ライフサイエンスコーパス: renal damage

1 resistance" state (ie, resistance to further renal damage).

2 of diabetic nephropathy and obesity-induced renal damage.

3 aid bacterial clearance but can also lead to renal damage.

4 protein excretion, and the amount of chronic renal damage.

5 in response to ischemia/reperfusion-induced renal damage.

6 tients to reduce the incidence and extent of renal damage.

7 function and ameliorate hypertension induced renal damage.

8 e may be more susceptible to immune-mediated renal damage.

9 these compensatory pathways following acute renal damage.

10 ld overcome HFD-induced metabolic memory and renal damage.

11 egies that limit or prevent ischemia-induced renal damage.

12 uced in a dose-dependent fashion cardiac and renal damage.

13 e novo production of nephrons in response to renal damage.

14 CR enzyme and cholesterol accumulation after renal damage.

15 utic potential for protection from ischaemic renal damage.

16 essed after in vivo ischemic and Fe-mediated renal damage.

17 urine flow protects adults from progressive renal damage.

18 peripheral vascular disease, and progressive renal damage.

19 after an infection actually have congenital renal damage.

20 nsin II challenge and were protected against renal damage.

21 n and glomerular hypertension eventuating in renal damage.

22 ers cause hemodynamic process that result in renal damage.

23 after ischemia also significantly inhibited renal damage.

24 vement of IgG glycosylation in mechanisms of renal damage.

25 ng hypertension while preventing cardiac and renal damage.

26 ompanied by a better renal function and less renal damage.

27 es metabolic memory and prevents HFD-induced renal damage.

28 pair capacity and thus, higher resistance to renal damage.

29 s show that ISD protects from injury-induced renal damage.

30 expression of p66Shc was linked to increased renal damage.

31 opriate activation of the AP, eventuating in renal damage.

32 of the Th17 immune response in experimental renal damage.

33 ADMA metabolism protects against progressive renal damage.

34 egy for protection against cisplatin-induced renal damage.

35 ce are more sensitive to tunicamycin-induced renal damage.

36 d VDR-null mice from severe diabetes-related renal damage.

37 in parenchymal cells predominantly mediates renal damage.

38 tinal and systemic disease, including severe renal damage.

39 suggesting absence of therapy-induced acute renal damage.

40 ine HK-2 as an in vitro model of Stx-induced renal damage.

41 y contribute to increased blood pressure and renal damage.

42 ucial in ameliorating streptozotocin-induced renal damage.

43 l growth factor, can lead to proteinuria and renal damage.

44 kidney, improved renal function, and reduced renal damage.

45 which administration of BMP-7 may attenuate renal damage.

46 imbalance in hypertensive cardiovascular and renal damage.

47 iographic contrast media fail to demonstrate renal damage.

48 hites, but ethnicity was not associated with renal damage (adjusted odds ratio 1.6, 95% confidence in

49 (RBF) and GFR and established the degree of renal damage after 6 weeks of RVD.

50 single therapy that effectively resolves the renal damage after ischemia.

51 synthesis also ameliorated diabetes-mediated renal damage and albuminuria in Cyp4a14KO male mice.

52 0 inhibition ameliorates diabetes-associated renal damage and atheroprogression in a mouse model of c

53 ip between the monoclonal gammopathy and the renal damage and because the significance of the monoclo

54 ittle is known about the pathogenesis of SLE renal damage and compromised renal function.

55 and humoral pathways leading to progressive renal damage and end-stage renal disease.

56 ARC function provides a protective effect on renal damage and fibrosis associated with ANG II hyperte

57 refore evaluated the contribution of CCL5 to renal damage and fibrosis in hypertensive and normotensi

58 position in the kidneys was dissociated from renal damage and from activation of renal endothelial an

59 n preclinical models of hypertension-induced renal damage and glomerulonephritis.

60 ls, histological examination revealed severe renal damage and immunohistochemical localization demons

61 L-2C-induced Treg expansion attenuates acute renal damage and improves renal recovery in vivo, sugges

62 levels were associated with accumulation of renal damage and lack of response to therapy.

