ライフサイエンスコーパス: hyperfiltration

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

2 tion of Px and UNx increased GFR, indicating hyperfiltration.

3 stained inhibition of renal vasodilation and hyperfiltration.

4 r weight and avoid adverse lipid profile and hyperfiltration.

5 and increased renal energy requirements from hyperfiltration.

6 omerular feedback (TGF) promoting glomerular hyperfiltration.

7 enchyma because of an increase in glomerular hyperfiltration.

8 ting a possible role in relieving glomerular hyperfiltration.

9 ng the TGF response and promoting glomerular hyperfiltration.

10 unexpectedly low proportion of patients with hyperfiltration.

11 ts with type 1 diabetes with potential renal hyperfiltration.

12 ak GFR by over two years were considered pre-hyperfiltration.

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

14 demographic characteristics including renal hyperfiltration.

15 buloglomerular feedback signals and mitigate hyperfiltration.

16 erglycemia, polyuria, renal hypertrophy, and hyperfiltration.

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

18 d to be essential for renal vasodilation and hyperfiltration.

19 Benfotiamine also inhibited diabetes-induced hyperfiltration.

20 es diabetic renal hypertrophy and glomerular hyperfiltration.

21 ccelerated by unilateral nephrectomy-induced hyperfiltration.

22 ikely contribute to the etiology of diabetic hyperfiltration.

23 uely responsible for the observed postpartum hyperfiltration.

24 filtration coefficient, and did not mitigate hyperfiltration.

25 oxide, which also contributes to glomerular hyperfiltration.

26 rictor responsiveness and promote glomerular hyperfiltration.

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

28 Midterm hyperfiltration, a marker for renal reserve capacity, wa

29 s at higher risk for adverse outcomes due to hyperfiltration: African American recipients (aHR 1.10,

30 s at higher risk for adverse outcomes due to hyperfiltration: African American recipients (aHR 1.10,

31 Adaptive hyperfiltration after donor nephrectomy is attributable

32 o [aHR], 2.74; 95% CI, 1.63-4.62; P < .001), hyperfiltration (aHR, 2.11; 95% CI, 1.17-3.80; P = .01),

33 ed serum uric acid level, reduced glomerular hyperfiltration and albuminuria, and suppression of adva

34 proved renal function, decreasing glomerular hyperfiltration and albuminuria.

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

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

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

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

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

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

41 opathy is multifactorial - oxidative stress, hyperfiltration and glomerular hypertension are all cont

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

43 The model predicts quantitatively how hyperfiltration and glomerular leak interact to promote

44 y post-PTA was higher in those with pre-PTA hyperfiltration and higher HbA1c concentrations; eGFR ch

45 Glomerular hyperfiltration and hypertrophy contribute to the pathop

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

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

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

49 erting enzyme inhibition (ACEi) can mitigate hyperfiltration and may be therapeutically beneficial in

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

51 -salt diet might help to mitigate glomerular hyperfiltration and preserve renal function for longer,

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

53 endent and MAS-receptor-dependent glomerular hyperfiltration and regulates the RAAS during acute and

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

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

56 In this study, the risks of albuminuria, hyperfiltration, and hypertension increased with heavy c

57 The level of risk of developing albuminuria, hyperfiltration, and hypertension, assessed by Cox regre

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

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

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

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

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

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

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

65 ovel opportunity to delay the progression of hyperfiltration-associated CKD as seen in transplant don

66 LKDs and 61 +/- 18 mL/min in recipients with hyperfiltration being more prominent in LKDs (30.4%) as

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

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

69 eceptors megalin and cubilin in PT cells and hyperfiltration both contribute significantly to increas

70 at downregulation of megalin and cubilin and hyperfiltration both contribute significantly to increas

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

72 Although hyperfiltration can cause glomerular injury, many studie

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

74 iabetic kidney disease were grouped into two hyperfiltration categories based on annual iothalamate G

75 reducing biomechanical strain and glomerular hyperfiltration, chaperone therapy, blocking aberrant si

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

77 ar filtration rate, and only one (1%) showed hyperfiltration (clearance, > 130 mL/min).

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

79 nimizing recipient weight may prevent future hyperfiltration damage.

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

81 ned as an albumin level of >=30 mg/24 h) and hyperfiltration (defined as an estimated glomerular filt

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

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

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

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

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

87 The hyperfiltration group had higher hemoglobin A1c, higher

88 transcriptional signature identified in the hyperfiltration group was enriched for endothelial stres

89 two years of biopsy were categorized as the hyperfiltration group, and 26 in whom biopsy preceded pe

90 d lower podocyte density compared to the pre-hyperfiltration group.

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

92 The study of hyperfiltration has focused on microvascular abnormaliti

93 However, the mechanisms underlying diabetic hyperfiltration have not been fully clarified.

94 Several factors in DN, including hyperfiltration, hypertrophy and reduced abundance of th

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

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

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

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

99 ls molecular pathomechanisms associated with hyperfiltration in early diabetic kidney disease involvi

100 Rats demonstrate renal vasodilation and hyperfiltration in pregnancy.

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

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

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

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

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

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

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

108 meability (P(alb) ) assay, and mitigation of hyperfiltration-induced injury in unilaterally nephrecto

109 luid-flow shear stress (FFSS) contributes to hyperfiltration-induced podocyte and glomerular injury r

110 arise from autoimmune, genetic, mechanical (hyperfiltration), infectious, toxic or monoclonal mechan

111 This raises concern for hyperfiltration injury.

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

113 The hyperfiltration is a dysfunctional state that may arise

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

115 Hyperfiltration is a state of high glomerular filtration

116 Glomerular hyperfiltration is common in early diabetes and is consi

117 The attenuation of glomerular hyperfiltration is posited to be a principal mechanism u

118 Hyperfiltration is very infrequent.

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

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

121 Hyperfiltration mainly occurs in response to signals pas

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

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

124 in SFK is associated with reduced glomerular hyperfiltration-mediated kidney disease up to 8 months o

125 ls, this indicates a reduction in glomerular hyperfiltration-mediated kidney dysfunction.

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

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

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

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

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

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

132 ion is challenged by the transition from the hyperfiltration phase to reduced eGFR and by tubular cre

133 e key pathophysiological drivers (glomerular hyperfiltration, podocyte injury, tubulointerstitial inf

134 abetes, SGLT2 inhibitors mitigate glomerular hyperfiltration predominantly through afferent arteriola

135 amine the impact of elevated plasma glucose, hyperfiltration, PT hypertrophy and reduced abundance of

136 Although hyperfiltration restores sodium and chloride excretion i

137 Glomerular hyperfiltration resulting from an elevated intraglomerul

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

139 tration rate (GFR), otherwise known as renal hyperfiltration (RHf), is associated with an increased r

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

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

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

143 cell disease-related kidney disease include hyperfiltration that occurs early in the disease course

144 Obesity is thought to increase renal hyperfiltration, thereby increasing albuminuria and the

145 lower glomerular capillary hypertension and hyperfiltration, thereby reducing the physical stress on

146 haemodynamic changes that promote glomerular hyperfiltration to compensate for the greater metabolic

147 ellular mechanisms of damage associated with hyperfiltration, transcriptional profiles of kidney biop

148 Treatment with SGLT2i for Hyperglycemia and Hyperfiltration Trial) is a 22-week, double-blind, rando

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

150 Glomerular hyperfiltration was also significantly reduced in diabet

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

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

153 vel mechanism of acute hyperglycemia-induced hyperfiltration wherein increases in luminal glucose at

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

155 es in SNGFR can alter protein excretion, and hyperfiltration with glomerular leak can combine to incr