Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oxyphil carcinoma of the parathyroid is an extremely rare tumour, only two previous patients having been reported. We report a 55-year-old woman with this condition, who presented with a picture of hyperparathyroidism, including hypercalcaemia, hypercalciuria, hypophosphataemia, increased alkaline phosphatase, and bony lesions. Biopsy of a bone lesion was consistent with brown tumour. Fine needle aspiration cytology and subsequent operative histology of the parathyroid lesion showed an oxyphil cell tumour with malignant characteristics. Following excision, the patient made a good recovery, complicated only by postoperative hypocalcaemia.
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PMID:Oxyphil cell carcinoma of the parathyroid: a rare cause of hyperparathyroidism. 858 61

The differential effects of sodium-induced renal hypercalciuria on the biochemical markers of bone metabolism and calcium homeostasis were studied in oophorectomized (Oophx) and sham-operated rats. The rats consuming a normal (0.4%) calcium semisynthetic diet were randomly allocated to either 0, 0.4, 0.6, 0.9, or 1.25% NaCl in their drinking water for 7 days. At that time fasting blood and urine specimens were collected and analyzed for bone-related biochemical variables. The urinary calcium/creatinine ratio was increased with increasing urinary sodium (p < 0.01) in both sham and Oophx animals. The hydroxyproline/creatinine ratio was elevated as a result of Oophx (p < 0.001) and was raised with increasing urinary sodium in both sham (p = 0.012) and Oophx animals (p = 0.007). Serum osteocalcin and alkaline phosphatase were elevated in Oophx rats (p < 0.02). While serum osteocalcin was raised with increasing urinary sodium in Oophx rats (p = 0.035), there was no effect on osteocalcin levels in sham-operated rats. This study demonstrates that sodium-induced renal hypercalciuria potentiates bone turnover in Oophx rats as compared with ovary-intact rats and indicates important implications for the effect of dietary salt on bone turnover with ovarian hormone deficiency.
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PMID:Increased urinary calcium excretion potentiates bone turnover in oophorectomized rats. 905 68

Routinely used renal function tests remain normal in uncomplicated hypercalciuria. The aim of this study was to assess the value of N-acetyl-beta-D-glucosaminidase (NAG), a sensitive marker of renal proximal tubular damage, in experimental hypercalciuria. Oral calcium providing 75 mg/kg per day elementary calcium and 20,000 IU/day vitamin D3 was administered for 15 days to 7 rabbits (Orytolagus cuniculus-New Zealand white) and 7 rabbits were given placebo as a control group. Serum calcium, phosphorus, and alkaline phosphatase, daily urinary calcium excretion and NAG/creatinine ratio were measured before and after drug administration. Kidneys were examined macroscopically and microscopically following the study period. Serum calcium, phosphorous and urinary calcium excretion increased, while alkaline phosphatase decreased significantly in response to drug treatment [10.8 +/- 1.5 vs. 12.2 +/- 1.3 mg/dl, 4.6 +/- 0.6 vs. 6.7 +/- 0.7 mg/ dl, 22.3 +/- 8.3 vs. 46.8 +/- 22.5 mg/kg per day, and 138.0 +/- 57.1 vs. 70.1 +/- 33.1 IU/l, respectively (P < 0.05)]. The NAG/creatinine ratio prior to the study (0.5 +/- 0.1 mU/ mg) was significantly different from that after the study (5.4 +/- 1.5 mU/mg, P < 0.01). In the control group, changes in serum and urinary parameters were not significant (P > 0.05). The relationship between the urinary NAG/ creatinine ratio and the daily urinary calcium excretion was statistically significant (r = 0.67, P < 0.05). In the study group, nephrocalcinosis was present in all rabbits except 1 (85.7%), whereas none of the control group rabbits had nephrocalcinosis. In conclusion, in rabbits urinary NAG excretion increases significantly in nephrocalcinosis induced by hypercalciuria.
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PMID:Urinary N-acetyl-beta-D-glucosaminidase activity in rabbits with experimental hypercalciuria. 926 Feb 50

