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)

Treatment of 6 healthy adult men with a beta-blocker, timolol, resulted in a rise in serum phosphate which was maintained for the 5 days of therapy. This rise was accompanied by a transient fall in urine phosphate and a rise in the tubular maximum for phosphate reabsorption per unit glomerular filtration rate (TmPO4/GFR). No change in circulating parathyroid hormone or growth hormone could be demonstrated.
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PMID:Serum and urine phosphate during short-term beta-adrenergic blockade in healthy men. 3 May 63

Three indices of circulating parathyroid hormone (PTH) activity were compared between two groups: the first a group of 23 patients from three large kindreds with autosomal dominant hypercalcemia without hypercalciuria [familial hypocalciuric hypercalcemia (FHH)] and the second a group of 64 patients with typical primary hyperparathyroidism (1HPT) manifesting comparable hypercalcemia. The group with 1HPT differed from normal with respect to plasma PTH 1HPT concentration (normal, less 0.2 ng/ml), urinary cAMP excretion per 100 ml glomerular filtrate (U cAMP/GF) (normal, 2.3 x/divided by 0.6 nmol/100 ml glomerular filtrate; mean, x/divided 1 SD), and renal tubular maximum of phosphate transport corrected for glomerular filtration rate (TMP/GFR; normal, 3.4 +/- 0.4 mg/dl; mean, +/- 1 SD). The group with 1HPT also diverged significantly from the group with FHH for all three indices: for PTH, 0.37 x/divided by .48 vs. 0.25 x/divided .46 (P less than 0.05); for UcAMP/GF, 4.3 x/divided by .53 vs. 2.6 x/divided .60 (P less than 0.0005); and for TMP/GFR, 2.0 +/- 0.6 vs. 2.6 +/- 0.7 (P less than 0.01). The between-group differences for all three indices were also significant after adjustment for their variation with serum calcium. However, only the difference in TMP/GFR remained significant after adjustment for covariance attributable to serum calcium concentration, age, and creatinine clearance. The group with FHH differed from normal for TMP/GFR but not for UcAMP/GF. However, analysis of changes in UcAMP/GF and serum calcium concentration around the time of parathyroidectomy in three patients with FHH suggested that the parathyroid glands contributed to the abnormalities of mineral homeostasis in at least one. It was concluded that higher serum concentrations of PTH do not account for the lower renal clearance of calcium and magnesium in FHH calcium concentration, the group with FHH showed indices suggesting lower circulating PTH activity than the group with 1HPT.
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PMID:Circulating parathyroid hormone activity: familial hypocalciuric hypercalcemia versus typical primary hyperparathyroidism. 23 92

Clearance studies were performed in order to examine the effect of expansion of extracellular fluid volume (ECFV) on the maximal reabsorptive capacity for inorganic phosphate (TmPi) in acutely parathyroidectomized (PTX) and intact rats. TmPi values were obtained in both control and volume expansion. In PTX rats, the TmPi values in control and expansion were 8.25 +/- 1.52 and 6.14 +/- 1.02 micronmol/min (mean values +/- S.D.), respectively; the TmPi/GFR values were 2.96 +/- 0.31 and 2.09 +/- 0.30 micronmol/ml, respectively. In intact rats, the TmPi values in control and expansion were 3.56 +/- 0.94 and 2.98 +/- 0.94 micronmol/min, respectively, and the TmPi/GFR values were 1.34 +/- 0.23 and 1.05 +/- 0.23 micronmol/ml, respectively. From these results it is concluded that expansion of ECFV decreases the TmPi values both in the absence and presence of parathyroid hormone.
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PMID:Effect of expansion of extracellular fluid volume on the maximal reabsorptive capacity for inorganic phosphate in parathyroidectomized and intact rats. 56 1

