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

Phosphate indices (serum phosphate, tubular reabsorption of phosphate, renal threshold phosphate concentration (TmP/GFR) and index of phosphate excretion) were studied in 88 hypercalcaemic subjects: 64 with primary hyperparathyroidism (HPT) and 24 with hypercalcaemia from other causes, predominantly malignant disease. HPT patients as a group could easily be separated from normal subjects (n = 16) and patients with functional hypoparathyroidism (n = 7) by use of the phosphate variables but these indices were of little discriminating value for the differential diagnosis between HPT and hypercalcaemia from other causes. There was no difference in the urinary cyclic adenosine monophosphate (cAMP) excretion between the two hypercalcaemic patient groups, but HPT patients had clearly elevated serum parathyroid hormone (PTH) levels compared with normal PTH concentrations in patients with other causes of hypercalcaemia. A positive correlation between cAMP and serum calcium and an inverse relationship between cAMP and TmP/GFR were found in patients with hypercalcaemic malignant disease. These findings suggest the existence of a humoral factor with PTH-like effects in malignant disease. Since PTH levels were low, the physiological actions were apparently not mediated by circulating PTH. No difference in the values for phosphate variables, PTH, cAMP or serum calcium was found between renal stone-forming and stone-free patients with HPT.
 ...
PMID:Clinical studies on phosphate handling in hypercalcaemia. 629 62

Glomeruli contain receptors for many hormones. Binding of angiotensin II (ANG II) or antidiuretic hormone (ADH) to glomerular mesangial cells elicits a contractile response. Other hormones induce synthesis of cyclic nucleotides (cAMP, cGMP). Glomeruli also synthesize several prostaglandins, renin, and ANG II. Micropuncture studies in Munich-Wistar rats have examined the effects of vasoactive drugs and hormones on the filtration process. Several vasodilators increase renal plasma flow in the dog and rat, but GFR remains relatively unchanged due to an offsetting fall in the ultrafiltration coefficient (Kf). Vasoconstrictor substances such as ANG II and norepinephrine cause declines in renal plasma flow and Kf, but GFR remains constant due to an increase in the transcapillary hydraulic pressure gradient. Antidiuretic peptides and parathyroid hormone also reduce Kf. Glomerular mesangial cells may regulate Kf by contracting and reducing glomerular capillary surface area. ANG II and ADH directly stimulate mesangial cell contraction in vitro. Other hormones appear to cause contraction by inducing local ANG II synthesis. These hormonal pathways are implicated in the pathogenesis of altered glomerular function in diverse forms of renal injury.
 ...
PMID:Hormonal modulation of glomerular function. 629 13

The pathogenesis of familial hypophosphatemic rickets (FHR) is incompletely understood. We therefore examined the effects of acute dietary phosphorus deprivation to see whether renal phosphate conservation and increased 1,25 dihydroxyvitamin D [1,25(OH)2D] plasma levels, which normally follow restriction of phosphorus intake, could be induced in patients with FHR. Six healthy male volunteers (age 26 +/- 3 yr) and seven male patients with FHR (age 24 +/- 3 yr) were placed on a low phosphorus diet supplemented with aluminum hydroxide and studied over a 4-d period. The patients with FHR excreted more than five times as much phosphorus per day at the conclusion of the study than did the controls (176 +/- 61 mg/24 h vs. 33 +/- 11 mg/h). In the normal subjects, maximum tubular reabsorptive capacity for phosphorus/glomerular filtration rate (TmP/GFR) rose progressively during phosphorus deprivation, and the rise from base line was more than two times greater than that seen in patients with FHR. Immunoreactive parathyroid hormone levels and nephrogenous cyclic AMP were initially normal in both groups and no change was seen in either group with phosphorus deprivation. In the normal subjects, 1,25(OH)2D levels rose progressively over the 96 h of the study (49 +/- 3 to 63 +/- 6 pg/ml, P less than 0.05), while mean circulating 1,25(OH)2D in the patients with FHR did not change (34 +/- 3 to 29 +/- 3 pg/ml). The changes in individual plasma 1,25(OH)2D levels correlated strongly with the change in individual nephrogenous cyclic AMP measurements in the patients with FHR (r = +0.93), while no such correlation was observed in the normal subjects. These data demonstrate a defective renal response to phosphorus deprivation in patients with FHR including a qualitatively abnormal response in 1,25(OH)2D generation.
 ...
PMID:Impaired phosphorus conservation and 1,25 dihydroxyvitamin D generation during phosphorus deprivation in familial hypophosphatemic rickets. 630 51