Twenty male Wistar rats, weighing 150 g, were placed in metabolic cages on a 30% sucrose diet for 7 days, before allocation to two groups: a control group (n = 5) and a lactose group (n = 15). They received respectively a 30% sucrose diet or a 30% lactose diet for 8 weeks, each containing 0.67% calcium and 0.38% phosphorus. After 4 (T1) and 8 (T2) weeks, the serum calcium (Ca) and citrate levels were significantly (P < 0.01) higher in rats fed the lactose diet. Serum alkaline phosphatase activity was increased in the lactose group (P < 0.01) at T1 and T2. The lactose-rich diet induced an increase in urinary Ca excretion at T1 and T2; citrate excretion was only enhanced at T2 (P < 0.001). No difference between the two groups was observed in urinary oxalate (Ox) excretion or creatinine clearance. Crystalluria analysis revealed a marked number (>300/mm3 at T1 and T2) of calcium oxalate dihydrate crystals (COD) in rats fed the lactose-rich diet, whereas no COD crystals were observed in sucrose-fed control rats at any time point. The formation of COD crystals in lactose-fed rats was related to an increase in calcium oxalate (CaOx) product (pCaOx), which was respectively 12.6 vs 3.9 at T1 and 10.5 vs 1.8 at T2, and an increase in CaOx ratio (Ca/Ox), which was 99.1 vs 7.5 and 67.5 vs 18.5 at T1 and T2, respectively. The high pCaOx and Ca/Ox ratios in the lactose group were due to hypercalciuria, in agreement with the number and the type of crystals. The present experimental model confirms that the ingestion of a 30% lactose diet increases urinary Ca excretion without changing urinary Ox excretion and shows for the first time that it induces a stable and marked crystalluria composed of COD. Such a non-nephrotoxic and stable model is of interest for the study of CaOx crystal formation secondary to hypercalciuria, and thus afterwards eventually for CaOx nephrolithiasis.
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PMID:A stable animal model of diet-induced calcium oxalate crystalluria. 953 98

Npt2 encodes a renal-specific, brush-border membrane Na+-phosphate (Pi) cotransporter that is expressed in the proximal tubule where the bulk of filtered Pi is reabsorbed. Mice deficient in the Npt2 gene were generated by targeted mutagenesis to define the role of Npt2 in the overall maintenance of Pi homeostasis, determine its impact on skeletal development, and clarify its relationship to autosomal disorders of renal Pi reabsorption in humans. Homozygous mutants (Npt2(-/-)) exhibit increased urinary Pi excretion, hypophosphatemia, an appropriate elevation in the serum concentration of 1,25-dihydroxyvitamin D with attendant hypercalcemia, hypercalciuria and decreased serum parathyroid hormone levels, and increased serum alkaline phosphatase activity. These biochemical features are typical of patients with hereditary hypophosphatemic rickets with hypercalciuria (HHRH), a Mendelian disorder of renal Pi reabsorption. However, unlike HHRH patients, Npt2(-/-) mice do not have rickets or osteomalacia. At weaning, Npt2(-/-) mice have poorly developed trabecular bone and retarded secondary ossification, but, with increasing age, there is a dramatic reversal and eventual overcompensation of the skeletal phenotype. Our findings demonstrate that Npt2 is a major regulator of Pi homeostasis and necessary for normal skeletal development.
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PMID:Targeted inactivation of Npt2 in mice leads to severe renal phosphate wasting, hypercalciuria, and skeletal abnormalities. 956 Feb 83

Hypercalcemia and hypercalciuria observed both in humans and in animals who were on long-term theophylline therapy, prompted us to investigate whether oral theophylline treatment at optimal doses causes any adverse side effects on bone metabolism in mild asthmatics. Therefore, serum osteocalcin (BGP) and total alkaline phosphatase (TALP, EC 3.1.3.1) as bone formation markers, serum prolidase I (EC 3.4.13.9) activity as a marker for collagen metabolism, urinary deoxypyridinoline (Dpd), hydroxyproline (Hyp) and fasting urinary calcium as bone resorption markers, were measured in 18 mild asthmatics who had been treated with theophylline over 1-10 years. Among measured bone turnover markers, BGP, TALP, and Hyp levels were found to be increased in mild asthmatics; and BGP showed the greatest percent mean increase (98%) over the healthy subjects. However, these increments did not exceed the upper reference limits. Serum prolidase I activity was also increased in mild asthmatics receiving theophylline. Our results indicate that theophylline therapy at optimal doses may not exert adverse side effects on bone homeostasis, but patients receiving supratherapeutic doses of theophylline should be under close examination in order to predict future bone mass status.
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PMID:Evaluation of the effect of low-dose oral theophylline therapy on some bone turnover markers and serum prolidase I activity in mild asthmatics. 1043 80

