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1 range of kidney diseases, including diabetic nephropathy.
2 evels in human and animal models of diabetic nephropathy.
3 ibitors did not slow progression of diabetic nephropathy.
4 herapeutic potential for NOX-E36 in diabetic nephropathy.
5 rug to the distal ileum in patients with IgA nephropathy.
6 cans and with sickle cell disease-associated nephropathy.
7 ing albuminuria-reducing effects in diabetic nephropathy.
8 fundamental initiating mechanism of oxalate nephropathy.
9 nts beta-cell loss and hyperglycemia but not nephropathy.
10 l models with lupus nephritis and folic acid nephropathy.
11 glomerular filtration rate (GFR) decline and nephropathy.
12 microangiopathy of diabetic retinopathy and nephropathy.
13 the renal proteome in mice with acute folate nephropathy.
14 diabetic nephropathy, and adriamycin-induced nephropathy.
15 ive heart failure, hypertension, or diabetic nephropathy.
16 n the pathogenesis and treatment of diabetic nephropathy.
17 al vascular function in hypertension-induced nephropathy.
18 n-human trials for the treatment of diabetic nephropathy.
19 n the medulla that contribute to sickle cell nephropathy.
20 for BKPyV reactivation and BKPyV-associated nephropathy.
21 s were pursued for the treatment of diabetic nephropathy.
22 s in many investigations of contrast-induced nephropathy.
23 he dose-limiting toxicity was late radiation nephropathy.
24 tions and the role of these AGEs in diabetic nephropathy.
25 h adenine-induced chronic tubulointerstitial nephropathy.
26 critical role in the development of diabetic nephropathy.
27 emerging as a critical mediator of diabetic nephropathy.
28 e pathophysiology of polyomavirus-associated nephropathy.
29 associated with tumefactive brain lesions or nephropathy.
30 erapeutic effects of fenofibrate on diabetic nephropathy.
31 unction associated with hypertension-induced nephropathy.
32 gy, diagnosis, and outcomes of recurrent IgA nephropathy.
33 male gender and presence of retinopathy and nephropathy.
34 meruli of SLE patients compared with control nephropathy.
35 e reduced in patients with advanced diabetic nephropathy.
36 improve clinical manifestations of diabetic nephropathy.
37 f IL-17A was sufficient to suppress diabetic nephropathy.
38 uding 61 with additional viremia and 22 with nephropathy.
39 e major autoantigen in idiopathic membranous nephropathy.
40 thereby upregulating NOX4 in early diabetic nephropathy.
41 processing of miRNAs implicated in diabetic nephropathy.
42 hibitors have been shown to improve diabetic nephropathy.
43 y associated with susceptibility to diabetic nephropathy.
44 nd renal damage during experimental diabetic nephropathy.
45 ivity of urine and blood indicates later BKV nephropathy.
46 sively in the second decade of life in ADCK4 nephropathy.
47 r in the setting of Adriamycin (ADR)-induced nephropathy.
48 tes are important features of HIV-associated nephropathy.
49 s, thyroid dysfunction, and contrast-induced nephropathy.
50 uced albuminuria with atrasentan in diabetic nephropathy.
51 rug, Ezetimibe (EZT) on severity of diabetic nephropathy.
52 e tubular epithelium also during obstructive nephropathy.
53 nts with a hypokalemic-alkalotic salt-losing nephropathy.
54 , we examined the role of IL-17A in diabetic nephropathy.
55 diagnosis of paraprotein-induced crystalline nephropathy.
56 l biopsies from human subjects with diabetic nephropathy.
57 the major autoantigen in primary membranous nephropathy.
58 hildren who are already at risk for diabetic nephropathy.
59 OS formation may be a pathomechanism of COQ2-nephropathy.
60 eath was higher among patients with diabetic nephropathy.
61 ted as a major pathogenic factor in diabetic nephropathy.
62 occasionally associated with development of nephropathy.
63 s assigned salient pathogenetic roles in IgA nephropathy.
64 de, reduced proteinuria in patients with IgA nephropathy.
65 not in line with any other known salt-losing nephropathy.
66 A nephropathy, lupus nephritis, and diabetic nephropathy.
67 erum nephritis as a model of immune-mediated nephropathy.
68 rvention in patients with primary membranous nephropathy.
