ライフサイエンスコーパス: GFR

1 GFR and body weight reduction were correlated.

2 GFR reduction was larger in hyperfiltering (GFR >120 mL/

3 GFR was assessed in conscious TRPC6 wild type and knocko

4 tors of early mortality were age (P < 0.02), GFR (P < 0.0001), TAAA2 or 3 (P = 0.001), coronary arter

5 nts (mean baseline age 41 years, HbA1c 9.2%, GFR 164 mL/min, and albumin-to-creatinine ratio 31 mg/g)

6 (3) GFR is evaluated using several methods available at the

7 tiple linear regression was used to derive a GFR equation.

8 y agreement, precision, and accuracy using a GFR of 75 mL/min/1.73 m (eSCr75-MDRD) or the median GFR

9 We subsequently developed and validated a GFR equation specifically for cirrhosis and compared the

10 rospectively identified 2887 patients with a GFR between 15 and 60 ml/min per 1.73 m2 referred betwee

11 were 42% of recipients that had an absolute GFR decrease greater than 20 mL/min per 1.73 m, and 39%

12 the LPAR antagonist BMS002 protects against GFR decline and attenuates development of DN through mul

13 <60: HR, 0.49; 95% CI, 0.36-0.67; P<0.01 and GFR >/=60: HR, 0.50; 95% CI, 0.38-0.66; P<0.01).

14 <60: HR, 0.66; 95% CI, 0.44-1.00; P=0.05 and GFR >/=60: HR, 0.68; 95% CI, 0.44-1.05; P=0.08) and HF/d

15 reduction in risk of death (GFR <60: 14% and GFR >/=60: 6%) and HF/death (GFR <60: 25 and GFR >/=60:

16 GFR >/=60: 6%) and HF/death (GFR <60: 25 and GFR >/=60: 15%).

17 tion by blood oxygen level-dependent MRI and GFR by iothalamate clearance.

18 usted for baseline age, sex, proteinuria and GFR.

19 ogenic activity, and improvements in RBF and GFR greater than those observed with placebo, ELP alone,

20 ase (RVD) reduces renal blood flow (RBF) and GFR and accelerates poststenotic kidney (STK) tissue inj

21 measured single-kidney blood flow (RBF) and GFR and established the degree of renal damage after 6 w

22 end points were full clinical remission and GFR loss >/=15 ml/min per 1.73 m(2) during the 3-year tr

23 of the relation between aortic stiffness and GFR was mediated by pulsatility index (95% confidence in

24 x, the relation between aortic stiffness and GFR was no longer significant (P=0.10).

25 Results Cr levels decreased and GFRs increased in both groups from before to after imagi

26 Serum Cr levels and GFRs for each time period were compared between groups b

27 on the rate of change in serum Cr levels and GFRs from before to after imaging.

28 han for the general population, and falls as GFR declines.

29 wever, at 1 year, as a group, they remain at GFR less than 60 (stage III chronic kidney disease).

30 4%) were taking metformin despite a baseline GFR below 40 mL per min per 1.73 m.

31 after LT, with subgroup analysis by baseline GFR, model for end-stage liver disease (MELD), age, sex,

32 In both GFR groups, cardiac resynchronization therapy with defib

33 nd control littermates did not differ in BP, GFR, or natriuresis under baseline conditions.

34 mia, daptomycin efficacy was not affected by GFR level and was similar to vancomycin's efficacy.

35 weight may be attributable to confounding by GFR and that confounding by GFR may be more important in

36 o confounding by GFR and that confounding by GFR may be more important in studies with sample collect

37 d stage acute and chronic kidney diseases by GFR and albuminuria.

38 Calculated GFR was significantly higher in black women than in whit

39 cirrhosis, the Royal Free Hospital cirrhosis GFR, using readily available variables; this remains to

40 atios (median, 98 vs 66 mg/g) but comparable GFRs (median, 109 vs 106 mL/min|1.73 m(2)).

41 llaboration (CKD-EPI) equations, we compared GFR estimated from creatinine (eGFRcreat), cystatin C (e

42 (68)Ga-GFR agreed well with (51)Cr-GFR for estimation of GFR using serial plasma counting.

