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1 d in renal biopsies from human subjects with diabetic nephropathy.
2 t among children who are already at risk for diabetic nephropathy.
3 effects of the VEGF-A isoform VEGF-A165b in diabetic nephropathy.
4 ays that mediate podocyte injury and loss in diabetic nephropathy.
5 d functional and histologic abnormalities in diabetic nephropathy.
6 Risk of death was higher among patients with diabetic nephropathy.
7 lium to protect blood vessels and ameliorate diabetic nephropathy.
8 d severe podocyte effacement, matching human diabetic nephropathy.
9 s are significantly elevated in experimental diabetic nephropathy.
10 versely with renal function in patients with diabetic nephropathy.
11 el therapeutic strategy for the treatment of diabetic nephropathy.
12 s whereby 20-HETE affects the progression of diabetic nephropathy.
13 orylation, which may, in turn, contribute to diabetic nephropathy.
14 on of angiogenic VEGF-A isoforms each worsen diabetic nephropathy.
15 ress, suggesting a possible role for ASK1 in diabetic nephropathy.
16 s cardinal signatures for the development of diabetic nephropathy.
17 thelial Adora2b signaling in protection from diabetic nephropathy.
18 n implicated as a major pathogenic factor in diabetic nephropathy.
19 lin effects in podocytes during experimental diabetic nephropathy.
20 barrier homeostasis and are dysregulated in diabetic nephropathy.
21 erged as a novel target for the treatment of diabetic nephropathy.
22 itical mediator of podocyte injury in type 2 diabetic nephropathy.
23 signaling of extracellular adenosine during diabetic nephropathy.
24 owed a selective induction of Adora2b during diabetic nephropathy.
25 e heart failure, ventricular remodeling, and diabetic nephropathy.
26 ory bowel disease, rheumatoid arthritis, and diabetic nephropathy.
27 cleotide polymorphisms at the B7-1 gene with diabetic nephropathy.
28 strategy for the prevention or treatment of diabetic nephropathy.
29 dora2b signaling in kidney protection during diabetic nephropathy.
30 between lupus nephritis, IgA nephritis, and diabetic nephropathy.
31 resent early markers of glomerular injury in diabetic nephropathy.
32 receptors (EGFRs) are activated in models of diabetic nephropathy.
33 c may provide a novel therapeutic target for diabetic nephropathy.
34 ofiles differ across the different stages of diabetic nephropathy.
35 or therapeutic intervention in patients with diabetic nephropathy.
36 vitro and in vivo disease models, including diabetic nephropathy.
37 n was observed in podocytes of patients with diabetic nephropathy.
38 FSGS, IgA nephropathy, lupus nephritis, and diabetic nephropathy.
39 xpression directly modulates the severity of diabetic nephropathy.
40 ar protease aPC to mitochondrial function in diabetic nephropathy.
41 mesangial hypertrophy in the progression of diabetic nephropathy.
42 s to metabolic disease complications such as diabetic nephropathy.
43 d risk of adverse events among patients with diabetic nephropathy.
44 he beneficial effects of aPC in experimental diabetic nephropathy.
45 at the EP1 receptor promotes renal damage in diabetic nephropathy.
46 strategy in the prevention and treatment of diabetic nephropathy.
47 nt of renal fibrosis in two animal models of diabetic nephropathy.
48 to the prediction of progression to clinical diabetic nephropathy.
49 tients with chronic kidney disease (CKD) and diabetic nephropathy.
50 -regulating protein p66(Shc) in experimental diabetic nephropathy.
51 cy of RAAS inhibitors in promoting repair of diabetic nephropathy.
52 and the EP1 receptor could be beneficial in diabetic nephropathy.
53 its derived ROS in promoting progression of diabetic nephropathy.
54 Glomerular hypertrophy is a hallmark of diabetic nephropathy.
55 eactive oxygen species) measures of advanced diabetic nephropathy.
