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)

The relation between urinary sodium excretion (NaE) and renal tubular calcium reabsorption (TmCa/GFR) was assessed in patients with hypercalcaemia associated with malignancy and primary hyperparathyroidism. On acute saline loading of seven normally hydrated patients with primary hyperparathyroidism and five patients with malignancy, raised values of TmCa/GFR were reduced to normal in most cases, in association with increases in NaE. The reduction in TmCa/GFR, which occurred, may have been due to a reduction in proximal tubular calcium reabsorption associated with sodium: this would have obscured the effect of humorally mediated increases in distal tubular calcium reabsorption, which are stimulated either by parathyroid hormone or by a putative humoral mediator in hypercalcaemia of malignancy. In patients who were normally hydrated NaE and TmCa/GFR were not significantly correlated. When data were included from patients who were dehydrated and from those undergoing acute saline loading, significant inverse correlations between NaE and TmCa/GFR were observed both in primary hyperparathyroidism (r = -0.49; p less than 0.02) and malignancy (r = -0.60; p less than 0.001). In clinical practice changes in TmCa/GFR associated with sodium seem to be of minor importance under normal circumstances, but they become evident at the upper and lower extremes of urinary sodium excretion. In clinical studies of renal calcium handling urinary sodium excretion must also be assessed, as interpreting TmCa/GFR data is difficult in states of excessive sodium loading or depletion.
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PMID:Influence of urinary sodium excretion on the clinical assessment of renal tubular calcium reabsorption in hypercalcaemic man. 372 17

Twenty patients with malignant hypercalcemia were treated with aminohydroxypropylidene bisphosphonate (AHPrBP, previously APD) a potent inhibitor of osteoclast-mediated bone resorption. To assess the efficacy of oral vs intravenous therapy, the patients were divided into two groups: group A received AHPrBP intravenously (30 mg/day), and group B received the drug orally (1200 mg/day) for 6 days. In both groups all the patients responded to AHPrBP with a rapid decrease in plasma calcium concentration after a mean time lag of 1 day. Within 9 days plasma calcium concentration fell from 3.42 +/- 0.13 (mean +/- SEM) to 2.26 +/- 0.13 mmol/l in group A and from 3.28 +/- 0.12 to 2.24 +/- 0.09 mmol/l in group B. There was no significant difference in plasma Ca level between both groups on days 4, 6, and 9, and plasma Ca was within the normal range in all patients on day 9. On both treatment regimens urinary calcium excretion fell dramatically and similarly. Plasma phosphate concentration decreased significantly on AHPrBP in both groups of patients, reaching values slightly below the normal range from day 4 to day 9. TmP/GFR decreased progressively on AHPrBP. However, this decrement was significant at day 6 only. Plasma parathyroid hormone concentration rose significantly in both groups from day 4 to day 9. We conclude that at the doses used in the present study treatment of tumor-induced hypercalcemia with AHPrBP is equally effective whether given orally or intravenously.
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PMID:Oral versus intravenous AHPrBP (APD) in the treatment of hypercalcemia of malignancy. 376 3

The aging kidney suffers reduction both in mass and in glomerular filtration rate. These changes may be totally or partially due to atherosclerosis and hypertension, which reduce renal blood flow. Superimposed on these processes, and perhaps responsible for primary loss of renal mass irrespective of renal vascular disease, is glomerular damage and involution that is a consequence of adaptive increases in glomerular perfusion pressure that occurs as the number of nephrons decline with age. The data available at this time do not allow us to distinguish between these two potential mechanisms of renal senescence. The decline in GFR is in turn responsible for reduced renal acidification and the reduced renal clearance of drugs that are normally removed by the kidney. Certain renal functions, however, are depressed to a greater extent than is GFR. Both the ability to maximally dilute the urine and to maximally concentrate it are controlled by serum ADH concentrations and by the action of that hormone on the collecting duct. Aged rats do not maximally secrete ADH under conditions of dehydration and the effect of ADH on the kidney is also attenuated. Elderly humans also cannot maximally suppress ADH secretion when serum osmolality is reduced. Likewise, the renin-angiotensin-aldosterone axis is poorly responsive to volume depletion in aging subjects. As a result, elderly individuals cannot maximally retain sodium under conditions of plasma volume contraction out of proportion to reduction in GFR. The kidney is the site of vitamin D1 hydroxylation. Hydroxylation of vitamin D is reduced out of proportion to any reduction in GFR in the rat. There are no data as yet available on the effect of aging and the production of erythropoietin, a principal regulator of red blood cell mass. Neither are there data available on changes that might occur with advancing age in the ability of the aging kidney to metabolize various hormones, such as parathyroid hormone, glucagon, and insulin. The mechanisms and the full biochemical and physiologic consequences of renal senescence remain to be fully elucidated.
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PMID:The aging kidney. 391

