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1 flux and acceleration of cardiomyopathy and nephropathy.
2 rminal SCR-1/2 domain pair that causes CFHR5 nephropathy.
3 escribed a new entity called vancomycin cast nephropathy.
4 es to tubulointerstitial changes in diabetic nephropathy.
5 om patients with varying degrees of diabetic nephropathy.
6 omeostasis, as well as to the development of nephropathy.
7 ent early kidney responses in human diabetic nephropathy.
8 d diseases, including IgA vasculitis and IgA nephropathy.
9 sion, congestive heart failure, and diabetic nephropathy.
10 ove to be stronger modifiers of the risk for nephropathy.
11 ly associated with isolated glomerulotubular nephropathy.
12 mation in tissue from patients with diabetic nephropathy.
13 ng a potential approach to treating diabetic nephropathy.
14 ne the possible role of FHL2 in hypertensive nephropathy.
15 e one of the main culprits of Balkan endemic nephropathy.
16 lay a role in the pathogenesis of membranous nephropathy.
17 structure and function and lost in diabetic nephropathy.
18 nt thresholds may be required for women with nephropathy.
19 hat underlie development of APOL1-associated nephropathy.
20 function in a mouse model of severe diabetic nephropathy.
21 d late complications such as retinopathy and nephropathy.
22 glomerular disease and hypertension-induced nephropathy.
23 comorbid illnesses, such as retinopathy and nephropathy.
24 a therapeutic target in people with diabetic nephropathy.
25 ures of the mechanism and pathology of CFHR5 nephropathy.
26 considered a risk factor for later diabetic nephropathy.
27 EnC) dysfunction and albuminuria in diabetic nephropathy.
28 e investigation in the treatment of diabetic nephropathy.
29 n, two key pathologic signatures of diabetic nephropathy.
30 the phenotype of progressive human diabetic nephropathy.
31 estation of T1DM, preceding hypertension and nephropathy.
32 l biopsies from human subjects with diabetic nephropathy.
33 not in line with any other known salt-losing nephropathy.
34 ding" determines the prognosis of membranous nephropathy.
35 nts with a hypokalemic-alkalotic salt-losing nephropathy.
36 the major autoantigen in primary membranous nephropathy.
37 hildren who are already at risk for diabetic nephropathy.
38 OS formation may be a pathomechanism of COQ2-nephropathy.
39 eath was higher among patients with diabetic nephropathy.
40 ted as a major pathogenic factor in diabetic nephropathy.
41 occasionally associated with development of nephropathy.
42 s assigned salient pathogenetic roles in IgA nephropathy.
43 de, reduced proteinuria in patients with IgA nephropathy.
44 A nephropathy, lupus nephritis, and diabetic nephropathy.
45 erum nephritis as a model of immune-mediated nephropathy.
46 rvention in patients with primary membranous nephropathy.
47 ved ROS in promoting progression of diabetic nephropathy.
48 pha relevant in the pathogenesis of diabetic nephropathy.
49 ation status correlated with the severity of nephropathy.
50 s a novel renoprotective therapy in diabetic nephropathy.
51 protects mitochondrial integrity in diabetic nephropathy.
52 e extra SCR-1/2 domain pair present in CFHR5 nephropathy.
53 /-) mice were more susceptible to Adriamycin nephropathy.
54 notypes observed for many monogenic forms of nephropathy.
55 in minimal change disease, or in membranous nephropathy.
56 d no effect on the manifestations of 2,8-DHA nephropathy.
57 al trials in patients with NASH and diabetic nephropathy.
58 ith increased ESKD risk in patients with IgA nephropathy.
59 enic role in the development of hypertensive nephropathy.
60 tective effects of Glp1r agonism in diabetic nephropathy.
61 is also elevated in patients with membranous nephropathy.
62 on in kidney compartments may mitigate APOL1 nephropathy.
63 ion is linked to the development of diabetic nephropathy.
64 se glomerulosclerosis, particularly diabetic nephropathy.
65 l disease affects development of ESKD in IgA nephropathy.
66 of earlier inflammatory bowel disease in IgA nephropathy.
67 thogenesis of other types of crystal-induced nephropathies.
68 nd promote functional improvement in chronic nephropathies.