The effects of chronic phosphate depletion on renal tubular function were evaluated by micropuncture and free water clearance studies in the dog. Proximal tubular punctures demonstrated that chronic hypophosphatemia led to a reduction in ratio of tubular fluid to plasma inulin in late superficial tubular from 1.59+/-0.08 in control animals to 1.29+/-0.06 in phosphate-depleted dogs, with proportional inhibition of calcium and sodium reabsorption. The chronic decrease in proximal tubular fluid reabsorption was confirmed by the analysis of sustained water diuresis in conscious, phosphate-depleted dogs, before and after repletion of body PO4 stores, and in control animals. Urine flow rate/100 ml glomerular filtration rate (V/GFR) was significantly higher in PO4 DEPLETION THAN CONTROL (15.8+/-1.1 VS. 10.7+/-0.82). In addition, acetazolamide infusion did not increase V/GFR in phosphate-depleted dogs (15.8+/-1.1 vs. 17.16+/-0.9), supporting the conclusion that inhibition of proximal tubular fluid reabsorption was responsible for the elevated urine flow rate. PO4 repletion over 5 days reduced V/GFR to 9.2+/-0.7 despite no change in urine osmolality and no change in GFR, further suggesting a specific reversible alteration in proximal tubular reabsorption in phosphate depletion. Although hypercalciuria was a constant finding in phosphate depletion (fractional excretion of calcium of 2.04+/-0.4% vs. 0.47+/-0.13% in controls), the enhanced distal delivery of calcium was not a crucial factor; acute phosphate infusion reduced urinary calcium excretion to control values without affecting the reduced proximal tubular reabsorption in either intact or thyroparathyroidectomized phosphate-depleted dogs the change in distal nephron calcium reabsorption was independent of parathyroid hormone (PTH) levels since infusion of PTH failed to alter urinary calcium excretion. We conclude that chronic phosphate depletion leads to a reversible, sustained inhibition in proximal tubular reabsorptive fuction as well as a specific decrease in distal nephron calcium reabsorption. This latter reabsorptive defect is sensitive to phosplate infusion but not corrected by PTH.
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PMID:Renal tubular effects of chronic phosphate depletion. 85 68

Quantitative bone histology (micromorphometry of undecalcified sections, analysis under polarized light; fluorescence microscopy with tetracycline double labelling) as well as serum and urinary chemistry (creatinine clearance, parathyroid hormone, ionized Ca, bone phosphatase, pH), were studied in 50 patients with incipient to advanced (glomerular filtration rate, 80 to 6 ml/min x 1.73 m2 renal insufficiency. In incipient renal failure, indirect evidence of parathyroid hormone excess was found in the skeleton (empty osteoclastic lacunae, woven osteoid). Osteoclastic surface resorption was abnormally high when GFR fell below 50ml/min x 1.73 m2. With the tetracycline double-labelling technique, a mineralization defect was demonstrable in many but not all patients.
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PMID:Bone histology in incipient and advanced renal failure. 94 Feb 74

Renal bicarbonate reabsorption (expressed per unit of glomerular filtration rate, GFR) has been reported to be diminished in uremic man and uremic rats. Both the increases in parathyroid hormone concentrations and in natriuretic forces have been considered to play a role in this change. The increased kaliuresis per nephron observed in chronic uremia could theoretically also contribute to inhibition of bicarbonate reabsorption. Despite the common use of normal dogs in studying bicarbonate reabsorption and of uremic dogs in studying alterations of renal function in disease, few studies of bicarbonate reabsorption in uremic dogs have been performed. In the present studies we have examined bicarbonate reabsorption in normal dogs and in dogs with experimental renal disease using a conventional bicarbonate titration technique. In unanesthetized normal dogs, the threshold for bicarbonaturia was 24.8 mEq/liter of GFR. A maximal reabsorptive rate (Tm/GFR) of 34.0 mEq/liter of GFR was obtained. In a second group of dogs, GFR was decreased to one-fifth normal. FENa was increased 16.9-fold over normal values: UKV/100 GFR and FEP were increased 5.8-fold and 10.9-fold, respectively. The threshold for bicarbonaturia in these dogs was increased to 30.5 mEq/liter of GFR and the maximal reabsorptive rate was increased to 41.2 mEq/liter of GFR. Thus, the capacity to reabsorb bicarbonate was increased despite the presence of high fractional excretion rates for sodium, potassium and phosphate. This increased reabsorptive capacity could not be accounted for by the effects of other known determinants of bicarbonate reabsorption.
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PMID:Bicarbonate reabsorption in the dog with experimental renal disease. 99 75

The aetiology of senile osteoporosis was investigated in a series of elderly normal persons (mean age 76.8 years) who were compared to 18-19 year old normal controls. Osteoporosis was estimated by standard radiological morphometric and densitometric techniques, in the metacarpals and thoraco-lumbar vertebrae. Serum parathyroid hormone levels were significantly higher in the elderly group, and correlated well with morphometric and densometric measurements of osteoporosis. Creatinine clearance was reduced in seven out of nine of the elderly group, and correlated well with the degree of osteoporosis. Serum thyrocalcitonin levels were reduced in the elderly. Tubular reaborption of phosphate and TmP/GFR were in the hyperparathyroid range in the elderly group and correlated well with the degree of osteoporosis. The hypothesis is advanced that the osteoporosis of old age is a result of parathyroid overactivity, caused by asymptomatic chronic renal failure. The suggestion is made that a diet low in phosphorus might reduce the incidence of osteoporosis in old age by reducing the parathyroid overactivity.
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PMID:The aetiology of senile osteoporosis: secondary hyperparathyroidism due to renal failure. 117 20

