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Query: UNIPROT:Q92565 (GFR)
 4,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Chronic renal failure represents the most common disorder responsible for chronic stable metabolic acidosis. This type of metabolic acidosis has been characterized as "hyperchloremic" in pre-end-stage disease and the "anion-gap" form as the GFR falls below 20 ml/min. The early hyperchloremic, hyperkalemic variety may result from disease of the juxtaglomerular apparatus, a distal acidification defect, or volume depletion. The anion-gap acidosis of advanced renal disease occurs as a result of the inability of the diminished nephron mass to keep pace with the metabolic acid load which depletes extracellular fluid bicarbonate. Total ammonium excretion diminishes despite an adaptive increase in ammonia production per nephron. The observation that the serum bicarbonate rarely falls below 15 mEq/L and the anion gap stays below 20 mEq/L despite positive hydrogen ion balance attests to the important role of extrarenal buffers. Bone buffers, primarily calcium carbonate, titrate a portion of the excess hydrogen ions at the expense of progressive loss of bone salts. Parathyroid hormone (PTH) appears to be involved in the control of bone buffering capacity. Both PTH-dependent and PTH-independent mechanisms must therefore be considered. PTH mediates bone buffering capacity by activating intracellular shifts of calcium, phosphorus, and carbonate or by stimulation of bone carbonic anhydrase. A direct effect of pH on bone mineral mobilization has been demonstrated. Adequate alkali therapy to maintain serum bicarbonate levels of 20-22 mEq/L may prevent bone dissolution and minimize risk of volume overload.
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PMID:Acid-base physiology in uremia. 716 51

We diagnosed non X-linked hypophosphataemic bone disease in a 38-month-old girl. Findings included: genu varum, shortened stature, fasting hypophosphataemia (2.3-2.5 mg/100 ml; 0.74-0.81 mmol/l), diminished theoretical renal threshold for phosphate (TmP/GFR), and osteomalacia without rickets. One patient (the father) had fasting hypophosphataemia (2.3-2.7 mg/100 ml; 0.74-0.87 mmol/l) and low TmP/GFR without osteomalacia or shortened stature. Treatment of the girl with 1,25-(OH)2D3 (1 microgram a day) raised the level of serum phosphorus, improved tubular reabsorption of phosphate, and healed the bone deformity; this combination of responses is not present in X-linked hypophosphataemia. There was no correction of hypophosphataemia or TmP/GFR with 1,25-(OH)2D3 treatment (1-3 micrograms a day) in the father.
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PMID:Autosomal hypophosphataemic bone disease responds to 1,25-(OH)2D3. 721 58

Nutritional data compiled during the Growth Failure in Children with Renal Diseases Clinical Trial were analyzed to determine the relationship between the dietary intake of divalent minerals and sodium, nutritional status, and serum calcium, phosphorus, and parathyroid hormone (PTH) concentrations and blood pressure in black versus white children. One hundred eighteen patients are included in this report; 25 were black (21%) and 93 were white (79%). Although more of the blacks were male, the age distribution, midarm circumference, midarm muscle circumference, blood pressure, and serum calcium, phosphorus, and PTH concentrations were comparable in the two groups. Phosphorus intake was within the recommended daily allowance in both groups; in contrast, calcium intake was inadequate in all patients: 81% of the recommended daily allowance in whites, and 74% in blacks. Sixteen children were noted to be hypertensive during the observation period; six patients were receiving a variety of antihypertensive medications, including diuretics in two children. Linear regression analysis revealed that systolic and diastolic blood pressures were directly related to calcium and phosphorus intake in black patients. In white children, only dietary phosphorus intake and diastolic blood pressure were directly related. There was no relationship between sodium intake or GFR and blood pressure in the white or black children. PTH levels were directly correlated with systolic and diastolic blood pressure in all children. The correlations between PTH and blood pressure were stronger in white versus black patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The relationship between calcium, phosphorus, and sodium intake, race, and blood pressure in children with renal insufficiency: a report of the Growth Failure in Children with Renal Diseases (GFRD) Study. 757 65

