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)

Serum 1,25(OH)2D and factors related to its production were studied in 39 patients with various degrees of renal insufficiency. Serum 1,25(OH)2D levels correlated positively with 1/serum creatinine values (r = 0.54, P less than 0.001) and negatively with serum phosphorus (r = -0.39, P less than 0.02) and age (r = -0.33, P less than 0.05). There was no significant correlation between 1,25(OH)2D levels and serum calcium or calcitonin or PTH, although the logarithm of PTH correlated inversely with 1,25(OH)2D levels (r = -0.47, P less than 0.01). Patients who had normal or supranormal 1,25(OH)2D levels despite low GFR tended to have low serum phosphorus values. Serum levels of bone Gla protein (BGP), a biochemical marker for bone metabolism, correlated negatively with 1/serum creatinine (r = -0.39, P less than 0.02) and positively with PTH (r = 0.57, P less than 0.001) and age (r = 0.33, P less than 0.05). Prophylaxis with 1,25(OH)2D should be considered in patients with significantly decreased serum 1,25(OH)2D levels, as seem to occur when serum creatinine is greater than 4.0 mg/dl. However, despite the statistically significant correlation between serum 1,25(OH)2D and 1/serum creatinine, direct measurement should be used to ascertain the serum concentration of 1,25(OH)2D in chronic renal insufficiency.
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PMID:Determinants of serum 1,25(OH)2D levels in renal disease. 660 33

The effect of magnesium (Mg) supplementation on bone metabolism has been studied in the normal young mouse. Weanling male mice were given Mg-supplemented drinking water (5 mM or 32 mM Mg) for 4 weeks. Mineral and skeletal changes were assessed by biochemical methods and by histomorphometric analysis of endosteal bone formation and resorption parameters evaluated on tetracycline double-labeled, undecalcified caudal vertebrae. Magnesium supplementation increased serum and urinary Mg concentrations and bone Mg content. Both the calcification rate and the extent of tetracycline double-labeled osteoid surface increased progressively in Mg-treated mice, whereas the mineralization lag time was shortened. The osteoblastic surface was reduced, leading to a fall in osteoid surface. Stimulation of bone mineralization was associated with a rise in extracellular calcium (Ca) and phosphorus (P) concentrations whereas serum 25-OHD and 1,25(OH)2D levels remained normal. The Mg supplementation increased the number of acid phosphatase stained chondroclasts and osteoclasts and the extent of resorbing surface showing histochemically stained osteoclasts. Although urinary OH-proline increased above normal, Ca, P, and cyclic adenylic acid (cAMP) excretion and phosphate concentration (TmP/GFR) remained normal, suggesting that parathyroid hormone (PTH) secretion was not altered. The trabecular bone volume remained normal, showing that the increased bone resorption was balanced by the stimulated bone mineralization. The results show that Mg supplementation influenced both bone formation and resorption in the young mouse, and that the stimulation of bone mineralization was the result of increased extracellular mineral availability.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of magnesium supplementation on bone turnover in the normal young mouse. 665 50

Hypophosphatemia is frequently found in patients with alcoholic cirrhosis, and its postulated causes include inadequate phosphorus (PO4) intake, reduced gastrointestinal absorption, and inappropriate PO4 loss in the urine. Of these, the first two would be expected to be associated with a high threshold concentration (Tm/GFR) and the last with a low Tm/GFR. 24 patients with alcoholic cirrhosis were studied. All had normal renal function. Simultaneous mid-morning serum and urine samples were obtained and analyzed for creatinine, Ca, PO4, and Mg. Median serum PO4 was 2.75 mg/dl, including 8 patients who were hypophosphatemic (serum PO4 less than 2.5 mg/dl). The median Tm/GFR was 2.3 mg/dl; 13 of the patients had values below 2.5 mg/dl. There was a significant correlation between serum PO4 and Tm/GFR (p less than 0.001). The median serum Ca was 8.5 mg/dl and did not correlate with Tm/GFR. The median serum Mg was 2.0 mg/dl. Serum magnesium was significantly correlated with Tm/GFR (p less than 0.05). We conclude that hypophosphatemia in alcoholic cirrhosis is associated with a low Tm/GFR and that this may be related to hypomagnesemia.
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PMID:Reduced renal phosphate threshold concentration in alcoholic cirrhosis. 673 65

