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)

In chronic uremia, the clinical disorders o calcium and phosphorus metabolism are influenced by the following factors: (1) intestinal absorption of calcium and phosphate, resulting in a negative calcium and phosphate balance at normal dietary intakes; (2) renal handling of calcium and phosphate: the fractional transport of calcium (the isoosmotic reabsorption taking place in the proximal tubule) is not affected by GFR modifications, whereas the Tm-limited reabsorption is severely impaired; the external phosphate balance is kept, even in the presence of a reduced nephron population, by means of a proportional reduction in TmPO4 values; (3) physiochemical state and turnover of body calcium and phosphate: in uremic patients, the distribution spaces, turnover rate of calcium, and accretion rate of bones are increased in comparison with the controls; the calcium infusion test in patients with renal osteomalacia is followed by a regular increase in plasma [PO4], whereas a significant decrease is observed in patients with renal osteitis fibrosa, due to the extreme 'avidity' of bones for calcium phosphate; the role of hyperphosphatemia is critical in keeping the plasma [Ca] lower than the expected values for a given metabolic set; moreover, an increased cell uptake of phosphate could counteract to some extent the reduced renal clearance of phosphate; (4) structural and biochemical modifications of bone tissue: uremic osteodystrophy consists mainly of two components: (a) osteomalacia, with osteoid excess, disappearance of the calcification front, and diffuse pathologic mineralization, and (b) osteitis fibrosa, with severe resorption of normally mineralized bone, slight osteoid excess, and almost normal calcification front; (5) hormonal factors: chronic stimulation of parathyroid glands may result in suppressible or even autonomous hyperparathyroidism. As to vitamin D, it has been suggested that the uremic kidney is not able to synthesize the 1,25-di-OH-cholecalciferol, the active metabolite of vitamin D: this results in an impaired intestinal absorption of calcium. On the contrary, the role of calcitonin in chronic uremia is still uncertain, since low values of plasma [Ca] are usually observed.
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PMID:Calcium and phosphorus metabolism in chronic uremia. 109 55

We investigated the tubular action of endothelin in rat nephron segments. The effects of endothelin on arginine vasopressin (AVP)-, parathyroid hormone-, glucagon-, calcitonin-, and isoproterenol-dependent cAMP accumulation were studied. The following nephron segments were microdissected: glomerulus (Gl), proximal convoluted tubule (PCT), cortical and medullary thick ascending limbs of Henle's loop (cTAL and mTAL, respectively), cortical collecting duct (CCD), outer medullary collecting duct (OMCD), and inner medullary collecting duct (IMCD). Endothelin dose dependently (10(-8)-10(-10)M) inhibited AVP-dependent cAMP accumulation in CCD, OMCD, and IMCD. This effect was independent of the presence or absence of phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine, Ca channel blocker nicardipine, or indomethacin, but was abolished in the presence of protein kinase C inhibitor H-7. Protein kinase C stimulator dioctanoyl glycerol mimicked the effect of endothelin. On the other hand, endothelin had no inhibitory effect on AVP-dependent cAMP accumulation in cTAL or mTAL, parathyroid hormone-dependent cAMP accumulation in Gl and PCT, or glucagon-, calcitonin-, and isoprotereol-dependent cAMP accumulation in OMCD. We conclude that endothelin specifically inhibits AVP-dependent cAMP accumulation in CCD, OMCD, and IMCD through activating protein kinase C. This effect possibly has a role in maintaining urine volume to counteract the decrease in GFR caused by endothelin itself.
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PMID:Effects of endothelin on peptide-dependent cyclic adenosine monophosphate accumulation along the nephron segments of the rat. 169 79

The kidneys account for approximately two-thirds of the metabolism of calcitonin, but relatively little is known regarding the details thereof. To further characterize this process, we examined the renal handling and metabolism of human calcitonin (hCT) by the isolated perfused rat kidney. We also studied the degradation of radiolabeled salmon calcitonin (sCT) by subcellular fractions prepared from isolated rabbit proximal tubules. The total renal (organ) clearance of immunoreactive hCT by the isolated kidney was 1.96 +/- 0.18 ml/min. This was independent of the perfusate total calcium concentration from 5.5 to 10.2 mg/dl. Total renal clearance exceeded the glomerular filtration rate (GFR, 0.68 +/- 0.05 ml/min), indicating filtration-independent removal. Urinary calcitonin clearance as a fraction of GFR averaged 2.6%. Gel filtration chromatography of medium from isolated kidneys perfused with 125I-labeled sCT showed the principal degradation products to be low molecular weight forms eluting with monoiodotyrosine. Intermediate size products were not detected. In the subcellular fractionation experiments, when carried out at pH 5.0, calcitonin hydrolysis exclusively followed the activities of the lysosomal enzyme N-acetyl-beta-glucosaminidase. Typically, at pH 7.5, 42% of total degradation occurred in the region of the brush-border enzyme alanyl aminopeptidase and 29% occurred in the region of the cytosolic enzyme phosphoglucomutase. Although 9% of the calcitonin-degrading activity was associated with basolateral membrane fractions, most of this activity could be accounted for by the presence of brush-border membranes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal metabolism of calcitonin. 283 22

