ライフサイエンスコーパス: proteinuric

1 nuric, 17 were microalbuminuric, and 19 were proteinuric.

2 n both animal models and humans exhibiting a proteinuric.

3 odels of glomerular injury and that its anti-proteinuric action may result from direct effects on cel

4 maller and less specific differences between proteinuric and control groups.

5 LL lesion were more often black and severely proteinuric and developed more end-stage renal disease (

6 injection of anti-Fx1A antiserum, rats were proteinuric and had a blunted natriuretic response to in

7 On day 7, the PHN rats were severely proteinuric, and most slit diaphragms were either absent

8 ce with the results seen in suPAR-associated proteinuric animal models, in which kidney damage is cau

9 yeloid cells was commonly found in the BM of proteinuric animals having high suPAR, and these cells e

10 c patients with FSGS-CELL (n = 39) were more proteinuric at presentation than patients with FSGS-CS (

11 n the urinary side of renal tubular cells in proteinuric, but not in normal renal tissues and colocal

12 Therefore, urine from rats made proteinuric by puromycin aminoglycoside administration w

13 Proteinuric chronic kidney disease (CKD), once a rare af

14 hree-way crossover study in 27 patients with proteinuric CKD to compare the effects of the ET(A) rece

15 h renal and systemic vascular dysfunction in proteinuric CKD.

16 P) are more frequent in individuals with the proteinuric disease focal and segmental glomeruloscleros

17 a dynamic actin cross-linking protein, cause proteinuric disease in humans and mice.

18 ivated in glomeruli and podocytes in several proteinuric disease models.

19 RPC6 in the pathology of nongenetic forms of proteinuric disease.

20 athway leading to foot process effacement in proteinuric diseases.

21 er, and hence an important common pathway in proteinuric diseases.

22 meruli is observed in several human acquired proteinuric diseases.

23 r heparanase expression is increased in most proteinuric diseases.

24 trated to be a trigger mechanism for various proteinuric diseases.

25 rvention in the nephrotic syndrome and other proteinuric diseases.

26 ve therapeutic potential in the treatment of proteinuric diseases.

27 anges in these junctions are the hallmark of proteinuric diseases.

28 ted tubular injury can occur in MN and other proteinuric diseases.

29 id target for pharmaceutical intervention in proteinuric disorders and provide an approach to investi

30 insight into molecular mechanisms underlying proteinuric disorders, highlight potentially complex int

31 ogenic-independent and MC1R-dispensable anti-proteinuric effect of melanocortin signaling.

32 Current thresholds for defining proteinuric flare appear to be set either too high or to

33 egree of proteinuria increase that defines a proteinuric flare in systemic lupus erythematosus (SLE)

34 Ideally, the threshold for proteinuric flare should be set sufficiently high that s

35 -based approach to setting the threshold for proteinuric flare, based on quantifying the spontaneous

36 c flares (all severe except for 1) and 2 had proteinuric flares (1 in each responder group).

37 y podocytes of hyposialylated Angptl4, a pro-proteinuric form of the protein.

38 ma3a gain-of-function in adult mice leads to proteinuric glomerular disease involving the three layer

39 r studies should evaluate the role of YAP in proteinuric glomerular disease pathogenesis and its pote

40 butes to the development of several types of proteinuric glomerular disease, but the involvement of i

41 First delineated from other proteinuric glomerular lesions in the 1980s, CG is now r

42 inuria reducing and podoprotective effect in proteinuric glomerulopathies via MC1R-independent mechan

43 mensional ultrastructural characteristics of proteinuric glomerulopathy in mice with CD2-associated p

44 Examination of albumin staining of proteinuric human kidneys also showed a heterogeneous pa

45 eclampsia was assessed by the development of proteinuric hypertension.

46 ) experienced renal flares (nephritic in 33, proteinuric in 8) after a mean followup of 117 months; 3

47 or more than 2 yr or enrolling more severely proteinuric individuals.

48 In rats with one proteinuric kidney (PAN-treated) and one normal kidney (

49 Podocyte injury is a major determinant of proteinuric kidney disease and the identification of pot

50 mice with adriamycin nephropathy, a model of proteinuric kidney disease that resembles human focal se

51 t podocyte-specific deletion of Yap leads to proteinuric kidney disease through increased podocyte ap

52 Podocyte injury results in proteinuric kidney disease, and genetic deletion of SD-a

53 ntal glomerulosclerosis (FSGS) is a cause of proteinuric kidney disease, compromising both native and

54 In both genetic and acquired forms of proteinuric kidney disease, dysregulation of podocyte TR

55 During proteinuric kidney disease, induction of cytoplasmic cat

56 s an appropriate therapeutic goal in chronic proteinuric kidney disease.

57 eutic benefit in a rat model of hypertensive proteinuric kidney disease.

58 is of podocyte injury and the progression of proteinuric kidney disease.

59 in the BM, leading to high plasma suPAR and proteinuric kidney disease.

60 to podocytes is a central pathomechanism of proteinuric kidney disease.

61 iovascular risk and slows the progression of proteinuric kidney disease.

62 ss effacement, which is a classic feature of proteinuric kidney disease.

63 strategy for the prevention or treatment of proteinuric kidney disease.

64 providing a potential therapeutic target for proteinuric kidney disease.

65 ls of biochemistry may be useful in treating proteinuric kidney disease.

66 lockade may be therapeutically beneficial in proteinuric kidney disease.