Since the effects of cyclosporine on mineral and bone metabolism are controversial, we studied calcium regulating hormones, calcium-phosphorus (Ca-P) metabolism, and bone remodeling, assessed by serum osteocalcin, in long-term renal transplant recipients (RT). Forty-seven normocalcemic patients with good renal function receiving cyclosporine (CT, n = 27) or not (NC, n = 20) were studied at baseline and after an oral Ca load. CT and NC had similar age, daily dose of steroids, GFR level, and duration of transplantation. Baseline evaluation included 24-hr urinary Ca, P, TRP, TmP/GFR, fasting serum intact PTH, 1,25-(OH)2D, 25OHD, osteocalcin, Ca, and P. Subjects of the two groups had excessive secretion of PTH, tubular P wasting, and high serum osteocalcin level, as is usual in RT. However, there was no difference between CT and NC regarding any baseline variable. Ten CT and ten NC, matched for duration of transplantation and serum PTH level, ingested 1g Ca to achieve an acute dynamic study of PTH secretion and Ca-P metabolism. In both CT and NC, this Ca load caused the same decreases in serum PTH (P < 0.001), NcAMP (P < 0.05), and urinary P (P < 0.001) and the same increases in serum and urinary Ca (P < 0.001), and in both TmP/GFR and TRP (P < 0.001). These results strongly suggest that cyclosporine treatment had no significant effect on calcium-regulating hormone secretion, P-Ca metabolism, and bone remodeling level. We therefore consider that cyclosporine is unlikely to have any prominent role in the abnormalities of bone endocrine and mineral metabolism that are common in long-term kidney recipients.
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PMID:Lack of evidence that cyclosporine treatment impairs calcium-phosphorus homeostasis and bone remodeling in normocalcemic long-term renal transplant recipients. 760 39

Phosphorus retention as a result of chronic renal failure (CRF) induces secondary hyperparathyroidism (HPT II) while supplemented low-phosphorus low-protein diets (LPD) prevent it. The aim of this study was to assess in seven patients with advanced CRF and biological HPT II the effects of a LPD providing daily 5 to 7 mg/kg phosphorus, 0.4 g/kg protein, 300 mg calcium (Ca) and supplemented with amino acids, ketoacids, CaCO3 and vitamin D2, on the relationship between ionized Ca (iCa) and PTH concentrations. Hyper- and hypocalcemia were induced by CaCl2 and Na2-EDTA infusion. After three months of LPD, serum phosphorus decreased from 1.59 +/- 0.15 to 1.26 +/- 0.24 mmol/liter (mean +/- SEM, P < 0.02), basal PTH levels from 251 +/- 25 to 127 +/- 16 pg/ml (P < 0.03), while basal iCa and GFR did not vary. The sigmoidal PTH-calcium curve shifted downward with maximal PTH decreased from 482 +/- 86 to 319 +/- 60 pg/ml (P < 0.02) and minimal PTH from 35 +/- 4 to 21 +/- 4 pg/ml (P < 0.05). On the other hand, the slope of the % maximal PTH-iCa curve, which is an indicator of the sensitivity of the parathyroid cell to changes in iCa concentrations, did not vary significantly. The set point of Ca and calcitriol levels were not modified. These results demonstrate a direct inhibition of PTH secretion over a wide range of iCa concentration by LPD in patients with advanced CRF and mild HPT II over a three months period. This effect is independent of changes in plasma calcitriol levels.
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PMID:Phosphorus and protein restriction and parathyroid function in chronic renal failure. 785 97