Advanced tumor osteopathy is characterized by abnormal bone turnover. Using a rat model of parathyroid hormone-related peptide (PTHrP)-mediated tumor osteolysis, the aim of the present study was to define the sequential changes in, and the association between, biochemical and histomorphometric indices of bone metabolism during the early stages of developing tumor osteopathy. Eight-month-old Wistar rats (n = 48) were subcutaneously inoculated with either 2 x 10(6) cells of the Walker carcinosarcoma 256, or saline on day 0, and treated with either saline or the bisphosphonate ibandronate until killing on day 8. Serum calcium (sCa), alkaline phosphatase (sTAP), and osteocalcin (sOC) and urinary calcium (uCa), deoxypyridinoline (uDPD), and pyridinoline (uPYD) were measured daily. In a second semilongitudinal experiment (n = 70), the number of osteoclasts and osteoblasts (N.Oc, N.Ob), trabecular bone volume (BV/TV), and osteoid volume (O.Ar) were assessed by histomorphometry. In untreated tumor-bearing animals, osteoclast numbers increased by 74% on day 3 (5.4 +/- 2.4 vs. 3.1 +/- 1.5/mm(2), p < 0.05), and trabecular bone volume fell by 24% on day 4 (12.5 +/- 2.0 vs. 15.8 +/- 1.2%, p < 0.05). Both time course and magnitude of these changes were closely reflected by an increase in uDPD (0.46 +/- 0.14 vs. 0. 31 +/- 0.15 nmol/12 h, p < 0.05) and uPYD on day 4 (1.44 +/- 0.25 vs. 1.03 +/- 0.3 nmol/12 h, p < 0.05), sCa (3.8 +/- 0.52 vs. 3.0 +/- 0. 13 mmol/L, p < 0.01), and uCa (0.13 +/- 0.08 vs. 0.03 +/- 0.01 mmol/12 h, p < 0.001) on day 6, and sTAP (254 +/- 127 vs. 120 +/- 40 U/L, p < 0.001) on day 7 (mean +/- SD), whereas sOC remained unchanged until day 8. When combining the results of the two experiments, a high correlation was found between the number of osteoclasts and the urinary excretion of PYD (r = 0.91) and DPD (r = 0.89). Treatment with ibandronate delayed hypercalcemia, abolished hypercalciuria, and accelerated bone resorption. We conclude that osteoclast activation is an early event in PTHrP-mediated osteolysis, which is closely reflected by the renal excretion of pyridinium cross-links of type I collagen. Therefore, specific biochemical markers of collagen breakdown may be useful as early indicators of developing tumor osteopathy.
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PMID:Association between histomorphometry and biochemical markers of bone turnover in a longitudinal rat model of parathyroid hormone-related peptide (PTHrP)-mediated tumor osteolysis. 1077 87

To determine whether an "atherogenic" diet (excess of cholesterol and neutral fat) induces pathological calcification in various organs, including the kidney, and abnormal oxalate metabolism, 24 male Sprague-Dawley rats were fed either normal lab chow (controls, n = 12) or the cholesterol- and fat-rich experimental diet (CH-F, n = 12) for 111 +/- 3 days. CH-F rats developed dyslipidemia [high blood levels of triglycerides, total, low-density lipoprotein (LDL)-, very low-density lipoprotein (VLDL)-, high-density lipoprotein (HDL)-bound cholesterol, total phospholipids], elevated serum total alkaline phosphatase and lactate dehydrogenase (LDH) levels, in the absence of changes in overall renal function, extracellular mineral homeostasis [serum protein-corrected total calcium, magnesium, parathyroid hormone (PTH), 1,25-dihydroxyvitamin D (1,25(OH)2D)], plasma glycolate and oxalate levels. There was a redistribution of bone calcium and enhanced exchange of this within the extraosseous space, which was accompanied by significant bone calcium loss, but normal bone histomorphometry. Liver oxalate levels, if expressed per unit of defatted (DF) dry liver, were three times higher than in the controls. Urinary glycolate, oxalate, calcium and total protein excretion levels were elevated, the latter showing an excess of proteins > 100 kD and a deficit of proteins > 30-50 kD. Urinary calcium oxalate supersaturation was increased, and calcium phosphate supersaturation was unchanged. There were dramatically increased (by number, circumference, and area) renal calcium phosphate calcifications in the cortico-medullary region, but calcium oxalate deposits were not detectable. Electron microscopy (EM) and elemental analysis revealed intratubular calcium phosphate, apparently needle-like hydroxyapatite. Immunohistochemistry of renal tissue calcifications revealed co-localization of phospholipids and calcium phosphate. It is concluded that rats fed the CH-F diet exhibited: (1) a spectrum of metabolic abnormalities, the more prominent being dyslipidemia, hyperoxaluria, hypercalciuria, dysproteinuria, loss of bone calcium, and calcium phosphate nephrocalcinosis (NC); and (2) an interaction between calcium phosphate and phospholipids at the kidney level. The biological significance of these findings for the etiology of idiopathic calcium urolithiasis in humans is uncertain, but the presented animal model may be helpful when designing clinical studies.
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PMID:Nephrocalcinosis and hyperlipidemia in rats fed a cholesterol- and fat-rich diet: association with hyperoxaluria, altered kidney and bone minerals, and renal tissue phospholipid-calcium interaction. 1122 20