69 ved ROS in promoting progression of diabetic nephropathy.
70 pha relevant in the pathogenesis of diabetic nephropathy.
71 ation status correlated with the severity of nephropathy.
72 is involved in the pathogenesis of diabetic nephropathy.
73 for a biomarker that predicts progression of nephropathy.
74 nd promote functional improvement in chronic nephropathies.
77 cant difference in survival between diabetic nephropathy (23.8%) and other patients with CKD (59.9%;
78 regular screening for retinopathy, 47.1% for nephropathy, 4.5% for neuropathy, and 5.7% for foot ulce
80 can Study of Kidney Disease and Hypertension nephropathy (AASK-N) is a tubulopathy, we obtained urine
81 lishes the pathological features of diabetic nephropathy, although it does not affect the hyperglycem
82 A antagonist memantine also reduced diabetic nephropathy, although it was less effective than MK-801.
83 ates of the risk of radiocontrast-associated nephropathy among adult patients hospitalized in the Uni
84 ntly, kidney biopsies from patients with IgA nephropathy and diabetic nephropathy exhibited substanti
85 e describe a case of crystalglobulin-induced nephropathy and discuss its pathophysiology and the diff
87 mesangial deposition is the hallmark of IgA nephropathy and Henoch-Schonlein purpura, the onset of w
89 alpha(-/-) mice with diabetes or obstructive nephropathy and in PPARalpha(-/-) tubular cells treated
90 self in multiple ways, ranging from indolent nephropathy and inflammation to proteinuria with glomeru
91 inflammation, and apoptosis in acute folate nephropathy and less kidney dysfunction and a lower mort
92 hogenesis of severe diabetic retinopathy and nephropathy and may explain why some individuals with ty
93 6 expression in rats with adriamycin-induced nephropathy and mice with hyperglycemia-induced renal in
96 t 18 years with biopsy-confirmed primary IgA nephropathy and persistent proteinuria despite optimised
97 zed 34 adult patients with biopsy-proven IgA nephropathy and proteinuria >1 g/d, maintained on angiot
98 n implicated in the pathogenesis of diabetic nephropathy and renal fibrosis; however, the causative r
100 d glomerulosclerosis (indicators of diabetic nephropathy) and attenuated albumin leakage into the ret
101 microvascular (retinopathy, neuropathy, and nephropathy) and macrovascular (cerebrovascular, coronar
104 the increased risk for FSGS, HIV-associated nephropathy, and hypertension-attributed ESRD among peop
106 t role in the development of type 1 diabetic nephropathy, and its inhibition could be a promising opt
108 iated with cumulative burden of retinopathy, nephropathy, and peripheral neuropathy among individuals
109 ollowing: a kidney biopsy with PV associated nephropathy, any urine cytology demonstrating "decoy" ce
110 with end-stage kidney disease caused by IgA nephropathy are transplanted every year, and each of the
111 further strengthen the view of HNF1B-related nephropathy as a mitochondrial disorder in adulthood.
113 lycystic kidney disease (ADPKD) and diabetic nephropathy associated with higher HRs for mortality [1.
114 veloped hyperglycemia, oxidative stress, and nephropathy at age 20 weeks compared with their db/m lit
116 ith risk of severe retinopathy and/or severe nephropathy because they modify an individual's ability
124 and an array of pediatric problems including nephropathy, blastoma, gonadal dysgenesis and genital di
126 in salt-sensitive (SS) hypertension-induced nephropathy, but the molecular mechanisms contributing t
127 jor pathogenic factor that promotes diabetic nephropathy, but the underlying mechanism remains incomp
128 locks these effects and improves CNI-induced nephropathy by decreasing renin production in the CDs.
