ライフサイエンスコーパス: extrarenal

1 D has been broadened by the discovery of the extrarenal 1alpha-hydroxylase (CYP27B1) in various vitam

2 For example, although the identification of extrarenal 1alpha-hydroxylase activity suggests that aut

3 but also may be important for providing the extrarenal 1alpha-hydroxylase that is present in most ti

4 ies support the concept that the MR also has extrarenal actions and that defects in sodium handling a

5 erapeutic strategy for prevention of AKI and extrarenal acute organ injury, and have demonstrated enc

6 ts (retransplants, highly sensitized, etc.), extrarenal allograft recipients, or alternative drug reg

7 have not discriminated between the roles of extrarenal and intrarenal dopamine in the overall regula

8 a (34%), systemic atherosclerosis (25%), and extrarenal aneurysms (6.5%).

9 consider screening, particularly those with extrarenal anomalies or genetic disorders, as preterm in

10 rst 72 hours of life, genetic disorders, and extrarenal anomalies.

11 nd was associated with genetic disorders and extrarenal anomalies.

12 first example of hypertonic induction of an extrarenal aquaporin, as well as the first association b

13 nstrate that regulation of blood pressure by extrarenal AT(1A) receptors cannot be explained by alter

14 kidney, the residual repertoire of systemic, extrarenal AT1 receptors is not sufficient to induce hyp

15 Overall, extrarenal cells did not substitute for any intrinsic EC

16 elative contribution of intrarenal cells and extrarenal cells to kidney regeneration is not clear.

17 ion (I/R) injury as well as the potential of extrarenal cells to substitute for injured local EC.

18 as smooth-muscle, epithelial, mesangial, and extrarenal cells.

19 ibutable to defective renal clearance and/or extrarenal clearance and metabolism, the latter possibly

20 c26a6 is a candidate for contributing to the extrarenal clearance of oxalate via the gut in CKD.

21 te the specific contribution of renal versus extrarenal collectrin on BP regulation and salt sensitiv

22 disease seems to be a distinct and important extrarenal complication of ADPKD.

23 Moreover, in patients with at least one extrarenal complication, chitotriosidase significantly c

24 significantly correlated with the number of extrarenal complications and was superior to white blood

25 ns of Klotho expression, and hence renal and extrarenal complications associated with Klotho loss.

26 to study the evolution of less commonly seen extrarenal complications of cystinosis in a group of pat

27 er characterized by renal cyst formation and extrarenal complications such as hypertension and vascul

28 management of the renal failure and serious extrarenal complications that may occur during the cours

29 nt age and comorbidity, presence and risk of extrarenal complications, estimated waiting time, the av

30 th growing cysts, hypertension, and multiple extrarenal complications, including liver cysts, intracr

31 erized by the development of renal cysts and extrarenal complications, such as cardiac hypertrophy.

32 evels in predicting the presence of multiple extrarenal complications.

33 e model induces more severe renal injury and extrarenal complications.

34 Basal renal and extrarenal CYP24 is usually low but is highly induced by

35 To determine the role of renal versus extrarenal D(5) receptors in BP regulation, we performed

36 but not with extrarenal disease activity or extrarenal damage.

37 injury underscores the reluctance to recover extrarenal DCD organs since lack of medical therapy to s

38 tations, such as R246Q, can have less severe extrarenal defects but still exhibit congenital nephroti

39 The extrarenal defects in this murine model include common b

40 ric kidney development and abrogated several extrarenal developmental defects.

41 lovesical fistula, and incidentally detected extrarenal disease (a liver mass, hepatic metastases, ly

42 < 0.0001 for both comparisons), but not with extrarenal disease activity or extrarenal damage.

43 I score (r = 0.452, P = 0.009), but not with extrarenal disease activity.

44 C57BL/6 mice were negative for BM-derived or extrarenal ECFCs.

45 vestigations reveal a range of unanticipated extrarenal effects of aldosterone, as well as a detailed

46 duction in peritubular cells and unwarranted extrarenal effects.

47 Hepatocytes are the primary source of extrarenal EPO in the adult and express HIF-1 and HIF-2,

48 The extrarenal etiology of systemic lupus is based on multip

49 ion (27%) or kidney biopsy (18%), and guided extrarenal evaluation (72%) in patients with an informat

50 The prevalence of death or serious extrarenal events was 18% and 20% in the experimental an

51 podocyte-specific transgenic expression when extrarenal expression of a transgene is problematic.