43 (51)Cr-GFR ranged from 10 to 220 mL/min (mean, 85 mL/min).

44 good agreement between (68)Ga-GFR and (51)Cr-GFR using serial plasma sampling, with a Bland-Altman bi

45 GFR ((68)Ga-GFR) and (51)Cr-EDTA GFR ((51)Cr-GFR), using serial plasma sampling and PET imaging.

46 FR <60: 14% and GFR >/=60: 6%) and HF/death (GFR <60: 25 and GFR >/=60: 15%).

47 68; 95% CI, 0.44-1.05; P=0.08) and HF/death (GFR <60: HR, 0.49; 95% CI, 0.36-0.67; P<0.01 and GFR >/=

48 ator was associated with reduction in death (GFR <60: HR, 0.66; 95% CI, 0.44-1.00; P=0.05 and GFR >/=

49 greater absolute reduction in risk of death (GFR <60: 14% and GFR >/=60: 6%) and HF/death (GFR <60: 2

50 correlation was for plasma sampling-derived GFR with PETlate (PCC of 0.90; 95% confidence interval,

51 phosphate retention arising from diminished GFR is a key early step in a pathologic cascade leading

52 presence of a significant renal dysfunction (GFR <60 mL/min/1.73 m(2)).

53 (68)Ga-EDTA GFR ((68)Ga-GFR) and (51)Cr-EDTA GFR ((51)Cr-GFR), using serial plasma sampling and PET i

54 (51)Cr-EDTA GFR was compared with the estimated GFR (eGFR) from seve

55 Cr) EDTA excretion measurements ((51)Cr-EDTA GFR) from white patients >/= 18 years of age with histol

56 imed to assess agreement between (68)Ga-EDTA GFR ((68)Ga-GFR) and (51)Cr-EDTA GFR ((51)Cr-GFR), using

57 dosing; however, the best method to estimate GFR in patients with cancer is unknown.

58 were to identify which equation to estimate GFR is superior for predicting adverse outcomes after PC

59 ynamic imaging provides a method to estimate GFR without plasma sampling, with the additional advanta

60 Estimated GFR (eGFR) was calculated with the Cockcroft-Gault, Modi

61 Estimated GFR by the MDRD4 results declined throughout the study p

62 e with CKD G3a or G3b defined by 2 estimated GFR (eGFR) values more than 90 days apart were recruited

63 16 OLT patients from 1996 to 2009, estimated GFR (eGFR) was assessed during the 12 months before OLT

64 recovered renal function to above estimated GFR of greater than 60 mL per min.

65 a or 56 to 65 years of age with an estimated GFR of 25 to 44 ml per minute per 1.73 m(2) were randoml

66 ther 18 to 55 years of age with an estimated GFR of 25 to 65 ml per minute per 1.73 m(2) of body-surf

67 in C, by itself or as a part of an estimated GFR, was a significant predictor of mortality.

68 cystatin C should be measured and estimated GFR should be calculated and reported using cystatin C (

69 utcomes among patients with early [estimated GFR (eGFR)>/=10 ml/min per 1.73 m(2)] versus later (eGFR

70 end point was percentage change in estimated GFR (eGFR) trajectory over the treatment period.

71 or diabetes, and lower tertile of estimated GFR.

72 , which was not detected by SCr or estimated GFR alone.

73 ing serum creatinine and reporting estimated GFR based on serum creatinine (eGFRcr) using the Chronic

74 )Cr-EDTA GFR was compared with the estimated GFR (eGFR) from seven published models and our new model

75 ry end point was the change in the estimated GFR from baseline to follow-up, with adjustment for the

76 slower decline than placebo in the estimated GFR over a 1-year period in patients with later-stage AD

77 The change from baseline in the estimated GFR was -2.34 ml per minute per 1.73 m(2) (95% confidenc

78 B did not alter the decline in the estimated GFR.

79 We estimated GFR by mean clearance of creatinine and urea from the sa

80 Therefore, we estimated GFR in 18,015 individuals from the IMPROVE-IT (ezetimibe

81 nce of the new derived formula with existing GFR formulae.