69 ferase causes 2,8-dihydroxyadenine (2,8-DHA) nephropathy, a rare condition characterized by formation
70 can Study of Kidney Disease and Hypertension nephropathy (AASK-N) is a tubulopathy, we obtained urine
71 g kidney donors at risk for APOL1-associated nephropathy about the gene and possibility of genetic te
73 y disease, including podocytopathy, diabetic nephropathy, albuminuria, autosomal dominant polycystic
75 of 12.6 years, 196 (4.95%) patients with IgA nephropathy and 330 (1.65%) matched controls developed i
76 for future inflammatory bowel disease in IgA nephropathy and conditional logistic regression to asses
77 ranulomas develop late in chronic UA crystal nephropathy and contribute to CKD progression because UA
78 d late in this process of chronic UA crystal nephropathy and contributed to the progression of pre-ex
79 cellular and molecular mechanisms of 2,8-DHA nephropathy and crystal clearance have clinical relevanc
80 tatus included risk of incident or worsening nephropathy and estimated glomerular filtration rate slo
82 injury and loss in the progression of Fabry nephropathy and indicates a need for therapeutic interve
83 6 expression in rats with adriamycin-induced nephropathy and mice with hyperglycemia-induced renal in
86 p1 suppression in zebrafish induced signs of nephropathy and reduced optic nerve size, the latter phe
87 , including cardiovascular disease, diabetic nephropathy and retinopathy, have a negative effect on t
88 scular disease (retinopathy, neuropathy, and nephropathy) and peripheral artery disease status on the
89 osed multiple myeloma, biopsy-confirmed cast nephropathy, and acute kidney injury that required dialy
92 and alpha(1) -m content in aristolochic acid nephropathy, and elevated beta(2) -m excretion with incr
93 the increased risk for FSGS, HIV-associated nephropathy, and hypertension-attributed ESRD among peop
95 es in the development of severe retinopathy, nephropathy, and neuropathy in those treated intensively
96 are found in 80% of patients with membranous nephropathy, and previous studies described three autoan
97 f RRVs may underlie cellular injury in APOL1 nephropathy, and that interventions that reduce RRV expr
98 diseases, such as rheumatoid arthritis, IgA nephropathy, ankylosing spondylitis, and inflammatory bo
99 ollowing: a kidney biopsy with PV associated nephropathy, any urine cytology demonstrating "decoy" ce
101 further strengthen the view of HNF1B-related nephropathy as a mitochondrial disorder in adulthood.
102 n), for a kidney transplant 2.8 (sickle cell nephropathy as primary cause of end-stage renal disease)
103 patients with early and late-stage diabetic nephropathy, as well as other nondiabetic glomerular dis
104 lycystic kidney disease (ADPKD) and diabetic nephropathy associated with higher HRs for mortality [1.
106 almia, ptosis and syndactyly with or without nephropathy, associated with homozygous frameshift mutat
107 veloped hyperglycemia, oxidative stress, and nephropathy at age 20 weeks compared with their db/m lit
111 ressive regimens, BK polyomavirus-associated nephropathy (BKPyVAN) is still a matter of concern.
112 idney graft failure through BKPyV-associated nephropathy (BKPyVAN), but markers predicting outcome ar
113 ), including development of BKPyV-associated nephropathy (BKPyVAN), can be useful for patient risk st
114 brosis and tubular atrophy (14.4%); BK virus nephropathy (BKVAN) 9.9%; and acute tubular necrosis (AT
117 mice developed the full picture of diabetic nephropathy, but diabetic retinopathy was prevented.