The mechanisms underlying the effects of recombinant human growth hormone (rhGH) on vitamin D, mineral, and bone metabolism are not known. We examined whether these effects are mediated by parathyroid hormone (PTH) by measuring renal phosphorus (P) and calcium (Ca) handling, serum calcitriol, and markers of bone turnover for 24 h before and 72 h after an infusion of hPTH(1-34) in eight healthy postmenopausal women at baseline and following short-term (1 week) and sustained (5 weeks) rhGH treatment. On short-term rhGH, serum phosphorus and basal TmP/GFR were unaffected, but the fall in TmP/GFR after hPTH infusion was exaggerated (integrated response: -99.2 +/- 22.3 versus -144.1 +/- 15.0 minute-mg/dl, P = 0.0021). Basal calcitriol levels rose from 115 +/- 17 to 163 +/- 16 pM (P = 0.0002), but the increase in calcitriol following hPTH infusion was unaffected by short-term rhGH. The basal Ca excretion index (CEI) rose from 0.054 +/- 0.005 to 0.073 +/- 0.007 mM (P = 0.0095), but markers of bone turnover were unaffected. With sustained rhGH treatment, serum P (1.47 +/- 0.05 mM), basal TmP/GFR (4.29 +/- 0.24 mg/dl), and basal CEI (0.067 +/- 0.005 mM) were elevated compared with control values, and the PTH-induced lowering of TmP/GFR was again enhanced (-158.7 +/- 22.8 minute-mg/dl, P = 0.0021). Basal calcitriol concentrations returned to control levels (108 +/- 10 pM), but the calcitriol response to hPTH remained unchanged. Markers of bone remodeling were elevated with sustained rhGH treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interactions of growth hormone and parathyroid hormone in renal phosphate, calcium, and calcitriol metabolism and bone remodeling in postmenopausal women. 786 23

We report the results of an oral tolerance test performed in 317 patients with kidney stones. In order to avoid PTH or AMPc measurements, and therefore to reduce costs and time to get the results, we measured the tubular maxima of phosphate per glomerular filtration rate (TmP04/GFR, the phosphate threshold). Urine collections from 7 to 9 h and from 9 to 13 h were obtained. The samples were analyzed for calcium, creatinine and phosphorus content. All patients ingested 1 g of calcium mixed in a meal at 9 o'clock. Venous blood samples were obtained for calcium, creatinine and phosphorus measurements, previous to the calcium ingestion. Urinary calcium to creatinine ratio, before and after the calcium-load, as well as TmP04/GFR were calculated. In 97 subjects (30.8%) there were no calcium metabolism abnormalities. Idiopathic hypercalciuria was present in 183 (57%) and primary hyperparathyroidism in 37 (11.7%). Idiopathic hypercalciuria was classified in four subgroups: absorptive hypercalciuria with normal serum phosphorus, absorptive hypercalciuria with low serum phosphorus (renal phosphate leak), renal hypercalciuria with normal phosphorus and renal hypercalciuria with low serum phosphorus.
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PMID:[Usefulness of oral calcium test in renal lithiasis]. 792 97

We investigated if renal handling of phosphate could predict height velocity in 28 normal variant short children (16 boys and 12 girls). Before and after human growth hormone was given for four consecutive days, the ratio of maximum tubular reabsorption rate for phosphorus to glomerular filtration rate (TmP/GFR) was calculated. Based on increments in TmP/GFR (delta TmP/GFR) with growth hormone administration, the patients were divided into two groups; children in whom the levels of delta TmP/GFR were 0.8 mg/dl GF or more (group A, n = 7) and those with levels less than 0.8 mg/dl GF (group B, n = 21). All children in group A and some in group B (n = 9) were injected with 0.5 IU/kg/week of recombinant human growth hormone for over one year. Height velocity during therapy was significantly greater in treated children in group A than in group B and was similar among treated (n = 9) and untreated (n = 12) children in group B. The present study suggests that change in renal handling of phosphate during short-term growth hormone administration can serve to select normal variant short children who will respond well to growth hormone therapy.
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PMID:Can renal handling of phosphate predict response to growth hormone therapy in normal variant short children by short-term treatment? 794 4


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