82 urinary protein, stenotic renal blood flow, GFR, microvascular structure, and oxygenation in vivo 4

83 The level of agreement for GFR determination was calculated using a Bland-Altman pl

84 loped and validated a new accurate model for GFR assessment in cirrhosis, the Royal Free Hospital cir

85 veloped a new multivariable linear model for GFR using statistical regression analysis.

86 m creatinine concentrations, and results for GFR from chromium-51 ((51)Cr) EDTA excretion measurement

87 Similar findings were observed for GFRs.

88 42% of patients with normal renal function (GFR > 90) at baseline, and this decreased to 18% at 1 ye

89 tients with rather preserved renal function (GFR>50 ml/min per 1.73 m(2)) and persistent proteinuria

90 (68)Ga-GFR agreed well with (51)Cr-GFR for estimation of GFR us

91 There was good agreement between (68)Ga-GFR and (51)Cr-GFR using serial plasma sampling, with a

92 ss agreement between (68)Ga-EDTA GFR ((68)Ga-GFR) and (51)Cr-EDTA GFR ((51)Cr-GFR), using serial plas

93 ived from donor and recipient Cockroft-Gault GFRs and adjusted for the single kidney adaptive respons

94 d based on glomerular filtration rate (GFR): GFR <60 and >/=60 mL/min per 1.73 m(2).

95 Among liver only patients, 25% had GFR less than 60 (mL/min per 1.73 m) at LT, and this inc

96 apy; P = 0.22); however, 3 patients now have GFR less than 20.

97 GFR reduction was larger in hyperfiltering (GFR >120 mL/min) than nonhyperfiltering patients and was

98 ortive care or additional immunosuppression (GFR>/=60 ml/min per 1.73 m(2): 6-month corticosteroid mo

99 The cumulative incidence of impaired GFR (sustained eGFR<60 ml/min per 1.73 m(2)) 10 years af

100 kwave therapy also decreased BP and improved GFR, microvascular density, and oxygenation in the steno

101 ly of functioning nephrons and adaptation in GFR of a single kidney.

102 l variables for time to GFR event (change in GFR of 50% or 25-ml/min per 1.73 m(2) decline), incident

103 osite outcome of incident ESRD and change in GFR: GSTM1 active/APOL1 high-risk hazard ratio, 2.13; 95

104 trophy (P=0.003) at diagnosis and changes in GFR (P<0.001), peritubular capillaritis Banff score (P=0

105 This study analyzed changes in GFR during long-term treatment with warfarin or dabigatr

106 Changes in GFR for up to 30 months were evaluated.

107 group of people with age-related decline in GFR and low associated risk as having CKD.

108 isease labeling of an age-related decline in GFR is appropriate.

109 PAR inhibition also prevented the decline in GFR observed in vehicle-treated mice, such that GFR at w

110 A more pronounced decline in GFR was associated with previous warfarin use and with t

111 age of 30 months, the mean +/- SE decline in GFR was significantly greater with warfarin (-3.68 +/- 0

112 groups experienced a significant decline in GFR.

113 ic range <65%) exhibited a faster decline in GFR.

114 A decrease in GFR >25% was less likely with DE 110 mg (hazard ratio: 0

115 recipients overall experience a decrease in GFR 1 year after transplantation.

116 An absolute, supraphysiologic elevation in GFR is observed early in the natural history in 10%-67%

117 oup most likely to experience improvement in GFR after transplantation.

118 Only 22% had an absolute improvement in GFR greater than 5 mL/min per 1.73 m.

119 D > 25 experienced any 1-year improvement in GFR, whereas all lower MELD groups experienced a signifi

120 The increase in GFR was uniform.

121 /- 9.0 y), with relatively mild reduction in GFR (mean +/- SD eGFR 53.5 +/- 11.8 mL/min/1,73 m2) and

122 In conclusion, severe reduction in GFR and ESRD after kidney donation were uncommon and wer

123 ssociated with a nonsignificant reduction in GFR in the hypertensive group (89+/-12 versus 95+/-16 ml

124 nce of albuminuria, age-related reduction in GFR with the corresponding increase in CKD (defined by a

125 due to the nephrectomy-related reduction in GFR, followed by an age-related decline that may be more

126 rular capsules corresponded to reductions in GFR.

