ライフサイエンスコーパス: hypercalciuria

1 Western diets induce metabolic acidosis and hypercalciuria.

2 ensity has been increasingly associated with hypercalciuria.

3 ns are often sufficient in the management of hypercalciuria.

4 ontribution exists in the pathophysiology of hypercalciuria.

5 ctomy did not prevent this magnesium-induced hypercalciuria.

6 eproducing the human phenotype of idiopathic hypercalciuria.

7 results from attempts in studying polygenic hypercalciuria.

8 citriol was associated with a higher risk of hypercalciuria.

9 restriction is only effective in absorptive hypercalciuria.

10 remature delivery, hypokalemic alkalosis and hypercalciuria.

11 y supplements and were found to have fasting hypercalciuria.

12 tients and are most commonly associated with hypercalciuria.

13 (NSHPT) or autosomal dominant hypocalcaemic hypercalciuria (ADHH) for CaSR mutations and performed i

14 Increasing dietary protein induces hypercalciuria and a negative calcium balance.

15 cance, significant linkage was found between hypercalciuria and a region of chromosome 1 at D1Rat169

16 oto (WKY) male rats, loci that are linked to hypercalciuria and account for a 6 to eight-fold phenoty

17 tubule dysfunction, including hyperkalemia, hypercalciuria and acidosis, often complicate their use.

18 n and CaR protein that may contribute to the hypercalciuria and calcium nephrolithiasis.

19 e in the management in patients in whom both hypercalciuria and decreased bone density are present.

20 estations, and Bartter's syndrome, featuring hypercalciuria and early presentation with severe volume

21 : Ksp-cre;Pth1r(fl/fl) Mutant mice exhibited hypercalciuria and had lower serum calcium and markedly

22 In aldosteronism, hypercalciuria and hypermagnesuria and accompanying decr

23 Under a high-Na+ diet, KO mice exhibited hypercalciuria and increased blood pressure, which were

24 Hydrochlorothiazide resolved hypercalciuria and increased bone mineral density at a r

25 These patients present not only with hypercalciuria and increased BTMs (mainly resorptive), b

26 d prove valuable in understanding idiopathic hypercalciuria and kidney stone disease in humans.

27 turing salt wasting, hypokalaemic alkalosis, hypercalciuria and low blood pressure.

28 ce have higher blood pressure, hyperkalemia, hypercalciuria and marked hyperplasia of the distal conv

29 Familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC) is a human d

30 Familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC) is an inheri

31 renal disorder familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC).

32 e renal tubular acidosis are associated with hypercalciuria and nephrocalcinosis.

33 They also developed hypercalciuria and renal calcium deposits and some had d

34 s a potential explanation for Cd(2+)-induced hypercalciuria and resultant renal stone formation.

35 on Ca metabolism that thus contribute to the hypercalciuria and stone formation.

36 abolism in RCTs, specifically hypercalcemia, hypercalciuria, and kidney stones, in participants who w

37 lactose-free diet, including hypercalcaemia, hypercalciuria, and nephrocalcinosis which, however, onl

38 linical and experimental monogenic causes of hypercalciuria, and outlines the initial results from at

39 The polyuria, hypercalciuria, and proteinuria of the -/- adults and fu

40 hrosis, low plasma potassium, high blood pH, hypercalciuria, and proteinuria.

41 ndingly elevated 1,25(OH)2 vitamin D levels, hypercalciuria, and rickets/osteomalacia.

42 retention of suture material, recurrent UTI, hypercalciuria, and urinary stasis.

43 artter syndrome (diagnosis during childhood, hypercalciuria, and/or polyuria), and 26.0% had Gitelman

44 Hypercalciuria, as determined by the urinary calcium-to-

45 late stone formation, even in the absence of hypercalciuria, but the molecular mechanisms that contro

46 Chronic hypercalciuria can contribute to osteoporosis, particula

47 Hypercalciuria developed in 27 percent of the patients i

48 ts in that affected individuals present with hypercalciuria due to increased serum 1,25-dihydroxyvita

49 hyroidism, patients with these mutations had hypercalciuria even at low serum calcium concentrations.