Blood levels of glucose, insulin (IRI), Calcium (Ca), phosphorus (P), alkaline phosphatase (AP), osteocalcin (OC), parathyroid hormone (PTH), calcitonin (CT), 25-hydroxyvitamin D3 (25OHD3), 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) and urinary excretion of Ca (Ca/Cr), P (TmP/GFR), hydroxyproline (OH-P/Cr) and cyclic AMP (cAMP/GFR) were determined in 16 obese children, aged 8 to 11 years, on a diet rich in calories and carbohydrates and in 15 controls of the same age. Blood glucose, IRI, Ca, P, PTH and CT were also determined in both groups of subjects, during an oral glucose tolerance test (OGTT). In basal conditions glucose, IRI, AP, OC, PTH, CT and 1,25(OH)2D3 levels were significantly higher, and 25OHD3 levels lower, in obese children than in controls. Urinary Ca/Cr, TmP/GFR were lower in obese than in non obese children, while OH-P/Cr and cAMP/GFR were higher. Bone mineral content (BMC), measured by photon absorptiometry, and BMC/bone width ratio were lower in obese than in non obese children. During OGTT serum Ca and P decreased and serum PTH and CT increased less in obese than in non obese children. In obese children receiving a diet with high carbohydrate content, an alteration of mineral metabolism occurred, characterized by secondary increase of PTH and 1,25(OH)2D3. Ca decreased and PTH and CT increased less markedly during OGTT.
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PMID:Mineral metabolism in obese children. 233 52

Twelve children (5 males and 7 females, mean age 8.5 years) with idiopathic hypercalciuria (IH), 9 with absorptive IH (1 type I and 8 type II) and 3 with renal IH, were followed in our outpatient hospital from September 1981 to March 1987. Mean (+/- 1 SD) free diet calciuria was 5.9 +/- 1.66 mg/kg/day. Diagnosis was made measuring urinary Ca/Cr ratio after controlled diet and calcium loading test. Serum parathormone (PTH), 1,25-(OH)2-D3 and calcitonin (TCT) values and renal threshold phosphate concentration (TmPO4/GFR) were also studied. Serum PTH was normal in all children. Serum TCT levels were significantly increased in the patients with IH compared with controls (p less than 0.001) while serum 1,25-(OH)2-D3 levels were significantly reduced compared with controls (p less than 0.001).
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PMID:Increased serum calcitonin, reduced serum 1,25-(OH)2-vitamin D and normal parathormone concentrations in idiopathic hypercalciuria. 325 62

We have studied the effects of bovine parathyroid hormone (PTH) and salmon calcitonin (CT) on plasma calcium (Ca) and phosphate levels and on renal function in intact and parathyroidectomized (PTX) chickens, using a simple technique that separates urine from feces. In immature males and egg-laying females, the intravenous injection of PTH (10-20 IU/kg body wt) caused a transient fall in plasma Ca and phosphate levels, which was followed by an increase to a maximal level 20-30 min after the injection. By contrast, adult cockerels seldom showed any variation in plasma Ca or phosphate levels. In all birds, treatment with PTH increased glomerular filtration rate, urine flow rate, phosphate clearance, and Ca clearance, although this peaked later and remained elevated longer than did the phosphate clearance. The infusion of CT (1-20 U/kg over 30 min) caused a significant decrease in plasma Ca only in PTX or partially PTX chickens. All birds showed an increased GFR, urine volume, and urinary Ca excretion. In parathyroid-intact birds, the renal clearance of phosphate also increased, but peaked later and remained high longer than did Ca clearance, suggesting an increased endogenous PTH secretion. We conclude that plasma Ca and phosphate homeostasis in the chicken, as in the mammal, depends on a balanced release of PTH and CT. However, in the chicken, the response time is faster, thus minimizing the fluctuations in plasma Ca and phosphate levels resulting from exogenous hormone administration. This rapid homeostatic response is less effective when Ca demands by the body are high as in the growing or laying bird.
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PMID:Changes in renal function of the chicken associated with calcitonin and parathyroid hormone. 360 10

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

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 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.
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PMID:Calcitonin decreases the renal tubular capacity for phosphate reabsorption. 661 73

Secondary hyperparathyroidism (SHP) is a well documented finding even in the early stages of chronic renal failure (CRF). A sigmoidal relationship, fitting a four parameter model, links PTH secretion rate and calcium concentration changes. To our knowledge, PTH secretory parameters have only been studied in uremic patients who are in dialysis treatment. As a result of these studies, a possible role for derangement in setpoint values (that is, the serum calcium concentration corresponding to the mid-range value on the sigmoidal curve) has been suggested in the pathogenesis of SHP in CRF. Our study was undertaken to gain insight into the calcium-PTH relationship curve in the first course of CRF and to assess whether a change in any of the secretory parameters is related to the beginning of SHP. We studied 27 male renal patients with a variable degree of renal function (creatinine clearance 12 to 164 ml/min) and 9 control subjects. In all patients and controls the following parameters were evaluated: (1) basal 1,25(OH)2 vitamin D, 25(OH)vitamin D, calcitonin (CT), intact PTH; (2) GFR by Cr51EDTA clearance; (3) the sigmoidal PTH-ionized calcium relation curve, by means of a hypocalcemic stimulating test (Na2-EDTA 37 mg/kg body weight/2 hr) and a hypercalcemic test (Ca gluconate giving 8 mg/kg of body weight/2 hr of Ca element), performed on two consecutive days.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Direct in vivo assessment of parathyroid hormone-calcium relationship curve in renal patients. 770 31


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