The change in phosphate metabolism after surgical correction of Cushing's syndrome was examined in 3 consecutive patients. During replacement therapy with hydrocortisone after successful operation, when serum cortisol levels were undetectable in the early morning, serum inorganic phosphate (PI) levels increased gradually with reduction of the replacement dose of hydrocortisone. Hyperphosphatemia developed 3-7 weeks after surgery when the patients was given 20-25 mg/day of hydrocortisone, and 2 patients demonstrated clinical manifestation of glucocorticoid deficiency. During these periods, there was a significant inverse relationship between serum Pi and the replacement dose of hydrocortisone in each patient. Thereafter, serum Pi started to decrease despite administration of the same amount of hydrocortisone and became normal by 26 weeks after surgery. Daily urinary Pi excretion was decreased compared to that before surgery, and the maximal tubular reabsorptive capacity for Pi (TmP/GFR) changed in parallel with serum Pi in all patients. Serum immunoreactive parathyroid hormone and urinary 3',5'-cyclic adenosine monophosphate excretion remained unchanged during the postoperative course. The serum concentrations of 1,25-dihydroxyvitamin D decreased from preoperatively normal values to subnormal levels after surgery with development of hyperphosphatemia and returned to normal with the fall of serum Pi. In summary, the present study demonstrates that surgical correction of hypercortisolism is accompanied by a transient hyperphosphatemia during the postoperative periods, probably due to increased renal Pi reabsorption, and that parameters of parathyroid function do not change during these periods. These results suggest that glucocorticoid has a direct action on Pi metabolism and that during the replacement therapy after surgical treatment of hypercortisolism hyperphosphatemia may develop due to relative glucocorticoid deficiency.
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PMID:Hyperphosphatemia after surgical correction of hypercortisolism in patients with Cushing's syndrome. 396 15

In order to evaluate the sex difference in the renal handling of inorganic phosphate (Pi) in the rat we performed clearance experiments using intact, thyroparathyroidectomized (TPTX), oophorectomized (OophX) and orchiectomized (OrchX) rats. During stepwise elevation of the Pi concentration in plasma (Pi-titration) to about 6 mmol/l the reabsorptive mechanism of Pi was saturated. The ratio Pi-reabs./GFR in intact males was higher than in females. A significant difference in this parameter was also observed in thyroparathyroidectomized rats: in females this value was 3.47 +/- 0.13, and in males it was 4.54 +/- 0.37 mumol/ml (P less than 0.001). Oophorectomy in the absence of parathyroid hormone (PTH) increased Pi-reabs./GFR from 3.18 +/- 0.36 to 4.12 +/- 0.24 mumol/ml (P less than 0.001); however, orchiectomy did not significantly change the reabsorption of Pi. In conclusion, the present results demonstrate a PTH independent sex difference in the renal handling of inorganic phosphate and are consistent with the hypothesis that estrogens may play a dominant role in this differentiation.
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PMID:PTH independent sex difference in renal handling of inorganic phosphate in the rat: effect of oophorectomy. 401 7