129 ion (STAT) signaling contributes to diabetic nephropathy by inducing genes involved in leukocyte infi
130 is of obesity-induced renal lipotoxicity and nephropathy by regulating the liver kinase B1/AMP-activa
131 (SOCS1) regulatory protein protects against nephropathy by suppressing STAT-mediated cell responses
132 infections, such as polyomavirus-associated nephropathy, calcineurin inhibitors (CNI), and genetic f
134 to dissect the molecular pathways underlying nephropathy caused by TFV and its more toxic analog, ade
135 target of the autoimmune disease, membranous nephropathy, characterised by production of anti-PLA2R a
136 nd show diminished physiological function in nephropathies characterized by altered tissue stiffness,
137 al nephritis (KIN) is a chronic interstitial nephropathy characterized by tubulointerstitial nephriti
141 methods, including determination of diabetic nephropathy class, as defined by the Renal Pathology Soc
143 from the Banff Working Group on Polyomavirus Nephropathy, comprising nine transplant centers in the U
147 lbuminuria and 162 individuals with diabetic nephropathy (DN) from the outpatient clinic at Steno Dia
149 rly relevant to the pathogenesis of diabetic nephropathy (DN) in which evidence suggests that metabol
156 t proteases aberrantly expressed in diabetic nephropathy (DN) may be involved in the generation of DN
157 rtant to find better treatments for diabetic nephropathy (DN), a debilitating renal complication.
158 lls (PTECs) has been highlighted in diabetic nephropathy (DN), but little is known about the underlyi
159 alyzed specimens from patients with diabetic nephropathy (DN), FSGS, IgA nephropathy (IgAN), membrano
170 f2 activation and ROS inhibition in diabetic nephropathy (dNP), the Nrf2 activator bardoxolone failed
171 cal segmental glomerulosclerosis or diabetic nephropathy exhibited diminished H3K27me3 and heightened
172 m patients with IgA nephropathy and diabetic nephropathy exhibited substantial activation of p53 and
173 r 1.73m(2), or development of overt diabetic nephropathy), eye events (a composite of requirement for
174 e followed a cohort of 112 patients with IgA nephropathy for a mean+/-SEM period of 14+/-10.2 years,
177 lial cells from patients with HIV-associated nephropathy (HIVAN) express HIV-1 transcripts, suggestin
179 Overall, both AT and EZT attenuated diabetic nephropathy; however, AT exhibited greater efficacy desp
180 is (HR, 0.80; 95% CI, 0.77-0.82), membranous nephropathy (HR, 0.88; 95% CI, 0.83-0.93), membranoproli
181 y (HRa, 0.74; 95% CI, 0.59-0.92), membranous nephropathy (HRa, 0.47; 95% CI, 0.29-0.75), and focal se
182 , 0.32-2.52) but present in immunoglobulin A nephropathy (HRa, 0.74; 95% CI, 0.59-0.92), membranous n
183 ant rates were highest for patients with IgA nephropathy (IgAN) (referent) and lower for all other gr
184 patients with GN studied, patients with IgA nephropathy (IgAN) had the lowest mortality rates and pa
190 ts with diabetic nephropathy (DN), FSGS, IgA nephropathy (IgAN), membranoproliferative GN (MPGN) (n=1
191 bout 6-8% of the disease heritability of IgA nephropathy (IgAN), suggesting that there are still a la
193 Most patients with idiopathic membranous nephropathy (IMN) have IgG4 autoantibodies against phosp
195 de attenuates the manifestations of diabetic nephropathy in a type 1 diabetic animal model, OVE26.
198 isms underlying the onset and progression of nephropathy in diabetic patients are not fully elucidate
199 heavy chain IIA are associated with diabetic nephropathy in European Americans and with sickle cell d
201 examined the role of Nox5 in human diabetic nephropathy in human mesangial cells and in an inducible
202 ructive nature of vancomycin-associated cast nephropathy in mice, which we detected using different i
203 ration of low-dose IL-17A prevented diabetic nephropathy in models of type 1 and type 2 diabetes.
216 II receptors (UTR) are increased in diabetic nephropathy, it remains unclear whether UII regulates GM
219 rade/class for disease entities, such as IgA nephropathy, lupus nephritis, and ANCA GN; and additiona
220 affecting the glomerulus, such as FSGS, IgA nephropathy, lupus nephritis, and diabetic nephropathy.