118 FA-treated diabetic mice were protected from nephropathy, but not in the absence of GPR43 or GPR109A.
119 jor pathogenic factor that promotes diabetic nephropathy, but the underlying mechanism remains incomp
120 ion (STAT) signaling contributes to diabetic nephropathy by inducing genes involved in leukocyte infi
121 is of obesity-induced renal lipotoxicity and nephropathy by regulating the liver kinase B1/AMP-activa
122 infections, such as polyomavirus-associated nephropathy, calcineurin inhibitors (CNI), and genetic f
125 to dissect the molecular pathways underlying nephropathy caused by TFV and its more toxic analog, ade
126 target of the autoimmune disease, membranous nephropathy, characterised by production of anti-PLA2R a
127 nd show diminished physiological function in nephropathies characterized by altered tissue stiffness,
128 bin (HbA1c), diabetes duration, retinopathy, nephropathy, chronic kidney disease (CKD), and anaemia a
130 methods, including determination of diabetic nephropathy class, as defined by the Renal Pathology Soc
131 nd Renal Events in Diabetes With Established Nephropathy Clinical Evaluation) trial in patients with
132 ncluding pure LCDD [n = 154], LCDD with cast nephropathy (CN) [n = 58]), HCDD (n = 23), or LHCDD (n =
133 gimens in patients with initial myeloma cast nephropathy (CN) and acute kidney injury (AKI) without n
136 from the Banff Working Group on Polyomavirus Nephropathy, comprising nine transplant centers in the U
137 ew entity, which we term COVID-19-associated nephropathy (COVAN), may particularly impact individuals
142 ferative glomerulonephritis (MPGN), diabetic nephropathy (DN) and obesity-related glomerulopathy (ORG
143 lbuminuria and 162 individuals with diabetic nephropathy (DN) from the outpatient clinic at Steno Dia
147 t proteases aberrantly expressed in diabetic nephropathy (DN) may be involved in the generation of DN
149 ximal tubule is a site of injury in diabetic nephropathy (DN), and progressive renal tubulointerstiti
150 lls (PTECs) has been highlighted in diabetic nephropathy (DN), but little is known about the underlyi
157 ented lipid-induced renal injury in diabetic nephropathy (DN). However, the role and regulation of pr
159 ignificantly less likely to develop diabetic nephropathy, exhibiting less albuminuria, glomerular hyp
160 r 1.73m(2), or development of overt diabetic nephropathy), eye events (a composite of requirement for
161 amaged rat mesangial cells leads to diabetic nephropathy, fibrosis, and proteinurea, which are inhibi
163 otic syndrome or biopsy-based minimal change nephropathy, FSGS, or membranous nephropathy, with 94% s
164 f PPM1A and PTEN levels in aristolochic acid nephropathy further suggests crosstalk between these rep
166 tween the apolipoprotein L1 gene (APOL1) and nephropathy has altered the epidemiology of chronic kidn
168 udies in models of experimental and clinical nephropathies have described accumulation of sphingolipi
171 cular Outcomes in Participants with Diabetic Nephropathy) have shown that the sodium-glucose cotransp
172 h graft loss attributed to chronic allograft nephropathy (hazard ratio [HR], 1.39; 95% confidence int
173 glutinin disease, hemolytic uremic syndrome, nephropathies, HELLP syndrome, transplant-associated thr
176 is (HR, 0.80; 95% CI, 0.77-0.82), membranous nephropathy (HR, 0.88; 95% CI, 0.83-0.93), membranoproli
178 ant rates were highest for patients with IgA nephropathy (IgAN) (referent) and lower for all other gr
179 ed glomerulonephritis (SAGN) and primary IgA nephropathy (IgAN) are separate disease entities requiri
186 common renal disease, immunoglobulin A (IgA) nephropathy (IgAN), is associated with glomerular deposi
188 Membranous nephropathy (MN, 24.96%) and IgA nephropathy (IgAN, 24.09%) were the most common primary
190 hropathy will identify biomarkers predicting nephropathy in individuals at high genetic risk and lead
192 ructive nature of vancomycin-associated cast nephropathy in mice, which we detected using different i
194 ; however, it causes polyomavirus-associated nephropathy in renal transplant patients and hemorrhagic
196 ed in several clinical hallmarks of diabetic nephropathy indicative of early disease development.
197 elevance of rodent models of 2,8-DHA crystal nephropathy induced by excessive adenine intake is unkno
200 vere acute kidney injury due to myeloma cast nephropathy is caused by pathogenic free light chain imm
209 denine-enriched diet in mice induced 2,8-DHA nephropathy, leading to progressive kidney disease, char
211 affecting the glomerulus, such as FSGS, IgA nephropathy, lupus nephritis, and diabetic nephropathy.