52 It is suggested that the hepatic extrarenal expression of klotho may function as a furthe

53 of mediators of epithelial Cl(-) flux whose extrarenal expression overlaps with WNK4.

54 sion of both, suggesting that both renal and extrarenal factors are important in the regulation of AT

55 However, in edematous disorders, extrarenal factors can override the 'innate wisdom' of t

56 s achieved by a dual mechanism that includes extrarenal factors such as insulin and beta-adrenergic a

57 cross-sectional study that aimed to evaluate extrarenal factors that may have influence on kidney gra

58 ependently associated with eGFR but not with extrarenal factors.

59 h autosomal dominant FSGS but without either extrarenal features or ultrastructural abnormalities of

60 lity is important to ensure compensation for extrarenal fluid losses.

61 Phenotype analysis of kidney and extrarenal function in knockout mice has been very infor

62 would be the definite proof of extrahepatic, extrarenal glucose production.

63 hout adversely affecting donor physiology or extrarenal graft survival.

64 to systemic EPO homeostasis and the role of extrarenal HIF-2 in erythropoiesis, in the absence of ki

65 the associated uremia did not seem to affect extrarenal HO-1 gene activity assessed in the liver, lun

66 Extrarenal immune-related adverse events occurred in 43%

67 Concomitant extrarenal immune-related adverse events were associated

68 Anesthetic effects on extrarenal injury (plasma creatine phosphokinase, lactat

69 Extrarenal involvement (e.g., skin and cornea) is freque

70 ted in all 8 patients with PTMA, and limited extrarenal involvement by PTMA was observed in 3 of thes

71 horough hematologic workup and evaluation of extrarenal involvement is mandatory for management.

72 atments, familial history of kidney disease, extrarenal involvement, congenital abnormalities of the

73 Secondary endpoints included hematologic and extrarenal involvement.

74 nsporters and channels involved in renal and extrarenal K(+) homeostasis.

75 electrolytes (i.e, UAG) indicates selective extrarenal loss of these electrolytes or nonsteady state

76 (PCLD) and are recognized as the most common extrarenal manifestation in autosomal dominant polycysti

77 Polycystic liver disease is the most common extrarenal manifestation of autosomal dominant polycysti

78 The principal extrarenal manifestation of autosomal dominant polycysti

79 racteristics of the liver disease, and other extrarenal manifestations in ADPKD.

80 study highlights an unexpected frequency of extrarenal manifestations in MIDD.

81 Extrarenal manifestations include an increased level of

82 Imaging is also helpful in detecting extrarenal manifestations of ADPKD, most significant of

83 This article reviews the renal and extrarenal manifestations of autoimmune reactivity in AP

84 exhibited similar hematologic evolution and extrarenal manifestations of STEC-HUS.

85 lmonary hemorrhage at onset; (3) presence of extrarenal manifestations versus renal limited disease;

86 Extrarenal manifestations, mostly of skin, were present

87 logy, renal and hematologic characteristics, extrarenal manifestations, prognosis, treatment, and pat

88 by renal and liver cysts, and cardiovascular extrarenal manifestations.

89 ttention has been paid to the description of extrarenal manifestations.

90 to adult-onset FSGS in the absence of overt extrarenal manifestations.

91 sediment or the persistence or appearance of extrarenal manifestations.

92 er disease; intracranial aneurysms and other extrarenal manifestations; lifestyle and psychosocial as

93 the other types, 35% of whom had symptomatic extrarenal (mostly hepatic and cardiac) involvement.

94 ey injury (AKI) is frequently complicated by extrarenal multiorgan injury, including intestinal and h

95 alignant mesothelioma is one of the very few extrarenal neoplasms in which the Wilms tumor suppressor

96 med before EC injury to allow distinction of extrarenal or BM-derived cells from intrinsic renal cell

97 ) remains unacceptably high, likely owing to extrarenal organ dysfunction.

98 e supports extensive, yet indistinguishable, extrarenal organ manifestations.

99 these principles in recipients of renal and extrarenal organ transplants.

100 ng the role of facilitated urea transport in extrarenal organs expressing UT-B.