127 The dynamic ABMR prediction model included GFR (P<0.001) and presence of interstitial fibrosis/tubu

128 rs that stabilize renal function or increase GFR, even in advanced phases of the disease.

129 BP through renal actions involving increased GFR and vascular and tubular effects.

130 ruct significantly attenuated Ang II-induced GFR decline in rats.

131 widely in response to dietary sodium intake, GFR, circulating hormones, neural signals, and local reg

132 able indicator of overall kidney function is GFR, which is measured either via exogenous markers (eg,

133 that the 40% elevation in the single-kidney GFR observed after donation could be attributed exclusiv

134 Single-kidney GFR remained stable after MSC but fell in the medical tr

135 omparable reduction in measured whole-kidney GFR.

136 g non-left bundle-branch block patients, low GFR predicted outcomes; however, no benefit from cardiac

137 mean, 79.6+/-16.0) mL/min per 1.73 m(2), low-GFR patients experienced higher risk of death (hazard ra

138 In the low-GFR group, there was greater absolute reduction in risk

139 In addition, lower GFR was associated with 3-4% higher PFAS concentrations

140 Patients with proteinuria or lower GFR should be monitored more closely.

141 hat aortic stiffness may contribute to lower GFR by transferring excessive flow pulsatility into the

142 d dialysis independent, compared with a mean GFR loss of 6.5 mL/min/year among those achieving only a

143 Estimated mean GFR values at year 10 for belatacept 4-weekly, belatacep

144 The mean GFR was 115+/-24 ml per minute, the mean number of nephr

145 Measured GFR (mGFR) has long been considered the gold standard me

146 of this study include the lack of a measured GFR and the potential lack of ethnic diversity in the st

147 As expected, LSD did not alter measured GFR and increased the abundance of total and cell-surfac

148 n the other hand, HSD did not alter measured GFR but decreased the abundance of the aforementioned tr

149 m(2), P=0.01), whereas CKD EPI and measured GFR did not change throughout the study period in the CN

150 lomerular filtration rate (GFR) and measured GFR were -0.30+/-0.66 and -1.51+/-1.33 ml per minute per

151 neurin inhibitors (CNIs) defined by measured GFR.

152 models (adjusted for demographics, measured GFR, proteinuria, body mass index, net endogenous acid p

153 dies are needed to monitor directly measured GFR, ensure that the bone remodeling and mineral effects

154 SRD disappeared upon adjustment for measured GFR.

155 ignificantly greater improvement in measured GFR (mGFR) at 12 months compared with those kept on CNI/

156 er serum uric acid level, and lower measured GFR.

157 nd placebo-treated groups in median measured GFR at 24 months (33 versus 42 ml/min per 1.73 m(2); P=0

158 FL was defined as >/=40% decline of measured GFR from baseline.

159 When compared to measured GFR, the formula with both creatinine and cystatin C, na

160 Primary outcome was measured GFR (iohexol plasma clearance).

161 Furthermore, correlation with measured GFR in 200 participants in the AASK study was 0.78 for b

162 sease epidemiology with "true," or measured, GFR (mGFR) and the impact of this difference on Model fo

163 In period 1 (n = 243), median GFR was 121 mL/min/1.73 m.

164 The median GFR in period 1 (2005-2006) was determined.

165 75 mL/min/1.73 m (eSCr75-MDRD) or the median GFR observed in period 1 (eSCrTRAUMA-MDRD).

166 73 m(2): 6-month corticosteroid monotherapy; GFR=30-59 ml/min per 1.73 m(2): cyclophosphamide for 3 m

167 At 6 months, GFR significantly decreased in 34 patients on CR and did

168 tion of all nephrons, and the single-nephron GFR assesses the function of individual nephrons.

169 The single-nephron GFR did not vary significantly according to age (among d

170 How the single-nephron GFR relates to demographic and clinical characteristics

171 However, single-nephron GFR remains relatively constant with healthy aging as do

172 ,000 per kidney, and the mean single-nephron GFR was 80+/-40 nl per minute.