Previous studies have shown that the adaptive response of tubular inorganic phosphate (Pi) transport to Pi deprivation is detectable in the whole kidney 24 h after switching rats from a high (HPD) to a low (LPD) Pi diet. In the present work we report on a more rapid adaptive response of the sodium (Na)-dependent Pi transport system located in the luminal membrane of the proximal tubule and its relation with changes in phosphatemia an parathyroid hormone status. Rats were fed HPD and trained to eat their daily ration within 1 h. After two weeks of equilibration half of the animals received a single LPD ration. 1, 2 and 4 h after the end of food consumption the animals were either sacrificed for renal cortical brush border membrane vesicle (BBMV) isolation or used for determining plasma Pi concentration, urinary excretion of Pi and cAMP. The results indicate that 2 and 4 h after the end of feeding, the Na-dependent Pi transport in BBMV was stimulated by 70 and 140% respectively in intact rats exposed for the first time to LPD. This response was preceded by a significant fall in plasma Pi concentration (HPD: 2.46 +/- 0.03, LPD: 2.04 +/- 0.05 mM), in the urinary excretion of Pi (HPD: 899.0 +/- 68.1; LPD: 6.5 +/- 3.3 mumol/ml GFR) and cAMP (HPD: 76.9 +/- 7.4, LPD: 48.2 +/- 1.4 pmol/ml GF). This last result suggested a rapid inhibition of PTH after one single LPD feeding.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanism of rapid phosphate (Pi) transport adaptation to a single low Pi meal in rat renal brush border membrane. 403 69

The hypotensive, hypercalcemic, and hyperphosphaturic responses to bovine synthetic 1-34 amino acid parathyroid hormone [bPTH(1-34)] were simultaneously evaluated in anesthetized laying hens, and compared to the same responses to oxidized (0.3% hydrogen peroxide) bPTH(1-34) prepared from the same commercial batch of hormone. The oxidized and nonoxidized hormones were administered intravenously into separate groups of animals, which were also receiving a constant intravenous infusion of inulin and p-aminohippuric acid (PAH) to serve as renal clearance test markers. bPTH(1-34) caused a 33.25 +/- 7.05 mm Hg decrease in mean arterial blood pressure. The corresponding change in response to the oxidized hormone preparation was a 10.75 +/- 1.49 mm Hg decrease, a significant reduction in hypotensive activity compared to the intact hormone. In contrast, oxidation had no influence on the hypercalcemic or hyperphosphaturic (relative clearance of phosphate, CPO4/CIn) responses to bPTH(1-34), both preparations causing significant and parallel increases in these variables. Both hormone preparations also caused increases in urine flow rate, GFR, CPAH, CCa/CIn, CK/CIn, CNa/CIn, and urine pH. However, on the basis of percentage change from the respective control periods, only CNa/CIn and urine pH showed significant differences between the two hormone preparations, with the intact hormone causing greater natriuresis and urine alkalinization than the oxidized hormone. The failure of peroxide oxidation to significantly affect the renal hyperphosphaturic response to bPTH(1-34) in chickens contrasts with results reported on mammalian species, and may be related to differences in the mechanism of renal phosphate transport between these groups.
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PMID:Avian renal responses to oxidized and nonoxidized bPTH(1-34). 404 23

