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1 eGFR and CFR were associated with diastolic and systolic
2 eGFR is now recommended by clinical practice guidelines,
3 eGFR was reassessed after 4 years in 124 available diabe
4 x was 24.7 kg/m(2) [IQR, 21.9-28.4 kg/m(2)], eGFR was 105 mL/min/1.73 m(2) [IQR, 95.7-113.0 mL], 9.7%
5 to <60 mL/minute/1.73 m2 (n = 144) or >=25% eGFR drop to <90 mL/minute/1.73 m2 (n = 599), and 322 co
12 in-to-creatinine ratio of 300 to 5000 and an eGFR of 25 to less than 75 ml per minute per 1.73 m(2).
13 ; 63% female; 22% black) studied, 35% had an eGFR <60 mL.min(-1).1.73 m(-2), a median left ventricula
16 in milligrams and creatinine in grams) or an eGFR decrease of at least 3.0 ml per minute per 1.73 m(2
19 Cohort Study which enrolled children with an eGFR of 30-90 ml/min per 1.73 m(2) and then assessed eGF
20 f cycles with uCrCl < 50 ml/min/1.73m(2) and eGFR >= 50 ml/min/1.73m(2) (i.e. a "false negative" resu
24 asured GFR is unavailable, the Avg (CrCl and eGFR) provides a better estimate of kidney function in k
25 mated iGFR, and their average [Avg (CrCl and eGFR)] essentially eliminated the GFR bias (median bias
27 hite primary care patients with diabetes and eGFR>=30 ml/min per 1.73 m(2) in a large health system (
29 s an inverse linear relation between PTH and eGFR in white women after accounting for 25(OH)D, PTH an
31 ls to estimate slopes with up to four annual eGFR assessments, and Cox proportional hazards models to
33 defined incident CKD (stage 3 or higher) as eGFR<60 ml/min per 1.73 m(2) and >=25% decline from base
34 ciated with clinical renal endpoints such as eGFR or proteinuria, there was a consistent pattern of i
38 ars after transplantation, although baseline eGFR 1 month after transplantation was lower in the inte
39 Male sex, diabetes mellitus, and baseline eGFR >=90 ml/min per 1.73 m(2) were associated with fast
40 was no interaction between race and baseline eGFR on odds for incident AKI (P value for interaction =
41 d race (Black, White, or other) and baseline eGFR with AKI incidence among patients who underwent PCI
42 iabetes, treatment with an ARNI and baseline eGFR, but suggested treatment-by-subgroup interactions f
43 no significant association between baseline eGFR <60 ml/min per 1.73 m(2) and risk for dementia or M
47 , higher glycated hemoglobin, lower baseline eGFR, and higher baseline urine albumin/creatinine ratio
49 ighest risk of ESRD with the lowest baseline eGFR group, there was a substantial increase in eGFR see
50 luated (median age 11 years; median baseline eGFR of 53 ml/min per 1.73 m(2)), 195 (30%) had a glomer
51 12,761 eligible individuals (median baseline eGFR, 103 ml/min/1.73 m2), 1,192 (9%) developed a CKD af
53 mean age, 64 years; postnephrectomy baseline eGFR, 48 ml/min per 1.73 m(2)), 117 progressive CKD even
54 int did not differ according to the baseline eGFR (<60 versus >=60 mL.min(-1).1.73 m(-2) (P-interacti
57 ersus 39.8 years; p < 0.0001) and had better eGFR (mean +/- SD 87.4 +/- 23.9 versus 80.1 +/- 20.7 mL/
58 end, placebo-treated CD subjects had better eGFR than projected by a prediction equation (mean diffe
64 al, dialysis, and total health care costs by eGFR (Kidney Disease Improving Global Outcomes-defined e
65 dults, declining kidney function measured by eGFR is associated with increased risk for probable deme
68 min per 1.73 m(2)), 24 with nondialysis CKD (eGFR <60 ml/min per 1.73 m(2)), and 20 with ESKD treated
72 combination of added kidney measures (creat-eGFR, cysC-eGFR, and urine albumin-to-creatinine ratio)
74 we aimed to (1) longitudinally compare CysC-eGFR and sCr-eGFR, (2) assess their predictive value for
75 n of added kidney measures (creat-eGFR, cysC-eGFR, and urine albumin-to-creatinine ratio) led to sign
77 timal pair of added kidney measures was cysC-eGFR and urine albumin-to-creatinine ratio (DeltaC=0.019
79 9-year-old individuals with mildly decreased eGFR (60-89 mL/min/1.73 m2), the model projected a furth
81 ey Disease Improving Global Outcomes-defined eGFR categories), adjusted for age, sex, and nonwhite ra
84 reased the risk of >= 40% decline in CKD-EPI eGFR (HR 1.5, p = 0.001) and doubling of serum creatinin
85 tment for clinical variables, annual CKD-EPI eGFR decreased by - 0.56 mL/min/BSA/year for each logari
88 ine Clearance (uCrCl) versus GFR estimation (eGFR) by the CKD-EPI formula versus both] is unclear.
