ライフサイエンスコーパス: hyperfiltration

1 sure to renal compensatory mechanisms (i.e., hyperfiltration).

2 erglycemia, polyuria, renal hypertrophy, and hyperfiltration.

3 as been suggested to play a role in diabetic hyperfiltration.

4 d to be essential for renal vasodilation and hyperfiltration.

5 Benfotiamine also inhibited diabetes-induced hyperfiltration.

6 es diabetic renal hypertrophy and glomerular hyperfiltration.

7 ccelerated by unilateral nephrectomy-induced hyperfiltration.

8 ikely contribute to the etiology of diabetic hyperfiltration.

9 uely responsible for the observed postpartum hyperfiltration.

10 filtration coefficient, and did not mitigate hyperfiltration.

11 ers is unlikely to be a result of glomerular hyperfiltration.

12 rictor responsiveness and promote glomerular hyperfiltration.

13 stained inhibition of renal vasodilation and hyperfiltration.

14 demographic characteristics including renal hyperfiltration.

15 two systems may account for diabetes-induced hyperfiltration; (3) the LNA-induced decrease in GFR in

16 Adaptive hyperfiltration after donor nephrectomy is attributable

17 elopment of ORG as a maladaptive response to hyperfiltration and albuminuria.

18 proved renal function, decreasing glomerular hyperfiltration and albuminuria.

19 abetic nephropathy exhibits renal glomerular hyperfiltration and an increase in renal plasma flow.

20 then contribute to hypertension, glomerular hyperfiltration and diabetic nephropathy.

21 It has been postulated that glomerular hyperfiltration and endothelial dysfunction are early fe

22 Microalbuminuria, a marker of glomerular hyperfiltration and endothelial dysfunction, has been de

23 protein in diabetes patients results in less hyperfiltration and glomerular hypertension and, therefo

24 otein intakes by diabetic individuals create hyperfiltration and glomerular hypertension eventuating

25 nd normalized by DFMO, which also attenuated hyperfiltration and hypertrophy.

26 a-tocopherol treatment to prevent glomerular hyperfiltration and increased albuminuria as well as PKC

27 rtant role for the development of glomerular hyperfiltration and increased albuminuria in diabetes an

28 possibly TGF, limits the degree of diabetic hyperfiltration and nephropathy.

29 ric oxide (NO)-dependent renal vasodilation, hyperfiltration and reduced myogenic reactivity of small

30 d glomerular endothelial cell proliferation; hyperfiltration and renal morphology were unchanged.

31 on hypertension on postdonation BP, adaptive hyperfiltration, and compensatory glomerular hypertrophy

32 reased in insulin-treated diabetic rats with hyperfiltration, and inhibition of kallikrein or blockad

33 emove metabolic waste products through renal hyperfiltration, and it could also link metabolic diseas

34 of the renin-angiotensin system, glomerular hyperfiltration, and structural changes in the kidney th

35 hat renal functional reserve is exhausted by hyperfiltration; and (2) ACEI restores the GFR response

36 and its exact role in states of TGF-induced hyperfiltration are still unclear.

37 The revived interest in glomerular hyperfiltration as a prognostic and pathophysiologic fac

38 eration and developed hypertension and renal hyperfiltration as well as renal injury with heightened

39 educed urinary albumin excretion, glomerular hyperfiltration, blood glucose levels, histological dete

40 Because of hyperfiltration, BNZ increased VLP and distal flow, but

41 ts manifest renal hypertrophy and glomerular hyperfiltration but not glomerular capillary hypertensio

42 Although hyperfiltration can cause glomerular injury, many studie

43 corresponding magnitude of postdonation BP, hyperfiltration capacity, or compensatory renocortical h

44 This phenomenon, known as glomerular hyperfiltration, classically has been hypothesized to pr

45 esis, nonimmunologic factors, in particular, hyperfiltration damage related to reduced renal mass, ha

46 nimizing recipient weight may prevent future hyperfiltration damage.