173 A higher single-nephron GFR was associated with a height of more than 190 cm, ob

174 A higher single-nephron GFR was associated with certain risk factors for chronic

175 The mean single-nephron GFR was calculated as the GFR divided by the number of n

176 lthy adult kidney donors, the single-nephron GFR was fairly constant with regard to age, sex, and hei

177 A higher single-nephron GFR was independently associated with larger nephrons on

178 r age is there an increase in single-nephron GFR.

179 ings were correlated with the single-nephron GFR.

180 , albuminuria, and C reactive protein as non-GFR determinants of eGFRcys.

181 and all-cause mortality and investigated non-GFR determinants of eGFRcys.

182 s an important role in enhancing accuracy of GFR estimation and predicting mortality in LT recipients

183 Network analysis of GFR-correlating transcripts highlighted two major cluste

184 For initial assessment of GFR, measuring serum creatinine and reporting estimated

185 d a PBPK model to reflect the association of GFR with birth weight (estimated from three studies of G

186 If confirmation of GFR is required because of conditions that affect serum

187 recommend that cystatin-C-based estimates of GFR be used to confirm or exclude the diagnosis in peopl

188 Estimation of GFR from serum concentrations of creatinine and cystatin

189 greed well with (51)Cr-GFR for estimation of GFR using serial plasma counting.

190 s that may help to improve the estimation of GFR.

191 Evaluation of GFR, required in the evaluation of living kidney donor c

192 that affect serum creatinine independent of GFR (eg, extremes of muscle mass or diet), or interferen

193 for proteinuria >3.0 g/24 h, independent of GFR and allograft histology.

194 e of higher phosphate levels, independent of GFR and other confounding factors.

195 lasma phosphate concentration independent of GFR.

196 e cardiovascular risk factors independent of GFR.

197 IR reduced (14)C-inulin clearance (index of GFR) and increased renal vascular resistance (measured b

198 tomy itself does not cause long-term loss of GFR at a higher rate than what is seen in the normal agi

199 vival, defined as a composite of 50% loss of GFR that persisted for at least 1 month, the start of re

200 od evidence for cystatin C being a marker of GFR and risk in people with CKD, its use to define CKD i

201 tion generally is assessed by measurement of GFR and urinary albumin excretion.

202 ssociated with significantly greater odds of GFR </=90 mL/min/1.73 m(2) (odds ratio, 2.0) and urine p

203 Performance of GFR-estimating equations with and without cystatin C, in

204 The end point of GFR loss >/=15 ml/min per 1.73 m(2) did not differ betwe

205 the guideline recommendations, principles of GFR measurement and estimation, and our suggestions for

206 irth weight (estimated from three studies of GFR and birth weight) and used it to simulate PFAS conce

207 Similar significant effects on GFR and renal function parameters were observed during c

208 onclusion, the physiologic effects of NPs on GFR and natriuresis do not involve podocytes.

209 imitations of this study include reliance on GFR estimated using the Modification of Diet in Renal Di

210 GFRcys) and serum creatinine (eGFRcr-cys) or GFR should be measured directly using a clearance proced

211 1 did not associate with microalbuminuria or GFR.

212 pposed to estimate SCr using a predetermined GFR of 75 mL/min/1.73 m.

213 the most accurate published model to predict GFR.

214 Ambrisentan preserved GFR at the level of nondisease controls and prevented th

215 who had IgAN with relatively well preserved GFR and persistent proteinuria.

216 cline among 3030 young adults with preserved GFR in the Coronary Artery Risk Development in Young Adu

217 travenously on days 1, 4, 8, and 11) prevent GFR decline by halting the progression of late donor-spe

218 Neither immunosuppressive regimen prevented GFR loss, and both associated with substantial adverse e

219 rial failed to show that bortezomib prevents GFR loss, improves histologic or molecular disease featu

220 PUA, GFR (inulin), effective renal plasma flow (para-aminohip

221 eir pre-donation glomerular filtration rate (GFR) after they experience compensatory hypertrophy and

222 iated with lower glomerular filtration rate (GFR) and higher blood pressure (BP) in patients with typ

223 in the estimated glomerular filtration rate (GFR) and measured GFR were -0.30+/-0.66 and -1.51+/-1.33

224 TRPC6 regulates glomerular filtration rate (GFR) and the contractile function of glomerular mesangia

225 y salt intake on glomerular filtration rate (GFR) and tubular Na(+) reabsorption.