Serum vitamin D metabolites, the renal tubular maximum reabsorptive rate for phosphate (TMP/GFR) nephrogenic cyclic AMP (NcAMPI, and CaE (urinary calcium excretion per litre of glomerular filtrate) were measured in 14 adults with familial hypocalciuric hypercalcaemia (FHH). The findings were compared with analyses in 14 patients with surgically proven primary hyperparathyroidism matched for serum calcium, creatinine clearance and vitamin D status (assessed by serum concentrations of 25 hydroxyvitamin D). Vitamin D metabolites were also measured in 16 normocalcaemic relatives of patients with FHH. The serum concentration of 24,25 dihydroxycholecalciferol was appropriate for the prevailing 25 hydroxyvitamin D and no difference was found between groups. The serum concentration of 1,25 dihydroxycholecalciferol was significantly greater in primary hyperparathyroidism (P less than 0.0005) compared with patients with FHH and their normocalcaemic relatives. TMP/GFR was reduced in both primary hyperparathyroidism (0.53 +/- 0.12 mmol/l GF, mean +/- SEM) and FHH (0.86 +/- 0.14 mmol/l GF). Patients with primary hyperparathyroidism showed an increase in NcAMP output in the urine (38.5 +/- 16 mmol/l GF) which was significantly greater (P less than 0.0001) than the normal NcAMP (13.5 +/- 9.2 nmol/l GF) found in FHH. CaE was low in FHH indicating increased renal tubular reabsorption of calcium. It is concluded that there is no abnormality of vitamin D metabolism in FHH comparable with the changes observed in primary hyperparathyroidism. It is suggested that the biochemical abnormalities in FHH cannot be explained solely upon an increased sensitivity of the renal tubules to the effects of endogenous parathyroid hormone.
 ...
PMID:Familial hypocalciuric hypercalcaemia: observations on vitamin D metabolism and parathyroid function. 631 24

We examined parathyroid gland function in 47 patients with idiopathic hypercalciuria in an effort to determine whether serum levels of parathyroid hormone (PTH) and/or urinary excretion of cyclic adenosine monophosphate (cyclic AMP) can discriminate between the various forms of hypercalciuria. Although we could separate our 47 patients into two groups, 21 patients with renal hypercalciuria (RH) and 15 patients with absorptive hypercalciuria (AH), there remained a group of 11 patients who did not exactly correspond to either group. Basal serum PTH was normal in the two groups: for RH, 10.32 +/- 0.93; for AH, 11.43 +/- 1.10 microliter Eq/ml. Similarly, urinary cyclic AMP did not differ between the two groups: for RH, 4.88 +/- 0.5; for AH, 4.87 +/- 0.55 nmoles/dl/min GFR. Moreover, the response of the parathyroid glands to acute hypocalcemia produced by intravenous infusion of EDTA was not different among patients with AH, RH, and control subjects. Only one patient showed a marked increase of serum PTH in response to acute hypocalcemia, and the bone biopsy revealed increased osteoclastic resorption. In conclusion, our data show that serum levels of PTH and urinary cyclic AMP do not differentiate between the various forms of idiopathic hypercalciuria. The EDTA test demonstrated that secondary hyperparathyroidism is very uncommon in these patients.
 ...
PMID:Absence of secondary hyperparathyroidism in most patients with renal hypercalciuria. 633 Apr 24

Aluminum (Al) may cause both osteomalacia and encephalopathy in dialysis patients. Little is known about the biology of Al. This study examined the initial distribution kinetics of Al and its biological effects after injections of 1 mg/kg/day into dogs for 3 to 5 weeks. Following one intravenous dose, the plasma half-life (x +/- SE) was 276 +/- 51.8 min, with an apparent volume of distribution of 1.30 +/- 0.17 liters or 5.90 +/- 0.30% body wt; 10 to 21% of administered Al was excreted in the urine over 150 min, and the renal contribution to plasma clearance of Al correlated with GFR (r = 0.77, P less than 0.05). The total plasma clearance of Al (4.43 +/- 2.83 ml/min) exceeded the renal contribution to plasma clearance (1.94 +/- 0.36 ml/min) in each dog, and in only two instances did the renal contribution reach 50% of total plasma clearance. Serum calcium rose from 9.4 +/- 0.2 to 11.1 +/- 0.3 mg/dl and immunoreactive parathyroid hormone (iPTH) fell by 27 +/- 4% following one Al injection. With repeated Al injections, serum calcium increased from baseline levels of 10.2 +/- 0.07 mg/dl to 11.1 +/- 0.22 and 11.3 +/- 0.46 mg/dl after 1 and 2 weeks, respectively. Renal function declined in all dogs, and serum creatinine exceeded 3.5 mg/dl in four; over the 5 weeks of study, serum calcium correlated with serum creatinine (r = 0.91, P less than 0.001). Liver, kidney, and spleen showed the highest tissue content of Al, and there was substantial uptake by bone; the parathyroid content of Al was modest.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Parenteral aluminum administration in the dog: I. Plasma kinetics, tissue levels, calcium metabolism, and parathyroid hormone. 642 8

