Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0235394 (wasting)
 8,040 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1 alpha-hydroxycholecalciferol was tried as a therapy for renal phosphate wasting in kidney allograft recipients with normal parathyroid gland activity. During a 3-week period of treatment we observed a significant rise in renal phosphate threshold concentrations and plasma phosphate levels paralleled by a significant decrease in serum immunoreactive parathyroid hormone levels and a significant increase in intestinal calcium absorption. It is suggested that 1 alpha-hydroxycholecalciferol acts on renal phosphate handling in a dual fashion: one is by suppression of parathyroid hormone and the other by restoration of 1,25-dihydroxycholecalciferol levels to an appropriate level.
 ...
PMID:Renal phosphate wasting after successful kidney transplantation: 1-alpha vitamin D therapy in patients with normal parathyroid gland activity. 703 94

The components of calcium and magnesium balance and the factors responsible for the maintenance of the serum concentration of these cations are reviewed. Within this framework, the causes and treatment of disturbances of the serum concentration are discussed. Hypercalcemia is usually a reflection of increased bone resorption and/or gut absorption with the kidney playing a secondary role. Hypocalcemia is usually due to either a disturbance in the parathyroid hormone-adenylate cyclase system or a disturbance in vitamin D metabolism. As vitamin D is required for expression of the action of PTH at bone and as PTH is a prime regulator of vitamin D metabolism, the absence of either component results in important disturbances in calcium balance. In contrast to calcium homeostasis, the kidney plays a major role in the determination and regulation of serum magnesium. The major causes of hypermagnesemia therefore are associated with loss of renal function, and hypomagnesemia is frequently due to renal magnesium wasting.
 ...
PMID:Disorders of calcium and magnesium homeostasis. 703 37

Clinical and pathophysiologic studies were performed in five unrelated children with primary distal renal tubular acidosis who were diagnosed during infancy and followed for 3 to 9 1/2 years. All patients had permanent defects in hydrogen ion secretion, sodium reabsorption, and concentrating capacity. A transient, age-related, proximal tubular defect in sodium and bicarbonate reabsorption was also present. Renal bicarbonate wasting was mainly observed during the first years of life and progressively decreased with advancing age. Glomerular filtration rate remained within normal limits. Following sustained therapy with sodium and potassium bicarbonate, the patients had optimal growth, arrest of progression of nephrocalcinosis, and lack of other characteristic features of the disease with the exception of polyuria. Dosage of alkali was mainly determined by the magnitude of the renal bicarbonate loss and decreased progressively from a maximum of 3.9 to 10.0 mEq/kg/day during the first year of life to about 3 mEq/kg/day at or beyond 6 years of age. The total dosage of alkali required could be derived by the sum of the urinary excretion of bicarbonate plus 2 mEq/kg/day, which represents mean endogenous acid production. Although calciuria was normal when metabolic acidosis was corrected, patients with higher urinary sodium excretion had higher urinary excretion of calcium and thus were at greater risk of developing nephrocalcinosis if therapy was not carefully controlled.
 ...
PMID:Natural history of primary distal renal tubular acidosis treated since infancy. 713 Nov 38

Of 100 consecutive patients with recurrent renal calculi, 43 had idiopathic hypercalciuria (IH) on outpatient evaluation. Hypercalciuria was classified as diet-dependent or fasting; all patients had normal serum iPTH and urinary cyclic AMP, and serum phosphate and TmPO4/GFR were reduced in IH compared to normocalciuric stone formers. In 16 patients with IH, clearance studies revealed an elevated urine flow are factored for GFR (V/GFR) as compared with normal controls (p less than 0.05). In 12 patients, serum PTH was normally suppressed by calcium infusion but TmPO4/GFR was persistently reduced. Acute and chronic phosphate administration significantly reduced urine calcium excretion but did not correct the abnormal V/GFR. We conclude that in IH of both the fasting and the diet-dependent type, there is a defect in the proximal tubular reabsorption of sodium and fluid as well as PTH-independent tubular phosphate wasting. The proximal tubular defect is not a consequence of hypercalciuria nor of phosphate depletion but may be a cause of these abnormalities.
 ...
PMID:Proximal tubular defects in idiopathic hypercalciuria: resistance to phosphate administration. 716 88