The renal handling of phosphorus was evaluated in rats with acute renal failure (ARF) induced by injection of mercuric chloride (HgCl(2)). Clearances of endogenous creatinine (Ccr) and of phosphorus (Cp) were measured in the following groups: 1. Intact animals (control); 2. Parathyroidectomized rats (PTX) with normal kidney function (PTX control); 3. Animals with mercury-induced acute renal failure (Hg-ARF); 4. PTX rats with Hg-ARF; 5. Rats with Hg-ARF maintained normophosphatemic with dietary phosphate restriction; 6. Animals with oliguric ARF following renal artery constriction; 7. Rats with unilateral Hg-ARF. In addition, radioinulin clearances were measured in 6 normal and in 14 azotemic animals and correlated with simultaneously recorded endogenous Ccr. Radioinulin clearance was also used as an estimate of GFR (glomerular filtration rate) in the animals of group 7. The Cp/GFR in the intact animals (group 1) was 0.25 +/-0.06 (mean +/-SD). PTX (group 2) caused a subsequent decrease in Cp/GFR to 0.11 +/-0.04 P < 0.0005. The ARF animals in group 3 were classified either as oliguric (U(vol) [urine volume] <2 ml/24 hr, Ccr 0.008 +/-0.005 ml/min) or nonoliguric (V(vol) >2 ml/24 hr, Ccr 0.136 +/-0.12). The Cp/GFR in the oliguric animals (0.16 +/-0.09) was lower than that in group 1, P < 0.0005, and failed to increase following administration of exogenous parathyroid hormone. The Cp/GFR in the oliguric animals in groups 5 and 7 was also lower than the clearance ratio in group 1, 0.030 +/-0.08 and 0.077 +/-0.006, respectively. In the nonoliguric ARF animals of group 3 the Cp/GFR (0.94 +/-0.29) was higher than that in group 1, P < 0.0005. In the nonoliguric ARF animals of group 4 the Cp/GFR 0.27 +/-0.08 did not differ from the clearance ratio in group 1, however it was higher than that in the PTX animals (group 2) P < 0.0005. Cp/GFR in the nonoliguric animals of group 5 was not different from that in the nonoliguric rats of group 3. In the animals with nonoliguric unilateral Hg-ARF Cp/GFR on the affected side 0.51 +/-0.16 was higher than that on the control (contralateral) side, 0.23 +/-0.07, P < 0.0005. These results indicate that the low Cp/GFR observed in the oliguric ARF animals was not related to the level of circulating parathyroid hormone nor to the presence or absence of azotemia but probably was due to a reduced renal cortical perfusion. The high Cp/GFR in the nonoliguric ARF animals could be explained by secondary hyperparathyroidism and impaired phosphorus reabsorption due to tubular injury.
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PMID:Renal handling of phosphorus in oliguric and nonoliguric mercury-induced acute renal failure in rats. 509 19

A study of 28 consecutively admitted patients with active acromegaly revealed the following results with regards to calcium and phosphate metabolism. When compared with controls, there was an increase in serum calcium levels corrected for total protein, urinary calcium was increased, but the tubular re-absorption of calcium was normal. There was a negative correlation between the urinary cAMP and calcium excretion indicating that hyperabsorption of calcium from the gut is the cause of the increased urinary calcium excretion. Serum phosphate values were increased in acromegalics and correlated well with TmP/GFR which was also increased. Immunoreactive parathyroid hormone (PTH) was increased in 5 patients, three of whom had hypercalcaemia. In the remaining patients the PTH values were scattered within the normal range. The urinary cAMP/creatinine ratio was increased in acromegalics, but most of this difference was abolished when urinary cAMP was expressed relative to 100 ml of glomerulus filtrate. It is concluded that parathyroid hyperactivity is a feature of acromegaly.
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PMID:Calcium and phosphate metabolism in acromegaly. 625 98

The ratio of maximum rate of renal tubular reabsorption of phosphate to glomerular filtration rate (TmPO4/GFR) was determined in 546 schoolchildren, aged between 6 and 17.9 years, using the nomogram of Walton and Bijvoet.1 TmPO4/GFR correlated with chronological age in girls and boys and in each remained significantly higher than in adults. TmPO4/GFR in the children correlated neither with fasting serum immunoreactive calcitonin and parathyroid hormone levels nor with the urinary cyclic AMP excretion. The study showed a parallel decrease in TmPO4/GFR, excretion of total hydroxyproline and serum alkaline phosphatase activities after puberty, with a significant relationship of both these indices of bone turnover to TmPO4/GFR values. This indicates that the high renal phosphate threshold of children may be an important factor for bone mineralisation by providing high extracellular inorganic phosphate concentrations during normal growth.
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PMID:Renal threshold phosphate concentration (TmPO4/GFR). 628 Jun 22


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