63 Both renal damage and PARS activation were attenuated by admi

64 othelial HIF-2 protects from hypoxia-induced renal damage and represents a potential therapeutic targ

65 very effectively arrested the progression of renal damage and, in some respects, reversed renal patho

66 ctrum antibiotics whose side effects include renal damage and, strangely, tendinopathies.

67 ilateral renal artery stenosis), established renal damage, and hypertension.

68 tor has been reported in tubular cells after renal damage, and Stat3 has been implicated in CKD progr

69 lar mechanisms that lead to diabetes-induced renal damage are incompletely defined.

70 nostic capability or help determine risk for renal damage are sorely needed.

71 Lastly, we showed reduced renal damage, as determined by renal biomarkers and hist

72 t to body weight (HW/BW) ratios, cardiac and renal damage assessed by histological examination, PAI-1

73 Treatment with FTY720 reduced renal damage assessed histologically and also reduced ap

74 implying that macrophages contribute to the renal damage associated with HUS.

75 ic mechanism responsible for the progressive renal damage associated with uromodulin gene mutations.

76 and renal damage (in trial 1) and those with renal damage but no decrease in the platelet count of mo

77 s, sympathetic nerve activity contributes to renal damage but the extent to which autonomic dysfuncti

78 c anti-DNA antibodies may also contribute to renal damage by directly influencing mesangial gene expr

79 Proteinuria may contribute to progressive renal damage by inducing tubulointerstitial inflammation

80 Renal damage caused by cold preservation and warm reperf

81 n extensively employed as an animal model of renal damage caused by Shiga toxins.

82 ciated with less functional and histological renal damage compared with control mice.

83 plus isoflurane anesthesia induced only mild renal damage (Cr, 0.9 +/- 0.1, minimal tubular necrosis;

84 an reverse this signature and the associated renal damage despite ongoing immune complex deposition.

85 reduced serum creatinine levels, diminished renal damage detected by histopathologic evaluation, and

86 Endothelin-1 (ET-1) promotes renal damage during cardiovascular disease; yet, the mol

87 idase, mediates the onset of proteinuria and renal damage during experimental diabetic nephropathy.

88 n of the microbiota significantly attenuated renal damage, dysfunction, and remote organ injury and m

89 Differential renal damage from anti-dsDNA antibodies may be due to di

90 children at high risk for VUR or at risk for renal damage from reflux-induced scarring.

91 erstitial injury when it is given 2 wk after renal damage has been established.

92 Although immune parameters that instigate renal damage have been characterized, their link to loca

93 etal urinary tract motility defects prior to renal damage.-Hurtado, R., Bub, G., Herzlinger, D.

94 sterone in the development of myocardial and renal damage in a model with high Ang II and low nitric

95 molecular markers to measure non-invasively renal damage in children with VUR.

96 Renal damage in D+HUS is caused by Shiga toxin (Stx), wh

97 potent regulatory role of LXRs in preventing renal damage in diabetes.

98 E production, normalized BP, and ameliorated renal damage in diabetic Cyp4a14KO mice.

99 hypothesized that the EP1 receptor promotes renal damage in diabetic nephropathy.

100 at heparanase contributes to proteinuria and renal damage in experimental glomerulonephritis by decre

101 res of the disease and demonstrates that the renal damage in HCDD relies on the production of an isol

102 ed that a positive MCU increases the risk of renal damage in hospitalized UTI patients by about 20%,

103 Because progressive renal damage in humans associates with proteinuria regar

104 age-specific LXR activation were analyzed on renal damage in hyperlipidemic-hyperglycemic mice.

105 t that CO itself may be protective and limit renal damage in ischemia induced ARF.

106 ssion of AM enhances cardiac hypertrophy and renal damage in male, but not female, mice with a renin

107 edly decreased the extent of albuminuria and renal damage in mouse models of DN.

108 ve protein (CRP) can prevent and reverse the renal damage in murine models of spontaneous lupus, as w

109 sis revealed a marked reduction in liver and renal damage in mutant mice treated with LPS, whereas bl

110 s suggest that IL-1beta blockade may prevent renal damage in nephrocalcinosis.