A 50-year-old Latin American man with tumoral calcinosis presented with hyperphosphatemia (6.62 +/- 1.04 SD mg/dl), elevated renal threshold phosphorus concentration (TmP) (7.3 mg/GFR), and 1,25-dihydroxyvitamin D [1,25-(OH)2D] (69 pg/ml) hypercalciuria (239 mg/day), and a high fractional intestinal calcium (Ca) absorption (0.74). Sodium cellulose phosphate therapy (20 g/day) lowered urinary Ca, and partially reduced serum phosphorus (P) and TmP to 5.91 +/- 0.63 mg/dl and 6.2 mg/GFR, respectively. Serum 1,25-(OH)2D remained elevated at 58-64 pg/ml. Amphojel therapy (4 oz/day) decreased urinary P to 23 +/- 21 mg/day and lowered serum P to 5.75 +/- 0.36 mg/dl (P < 0.05). TmP increased to a value of 8.0 mg/GFR while serum 1,25-(OH)2D continued to remain elevated at 53 pg/ml. This case illustrates the probable operation of dual abnormalities in tumoral calcinosis represented by augmented renal conservation of P and an elevation in the circulating concentration of 1,25-(OH)2D.
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PMID:Tumoral calcinosis: evidence for concurrent defects in renal tubular phosphorus transport and in 1 alpha,25-dihydroxycholecalciferol synthesis. 677 76

In ten male hypophosphataemic hypercalciuric recurrent renal stone formers with absorptive hypercalciuria and ten male normophosphataemic normocalciuric control persons, fasting plasma and urine chemistry was studied throughout the day under basal conditions and following an oral phosphorus load. After overnight fasting, plasma phosphorus and TMP/GFR were lower and urinary calcium higher in patients than in controls. Both in patients and controls, plasma phosphorus rose throughout the morning hours. In the afternoon, plasma phosphorus was almost equal in patients and controls. The circadian rise of plasma phosphorus despite no increase of urinary phosphorus argues against the presence of a fixed renal tubular phosphorus leak in absorptive hypercalciuria, at least in the fasting state. Patients differed from controls not only with respect to urinary calcium, but also with respect to fasting absolute and fractional urinary excretion of sodium and chloride. Increased fractional urinary sodium was found both in normotensive and hypertensive patients. Since tubular reabsorption of phosphorus and the setting of fasting plasma phosphorus depend, among other factors, on tubular handling of sodium, the finding may be relevant for the genesis of transient fasting hypophosphataemia in absorptive hypercalciuria.
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PMID:Is there a renal phosphorus leak in recurrent renal stone formers with absorptive hypercalciuria? 677 72

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

Changes in phosphatemia and in maximum renal threshold phosphate concentration (TmP/GFR) have been measured before and 45 and 75 min after oral ingestion of 75 g of glucose in 10 hypercalciuric lithiasic patients (HCI), 8 normocalciuric lithiasic patients (NCI) and 7 control subjects. After glucose ingestion, whereas plasma phosphorus decreased in all 3 groups, TmP/GFR decreased significantly in HCI and NCI but not in controls. A slight increase in calcium excretion was noted in the subjects with HCI and NCI after glucose load. Plasma concentration of 1,25(OH)2D was measured in 8 HCI and 7 controls before and after glucose: there was a significant increase in HCI 45 min after glucose and no modification in control subjects. These results show that a glucose load causes a decrease in TmP/GFR in lithiasic subjects. The results demonstrate the existence in lithiasic patients of perturbations of renal handling of phosphates which could, at least in part, be related to glucose metabolism. This trouble could contribute to the elevation of the serum 1,25(OH)2D observed in these patients.
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PMID:[Evidence for a glucose-dependent renal phosphorus leak in normo- and hypercalciuric stone-formers (author's transl)]. 689 6

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

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

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


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