This difference was maintained after removal of the thyroparathyroid glands; adult, 2.89 +/- 0.25, young, 4.56 +/- 0.25 mumol/ml. It was not associated with a difference in the urinary excretion of cAMP, GFR, renal handling of sodium, plasma calcium, or acid-base status. Administration of growth hormone preparations to adult rats did not raise max TRPi/ml GF to the level observed in young intact animals. With regard to the tubular Pi adaptation to Pi restriction, lowering the phosphorus content in the diet from 0.8 to 0.2 g/100 g resulted in an attenuated and delayed enhancement in max TRPi/ml in adult as compared with the response observed in young growing rats. These results show that the decrease in tubular reabsorption of Pi that occurs when rats become adult in a parathyroid hormone-independent phenomenon. It is suggested that this change is an adaptation of the tubular Pi transport to a reduction in the utilization of Pi in relation to the diminished growth rate of the animals.
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PMID:Tubular handling of Pi in young growing and adult rats. 709 22

The renal handling of inorganic phosphate was studied by measuring the urinary excretion rate of phosphate (UPO4V), phosphate-(Cr51) EDTA clearance ratio (CPO4/GFR) and maximal tubular reabsorption of phosphate per litre glomerular filtrate (TmPO4/GFR) during fasting in 26 ambulatory Type 1 (insulin-dependent) diabetic children without clinical signs of microangiopathy (age: 7-14 years; duration of disease: 3-14 years). Similar measurements were made in 28 healthy schoolchildren (age: 8-14 years). UPO4 V and CPO4/GFR were significantly enhanced in the diabetic children (p less than 0.001) and correlated with the degree of hyperglycaemia (p less than 0.005). TmPO4/GFR was significantly suppressed in the diabetic children (1.23 versus 1.73 mmol/l, p less than 0.001). This disturbance was neither related to changes in serum parathyroid hormone nor to growth hormone concentrations but was inversely correlated with the degree of hyperglycaemia (r = -0.61, p less than 0.001) and with tubular reabsorption of glucose (r = -0.53, p less than 0.01). In spite of the markedly lowered TmPO4/GFR in the diabetic subjects, the mean maximal (TmPO4) and absolute tubular phosphate reabsorption rates were equal to those of the 28 healthy subjects. Both in the diabetic and healthy subjects, these parameters were positively correlated with glomerular filtration rate which was significantly elevated in the diabetic children (138 versus 109 ml/min per 1.73 m2, p less than 0.01). The study demonstrates a dysfunction in tubular phosphate reabsorption in diabetic children which is related to glycaemic regulation.
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PMID:Dysfunction of tubular phosphate reabsorption related to glomerular filtration and blood glucose control in diabetic children. 717 17

Fifty-six consecutive patients with sarcoidosis, 31 subacute and 25 chronic, were investigated for abnormalities of calcium and phosphate metabolism with particular reference to parathyroid function. No abnormality of serum calcium, phosphate, creatinine or alkaline phosphatase was found. Serum levels of 25-OH cholecalciferol were normal and parathyroid hormone levels were normal in all but one patient. Maximum renal tubular reabsorption capacities for calcium and phosphate (TmCa/GFR, TmP/GFR) in relation to glomerular filtration rate in the fasting state, were abnormal in some patients but this did not correlate with any other abnormality in parathyroid function. There was significant hypercalciuria (greater than 10 mmol calcium per 24 hours) in 7.5% of our patients and this is believed to be due to increased calcium flow.
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PMID:Calcium and phosphate metabolism in sarcoidosis with particular reference to parathyroid function. 725 66


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