111 is instrumental, we compared the severity of renal damage in NGAL wild-type mice and NGAL-knockout mi

112 Despite advances in therapeutics, renal damage in particular continues to be an important

113 VUR is hence a weak predictor of renal damage in pediatric patients hospitalized with UTI

114 ibody-induced hypertension, proteinuria, and renal damage in pregnant mice, demonstrating that autoan

115 Renal damage in response to 5/6 nephrectomy was greatly

116 ay be a novel therapeutic approach to reduce renal damage in SLE.

117 Furthermore, the pathogenesis of renal damage in such patients is probably complex becaus

118 ay be important in the cascade(s) leading to renal damage in systemic Lupus erythematosus.

119 candesartan caused a significant increase in renal damage in the Dahl salt-sensitive model of hyperte

120 cilexetil significantly reduced cardiac and renal damage in the nitric oxide synthase inhibitor mode

121 pe mice, VDR-null mice developed more severe renal damage in the obstructed kidney, with marked tubul

122 imary VUR as an effective screening test for renal damage in this population.

123 e beneficial in ameliorating the progressive renal damage in uromodulin-associated kidney diseases.

124 Patients with low platelet counts and renal damage (in trial 1) and those with renal damage bu

125 Aging of the kidney is associated with renal damage, in particular mesangial matrix expansion (

126 This renal damage increases in relation to the time of exposu

127 ly to improve metabolic disorder and relieve renal damage induced by diabetes.

128 esized to be instrumental in the etiology of renal damage induced by proteinuria.

129 c reticulum (ER), but the pathophysiology of renal damage is unclear.

130 a-MSH significantly reduced ischemia-induced renal damage, measured by changes in renal histology and

131 administered after the development of severe renal damage (MST after proteinuria onset was 12.5 weeks

132 viewed as the major risk factor for acquired renal damage, now shares this role with nonreflux nephro

133 Renal damage occurred more frequently among Hispanics an

134 ere found to be protected from the liver and renal damage of tyrosinemia as hypothesized.

135 ins after AKI, and it is highly expressed in renal damage of various etiologies.

136 Renal damage or dysfunction was examined by immunohistoc

137 mination verified the absence of significant renal damage or immune deposition in responding mice.

138 s, and prognostic implications of persistent renal damage (RD) in patients with preexistent moderate-

139 e role of statin pre-treatment in preventing renal damage remains uncertain.

140 ded to either ischemic or folic acid-induced renal damage similarly to control mice.

141 y correlated with renal disease activity and renal damage (Spearman's r >/= 0.47, P < 0.0001 for both

142 non-renal transplant recipients demonstrate renal damage that affects primarily the preglomerular ar

143 Renal damage that is characterized by activation of Ang

144 he primary virulence factors responsible for renal damage that may follow diarrheal disease.

145 that includes the reduction of iron-induced renal damage, the regulation of nicotinamidase activity,

146 hrectomized Wistar rats mediated the greater renal damage, the study was repeated, with Wistar rats (

147 zes to kidney tissue and eventually leads to renal damage through a process that first involves the b

148 TLR4, these results support the concept that renal damage triggers an innate immune response, which c

149 In summary, renal damage upon 5/6 nephrectomy was markedly reduced i

150 nicotinic acetylcholine receptor agonists on renal damage using a mouse model of lipopolysaccharide (

151 mpact of arginase activity and expression on renal damage was evaluated in spontaneously diabetic Ins

152 myocardial infarction, stroke, or persistent renal damage) was significantly lower in the statin grou

153 Urinary albumin excretion, an index of renal damage, was also lower in CDU-treated hypertensive

154 rmine susceptibility to hypertension-induced renal damage, we derived an experimental animal model in

155 ers that monitor recovery from agent-induced renal damage, we scored changes in the levels of urinary

156 sis, respectively, and all six parameters of renal damage were changed in parallel, and ARB treatment

157 Although progressive renal damage with proteinuria only occurred in F1 mice,