In patients with uncomplicated idiopathic hypercalciuria renal function is normal except for increased renal calcium excretion. In this study, the level of fractional urinary enzyme excretion was assessed in relation to calciuria. Fourteen patients with a mean age of 5.8 +/- 0.8 years who had daily urinary calcium excretion more than 4 mg/kg and with otherwise normal renal function tests were included in the study. None of the patients manifested either renal calculus or nephrocalcinosis. Fourteen normal children with a mean age of 5.4 +/- 0.74 were included in the control group. The level of the urinary N-acetyl beta-D glucosaminidase (NAG) to creatinine ratio, fractional aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH) excretion were not significantly different compared to the control group (p > 0.05). The patients were subdivided according to the type of hypercalciuria. The levels of NAG/creatinine ratio, fractional ALT, AST, ALP, LDH excretion were not significantly different in the absorptive type of calciuria group compared to the control group (p > 0.05). In conclusion, hypercalciuria during childhood which is 6.46 +/- 1.83 mg/kg/day is not related to the levels of NAG/creatinine ratio, fractional ALT, AST, ALP and LDH excretion in urine.
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PMID:Investigation of relationship between idiopathic hypercalciuria and urinary enzyme activities. 1122 47

Our cross-sectional study aimed at the early determination of changes in bone metabolism in terms of bone mineral density (BMD) and bone turnover in persons with complete spinal cord injury (SCI) during the acute phase of paraplegia. Combined dual-energy x-ray absorptiometry (DXA) and specific biochemical markers of bone turnover were used to determine bone metabolism. Seven persons with SCI (age, 31.3 +/- 9.5 years) who had sustained injury an average of 3 months earlier (103 +/- 10.8 days) were compared with 10 able-bodied controls (27.5 +/- 4.3 years). Four paraplegics and 3 quadriplegics composed the SCI group. BMD was measured by DXA, while bone turnover was evaluated by serum osteocalcin (OC), bone alkaline phosphatase (B-ALP), and serum and urinary type I collagen C-telopeptide (CTXs and CTXu). Regional BMD (proximal femur, lumbar spine, radius, lower limb) was similar in the 2 groups except in the upper limb (P <.05). CTXs and CTXu were significantly higher in SCI (P <.01 and P <.001, respectively), whereas among the bone formation markers used, only serum OC was affected by immobilization (P <.05). The SCI group developed hypercalciuria (0.76 +/- 0.37 v 0.35 +/- 0.14), whereas calcemia was normal (2.42 +/- 0.09 v 2.31 +/- 0.10). Intact parathyroid hormone (iPTH) and 1.25 (OH)(2) vitamin D levels were suppressed in persons with SCI (P <.001) by 80.6% and 66%, respectively. In conclusion, it was not possible to detect any variation in BMD from the DXA technique at this early stage of demineralization, but the sensitivity and early response of the biochemical markers strongly suggested their usefulness for the early identification of persons with SCI at risk of severe osteoporosis.
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PMID:Use of bone biochemical markers with dual-energy x-ray absorptiometry for early determination of bone loss in persons with spinal cord injury. 1214 66


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