ライフサイエンスコーパス: hyperoxaluria

1 xalate intake contributed to the severity of hyperoxaluria.

2 d with exposure to ethylene glycol or severe hyperoxaluria.

3 o 98% after multiple doses in a rat model of hyperoxaluria.

4 osis in oxalate nephropathy, such as primary hyperoxaluria.

5 Primary hyperoxaluria 1 (PH1; Online Mendelian Inheritance in Ma

6 tential drug target for treatment of primary hyperoxaluria, a genetic disorder where overproduction o

7 f cinnamon and turmeric may increase risk of hyperoxaluria, a significant risk factor for urolithiasi

8 BACKGROUND AND AIMS: Hyperoxaluria after Roux-en-Y gastric bypass (RYGB) is g

9 Hyperoxaluria after RYGB correlated with steatorrhea and

10 stic fibrosis have an increased incidence of hyperoxaluria and calcium oxalate nephrolithiasis.

11 al absorption of oxalate, thereby preventing hyperoxaluria and calcium oxalate urolithiasis.

12 lora is associated with an increased risk of hyperoxaluria and calcium-oxalate urolithiasis.

13 Slc26a6-null mice have significant hyperoxaluria and elevation in plasma oxalate concentrat

14 The combination of hyperoxaluria and hypocitraturia can trigger Ca(2+)-oxal

15 pendent succinate uptake, as well as urinary hyperoxaluria and hypocitraturia, but no change in urina

16 spite their clinical significance in primary hyperoxaluria and idiopathic calcium oxalate nephrolithi

17 n of oxalate, thereby increasing the risk of hyperoxaluria and its complications (eg, nephrocalcinosi

18 therapy is an efficient procedure to prevent hyperoxaluria and its complications.

19 ven 0.75% ethylene glycol for 2 wk to induce hyperoxaluria and kidney calcium oxalate crystal deposit

20 absence from the gut increases the risk for hyperoxaluria and recurrent kidney stone disease, and th

21 trol rats and experimental rats with induced hyperoxaluria and renal CaOx crystallization.

22 d caused by fat malabsorption, magnitudes of hyperoxaluria and steatorrhea should correlate.

23 pears to be a risk factor for development of hyperoxaluria and/or recurrent calcium oxalate kidney st

24 e transporter SLC26A6 develop hyperoxalemia, hyperoxaluria, and calcium-oxalate stones as a result of

25 th cystic fibrosis have an increased risk of hyperoxaluria, and of subsequent nephrocalcinosis and ca

26 ient repopulation of the liver to ameliorate hyperoxaluria, and therefore should be evaluated further

27 absence of O. formigenes and the presence of hyperoxaluria are correlated in cystic fibrosis (CF) pat

28 e molecular aspect and management of primary hyperoxalurias as well as nephropathic cystinosis provid

29 cate an association between the induction of hyperoxaluria/CaOx nephrolithiasis and the expression of

30 Persistent hyperoxaluria causes nephrocalcinosis and urolithiasis,

31 lated probands with PH1 from the Mayo Clinic Hyperoxaluria Center, to date the largest with availabil

32 ad to multiple complications associated with hyperoxaluria, especially recurrent calcium oxalate urol

33 Furthermore, hyperoxaluria in the OPN wild-type mice was associated w

34 for the increased lipid peroxidation during hyperoxaluria-induced nephrolithiasis.

35 Hyperoxaluria is a major risk factor for kidney stones a

36 Primary hyperoxaluria is a rare autosomal recessive metabolic di

37 Hyperoxaluria is discussed relative to mutations in AGXT

38 If hyperoxaluria is indeed caused by fat malabsorption, mag

39 he importance of O. formigenes in regulating hyperoxaluria, laboratory rats known to be noncolonized

40 on mediated by SLC26A6 may contribute to the hyperoxaluria observed in this mouse model of cystic fib

41 nes were hyperoxaluric, with the most severe hyperoxaluria occurring in young patients.

42 tive in the treatment of primary and enteric hyperoxaluria or even idiopathic calcium oxalate nephrol

43 Primary hyperoxaluria (PH) is a rare autosomal recessive disease

44 (AGT), the metabolic error in type 1 primary hyperoxaluria (PH1).

45 ymatic defect responsible for type 1 primary hyperoxaluria (PH1).

46 ubular crystal deposition and progression of hyperoxaluria-related CKD.

47 Despite identical levels of hyperoxaluria, Tnfr1-, Tnfr2-, and Tnfr1/2-deficient mic

48 Primary Hyperoxaluria Type 1 (PH1) is a rare autosomal recessive

49 Primary hyperoxaluria type 1 (PH1) is an inborn error of metabol

50 Primary hyperoxaluria type 1 (PH1) is caused by defects in perox

51 Primary hyperoxaluria type 1 (PH1), an inherited rare disease of

52 ion of intracellular oxalate and the primary hyperoxaluria type 1 (PH1).

53 calcium oxalate kidney stone disease primary hyperoxaluria type 1 (PH1).

54 thal hereditary kidney stone disease primary hyperoxaluria type 1 (PH1).

55 g glycolate and glyoxylate levels in primary hyperoxaluria type 1 patients who have the inability to

56 In a mouse model of primary hyperoxaluria type 1, rectal administration of O. formig

57 is enzyme is the underlying cause of primary hyperoxaluria type 2 (PH2) and leads to increased urinar

58 e (PLP)-dependent enzymes, including primary hyperoxaluria type I (PH1).

59 or end-stage renal disease caused by primary hyperoxaluria type I (PH1).

60 Primary hyperoxaluria type I is a severe kidney stone disease ca

61 results in the kidney stone disease, primary hyperoxaluria type I, identifying mutations that specifi

62 oxylate aminotransferase, mutated in primary hyperoxaluria type I.

63 Primary hyperoxaluria type II (PH2) is a rare monogenic disorder

64 Primary hyperoxaluria type-1 (PH1) is an autosomal recessive dis

65 To determine the importance of OPN in vivo, hyperoxaluria was induced in mice targeted for the delet

66 common in obese patients before bypass, but hyperoxaluria was not caused by excess unabsorbed fatty

67 s) may be effective for treatment of primary hyperoxaluria, we propose that the methods described her

68 Steatorrhea and hyperoxaluria were common in obese patients before bypas

69 Steatorrhea and hyperoxaluria were defined as fecal fat >7 g/day and uri