50 ecurrent calcium nephrolithiasis and fasting hypercalciuria have a higher incidence of osteopenia and

51 Hereditary hypophosphatemic rickets with hypercalciuria (HHRH) is a rare disorder of autosomal re

52 use hereditary hypophosphatemic rickets with hypercalciuria (HHRH), a disorder characterized by renal

53 ncreased the percentage of participants with hypercalciuria, hypercalcemia, and nausea by 24% (CI, 20

54 Hypercalciuria, hypercalcemia, and nausea were more comm

55 xhibit increased nephrocalcinosis or develop hypercalciuria, hypercalcemia, anti-KRN23 antibodies, or

56 ight males, ages 7 to 34 yr, with idiopathic hypercalciuria (IH) served as controls.

57 from those changes encountered in idiopathic hypercalciuria (IH).

58 , hypercalcemia occurred in 2.8% to 9.0% and hypercalciuria in 12.0% to 33.0% of participants; events

59 This suggests that hypercalciuria in Dent's disease is a direct consequence

60 Hypercalciuria in genetic hypercalciuric stone-forming (

61 Hypercalciuria in inbred genetic hypercalciuric stone-fo

62 Surprisingly, hypercalciuria in RZ mice is abolished by dietary calciu

63 identifying genetic loci that contribute to hypercalciuria in the GHS rat, an F2 generation of 156 r

64 Identification of genes that contribute to hypercalciuria in this animal model should prove valuabl

65 his nephron segment, the pathogenesis of the hypercalciuria in this disease is unknown.

66 ome, characterized by hypokalemic alkalosis, hypercalciuria, increased serum aldosterone, and plasma

67 This augmented hypercalciuria increases the risk of renal complications

68 Idiopathic hypercalciuria is a common disorder in children and can

69 Hypercalciuria is a complex trait.

70 Hypercalciuria is a major risk factor for nephrolithiasi

71 Hypercalciuria is an important, identifiable, and revers

72 Hypercalciuria is discussed relative to mutations in the

73 Hypercalciuria is the major risk factor promoting stone

74 Hypercalciuria is the most common risk factor for kidney

75 Hypercalciuria is the most common risk factor for kidney

76 ndamental step in dissecting the genetics of hypercalciuria is understanding its pathophysiology.

77 ary calcium deprivation, suggesting that the hypercalciuria may be attributable to gastrointestinal h

78 Although originally thought to be related to hypercalciuria, more recent studies in humans and resear

79 X-linked inherited disorder characterized by hypercalciuria, nephrocalcinosis, nephrolithiasis, low m

80 sulting in low-molecular-weight proteinuria, hypercalciuria, nephrolithiasis, and renal failure.

81 The hypercalciuria noted on spot testing of the urinary calc

82 ous for a SLC34A3 mutation frequently showed hypercalciuria, often in association with mild hypophosp

83 ctive of PTx: calcium >11.5 mg/dL (OR 2.27), hypercalciuria (OR 3.28, P < 0.0001), and age < 50 years

84 D supplementation on risk of hypercalcemia, hypercalciuria, or kidney stones was not modified by bas

85 f the following side effects: hypercalcemia, hypercalciuria, or kidney stones.

86 d osteocalcin (P </= 0.001 for each) despite hypercalciuria (P = 0.029).

87 Their greater hypercalciuria presumably reflected activation of Ca(2+)

88 omise the attempt to dissect the genetics of hypercalciuria, summarizes the clinical and experimental

89 to CaR mutations also show disproportionate hypercalciuria that may increase the risk of nephrocalci

90 rease renal tubule Ca reabsorption and cause hypercalciuria through suppression of Ca-sensitive potas

91 This is the first QTL for hypercalciuria to be isolated in a congenic animal.

92 lcium nephrolithiasis and idiopathic fasting hypercalciuria (urinary calcium/creatinine ratio >0.11)

93 Null mice were hypocitraturic, but hypercalciuria was absent.

94 Idiopathic hypercalciuria was diagnosed in 15.6%, primary hyperpara

95 No hypercalcemia or hypercalciuria was observed.

96 Similar increased risk of hypercalciuria was shown in 14 studies for the vitamin D

97 adults and is most commonly associated with hypercalciuria, which may be due to monogenic renal tubu

98 lted in increased risks of hypercalcemia and hypercalciuria, which were not dose related.

99 al associations and management of idiopathic hypercalciuria will be discussed.

100 din-16 and -19 cause familial hypomagnesemic hypercalciuria with nephrocalcinosis, whereas polymorphi

101 odel that closely resembles human idiopathic hypercalciuria, with excessive intestinal calcium absorp