56 actor-1alpha relevant in the pathogenesis of diabetic nephropathy.
57 ributes to the tubulointerstitial lesions of diabetic nephropathy.
58 ous TLR4 ligand high-mobility group box 1 in diabetic nephropathy.
59 ve stress and accelerates the development of diabetic nephropathy.
60 the stage for tubulointerstitial injury and diabetic nephropathy.
61 nsequences in the underlying pathogenesis of diabetic nephropathy.
62 ignated LNA-anti-miR-192, in mouse models of diabetic nephropathy.
63 regulated in the tubulointerstitium in human diabetic nephropathy.
64 ia, which is involved in the pathogenesis of diabetic nephropathy.
65 e for generation of superoxide anions during diabetic nephropathy.
66 ies that are involved in the pathogenesis of diabetic nephropathy.
67 d translational approach to the treatment of diabetic nephropathy.
68 therapeutic strategies for the prevention of diabetic nephropathy.
69 y promote tubulointerstitial inflammation in diabetic nephropathy.
70 f a wide range of kidney diseases, including diabetic nephropathy.
71 ve stress contributes to the pathogenesis of diabetic nephropathy.
72 receptor signaling may be renoprotective in diabetic nephropathy.
73 ting that it may be a therapeutic target for diabetic nephropathy.
74 protein levels in human and animal models of diabetic nephropathy.
75 for treating chronic kidney diseases such as diabetic nephropathy.
76 in the development of renal diseases such as diabetic nephropathy.
77 tol and is implicated in the pathogenesis of diabetic nephropathy.
78 a promising agent for individuals with overt diabetic nephropathy.
79 /6J-Ins2(Akita)) as a targeted treatment for diabetic nephropathy.
80 protective effects of thiazolidinediones in diabetic nephropathy.
81 prove renal outcomes in patients with type 2 diabetic nephropathy.
82 ystem inhibitors did not slow progression of diabetic nephropathy.
83 sting a therapeutic potential for NOX-E36 in diabetic nephropathy.
84 long-lasting albuminuria-reducing effects in diabetic nephropathy.
85 f congestive heart failure, hypertension, or diabetic nephropathy.
86 nvolved in the pathogenesis and treatment of diabetic nephropathy.
87 o first-in-human trials for the treatment of diabetic nephropathy.
88 activators were pursued for the treatment of diabetic nephropathy.
89 complications and the role of these AGEs in diabetic nephropathy.
90 , play a critical role in the development of diabetic nephropathy.
91 stress is emerging as a critical mediator of diabetic nephropathy.
92 or the therapeutic effects of fenofibrate on diabetic nephropathy.
93 urine were reduced in patients with advanced diabetic nephropathy.
94 HIF-1 may improve clinical manifestations of diabetic nephropathy.
95 ression of IL-17A was sufficient to suppress diabetic nephropathy.
96 ssing and thereby upregulating NOX4 in early diabetic nephropathy.
97 volved in processing of miRNAs implicated in diabetic nephropathy.
98 uctase inhibitors have been shown to improve diabetic nephropathy.
99 e strongly associated with susceptibility to diabetic nephropathy.
100 einuria and renal damage during experimental diabetic nephropathy.
101 ns of reduced albuminuria with atrasentan in diabetic nephropathy.
102 owering drug, Ezetimibe (EZT) on severity of diabetic nephropathy.
103 Here, we examined the role of IL-17A in diabetic nephropathy.
104 y significant difference in survival between diabetic nephropathy (23.8%) and other patients with CKD
105 lmost abolishes the pathological features of diabetic nephropathy, although it does not affect the hy
106 milar NMDA antagonist memantine also reduced diabetic nephropathy, although it was less effective tha
108 has been proposed to be a unifying cause for diabetic nephropathy and a target for novel therapies.
