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1 diagnosed in 56 patients (17 with end-stage renal disease).
2 disease (SCI-Diabetes: 62 years; 35% cardio-renal disease).
3 sation for heart failure, and progression of renal disease.
4 patients with type 1 diabetes and end stage renal disease.
5 ncreasing albuminuria and the progression of renal disease.
6 1, onwards along with the specified cause of renal disease.
7 ction mutations contribute to cardiac and/or renal disease.
8 a requisite for the development of end-stage renal disease.
9 s and the leading genetic cause of end-stage renal disease.
10 (DN) remains the leading cause of end-stage renal disease.
11 erse outcomes compared with patients without renal disease.
12 nd, thus, can prevent progression to chronic renal disease.
13 eloped a TMA due to CD and reached end-stage renal disease.
14 tion, end-stage liver disease, and end-stage renal disease.
15 osis, a condition that can lead to end-stage renal disease.
16 ne glycol poisoning, can result in end-stage renal disease.
17 lated hospitalization or death, or end-stage renal disease.
18 s, with inescapable progression to end-stage renal disease.
19 urce of diagnostic and prognostic markers of renal disease.
20 is an indicator of microvascular damage and renal disease.
21 ove care and retard progression to end-stage renal disease.
22 filtration rate via Modification of Diet in Renal Disease.
23 ority of patients who undergo MitraClip have renal disease.
24 ive uropathy (OR, 12.4; P < 0.01) as primary renal disease.
25 associated with a 10-year risk of end-stage renal disease.
26 not be applicable for patients with eye and renal disease.
27 erpretation of urine protein measurements in renal disease.
28 reatment to prevent progression to end-stage renal disease.
29 knowledged as the best therapy for end-stage renal disease.
30 tial fibrosis, eventually leading to chronic renal disease.
31 ependent contributions of these disorders to renal disease.
32 uced risk of future progression to end-stage renal disease.
33 T2 inhibition in the progression of diabetic renal disease.
34 ients, including patients with non-end-stage renal disease.
35 proof of causality of these risk alleles for renal disease.
36 e perspective of chronic cardiometabolic and renal disease.
37 receptors in causing pain during diabetes or renal disease.
38 , ICU stay less than 24 hours, and end-stage renal disease.
39 ary disease, peripheral vascular disease, or renal disease.
40 ferred treatment for patients with end-stage renal disease.
41 ill enable improvements in MSC therapies for renal disease.
42 enesis, has been suggested as a biomarker of renal disease.
43 , eGFR decline of 30% or more, and end-stage renal disease.
44 el, end-stage renal disease, or death due to renal disease.
45 kidney disease, eGFR decline, and end-stage renal disease.
46 nterval, 1.82-2.12) in people without cardio-renal disease.
47 s) of induction and the role of periostin in renal disease.
48 n is a lifesaving intervention for end-stage renal disease.
49 is is associated with cancer progression and renal disease.
50 L users in order to delay the progression of renal disease.
51 ider continuity, for patients with end-stage renal disease.
52 serum hsCRP levels in adults with end-stage renal disease.
53 e likely to vary depending on the underlying renal disease.
54 tioning of the kidneys, leading to end-stage renal disease.
55 heart failure hospitalization and end-stage renal disease.
56 modifying medications than those with cardio-renal disease.
57 physiology and spectrum of Fontan-associated renal disease.
58 use of senotherapeutics in the management of renal disease.
59 high blood levels in patients with advanced renal diseases.
60 co-existing form of heart failure (HF) with renal diseases.
61 f MYOCD in the DCM patients with and without renal diseases.
62 s new drug targets to treat APOL1-associated renal diseases.
63 t alleles are at elevated risk of developing renal diseases.
64 rogression of immune- and nonimmune-mediated renal diseases.
65 es of these genes in kidney cell biology and renal diseases.
66 TGF-beta signaling, including biomarkers of renal diseases.
67 tions, and tissue repair and regeneration in renal diseases.
68 erly, especially among persons with existing renal diseases.
69 ecules was shown to be promising in treating renal diseases.
70 The most common grouped causes of death were renal disease (102, 23.4%), neoplasia (37, 8.5%) and mas
71 d categories, including congenital or cystic renal disease (127 of 531 patients [23.9%]) and nephropa
73 ared with 1.5%; p = 0.0041), and preexisting renal disease (9.1% compared with 3.0%; p < 0.0001) had
74 rtality as well as increased risk of chronic renal disease, a finding that is especially relevant amo
76 erapeutic option for patients with end-stage renal disease after orthotopic liver transplantation (OL
78 me to the first occurrence of cardiovascular-renal diseases, all-site cancer, and/or death, based on
79 rimposed upon clinical cardiovascular and/or renal disease, alone or as part of a systemic disorder.