90 trait and disease are associated with faster eGFR decline in black patients, with faster decline in s
91 Low hemoglobin S was associated with faster eGFR decline in sickle cell trait but may be confounded
92 ted hemoglobin A were associated with faster eGFR decline, but elevated hemoglobins F and A(2) were r
93 eir listing estimated glomerular filtration (eGFR) as well as based on their eGFR at the time of tran
94 ; P=7.8E-6 for urate) and mice (P=0.0003 for eGFR; P=0.0002 for urate) and confirmed as the primary c
95 tubule was enriched in humans (P=8.5E-5 for eGFR; P=7.8E-6 for urate) and mice (P=0.0003 for eGFR; P
97 S loci were enriched in kidney (P=9.1E-8 for eGFR; P=1.2E-5 for urate) and liver (P=6.8.10(-5) for eG
98 CKD progression and mortality, adjusting for eGFR, albuminuria, and other confounding characteristics
102 cipants at all CKD stages when corrected for eGFR and age, but not when adjusted for serum phosphate.
103 en consortium provided GWAS summary data for eGFR, urinary albumin-creatinine ratio (UACR), BUN, and
104 he tertile with both normal kidney function (eGFR 84 +/- 11.7 ml/min/1.73m(2)) and norm-albuminuria a
106 ted I-iothalamate GFR (iGFR), estimated GFR (eGFR), underestimated iGFR, and their average [Avg (CrCl
108 we concentrated on clinical (estimated GFR [eGFR], proteinuria, time posttransplant, donor-specific
110 r glomerular area was associated with higher eGFR (p-value<=0.001) and increased graft survival after
112 undergoing TAVR, even with baseline impaired eGFR, CKD stage is more likely to stay the same or impro
117 en or continued TDF, we estimated changes in eGFR and urine protein-to-creatinine ratio (UPCR) after
118 e ADC values were correlated with changes in eGFR, serum creatinine (SCr), systolic blood pressure (S
120 dent CKD (1.28, 1.18-1.39), >=30% decline in eGFR (1.23, 1.15-1.33), and end-stage renal disease (ESR
125 t CKD, 5.8% (5.0-7.0%) with >=30% decline in eGFR, and 17.0% (13.1-20.4%) with ESRD or >=50% decline
127 posite progression outcome (>=40% decline in eGFR, with eGFR<60 ml/min per 1.73 m(2), or ESKD), and l
130 sformed PA, there was an average decrease in eGFR of 0.38 ml/min/1.73 m2 (95% CI: -0.75, -0.01; p = 0
132 imary analysis, we detected no difference in eGFR for the intervention and control groups 2 years aft
134 R group, there was a substantial increase in eGFR seen during follow-up with a mean gain of 11 mL/min
138 , 1.07-1.39), and increased risk of incident eGFR <60 ml/min/1.73 m(2) (hazard ratio:1.20, 95% CI: 1.