109 pathway, a key factor in the development of diabetic nephropathy and an inhibitor of autophagy, is i
110 pertension and podocyte injury contribute to diabetic nephropathy and are strong predictors of diseas
111 kidney and in pathologic conditions such as diabetic nephropathy and CKD; upregulation of Nox4 may b
112 c variation influence the risk of developing diabetic nephropathy and ESRD in patients with type 1 di
113 indicate that excess sema3a promotes severe diabetic nephropathy and identifies novel potential ther
115 show that renal Nox5 is upregulated in human diabetic nephropathy and may alter filtration barrier fu
116 r regulator of inflammation and apoptosis in diabetic nephropathy and may be a useful therapeutic mol
117 lear bile acid receptor in the prevention of diabetic nephropathy and obesity-induced renal damage.
119 hogenesis of several renal diseases, such as diabetic nephropathy and polycystic kidney disease.
120 ndings identify miR-29c as a novel target in diabetic nephropathy and provide new insights into the r
121 patients with type 2 diabetes for studies of diabetic nephropathy and recorded their characteristics
122 ) has been implicated in the pathogenesis of diabetic nephropathy and renal fibrosis; however, the ca
123 podocytes contributes to the development of diabetic nephropathy and represents a common pathway thr
125 inuria and glomerulosclerosis (indicators of diabetic nephropathy) and attenuated albumin leakage int
126 proteinuria in two independent mouse models, diabetic nephropathy, and adriamycin-induced nephropathy
127 ent age, donor age, longer dialysis vintage, diabetic nephropathy, and congestive heart failure.
128 important role in the development of type 1 diabetic nephropathy, and its inhibition could be a prom
130 Adora2b(-/-) mice experienced more severe diabetic nephropathy, and studies in mice with tissue-sp
131 d PKC-beta contribute to the pathogenesis of diabetic nephropathy, and that dual inhibition of the cl
132 also induced in vivo in two murine models of diabetic nephropathy, and treatment with CTLA4-Ig preven
133 abetic fatty rats and patients with advanced diabetic nephropathy, and were normalized by pharmacolog
135 Since CAN often develops in parallel with diabetic nephropathy as a confounder, we aimed to invest
137 minant polycystic kidney disease (ADPKD) and diabetic nephropathy associated with higher HRs for mort
138 the hypothesis of a reactive rise of ADM in diabetic nephropathy, blunted in risk alleles carriers,
139 of tubulointerstitial and matrix proteins in diabetic nephropathy, but how this occurs is not well un
140 y and resulting albuminuria are hallmarks of diabetic nephropathy, but targeted therapies to halt or
141 a is a major pathogenic factor that promotes diabetic nephropathy, but the underlying mechanism remai
142 , we wanted to explore the role of Ang II in diabetic nephropathy by a translational approach spannin
143 ranscription (STAT) signaling contributes to diabetic nephropathy by inducing genes involved in leuko
144 for early atherosclerosis, type 2 diabetes, diabetic nephropathy, cardiovascular disease and all-cau
145 Chronic exposure to high glucose leads to diabetic nephropathy characterized by increased mesangia
147 standard methods, including determination of diabetic nephropathy class, as defined by the Renal Path
148 2 in the renal tubules of human kidneys with diabetic nephropathy compared with expression of TLR4 an
149 , and human kidney tissue from patients with diabetic nephropathy demonstrated lower gene expression
152 profibrotic protein, is highly expressed in diabetic nephropathy (DN) and implicated in its pathogen