83 lence rates of diabetes mellitus and chronic renal disease and are more likely to present with gangre
85 omyopathy that was associated with end-stage renal disease and characterized by severe functional abn
88 the leading cause of blindness and end-stage renal disease and contributes to both microvascular and
89 ogic assays characterize the presentation of renal disease and enable useful pharmacologic interventi
91 pment and progression of cardiometabolic and renal disease and is associated with increased cardiovas
92 airment is common in patients with end-stage renal disease and is associated with poor outcomes on di
93 donation are at increased risk of end-stage renal disease and may benefit from intensive postdonatio
94 is with unusual systemic features, including renal disease and platelet dysfunction, caused by the de
95 al immunoglobulin (MIg) in the occurrence of renal disease and raises the issue of the therapeutic ma
96 resenting up to 30% of patients in end-stage renal disease and renal transplantation, is the main ind
97 ine new light on the pathogenesis of various renal diseases and provide a basis for further hypothesi
98 significantly more likely to have diabetes, renal disease, and chronic pulmonary disease and had sig
99 atheters, diabetes mellitus, AIDS, end-stage renal disease, and cirrhosis), need for intensive care,
100 aboration (CKD-EPI), Modification of Diet in Renal Disease, and Cockcroft-Gault equations, and we eva
101 nce of diabetes, prior stroke, hypertension, renal disease, and congestive heart failure than white m
104 ary endothelial dysfunction, liver fibrosis, renal disease, and exercise intolerance are common in ad
106 analysis found that only age, high-risk MM, renal disease, and suboptimal MM control remained indepe
107 involved in the pathogenesis of cardiac and renal diseases, and in the progression of tumour growth
108 ies (cardiovascular, respiratory, liver, and renal diseases, and non-AIDS defining cancers because of
109 , and assess relevant risk factors including renal disease, antiphospholipid antibody, and anti-Ro/SS
110 re (adjusted odds ratio [aOR] 1.38), chronic renal disease (aOR 1.19), age >85 years (aOR 1.17), prio
112 on and depletion as novel therapies to treat renal disease are discussed, and we explore unanswered q
117 ts to identify subjects at risk of end-stage renal disease, as well as biomarkers to measure response
120 me in models of stress urinary incontinence, renal disease, bladder dysfunction and erectile dysfunct
121 e interval, 1.01-1.17) in people with cardio-renal disease but 1.96 (95% confidence interval, 1.82-2.
122 undergoing peritoneal dialysis for end-stage renal disease but without cirrhosis were included as con
123 rsus NHWs) in the first year after end-stage renal disease, but by Year 4, access to transplantation
124 SGLT2i reduced the risk of progression of renal disease by 45% (0.55 [0.48-0.64], p<0.0001), with
125 ey disease (ADPKD) is an inherited monogenic renal disease characterised by the accumulation of clust
126 R2 transgenic mice exhibited signs of severe renal disease characteristic of FSGS with proteinuria, l
127 Background Glomerulonephritis refers to renal diseases characterized by glomerular and tubuloint
128 isease (ADPKD) is the most common hereditary renal disease, characterized by cyst formation and growt
129 mic underlying diseases, including end-stage renal disease, cholestatic liver disease, endocrine/meta
131 itus or peripheral vascular disease, primary renal disease classification, and angiotensin converting
133 from 2.4 to 3.8, p <0.05) included end-stage renal disease, coronary artery disease, and neurologic d
134 cardiovascular disease, end-stage liver and renal disease, death) was compared between regimens usin
135 less than 60 mL/min per 1.73m(2), end-stage renal disease (defined as dialysis for at least 90 days,
136 he inflammatory process underlying end-stage renal disease development in both types of diabetes.
137 ablish a connection between sex hormones and renal disease development or progression, development of
139 nce of African American ethnicity, end-stage renal disease, diabetes, fair/poor self-rated health, ph
140 ublic insurance or no insurance at end-stage renal disease diagnosis, more regional acute care hospit
142 ute myocardial infarction, stroke, end-stage renal diseases, end-stage liver diseases, or death.