221 lusion, the risk of radiocontrast-associated nephropathy may be overstated in the literature and over
222 , at least at this stage and severity of IgA nephropathy, may reflect a failure of rituximab to reduc
223 mainstay for the treatment of minimal change nephropathy (MCN), which is characterised by an absence
224 pared with IgAN (referent), FSGS, membranous nephropathy, membranoproliferative GN, lupus nephritis,
225 rogate for long-term prognosis in membranous nephropathy (MGN), variability in proteinuria levels and
226 arget antigen identified in adult membranous nephropathy (MN) along with the major antigen phospholip
229 two major autoantigens in primary membranous nephropathy (MN), and define two molecular subclasses of
231 tract (n = 637 [70.9%]), tubulointerstitial nephropathies (n = 92 [10.2%]), glomerulopathies (n = 69
235 enal function loss in patients with diabetic nephropathy on chronic stable renin-angiotensin system i
237 nged from 0.49 for DN to 0.92 for membranous nephropathy or ADPKD) than by lower rates of deceased do
238 tic syndrome caused by idiopathic membranous nephropathy or focal segmental glomerulosclerosis were c
240 or an association with severe retinopathy or nephropathy or their combination in the FinnDiane cohort
245 ation: glomerulonephritis (P = 0.009), viral nephropathies (P = 0.002), interstitial fibrosis and tub
250 disease, inhibition of Jmjd3 and UTX abated nephropathy progression in mice with established glomeru
251 enal outcomes included incident or worsening nephropathy (progression to macroalbuminuria, doubling o
252 , during angiotensin II-induced hypertensive nephropathy provided novel insights into FSGS pathogenes
258 ects with type 2 diabetes mellitus and overt nephropathy receiving angiotensin converting enzyme inhi
261 98 patients with biopsy-proven myeloma cast nephropathy requiring hemodialysis treated at 48 French
262 g adolescence in ADCK4 than in WT1 and NPHS2 nephropathy, resulting in similar cumulative ESRD rates
265 ression of Nox5 in a mouse model of diabetic nephropathy showed enhanced glomerular ROS production, a
266 f NADPH oxidase in animal models of diabetic nephropathy since Nox5 is absent in the mouse genome.
267 Therapy for the Treatment of Progressive IgA Nephropathy (STOP-IgAN) Trial, 162 patients with IgAN an
269 entified in sows with porcine dermatitis and nephropathy syndrome (PDNS) and reproductive failure.
271 become the first specific treatment for IgA nephropathy targeting intestinal mucosal immunity upstre
272 s with or without treatment for presumed BKV nephropathy (tBKVN) using data from the United States Tr
273 with respect to annual eye examinations and nephropathy tests (P<0.001 for both comparisons); there
274 d a higher prevalence in recipients with BKV nephropathy than in those with viruria and viremia (P =
278 tubular Tyro3 and Mer expression in diabetic nephropathy tissue and glomerular depositions of protein
279 al [95% CI], 1.05-1.31) for immunoglobulin A nephropathy to 2.09 (95% CI, 1.56-2.78) for membranoprol
280 otein interactions at each stage of diabetic nephropathy to provide an overview of the events underly
283 g patients newly diagnosed with myeloma cast nephropathy treated with hemodialysis using a high-cutof
284 of the incidence of radiocontrast-associated nephropathy vary widely and suffer from misclassificatio
285 rotects kidneys against oxidative stress and nephropathy via stimulation of Sirtuin-1 expression and
286 atory burden or different etiology (diabetes nephropathy vs. other etiologies) of CKD could be associ
287 , although the incidence of contrast-induced nephropathy was higher in post-CABG patients (4.6% versu
288 elial glycocalyx is also reduced in diabetic nephropathy, we hypothesized that MCP-1 inhibition resto
289 ncing in a mouse model of folic acid-induced nephropathy, we identified ten genes that track kidney f
292 ly deficient in IL-17A developed more severe nephropathy, whereas administration of low-dose IL-17A p
293 renal cannabinoid-1 receptor (CB1R) induces nephropathy, whereas CB1R blockade improves kidney funct
294 n in a mouse model of unilateral obstructive nephropathy, which cannot be diagnosed with routine kidn
295 stitium in obstructive and aristolochic acid nephropathy, which correlates with progression of fibrot
296 ay hold promise in the treatment of diabetic nephropathy, which could eventually lead to applications
297 ovirus disease, herpes zoster, BK virus, and nephropathy, which led to the discontinuation of its dev
298 ed AS-IV to be beneficial to type 2 diabetic nephropathy, which might be associated with the inhibiti
299 ix affected individuals also had early-onset nephropathy with features of tubulo-interstitial nephrit
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