In hypoparathyroidism the absence of parathyroid hormone leads to a reduction in the absorption of calcium by renal tubular cells. In spite of treatment with vitamin D, hypercalciuria persists and normocalcaemia can only be maintained by providing the kidney with a large load of calcium. Thiazide diuretics enhance tubular calcium reabsorption and it has been suggested that they can be used as an alternative to vitamin D. Bendrofluazide in a dose of 10 mg daily was given to 9 patients with severe hypoparathyroidism in addition to their usual treatment with calcium and vitamin D. Following the introduction of Bendrofluazide the calculated renal threshold for calcium reabsorption (TmCa/GFR) increased by a mean value of 0.14 mmol/l, and the mean rise in serum calcium was 0.13 mmol/l. This increase was due to a direct effect of the drug and was not caused by salt restriction or changes in glomerular filtration rate. The rise in serum calcium is modest compared to the rise following the introduction of vitamin D and except for patients with mild hypoparathyroidism, thiazides are not an alternative to vitamin D. They may however reduce the oral calcium load required to maintain normocalcaemia.
 ...
PMID:Effect of bendrofluazide on calcium reabsorption in hypoparathyroidism. 648 26

The effects of pharmacologic doses of synthetic salmon calcitonin on the renal tubular capacity of phosphate (Pi) transport were determined in the presence and absence of maximally phosphaturic doses of parathyroid hormone (PTH). Thyroparathyroidectomized rats were given graded infusions of Pi (1, 2, and 3 mumol/min) to prevent the hypophosphatemic effects of calcitonin and to determine the maximum transport of Pi for the kidney (TmPi/GFR). The maximum transport of Pi for the rats treated with calcitonin was 2.46 +/- 0.27 mumol/ml. This value was significantly less than that of 3.88 +/- 0.32 mumol/ml (P less than 0.05) for the control animals but was significantly greater than the maximum transport of Pi of 1.16 +/- 0.05 mumol/ml (P less than 0.05) for the rats treated with PTH. Furthermore, there was no significant difference between the maximum transport of Pi for the rats treated with PTH and that of 1.04 +/- 0.05 mumol/ml for the rats treated with PTH plus calcitonin. We conclude that pharmacologic doses of calcitonin decrease the tubular capacity for Pi reabsorption of the kidney and that the effect is significantly smaller than that of maximally phosphaturic doses of PTH.
 ...
PMID:Calcitonin decreases the renal tubular capacity for phosphate reabsorption. 661 73

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)
 ...
PMID:Influence of magnesium supplementation on bone turnover in the normal young mouse. 665 50

The renal handling of inorganic phosphate was measured in 17 idiopathic nephrolithiasis patients with normal glomerular filtration rate and effective renal plasma flow. TmPO4/GFR was less than 2.5 mg/dl in nine subjects (Group I) and greater than or equal to 2.5 in eight (Group II). The former had serum PO4 of 2.5 +/- 0.13 mg/dl and the latter, 3.5 +/- 0.11 mg/dl (p less than 0.01). Four in Group I and five in Group II were hypercalciuric. There was no significant difference in the serum parathyroid hormone and 1,25(OH)2D3 between the two groups. However, renal tubular functions were abnormal in both groups. The low TmPO4/GFR in 53 per cent of the patients is another manifestation of tubular functional abnormality seen in idiopathic nephrolithiasis.
 ...
PMID:Renal threshold phosphate concentration in patients with idiopathic nephrolithiasis: correlations with tubular functions, serum parathyroid hormone and 1,25(OH)2D3. 668 10


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>