153 Loss of podocytes is an early feature of diabetic nephropathy (DN) and predicts its progression.
154 n, and with the global epidemic of diabetes, diabetic nephropathy (DN) became the leading cause of en
157 nt normoalbuminuria and 162 individuals with diabetic nephropathy (DN) from the outpatient clinic at
162 particularly relevant to the pathogenesis of diabetic nephropathy (DN) in which evidence suggests tha
173 re particularly vulnerable to development of Diabetic nephropathy (DN) leading to End Stage Renal Dis
174 sized that proteases aberrantly expressed in diabetic nephropathy (DN) may be involved in the generat
175 served mitochondrial protein associated with diabetic nephropathy (DN) that amplifies profibrotic tra
176 t is important to find better treatments for diabetic nephropathy (DN), a debilitating renal complica
177 mic reticulum (ER) stress is associated with diabetic nephropathy (DN), but its pathophysiological re
178 helial cells (PTECs) has been highlighted in diabetic nephropathy (DN), but little is known about the
179 instruments in defining the pathogenesis of diabetic nephropathy (DN), but they only partially recap
180 We analyzed specimens from patients with diabetic nephropathy (DN), FSGS, IgA nephropathy (IgAN),
181 As high glucose and oxidative stress mediate diabetic nephropathy (DN), the contribution of TxNIP was
183 k factor in the pathogenesis of both CVD and diabetic nephropathy (DN), with CVD identified as the pr
184 lications of diabetes and obesity, including diabetic nephropathy (DN), without any US Food and Drug
185 proach to assess the functional context of a diabetic nephropathy (DN)-associated SNP located in the
199 (n = 6839), type 2 diabetes (T2D; n = 7710), diabetic nephropathy (DN; n = 2452), % body fat (n = 555
200 fit of Nrf2 activation and ROS inhibition in diabetic nephropathy (dNP), the Nrf2 activator bardoxolo
202 s with focal segmental glomerulosclerosis or diabetic nephropathy exhibited diminished H3K27me3 and h
203 psies from patients with IgA nephropathy and diabetic nephropathy exhibited substantial activation of
204 mL/min per 1.73m(2), or development of overt diabetic nephropathy), eye events (a composite of requir
205 n a cohort of 3652 patients from the Finnish Diabetic Nephropathy (FinnDiane) Study with type 1 diabe
207 nge 0-2.9 microM for patients with diagnosed diabetic nephropathy, gout or hyperuricemia, and can rea
209 docyte membrane component that is reduced in diabetic nephropathy, has been shown to activate phospho
210 ubunit of N-type calcium channel, Cav2.2, in diabetic nephropathy, however, remains to be clarified.
212 -1 blockade attenuates the manifestations of diabetic nephropathy in a type 1 diabetic animal model,
213 osine kinase activity, on the progression of diabetic nephropathy in a type 1 diabetic mouse model.
214 is an oral antifibrotic agent that benefits diabetic nephropathy in animal models, but whether it is
215 Administration of lipoic acid abrogates diabetic nephropathy in animal models, but whether lower
216 ciency may contribute to the pathogenesis of diabetic nephropathy in both experimental models and hum
217 e myosin heavy chain IIA are associated with diabetic nephropathy in European Americans and with sick
218 Thus, we examined the role of Nox5 in human diabetic nephropathy in human mesangial cells and in an
219 Hypertension is a prerequisite for advanced diabetic nephropathy in humans, so its rarity in typical
222 administration of low-dose IL-17A prevented diabetic nephropathy in models of type 1 and type 2 diab
223 ese susceptibility loci were associated with diabetic nephropathy in patients from the Joslin Study o
224 ere independent predictors of progression to diabetic nephropathy in this normoalbuminuric cohort.
225 with erlotinib attenuates the development of diabetic nephropathy in type 1 diabetes, which is mediat
226 ubsequently been shown to be associated with diabetic nephropathy in unrelated patients with type 2 d
241 UII and UII receptors (UTR) are increased in diabetic nephropathy, it remains unclear whether UII reg
243 nd -4 in several glomerulopathies, including diabetic nephropathy, little is known regarding the role
244 isease [CD] and ulcerative colitis [UC]) and diabetic nephropathy (macroalbuminuria and end-stage ren
246 ents and signaling pathways activated during diabetic nephropathy may be similar in different cell ty
247 of native kidney disease were primary FSGS, diabetic nephropathy, membranous nephropathy, immunoglob
248 affected by Tgfb1 genotype, many features of diabetic nephropathy (mesangial expansion, elevated plas
249 replacing leptin could reverse the advanced diabetic nephropathy modeled by the leptin-deficient BTB
251 nal vessel calibers as 16-year predictors of diabetic nephropathy, neuropathy, and proliferative reti
252 slowing renal function loss in patients with diabetic nephropathy on chronic stable renin-angiotensin
256 ached statistical significance with advanced diabetic nephropathy (P = 0.037 [adjusted P = 0.222]).