143 s most commonly caused by genetic disorders, renal disease, endocrine disorders, or cardiovascular ab
144 rbate azotemia, increase clinical markers of renal disease, enhance glomerular immune complex deposit
145 on rate based on the Modification of Diet in Renal Disease equation (119.5 +/- 57.2 vs 93.0.0 +/- 32.
146 on rate based on the Modification of Diet in Renal Disease equation (147.9 +/- 50.2 vs 126.0 +/- 41.9
148 The CKD-EPI and Modification of Diet in Renal Disease equations demonstrated strong agreement, p
150 ng donors who subsequently develop end-stage renal disease (ESRD) also have higher graft failure, sug
155 on between serum 1,5-AG levels and end-stage renal disease (ESRD) from baseline (1990-1992) through 2
156 00 people and slowly progresses to end-stage renal disease (ESRD) in about half of these individuals.
157 he chronic kidney disease (CKD) or end stage renal disease (ESRD) is generally caused due to the prog
159 ine in eGFR (1.23, 1.15-1.33), and end-stage renal disease (ESRD) or >=50% decline in eGFR (1.17, 1.0
160 ing sociocultural factors preclude end-stage renal disease (ESRD) patients from initiating kidney tra
161 ant is the best treatment for most end-stage renal disease (ESRD) patients, but proportionally few ES
162 atitis C virus (HCV) infection and end-stage renal disease (ESRD) remains controversial without consi
163 ort studies that generate lifetime end-stage renal disease (ESRD) risks for young living kidney donor
164 sthma, diabetes mellitus (DM), and end-stage renal disease (ESRD) were calculated by Poisson regressi
166 ons are important complications of end-stage renal disease (ESRD) with few studies having investigate
168 sease (CKD) to predict the risk of end stage renal disease (ESRD), i.e., the need for dialysis or a k
169 , 5%, and 8% of patients developed end-stage renal disease (ESRD), major cardiovascular event (mCVE),
177 were strongly associated with cardiovascular/renal disease events and all-cause mortality (p < 0.0001
179 ease events, and 255 of 35 620 had end-stage renal disease events), about 17% were older than 50 year
180 e subsequent incidence of cardiovascular and renal disease events, follow-up information was obtained
183 ll nephropathy as primary cause of end-stage renal disease), for a liver transplant 14.3 (recipient s
184 were assessed by the Modification of Diet in Renal Disease formula (MDRD-4) up to 5 years after LT.
187 ETHODSWe used next-generation sequencing for renal disease genes to genotype cohorts of patients with
190 osis, non-alcoholic steatohepatitis, chronic renal disease, heart failure, diabetes, idiopathic pulmo
191 e-sensitive populations, including end-stage renal disease, heart failure, obesity, advanced age, or
192 tcome analyses controlled for sex, end-stage renal disease, heart failure, sepsis severity (severe se
193 cipients' age, cause and length of end-stage renal disease, hemoglobin, albumin, selected comorbiditi
194 th older age, lower body mass index, chronic renal disease, higher Sequential Organ Failure Assessmen
195 t predictors of MACE were cardiogenic shock, renal disease, history of peripheral vascular disease, m
197 hown to independently predict progression of renal disease, however, whether FGF23 and FGFR4 also con
198 lso associated with development of end-stage renal disease (HR, 2.40; 95% CI, 0.76-7.58) and acute ki
199 al {CI}, 1.48-9.92]; P = .004) and end-stage renal disease (HR, 4.27 [95% CI, 1.89-9.11]; P = .001) w
202 the largest reported cohort of patients with renal disease in Bardet-Biedl syndrome and identifies ri
204 be involved in the development of end-stage renal disease in diabetes, but which specific circulatin
210 he GRS performed better in the prediction of renal disease in the 'later onset' compared with the 'ea
213 icant positive correlation between a GRS and renal disease in two independent European GWAS (Pcohort1
214 role of uric acid (UA) in the development of renal disease, in which endothelial dysfunction is regar
215 ysate temperature in patients with end-stage renal disease is associated with a decrease in the frequ
220 ase in the number of patients with end-stage renal disease leads to a growing waiting list for kidney
223 llow-up visit in the Modification of Diet in Renal Disease (MDRD) Study from 482 participants in stud
224 nsion (AASK) and 761 Modification of Diet in Renal Disease (MDRD) Trial participants previously rando
226 ration (CKD-EPI) and Modification of Diet in Renal Disease (MDRD-4, MDRD-6) equations for mGFR < 30 m