140 of the association of PM(2.5) with incident eGFR <60 ml/min/1.73 m(2), 4.8% (4.2-5.8%) with incident
141 ant multivariable predictors of AKI included eGFR before imaging (OR: 0.99; 95% CI: 0.98, 0.995; P =
142 ) and validated (2015) a model incorporating eGFR using national data (n = 17,095) to predict WL mort
147 dG were analyzed in relation to longitudinal eGFR (per log-unit increase in 8-OHdG, beta = 0.81, 95%
150 hat failure was strongly associated with low eGFR, AKI, CKD, and glomerular deterioration, but not wi
157 ts stopped RAS inhibition at higher or lower eGFR, across prespecified subgroups, after adjustment an
158 sex, race, and estimated blood volume, lower eGFR was associated with reduced 25(OH)D clearance (beta
165 though proteinuria remained stable, the mean eGFR decline during part A was slower with clazakizumab
169 Median age was 58 years (IQR, 52-65), median eGFR was 95 ml/min per 1.73 m(2) (IQR, 74-100) using the
171 ian age was 71 years, 54.7% were men, median eGFR was 51.3 mL/min/1.73 m(2)) and observed that the nu
173 y associated with increased BMI in both men [eGFR-adjusted beta 0.443 (0.163-0.724)] and women [0.594
175 study of 87 adults, including 43 with normal eGFR (>=60 ml/min per 1.73 m(2)), 24 with nondialysis CK
176 5(OH)D clearance in participants with normal eGFR, but not in those with CKD or kidney failure (P for
177 /d, and 263 ml/d in participants with normal eGFR, CKD, and kidney failure, respectively (P=0.02).
178 Coronary microvascular dysfunction, but not eGFR, was independently associated with abnormal cardiac
180 ed difference between predicted and observed eGFR from 17.6 (using original htTKVs) to 4.0 ml/min per
181 ies study, we quantified the associations of eGFR (based on creatinine and cystatin C) and ACR with c
184 to severe CKD, we observed steep declines of eGFR were associated with progressively increasing risks
185 dpoint either as a percentage of decrease of eGFR (e.g. >= 30%) or an absolute decline (e.g. >= 5 ml/
190 levels were associated with a lower rate of eGFR decline in models adjusted for age, gender, hyperte
195 ucted an epigenome-wide association study of eGFR among 567 HIV-positive and 117 HIV-negative male pa
196 hese findings support the potential value of eGFR slopes in clinical assessment of adults with CKD.
198 ian age 72 years, 36% female) with new-onset eGFR <30 ml/min per 1.73 m(2), 1553 (15%) stopped RAS in
199 MRI in a patient with acute kidney injury or eGFR less than 30 mL/min per 1.73 m(2) should be balance
203 sis using K-fold cross validation to predict eGFR loss of >= 3 ml/min/1.73m(2)/year showed that UPPod
208 5 years old, diabetes mellitus, preoperative eGFR, and nephrectomy type (partial/radical)-to fit logi
209 ndent population with a relatively preserved eGFR at baseline and at least 5 years of follow up.