isoniazid, 300 mg daily for 14 days, reduced serum calcium and phosphate levels (P less than 0.001) in eight healthy subjects. After a single dose of isoniazid the concentration of 1 alpha-,25-dihydroxyvitamin D, the most active metabolite of vitamin D, fell by 47% (P less than 0.01) and was reduced throughout the study. Levels of 25-hydroxyvitamin D, the major circulating form of the vitamin, declined in all subjects and to below normal range in six (P less than 0.01). Parathyroid hormone levels rose by 36% (P less than 0.01) in response to the relative hypocalcemia produced. Isoniazid inhibited hepatic mixed-function oxidase activity, as evidenced by a reduction in antipyrine and cortisol oxidation, and a similar inhibition of the hepatic 25-hydroxylase and renal 1 alpha-hydroxylase would explain the reduction in the corresponding vitamin D metabolites. This perturbation of vitamin D metabolism differs from the vitamin D wasting effects after rifampicin. Patients with tuberculosis treated with isoniazid and rifampicin may show changes similar to those shown here in calcium and phosphate homeostasis and thus may be at risk of developing metabolic bone disorders.
 ...
PMID:Effect of isoniazid on vitamin D metabolism and hepatic monooxygenase activity. 727

Hypophosphatemic osteomalacia that remits after resection of a coexisting tumor has been described in 35 patients. Because the associated neoplasms have been of mesenchymal origin, it has been inferred that this tumor-induced osteomalacia syndrome is uniquely related to tumours of this derivation. However, in the present investigation we studied subjects with coincident hypophosphatemia and prostatic carcinoma to ascertain whether this endodermal malignancy causes the tumor-induced osteomalacia syndrome. The hypophosphatemic patients had renal phosphate wasting, gastrointestinal malabsorption of calcium and phosphate, and negative phosphate balance. Moreover, bone biopsies showed histomorphologic changes indicative of osteomalacia. Although widespread metastases precluded establishing the diagnosis of tumor-induced osteomalacia by resection of the tumor, a series of studied excluded alternate causes for the osteomalacia. Further, affected subjects had a normal serum concentration of 25-hydroxyvitamin D, 28.0 +/- 8.3 ng/mL, and serum 1,25-dihydroxyvitamin D levels were low, 15.0 +/- 1.0 pg/mL, characteristic of the tumor-induced osteomalacia syndrome. Thus, prostatic carcinoma, although an endodermal malignancy, may cause the tumor-induced osteomalacia syndrome.
 ...
PMID:Hypophosphatemic osteomalacia: association with prostatic carcinoma. 740 80

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.
 ...
PMID:Lack of evidence that cyclosporine treatment impairs calcium-phosphorus homeostasis and bone remodeling in normocalcemic long-term renal transplant recipients. 760 39

X-linked recessive nephrolithiasis (XRN) was described in a large kindred in which nephrolithiasis; proximal tubular dysfunction, proteinuria, nephrocalcinosis, and renal failure occur only in males. Carrier females are asymptomatic, but formal studies of them have not been done. The gene for XRN has been mapped to the pericentromeric region of the X chromosome, close to the loci for several eye disease genes. We studied six affected males, 13 carrier females, and 25 normal members of this family including 7 females whose genetic haplotype predicted them to be carriers. Studies were done in the Clinical Research Unit on a diet containing 400 mg of calcium and 2 g of sodium, and by an additional outpatient urine collection was obtained on a 1-g calcium intake. Hypercalciuria occurred in five of six affected males, 4 of 12 carrier females, and three of seven predicted carriers. Significant proteinuria was present in all affected males and in no other subjects. Low-molecular-weight proteinuria was present in all affected males: the excretion of alpha 1-microglobulin exceeded normal by 3- to 14-fold, of beta 2-microglobulin exceeded normal by 100- to 400-fold, and of retinol-binding protein exceeded normal by 1,000- to 3,000-fold. The excretion of these proteins was less strikingly elevated in carrier females, but the excretion of alpha 1-microglobulin was abnormal in 9 of 15 carriers, beta 2-microglobulin was abnormal in 12 of 15, and retinolbinding protein in was abnormal 12 of 13, and this pattern was similar in predicted carriers. The urinary concentrating ability was abnormal in four affected males with renal insufficiency but normal in all other subjects. Urinary wasting of potassium, phosphorous, and glucose occurred infrequently, and no subject was hypouricemic. Formal ophthalmologic studies were normal in five affected males. Thus, the most consistent urinary abnormalities in XRN are hypercalciuria and low-molecular-weight proteinuria, the latter of which appears to be a marker for the carrier state.
 ...
PMID:Characterization of carrier females and affected males with X-linked recessive nephrolithiasis. 770 83