212 lusion, the risk of radiocontrast-associated nephropathy may be overstated in the literature and over
213 , at least at this stage and severity of IgA nephropathy, may reflect a failure of rituximab to reduc
214 pared with IgAN (referent), FSGS, membranous nephropathy, membranoproliferative GN, lupus nephritis,
215 rogate for long-term prognosis in membranous nephropathy (MGN), variability in proteinuria levels and
221 two major autoantigens in primary membranous nephropathy (MN), and define two molecular subclasses of
226 odocytes, and a new puromycin aminoglycoside nephropathy model of INF2 transgenic mice were used to d
227 in (ogen)-induced podocyte injury in the PAN nephropathy model, with amiloride having podocyte-protec
230 utoimmunity-driven type-1 diabetes, diabetic nephropathy, multiple sclerosis, asthma, atherosclerosis
233 imal tubulopathy (n=2), and light chain cast nephropathy (n=1).Second, we conducted a literature revi
235 microscopy.Part-2: Whereas light chain cast nephropathy occurred the earliest and had the worst graf
237 al disease (127 of 531 patients [23.9%]) and nephropathy of unknown origin (48 of 281 patients [17.1%
238 l cells that play a pivotal role in diabetic nephropathy, one of the leading causes of renal failure,
239 nged from 0.49 for DN to 0.92 for membranous nephropathy or ADPKD) than by lower rates of deceased do
240 flozin reduced risk of incident or worsening nephropathy or cardiovascular death by 43% (hazard ratio
247 study, we compared 3963 biopsy-verified IgA nephropathy patients with 19,978 matched controls betwee
249 y, VEGFC reduced the development of diabetic nephropathy, prevented VEGF receptor alterations in the
251 disease, inhibition of Jmjd3 and UTX abated nephropathy progression in mice with established glomeru
252 an reactivate in transplant patients causing nephropathy, progressive multifocal leukoencephalopathy,
253 andomly assigned patients who had membranous nephropathy, proteinuria of at least 5 g per 24 hours, a
255 studies in a puromycin aminonucleoside (PAN) nephropathy rat model treated with amiloride, an inhibit
257 patients with PLA(2)R1-associated membranous nephropathy recognize at least two epitope regions in th
258 severe acute kidney injury, and myeloma cast nephropathy relative to treatment with standard high-flu
260 in glomerular podocytes in adriamycin (ADR) nephropathy, remnant kidney after 5/6 renal ablation, an
261 98 patients with biopsy-proven myeloma cast nephropathy requiring hemodialysis treated at 48 French
266 ression of Nox5 in a mouse model of diabetic nephropathy showed enhanced glomerular ROS production, a
268 odels of mesangioproliferative GN and in IgA nephropathy, suggesting that GATA3 plays a critical role
269 entified in sows with porcine dermatitis and nephropathy syndrome (PDNS) and reproductive failure.
270 become the first specific treatment for IgA nephropathy targeting intestinal mucosal immunity upstre
271 s with or without treatment for presumed BKV nephropathy (tBKVN) using data from the United States Tr
275 to increased circulating IgA levels, and IgA nephropathy, the most common form of primary GN and a le
276 l-risk variant protein in the development of nephropathy; this is true in both native kidney disease
277 Dietary fiber protects against diabetic nephropathy through modulation of the gut microbiota, en
278 tubular Tyro3 and Mer expression in diabetic nephropathy tissue and glomerular depositions of protein
279 otein interactions at each stage of diabetic nephropathy to provide an overview of the events underly
280 g patients newly diagnosed with myeloma cast nephropathy treated with hemodialysis using a high-cutof
281 schemia/reperfusion-induced injury, diabetic nephropathy, ureteral obstructive disease, and kidney al
282 cysts are due to genetic diseases (eg, HNF1B nephropathy, various ciliopathies, and tuberous sclerosi
283 atory burden or different etiology (diabetes nephropathy vs. other etiologies) of CKD could be associ
286 to five subgroups, interestingly, membranous nephropathy was the most common pathologic type, both in
287 tides in a mouse model of chronic folic acid nephropathy we can reduce fibrosis by 50% and prevent th
288 elial glycocalyx is also reduced in diabetic nephropathy, we hypothesized that MCP-1 inhibition resto
289 wly diagnosed PLA(2)R1-associated membranous nephropathy, we investigated the clinical role of epitop
290 ey biopsy sections from people with diabetic nephropathy, we show that Notch signaling is indeed up-r
291 fect on development of experimental diabetic nephropathy, we used streptozotocin to induce diabetes i
293 renal cannabinoid-1 receptor (CB1R) induces nephropathy, whereas CB1R blockade improves kidney funct
294 th de novo multiple myeloma and myeloma cast nephropathy who required haemodialysis for acute kidney
295 er detection of progression risk in diabetic nephropathy will allow earlier intervention to reduce pr
296 ding of the pathogenesis in APOL1-associated nephropathy will identify biomarkers predicting nephropa
297 ix affected individuals also had early-onset nephropathy with features of tubulo-interstitial nephrit
300 disorders that, although unrelated to their nephropathy, would also lead to subspecialty referral an