227 v) scores, renal function, and the burden of renal disease measured by area under the curve (serum cr
228 Monoclonal immunoglobulin (MIg) associated renal disease (MIgARD) comprises a group of disorders ca
229 Monoclonal immunoglobulin (MIg)-associated renal disease (MIgARD) comprises a group of disorders ca
233 for potential drug repurposing, as baseline renal disease must be considered when selecting medicati
234 icians involved in the care of patients with renal disease must be familiar with the local epidemiolo
235 of creatinine > 75 mL/min) patients with no renal disease (n = 24); Group 2 (clearance of creatinine
236 of creatinine of 11-75 mL/min) patients with renal disease (n = 67); Group 3 (clearance of creatinine
239 d spectrum of BBS phenotypes spans diabetes, renal disease, obesity, sleep apnea, cardiovascular dise
240 s for severe infection included pre-existing renal disease (odds ratio [OR], 7.4; 95% CI, 2.5-22.0),
241 tio, 0.18; CI, 0.13-0.25), or with end-stage renal disease (odds ratio, 0.23; CI, 0.13-0.40), heart f
242 nsion (odds ratio, 2.6; 95% CI, 1.2-5.6) and renal disease (odds ratio, 3.5; 95% CI, 1.9-6.5) were as
244 the human study, participants with end-stage renal disease on peritoneal dialysis (PD) underwent rand
246 the majority of patients reaching end-stage renal disease or dying with little or no chances of kidn
248 ease (OR 2.62; 95% CI 1.53-4.47; p < 0.001), renal disease (OR 2.13; 95% CI 1.84-2.46; p < 0.001), an
250 glomerular filtration rate (eGFR), end-stage renal disease, or death from renal causes), the individu
251 associated with excess mortality, end-stage renal disease, or morbidity, in at least 10 years follow
252 tion, end-stage liver disease, and end-stage renal disease outcomes that could be prevented with inte
255 073) and lesser reductions in progression of renal disease (p for interaction=0.0258) in patients wit
257 stereology, with a possible application for renal disease patients who are often not suitable for co
259 iving-donor kidney transplants for end-stage renal disease patients with willing but incompatible liv
262 ors of major adverse cardiac events included renal disease, prior myocardial infarction, silent ische
265 plications of LPI, including growth failure, renal disease, pulmonary alveolar proteinosis, autoimmun
266 plant recipients with aHUS-related end-stage renal disease received eculizumab: 10 from day 0 and 2 a
267 isation for heart failure and progression of renal disease regardless of existing atherosclerotic car
270 ng, type II diabetes mellitus, and end-stage renal disease requiring dialysis presented to the emerge
271 ng, type II diabetes mellitus, and end-stage renal disease requiring dialysis presented to the emerge
272 e age in T2D was 63 years and 28% had cardio-renal disease (SCI-Diabetes: 62 years; 35% cardio-renal
274 n-infantile disease (11%, all with end-stage renal disease) showed mild, likely PH1-related retinal f
275 d in a striking acceleration in the onset of renal disease, SLO germinal center formation, and autore
276 ents with both type 1 diabetes and end-stage renal disease, SPK recipients had similar progression of
277 ional ISAR (Risk Stratification in End-Stage Renal Disease) study, data on dynamic retinal vessel ana
278 ng System stage 3 (ISS3), high-risk disease, renal disease, suboptimal myeloma control (active or pro
279 ay substantially reduce risk for cardiac and renal disease, suggesting that it may be necessary to ch
281 at higher risk for progression to end-stage renal disease than those who have chronic kidney disease
282 AKUT as a feature (syndromic CAKUT) or cause renal diseases that may manifest as phenocopies of CAKUT
284 than 65 years of age), such as in end-stage renal disease, this therapy has not been optimized for o
288 n immunodeficiency virus (HIV) and end-stage renal disease was on the kidney transplant waitlist awai
289 rious associations of lymphangiogenesis with renal disease, we here tested the hypothesis that VitD h
290 rlying cardiovascular disease, diabetes, and renal disease were significantly associated with higher
292 poor outcomes, particularly in stage 4 or 5 renal disease where 1-year mortality is observed in near
293 APOL1 was strongly associated with incident renal disease, whereas no significant association with t
294 agonist anti-Ox40 mAbs potently exacerbated renal disease, which was accompanied by activation of ki
297 y disease, particularly those with end-stage renal disease who require dialysis and/or kidney transpl
299 y donors have an increased risk of end-stage renal disease, with hypertension and diabetes as the pre