To determine if an increase in the endogenous secretion of parathyroid hormone could decrease sodium reabsorption by the proximal tubule, the ionized calcium concentration of blood perfusing the parathyroid gland of eight unilaterally thyroid parathyroidectomized dogs (TPTX) was reduced by infusion of an isotonic sodium citrate plus sodium chloride solution into the blood supply of the parathyroid gland. The fractional clearance of phosphate increased significantly (+9.3 +/- 2.8 ml/min per 100 ml GFR), while fractional sodium reabsorption by the proximal tubule decreased (-.06 +/- .02; P less than .025). In seven normal control dogs that received isotonic sodium chloride infusion, neither fractional sodium reabsorption by the proximal tubule nor the fractional clearance of phosphate was significantly altered. In five bilaterally TPTX dogs that received a sodium citrate plus sodium chloride infusion, sodium reabsorption by the proximal tubule was not significantly altered. There were no significant changes in glomerular filtration rate or renal plasma flow in any of these groups. The data demonstrate that alterations in endogenous parathyroid hormone secretion can play a significant role in the regulation of sodium reabsorption by the proximal tubule.
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PMID:Effect of parathyroid hormone secretion on sodium reabsorption by the proximal tubule. 120 Jan 36

Acute renal denervation (DNX) has been reported to increase urinary phosphate (Pi) excretion in rats with intact parathyroid glands and also in rats which were thyroparathyroidectomized (TPTX). The present study was performed to determine the effects of acute renal denervation on the tubular transport of Pi in rats in the absence of parathyroid hormone (PTH) and in rats with constant PTH levels. In TPTX rats, the reabsorbed Pi normalized for the glomerular filtration rate (Reab Pi/GFR) was 2.38 +/- 0.16 mumol/ml in the DNX kidney compared to 2.56 +/- 0.16 mumol/ml (p < 0.05) in the contralateral innervated (INN) kidney at endogenous plasma phosphate levels (n = 6). The lower values for the Reab Pi/GFR in the DNX kidney persisted at elevated plasma phosphate concentrations during phosphate infusions. Infusion of PTH resulted in markedly lower Reab Pi/GFR values in the innervated kidney (1.47 +/- 0.21 mumol/ml) at endogenous plasma phosphate levels than in the vehicle-infused group. Furthermore, the Reab Pi/GFR in the DNX kidney was decreased (1.21 +/- 0.14 mumol/ml, n = 6) compared to the contralateral INN kidney. These studies demonstrate that acute renal DNX decreases the tubular transport of Pi both in the absence and in the presence of constant PTH levels.
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PMID:Acute renal denervation decreases tubular phosphate reabsorption. 129 56

The aim of the study was to investigate the interrelation between induced hypercalcaemia and serum intact parathyroid hormone (S-PTH(1-84)) in normal man and in patients with primary hyperparathyroidism (PHPT) by measuring blood ionized calcium (B-Ca++) and S-PTH(1-84) before and during a controlled calcium infusion. Guided by frequent measurements of B-Ca++, we adjusted the calcium infusion rate continuously, thereby keeping B-Ca++ in a steady state at a pre-determined level approximately 0.25 mmol l-1 above baseline values. This calcium clamp technique (CCT) applied to 14 normal volunteers for 120 min established a standardized reference for parathyroid suppression and the renal physiological PTH response. The reproducibility of the method and the results obtained by the CCT were satisfactorily assessed in six of the 14 normal subjects. In normal subjects B-Ca++ was raised from 1.25 +/- 0.3 mmol l-1 (mean +/- SD) to 1.49 +/- 0.02 mmol l-1 suppressing S-PTH(1-84) to 264 +/- 9.9% of pre-infusion levels. We applied the CCT to 10 patients with PHPT for 120 min raising B-Ca++ from 1.41 +/- 0.09 mmol l-1 to 1.69 +/- 0.08 mmol l-1, thereby suppressing S-PTH(1-84) to 47.9 +/- 16.3% of pre-infusion levels. The renal handling of calcium and phosphate during CCT demonstrates the biological effects of suppressed activity of PTH on the renal tubules showing increments in the maximal tubular phosphate reabsorption in relation to the glomerular filtration rate (TmP/GFR) and decreased tubular reabsorption fraction of calcium. The described CCT is a safe and reliable dynamic test.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcium clamp technique: suppression of serum intact PTH by induced hypercalcaemia in normal man and primary hyperparathyroidism. 141 Dec 58


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