257 rotective effects against the progression of diabetic nephropathy, partly by protecting podocytes.
258 a suggest that EP1 activation contributes to diabetic nephropathy progression at several locations, i
261 cytokines, inhibiting the pathomorphology of diabetic nephropathy, renal lipid accumulation, and impr
262 n rodents has limited utility to model human diabetic nephropathy, renin-dependent hypertension and h
264 c overexpression of Nox5 in a mouse model of diabetic nephropathy showed enhanced glomerular ROS prod
265 isoform of NADPH oxidase in animal models of diabetic nephropathy since Nox5 is absent in the mouse g
266 e MPs were assessed in three mouse models of diabetic nephropathy: streptozotocin (STZ)-treated, OVE2
267 and (U.K.-R.O.I.) collection and the Finnish Diabetic Nephropathy Study (FinnDiane), combined with re
268 collections previously identified four novel diabetic nephropathy susceptibility loci that have subse
270 denotes their common nuclear genome (type 2 diabetic nephropathy (T2DN) rats) and mtFHH or mtWistar
271 d products (AGEs) are important mediators of diabetic nephropathy that act through the receptor for A
272 presents a therapeutic strategy for treating diabetic nephropathy that preserves the homeostatic func
274 h glucose paves the way for complications of diabetic nephropathy through the production of reactive
275 dence that KCa3.1 mediates renal fibrosis in diabetic nephropathy through the TGF-beta1/Smad signalin
276 loss of tubular Tyro3 and Mer expression in diabetic nephropathy tissue and glomerular depositions o
278 rotein-protein interactions at each stage of diabetic nephropathy to provide an overview of the event
279 entifies ASK1 as a new therapeutic target in diabetic nephropathy to reduce renal inflammation and fi
280 ssigned 317 patients with proteinuric type 2 diabetic nephropathy to twice-daily placebo; Pyridorin,
282 glomerular injury in experimental and human diabetic nephropathy via persistent activation of Notch1
283 the role of podocyte COX-2 in development of diabetic nephropathy, we employed a streptozotocin model
284 he endothelial glycocalyx is also reduced in diabetic nephropathy, we hypothesized that MCP-1 inhibit
285 sms leading to glomerular podocyte injury in diabetic nephropathy, we performed quantitative proteomi
286 Vegfa in the development and progression of diabetic nephropathy, we used an inducible Cre-loxP gene
289 mbinant human VEGF-A165b reduced features of diabetic nephropathy when initiated during early or adva
291 tion of CD73 was associated with more severe diabetic nephropathy, whereas treatment with soluble nuc
292 number may hold promise in the treatment of diabetic nephropathy, which could eventually lead to app
293 exhibit only the earliest features of human diabetic nephropathy, which limits our ability to invest
294 ings showed AS-IV to be beneficial to type 2 diabetic nephropathy, which might be associated with the
295 l disease (ESRD) worldwide, most people with diabetic nephropathy will never develop ESRD but will in
296 ker diabetic fatty (ZDF) rats develop type 2 diabetic nephropathy with albuminuria, reduced glomerula
297 duce diabetes, wild-type mice developed mild diabetic nephropathy with microalbuminuria, mesangial ma
298 ) has been implicated in the pathogenesis of diabetic nephropathy with proteinuria and peritubular ex
299 cyte dysfunction is a detrimental feature in diabetic nephropathy, with loss of nephrin integrity con
300 critical mediator of vascular dysfunction in diabetic nephropathy, yet VEGF-A knockout and overexpres
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