The effect of maternal diabetes mellitus on renal calcium excretion in pregnant rats and their offspring has been examined in order to ascertain the role of the kidney in the disturbed calcium homeostasis of infants born to diabetic mothers. Diabetic pregnant (DP) rats exhibited severe hypercalciuria which greatly exceeded the urinary calcium losses (UCaV) in non-diabetic pregnant (CP) or non-pregnant diabetic (D) rats. Means +/- S.E.M. for UCaV at day 21 (mmol/24 h) were: DP = 1.12 +/- 0.09 (n = 7); CP = 0.06 +/- 0.01 (n = 7); D = 0.63 +/- 0.06 (n = 7) (P < 0.001 DP vs CP and DP vs D). The profile for urinary calcium excretion in the three groups was different from that of other measured ions. The degree of natriuresis, for example, was comparable in DP and D rats at all stages studied. Although magnesium output was significantly greater in DP than D rats on days 14 and 21, this appeared to result from an additive effect of the magnesiuresis seen when pregnancy and diabetes were studied separately. The marked renal calcium wasting of diabetic pregnancy will have implications for overall calcium balance in the mother. For example, an enhanced intestinal calcium absorption was seen in DP rats in the second half of gestation. Means +/- S.E.M. for day 21 (mmol/24 h) were: DP = 3.8 +/- 0.8 (n = 7); CP = 1.4 +/- 0.3 (n = 7); D = 1.6 +/- 0.3 (n = 7) (P < 0.05 DP vs CP and DP vs D).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:The effect of diabetes mellitus on urinary calcium excretion in pregnant rats and their offspring. 779 15

The influence of cardiac stunning on the oxidation of fatty acids and the oxidative phosphorylation in mitochondria was investigated. Rat hearts were perfused for 15 min according to the working mode with a Krebs-Henseleit buffer containing glucose (11 mM). The hearts were then maintained in normoxic conditions (C group) or subjected to a 15-min global no-flow normothermic ischemia followed by a 30-min reperfusion (R group). Throughout the perfusion, the aortic and coronary flows, and the heart rate and oxygen consumption were monitored. At the end of the perfusion procedure, a bolus of 1-14C palmitate was injected in the coronary arterial bed to evaluate the fatty acid oxidation. Two sub-populations of mitochondria were isolated from each heart by either mechanical (ME mitochondria) or enzymic (EE mitochondria) extraction and their respiration properties were evaluated. Furthermore, the mitochondrial energy production (ATP and creatine phosphate) was assessed. During ischemia, the aortic flow was suppressed and recovered only to approximately 50% of the preischemic value during reperfusion. This mechanical stunning was associated with an important reduction of the stroke volume (-37%, p < 0.01) and a slight decrease in heart rate (-20%, p < 0.001). At the end of reperfusion, the beta-oxidation rate constituted 55 +/- 1.7% of the cell palmitate and was similar to that assessed in the C group. The oxygen consumption was decreased to 216 +/- 31.0 microL O2/min/gww and the venous O2 concentration increased to 5.1 +/- 0.572 microL O2/mL (instead of 2.9 +/- 0.342 microL O2/mL in the C group), although due to large SD, only the latter was statistically significant. A decrease in metabolic efficiency (42 +/- 14.4 vs 106 +/- 16.8 mL/microL O2 in the C group) and an increase in palmitate oxidation to oxygen consumption ratio (77 +/- 10.1 vs 47.6 +/- 4.25% beta-oxidized palmitate/microL O2 in the C group) were observed. This increased fatty acid contribution in the oxidation metabolism could be responsible for some oxygen wasting and could contribute to decrease the energy available for the contraction despite the normal cardiac oxygen uptake. Furthermore, the respiration parameters of the mitochondria were similar in the C and R groups when glutamate (20 mM) or palmitoylcarnitine (25 microM) were used as substrate. ME mitochondria of R group displayed a reduced rate of ATP production (118 +/- 29.5 vs 180 +/- 14.5 nmoles/min/mg proteins in the C group) without altered creatine phosphate production. The presence of calcium in the medium (10(-5) M) provoked a decrease in ATP production.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Cellular and mitochondrial energy metabolism in the stunned myocardium. 782 5


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