67 on barrier and podocyte dysfunction leads to proteinuric kidney disease.

68 and defines a molecular mechanism underlying proteinuric kidney disease.

69 tial therapeutic target for the treatment of proteinuric kidney disease.Podocytes are essential compo

70 ) underlies the pathogenesis of all forms of proteinuric kidney disease; however, the specific geneti

71 ated overexpression of ShcA in several human proteinuric kidney diseases compared with normal conditi

72 docyte loss is central to the progression of proteinuric kidney diseases leading to end-stage kidney

73 In human proteinuric kidney diseases such as diabetic nephropathy

74 py is the standard of care for patients with proteinuric kidney diseases, but their use is challengin

75 wild-type TRPC6 is a common feature of human proteinuric kidney diseases, with highest induction obse

76 e of cytoskeletal and structural proteins in proteinuric kidney diseases.

77 provides a novel molecular target to tackle proteinuric kidney diseases.

78 c therapy in the treatment of FSGS and other proteinuric kidney diseases.

79 ssays for identifying novel therapeutics for proteinuric kidney diseases.

80 renal protection against the development of proteinuric kidney diseases.

81 rstanding of the pathogenesis of progressive proteinuric kidney diseases.

82 y represent a novel therapeutic strategy for proteinuric kidney diseases.

83 g and shed further light on the treatment of proteinuric kidney diseases.

84 CsA is also used for the treatment of proteinuric kidney diseases.

85 mma-secretase inhibitor) protected rats with proteinuric kidney diseases.

86 ry and provides a molecular target to tackle proteinuric kidney diseases.

87 In vivo, we observed activated PKC-delta in proteinuric kidneys of streptozotocin-induced diabetic m

88 al tissues and colocalized with properdin in proteinuric kidneys.

89 The GBM of proteinuric mice appeared thickened and "moth-eaten," an

90 cant difference in allele frequencies in the proteinuric, microalbuminuric, or normoalbuminuric group

91 romoter region of KLF15 In three independent proteinuric murine models, podocyte-specific loss of Klf

92 ile of MES who were also microalbuminuric or proteinuric (n = 16) were classified as "fast-track" for

93 the renal transplant population, as it is in proteinuric nephropathies.

94 ia changes have a prognostic significance in proteinuric nephropathies.

95 mmon pathways that lead to kidney failure in proteinuric nephropathies.

96 in 1467 individuals with T1D (718 cases with proteinuric nephropathy and 749 controls without nephrop

97 or secondary membranous nephropathy or other proteinuric or autoimmune diseases and from normal contr

98 Renal flares were classified as either proteinuric or nephritic based on changes in urinary pro

99 .012) and negatively with podocyte number in proteinuric patients (r = -0.48, P = 0.040).

100 In contrast, 71% of glomeruli from proteinuric patients had glomerulotubular junction abnor

101 nd-stage renal disease (ESRD) in a cohort of proteinuric patients with type 1 diabetes (T1D) and norm

102 otubular junction abnormalities, frequent in proteinuric patients with type 1 diabetes, may contribut

103 atients, five microalbuminuric patients, six proteinuric patients, and five control subjects were stu

104 absorption of phosphate increased during the proteinuric phase compared with the remission phase in n

105 e FHH.BN-Rab38 congenic line recapitulated a proteinuric phenotype indistinguishable from the FHH str

106 Proteinuric rats developed tubulointerstitial disease th

107 Compared with controls, proteinuric rats exhibited significantly lower eliminati

108 In study A, proteinuric rats were given sheep anti-Fx1A to induce ex

109 In vivo, proteinuric rats were treated with vehicle or paricalcit

110 oss of renal mass and was reduced further in proteinuric rats with 0.6 kidneys.

111 hat were not different from sera pooled from proteinuric rats with HN induced with nephritogenic Fx1A

112 Compared with vehicle-treated proteinuric rats, paricalcitol showed markedly reduced r

113 locks TRPC5 channel activity in glomeruli of proteinuric rats.

114 e may have relevance for the pathogenesis of proteinuric renal disease in human patients.

115 In acquired proteinuric renal disease, glomerular TRPC6 expression i

116 may have potential as a therapeutic agent in proteinuric renal disease.

117 Renal tubular atrophy accompanies many proteinuric renal diseases, suggesting that glomerular p

118 venting complement-derived tubular injury in proteinuric renal diseases.

119 Because podocyte injury is central to proteinuric states, such as the nephrotic syndrome, the

120 onfirm the presence of an inhibitor in other proteinuric states, the urine from two patients with pro

121 en compared with patients with other chronic proteinuric states, those with FSGS displayed a prolifer

122 te glycosaminoglycans and is up-regulated in proteinuric states.

123 te TRPC6 protein expression was increased in proteinuric streptozotocin-induced diabetic rats.

124 In mouse models of Pierson's or Alport's proteinuric syndromes resulting from defects in GBM stru

125 Thus, an additional mechanism by which anti-proteinuric therapies are beneficial in the treatment of

126 Renal biopsies from eight proteinuric type 1 D patients with normal to moderately

127 rial, we randomly assigned 317 patients with proteinuric type 2 diabetic nephropathy to twice-daily p

128 Proteinuric urine contained a powerful specific inhibito

129 Proteinuric urine was fractionated by thin-layer chromat

130 ed effects on renal tubular cells exposed to proteinuric urine, equivalent levels of proteinuria were

131 and mostly occurs in patients who are highly proteinuric with early CKD.