ライフサイエンスコーパス: DKD

1 DKD is a prototypical disease of gene and environmental

2 DKD samples were significant for their racial diversity

3 on on diabetic mouse models would accelerate DKD.

4 FR decline in persons with early or advanced DKD.

5 were roughly two-fold higher in the advanced DKD population (NEPHRON-D) than in the early DKD populat

6 tients with type 1 diabetes and albuminuria (DKD(+)) when compared with diabetic patients with normoa

7 (OR 1.43, 95% CI 1.20-1.72, P < 0.001), and DKD (OR 1.33, 95% CI 1.17-1.51, P < 0.001).

8 e profile between DKD-resistant C57BL/6J and DKD-susceptible DBA/2J (D2) glomeruli and demonstrated a

9 idence for a causal link between obesity and DKD in type 1 diabetes.

10 ared the early transcriptome profile between DKD-resistant C57BL/6J and DKD-susceptible DBA/2J (D2) g

11 atistically differentially regulated in both DKD glomeruli and tubuli and was associated with increas

12 ry bulb neurons, the phenotypes of complexin DKD and DKO neurons.

13 Furthermore, the complexin DKD but not the complexin DKO caused a compensatory incr

14 f early (ACCORD) and advanced (VA NEPHRON-D) DKD.

15 ight glucose control significantly decreases DKD incidence, indicating that hyperglycemia-induced met

16 We find that complexin-deficient DKD and DKO neurons invariably exhibit a ~50% decrease i

17 dent or progressive diabetic kidney disease (DKD) in persons with type 2 diabetes.

18 Diabetic kidney disease (DKD) is a microvascular complication that leads to kidne

19 Diabetic kidney disease (DKD) is a serious complication of hyperglycemia.

20 Diabetic kidney disease (DKD) is associated with oxidative stress and mitochondri

21 apeutics to prevent diabetic kidney disease (DKD) is limited by a lack of animal models exhibiting pr

22 Diabetic kidney disease (DKD) is the leading cause of ESRD.

23 Diabetic kidney disease (DKD) is the leading cause of kidney failure worldwide an

24 Diabetic kidney disease (DKD) is the single leading cause of kidney failure in th

25 Diabetic kidney disease (DKD) is the single most common cause of albuminuria and

26 , the prevalence of diabetic kidney disease (DKD) may increase due to the expanding size of the diabe

27 ogenetic markers of diabetic kidney disease (DKD) progression to ESRD are lacking.

28 tion/progression of diabetic kidney disease (DKD) remain poorly understood.

29 Diabetic kidney disease (DKD) remains the most common cause of end-stage kidney d

30 ent risk factor for diabetic kidney disease (DKD), but establishing causality from observational data

31 the progression of diabetic kidney disease (DKD), but their contribution to organ damage in DKD rema

32 amaged podocytes in diabetic kidney disease (DKD).

33 logical mediator of diabetic kidney disease (DKD).

34 as been linked with diabetic kidney disease (DKD).

35 DKD population (NEPHRON-D) than in the early DKD population (ACCORD).

36 nfirmed in biopsies from patients with early DKD (n = 70) when compared with normal living donors (n

37 t three residues of DesA3 showed that either DKD or LEA gave the best enhancement of stability for th

38 port characterizes clinical and experimental DKD and negatively influences podocyte function.

39 is no effective therapeutic intervention for DKD.

40 d in combination with first line therapy for DKD.

41 red human podocytes with sera collected from DKD patients, who displayed elevated TNF levels, and foc

42 vel, poor prognostic indicators of time from DKD to ESRD.

43 In human DKD, increased urine 8-oxo-deoxyguanosine was associated

44 icroarray analysis and comparison with human DKD showed common pathways affected in human disease and

45 ), but their contribution to organ damage in DKD remains largely unknown.

46 thelial cells representing an early event in DKD progression, and suggest that cross talk between glo

47 ce to determine the possible role of FHL2 in DKD and to clarify its association with the Wnt pathway.

48 e prognostic value of histologic findings in DKD for time to ESRD in native kidney specimens from bio

49 rises, this finding predicts an increase in DKD prevalence unless intervention should occur.

50 elated urinary metabolites were increased in DKD, but fumarate levels were uniquely reduced by the NO

51 arkers of inflammation and renal outcomes in DKD.

52 1,700 differentially expressed probesets in DKD glomeruli and 1,831 in diabetic tubuli, and 330 prob

53 cular endothelial growth factor signaling in DKD glomeruli.

54 may serve as a future therapeutic target in DKD.

55 ecule-1 (KIM-1) for the outcomes of incident DKD (ACCORD) and progressive DKD (VA-NEPHRON-D).

56 case-control study (n=190 cases of incident DKD and 190 matched controls) and a prospective cohort s

57 tified 338 genes altered in diabetes-induced DKD glomeruli, and PLK2 exhibited the most dramatic chan

58 ure experiments and a streptozotocin-induced DKD model in FHL2 gene-knockout mice to determine the po

59 ted multiple signaling pathways are involved DKD pathogenesis.

60 nd of mouse neurons with a double knockdown (DKD) of complexin-1 and -2 suggested that complexin main

61 ith diabetic patients with normoalbuminuria (DKD(-)) and similar duration of diabetes and lipid profi

62 al therapeutic agent for the amelioration of DKD.

63 characteristic change in the development of DKD.

64 matrix accumulation in the F1 Akita model of DKD.

65 nd podocytes of patients and mouse models of DKD.

66 during tubular injury in the pathogenesis of DKD and suggest d-glucarate as a potential therapeutic a

67 at C1-Ten contributes to the pathogenesis of DKD by inducing podocyte hypertrophy under high glucose

68 that may play a role in the pathogenesis of DKD or could serve as biomarkers.

69 present a distinct pathogenetic phenotype of DKD will require a large study with a broad spectrum of

70 betes, without a change in the prevalence of DKD among those with diabetes.

71 Prevalence of DKD in the United States increased from 1988 to 2008 in

72 The prevalence of DKD in the US population was 2.2% (95% confidence interv

73 The prevalence of DKD increased in direct proportion to the prevalence of

74 Among persons with diabetes, prevalence of DKD was stable despite increased use of glucose-lowering

75 lomerulosclerosis even in a different set of DKD samples.

76 uminuria, end-stage renal disease (ESRD), or DKD defined as presence of macroalbuminuria or ESRD.

77 th development of macroalbuminuria, ESRD, or DKD over time.

78 analysis showed no association with overall DKD, higher odds of macroalbuminuria (for every 1 kg/m(2

79 mes of incident DKD (ACCORD) and progressive DKD (VA-NEPHRON-D).

80 results identify novel models of progressive DKD that provide researchers with a facile and reliable

81 oxo-deoxyguanosine was associated with rapid DKD progression, and biopsies from patients with DKD sho

82 Our studies show that DKD susceptibility was linked to mitochondrial dysfuncti

83 Moreover, the DKD consistently increased spontaneous exocytosis, but t

84 FHL2 knockout significantly attenuated these DKD-induced changes.

85 a key link connecting metabolic pathways to DKD pathogenesis, and measuring urinary fumarate levels

86 test whether obesity is causally related to DKD using Mendelian randomization, which exploits the ra

87 kk1) also showed increased susceptibility to DKD.

88 esearch efforts will be needed to understand DKD pathogenesis and to identify novel drug targets.

89 While DKD is considered a microvascular complication of diabet

90 characteristic glomerular changes noted with DKD, including glomerular hypertrophy, mesangial matrix

91 progression, and biopsies from patients with DKD showed increased mitochondrial DNA damage associated