47 diabetic mice, COMT(-/-) mice had decreased hyperfiltration, decreased macula densa cyclooxygenase-2

48 recruited to maintain renal vasodilation and hyperfiltration during chronic NO synthase blockade in c

49 rto proposed mechanisms involved in diabetic hyperfiltration, focusing on ultrastructural, vascular,

50 inephrectomy alone demonstrated compensatory hyperfiltration following reduction in renal mass.

51 The 153 patients with hyperfiltration (GFR >130 ml x min(-1) x 1.73 m(-2)) had

52 mpanied by marked albuminuria, nephromegaly, hyperfiltration, glomerular ultrastructural alterations,

53 ent in renal function, whereas patients with hyperfiltration (>120 mL . min(-1) . 1.73 m(-2); n = 12)

54 The study of hyperfiltration has focused on microvascular abnormaliti

55 nditions, including glomerular hypertension, hyperfiltration, hypertrophy, and outflow of filtrate fr

56 ration of RLX elicits renal vasodilation and hyperfiltration in conscious adult, intact female rats.

57 ble evidence on the clinical significance of hyperfiltration in diabetes and discuss currently availa

58 ed to investigate the contribution of TGF to hyperfiltration in diabetic Ins2(+/-) Akita mice.

59 Rats demonstrate renal vasodilation and hyperfiltration in pregnancy.

60 , completely reversed renal vasodilation and hyperfiltration in relaxin-treated rats.

61 r 2 inhibitor empagliflozin attenuated renal hyperfiltration in subjects with T1D, likely by affectin

62 ibition with empagliflozin 25 mg QD on renal hyperfiltration in subjects with type 1 diabetes mellitu

63 w 50% may induce glomerular hypertension and hyperfiltration in surviving units, which in turn lead t

64 indicates that TGF is not required to cause hyperfiltration in the Akita model of diabetes.

65 Their results suggest that adaptive hyperfiltration in the remaining kidney occurs without g

66 they experience compensatory hypertrophy and hyperfiltration in their remaining kidney.

67 This raises concern for hyperfiltration injury.

68 abdominal obesity, CR ameliorates glomerular hyperfiltration, insulin sensitivity, and other cardiova

69 The hyperfiltration is a dysfunctional state that may arise

70 with type 2 diabetes with abdominal obesity, hyperfiltration is a risk factor for accelerated glomeru

71 ephrogenesis, systolic blood pressure, renal hyperfiltration, kidney injury, and reactive oxygen spec

72 Intraglomerular hypertension and glomerular hyperfiltration likely contribute to the pathogenesis of

73 focused on microvascular abnormalities, but hyperfiltration may actually result from a prior increas

74 male recipient functional demand results in hyperfiltration-mediated glomerular injury and that this

75 inhibitors abrogates renal vasodilation and hyperfiltration, NO most likely mediates the renal circu

76 nal hypertrophy, glomerular enlargement, and hyperfiltration observed in diabetic wild-type mice and

77 r angiotensin II (AngII) are involved in the hyperfiltration observed in rats with streptozotocin-ind

78 ons of AngII, alone, are responsible for the hyperfiltration observed in streptozotocin-induced diabe

79 tudy was to determine whether the glomerular hyperfiltration of pregnancy is maintained even after Ca

80 GFR in either virgin or pregnant rats; thus, hyperfiltration persisted in the latter despite chronic

81 consistent with the hypothesis that diabetic hyperfiltration results from normal physiologic actions

82 ering blood pressure and diabetic glomerular hyperfiltration, SGLT2 inhibitors may induce protective

83 t arteriolar dilation that occurs during the hyperfiltration stage of insulin-dependent diabetes mell

84 ed in individuals stratified based on having hyperfiltration (T1D-H, GFR >/= 135 mL/min/1.73m(2), n=2

85 Comparable renal vasodilation and hyperfiltration was also observed in ovariectomized rats

86 Glomerular hyperfiltration was also significantly reduced in diabet

87 During clamped euglycemia, hyperfiltration was attenuated by -33 mL/min/1.73m(2) wi

88 namate, 10 mg/kg IV), renal vasodilation and hyperfiltration were abolished; ie, the combined treatme

89 BNZ caused glomerular hyperfiltration, which was prevented with inhibitors of