101 ICU extubation should not eliminate extrarenal organs from consideration and may be preferab

102 o increase the utilization of both renal and extrarenal organs from donors after cardiac death (DCD),

103 Circulating Angptl4 was secreted by extrarenal organs in response to an elevated plasma rati

104 In addition to renal functions, extrarenal organs may be affected from cystine accumulat

105 red, 21 not transplanted, 8 en bloc, 23 with extrarenal organs, and 6 with missing records), 228 reci

106 significant differences in graft survival of extrarenal organs.

107 has a significant effect on the function of extrarenal organs.

108 production of this steroid hormone in >/=10 extrarenal organs.

109 Furthermore, CAIX expression is apparent in extrarenal organs.

110 , we observed CAIX expression in a number of extrarenal organs.

111 gest glucarpidase may improve both renal and extrarenal outcomes in patients with MTX-AKI.

112 nal oxalate elimination in humans to enhance extrarenal oxalate clearance.

113 diseases that are frequently associated with extrarenal pathologies such as retinal degeneration, obe

114 he present study characterizes the renal and extrarenal pathology in the BALB/c-cpk/cpk murine model

115 k/cpk murine model displays renal as well as extrarenal pathology similar to that found in human ARPK

116 -20 mice faithfully reproduced the renal and extrarenal phenotypes associated with human NPH, includi

117 time, in a local feedback loop, the elevated extrarenal pools of Angptl4 reduced tissue FFA uptake in

118 potassium and the neurohumoral mediators of extrarenal potassium disposal with maximal exercise.

119 levels may contribute to the maintenance of extrarenal potassium homeostasis in ESRD.

120 onal source of renin and constitute a unique extrarenal renin-angiotensin system.

121 oups provides evidence against any important extrarenal response to acute PO4 loads.

122 This pathway may explain renal and extrarenal responses to altered K(+) intake that occur i

123 abdoid tumors of the brain and 7 renal and 4 extrarenal rhabdoid tumors for mutations in the candidat

124 nvestigate the human placenta as a potential extrarenal site of EPO production.

125 press renin gene expression at inappropriate extrarenal sites where cellular proteases, to which pror

126 ipants of developmental vascular assembly in extrarenal sites.

127 bdoid tumors of the brain, kidney, and other extrarenal sites.

128 lupus nephritis than in patients with active extrarenal SLE, inactive SLE, and other glomerular disea

129 patients with moderately-to-severely active extrarenal SLE.

130 Associated renal or extrarenal symptoms should alert the nephrologist to HNF

131 D onset, performing clinical examination for extrarenal symptoms, and considering genetic testing.

132 Patients who exhibited extrarenal symptoms, had a familial history of the disea

133 l relevance, also with respect to additional extrarenal symptoms.

134 congenital nephrotic syndrome but only mild extrarenal symptoms; the mechanisms underlying the devel

135 Extrarenal thrombi were detected in the gastrointestinal

136 and may resemble those changes described for extrarenal tissues and (2) increased NHE-3 activity due

137 xpression in podocytes without expression in extrarenal tissues in adult or embryonic mice.

138 the kidney, is also expressed in many other extrarenal tissues including the pancreas.

139 ension, whereas the absence of RGS2 from all extrarenal tissues including the peripheral vasculature

140 AT(1) receptor actions in the kidney and in extrarenal tissues to determining the level of blood pre

141 e tested the ability of fibrotic kidneys and extrarenal tissues to produce EPO.

142 lore the relative contributions of renal and extrarenal tissues to the low blood pressure seen in the

143 of RGS2 actions in the kidney from those in extrarenal tissues with regard to BP regulation.

144 cts in renal epithelial cells directly or in extrarenal tissues, and whether inhibition of calcineuri

145 Prorenin is expressed in certain extrarenal tissues, but normally only the kidneys proces

146 Moreover, autoimmune injury in extrarenal tissues, including skin, heart, and joints, w

147 In extrarenal tissues, WNK4 is found almost exclusively in

148 e examined the distribution of WNK1 in these extrarenal tissues.

149 ents support our hypothesis that LPS acts on extrarenal TLR4, thereby leading to systemic TNF release

150 temic TNF release triggered by LPS acting on extrarenal TLR4.

151 l transplantation experiments confirmed that extrarenal transcription of transgenic albumin was unlik

152 stration compared with innervated kidneys in extrarenal transplantation.

153 Extrarenal tumors were also noted in the spleen and uter

154 e data support the hypothesis that increased extrarenal vascular ET-1 production in response to HS in

155 Extrarenal viral inclusions were documented in the gastr