213 eline (estimated glomerular filtration rate (eGFR) <= 60 mL/min/BSA) (n = 118), we collected clinical
214 s with estimated glomerular filtration rate (eGFR) 59 to 30 mL/min/1.73 m2 on two consecutive previou
216 sures, estimated glomerular filtration rate (eGFR) and urinary albumin-to-creatinine ratio (ACR), wit
219 ied by estimated glomerular filtration rate (eGFR) before imaging (>=60 mL/min/1.73 m(2) or <60 mL/mi
221 of the estimated glomerular filtration rate (eGFR) in patients with chronic kidney disease who are at
222 a mean estimated glomerular filtration rate (eGFR) of 13 +/- 11 mL/min/1.73 m2, and 82% had stage 3 a
223 00, an estimated glomerular filtration rate (eGFR) of 25 to less than 60 ml per minute per 1.73 m(2)
224 d with estimated glomerular filtration rate (eGFR) over time and a log-unit increase in baseline 8-OH
226 Median estimated glomerular filtration rate (eGFR) was 43.7 ml/min/1.73 m(2) (interquartile range: 30
230 seline estimated glomerular filtration rate (eGFR) with the Chronic Kidney Disease Epidemiology Colla
231 t-TAVR estimated glomerular filtration rate (eGFR), and assess association of post-TAVR eGFR with mor
232 -CRP), estimated glomerular filtration rate (eGFR), and homeostasis model assessment of insulin resis
235 ion in estimated glomerular filtration rate (eGFR), end-stage renal disease, or death from renal caus
242 eline (estimated glomerular filtration rate [eGFR] <60 ml/min/1.73 m(2) or albumin-to-creatine ratio
244 kidney function (glomerular filtration rate, eGFR) and overall survival at 2 years posttransplant.
245 ey function, measured by clinically relevant eGFR subgroups or by albuminuria, including patients wit
247 Poor outcomes in individuals with rising eGFR are potentially attributable to sarcopenia, hemodil
248 (1) longitudinally compare CysC-eGFR and sCr-eGFR, (2) assess their predictive value for early postop
252 monitoring seems safe, results in a similar eGFR, and personalizes immunosuppressive therapy by lowe
253 Lower baseline and longitudinal post-TAVR eGFR were associated with lower intermediate-term surviv
256 nd adjusted for ESKD risk factors other than eGFR (<median level: cause-specific hazard ratio [HR] 0.
260 ed CKD progression by a >=50% decline in the eGFR, initiation of maintenance dialysis, or kidney tran
264 were related to molecular AKI and CKD and to eGFR, not rejection activity, presumably because rejecti
265 nly urinary markers significantly related to eGFR slope were UPPod:CR (P < 0.01) and albuminuria (P <
272 tors for ESKD and/or death at 18 months were eGFR <15 ml/min per 1.73 m(2) at diagnosis (IRR 3.09 [95
274 efined as eGFR <60 ml/min per 1.73 m(2) with eGFR decline >=1 ml/min per 1.73 m(2) per year, or urine
275 ses of NaHCO(3) over 28 weeks in adults with eGFR 20-44 or 45-59 ml/min per 1.73 m(2) with urinary al
277 [CI]: 0.52, 1.86; adjusted P = .95) and with eGFR less than 60 mL/min/1.73 m(2) was 5.6% (two of 36)
279 the adjusted model, factors associated with eGFR <90 mL/min/1.73 m2 included white race, older age,
280 nd LTV1, were all negatively associated with eGFR (cg06329547, P = 5.25 x 10-9; cg23281907, P = 1.37
281 ites that were significantly associated with eGFR (false discovery rate Q value < 0.05) among HIV-pos
285 thalate metabolites were not associated with eGFR, proteinuria, or blood pressure, but PA was associa
287 ression outcome (>=40% decline in eGFR, with eGFR<60 ml/min per 1.73 m(2), or ESKD), and linear mixed
288 .91 (CI, 2.4-3.5) in the patient groups with eGFR of 45-59, 30-44, and <30 mL/min/1.73 m, respectivel
289 1.04 (0.91-1.19) in the patient groups with eGFR of 45-59, 30-44, and <30 mL/min/1.73m, respectively
294 before the label change, Black patients with eGFR of 30-44 ml/min per 1.73 m(2) were prescribed metfo
295 m(2), 40 examinations (in 39 patients) with eGFR less than 15 mL/min/1.73 m(2), and 34 examinations
297 were 109 examinations (in 94 patients) with eGFR of 15-29 mL/min/1.73 m(2), 40 examinations (in 39 p
298 ncluded 299 examinations (242 patients) with eGFR of 30-44 mL/min/1.73 m(2) and 183 examinations (157