226 The glomerular filtration rate (GFR) assesses the function of all nephrons, and the sing

227 kidney size and glomerular filtration rate (GFR) at the time of donation.

228 ficant change in glomerular filtration rate (GFR) before or after therapy (64.2 +/- 16.5 mL/min per b

229 in the estimated glomerular filtration rate (GFR) but also caused more elevations in aminotransferase

230 Glomerular filtration rate (GFR) can accurately be determined using (51)Cr-ethylened

231 for accelerated glomerular filtration rate (GFR) decline and nephropathy.

232 The glomerular filtration rate (GFR) decreased in both groups about 50% within 6 months.

233 ical volume, and glomerular filtration rate (GFR) early after the procedure, and these changes were s

234 e performance of glomerular filtration rate (GFR) equations incorporating both cystatin C (CysC) and

235 tatin C improves glomerular filtration rate (GFR) estimation and mortality prediction, in comparison

236 Purpose The glomerular filtration rate (GFR) is essential for carboplatin chemotherapy dosing; h

237 n improvement in glomerular filtration rate (GFR) of 6.1 mL/min/year among those achieving a complete

238 unction shown by glomerular filtration rate (GFR) of less than 60 mL/min per 1.73 m(2), or markers of

239 Changes in glomerular filtration rate (GFR) the year before and after OLT have not been well de

240 se to changes in glomerular filtration rate (GFR) to maintain glomerulotubular balance.

241 best theoretical glomerular filtration rate (GFR) to use in this estimation.

242 ean preoperative glomerular filtration rate (GFR) was 75.1 +/- 14.9 mL/min/1.73 m.

243 The glomerular filtration rate (GFR) was calculated by means of the Modification of Diet

244 The glomerular filtration rate (GFR) was directly measured (using iohexol) along with 12

245 Glomerular filtration rate (GFR) was measured annually.

246 iology (albumin, glomerular filtration rate (GFR)), with log-transformed plasma PFAS concentrations.

247 sed estimates of glomerular filtration rate (GFR), UK and international guidelines recommend that cys

248 attributable to glomerular filtration rate (GFR), which is related to PFAS concentration and birth w

249 " and calculated glomerular filtration rate (GFR).

250 with a decreased glomerular filtration rate (GFR).

251 les of estimated glomerular filtration rate (GFR).

252 created based on glomerular filtration rate (GFR): GFR <60 and >/=60 mL/min per 1.73 m(2).

253 xist to estimate glomerular filtration rate (GFR); however, there is no consensus on which is superio

254 es the change in glomerular filtration rate (GFR, mL/min per m) in the first year after LT, with subg

255 ith an estimated glomerular filtration rate [GFR] >60 ml per minute per 1.73 m(2) of body-surface are

256 Cr levels and glomerular filtration rates (GFRs) were grouped according to when they were obtained

257 reased urinary albumin excretion and reduced GFR in patients with diabetes, conservative dose selecti

258 lar-glomerular feedback response and reduced GFR.

259 in loss of the tubule brush border, reduced GFR, pericardial edema, and increased mortality.

260 d versus baseline), hypoalbuminemia, reduced GFR, and marked glomerular damage.

261 se may be contraindicated because of reduced GFR from the Folic Acid for Vascular Outcome Reduction i

262 ic whites, whereas the prevalence of reduced GFR increased without significant differences by age or

263 e estimated the risk of proteinuria, reduced GFR, and ESRD in 3956 white kidney donors, assessed the

264 cute volume expansion, significantly reduced GFR, urine flow, and sodium excretion.

265 a diverse group of individuals with reduced GFR from a variety of causes.

266 uation, with three recommendations regarding GFR.

267 hese results suggest that TRPC6 may regulate GFR by modulating MC contractile function through multip

268 ance imaging, we related arterial stiffness, GFR, urinary albumin excretion, and potential mediators,

269 We found that GFR was significantly greater, and serum creatinine leve

270 observed in vehicle-treated mice, such that GFR at week 20 differed significantly between vehicle an

271 unfortunate few, recent studies suggest that GFR loss at donor nephrectomy increases the risk of even

272 The GFR was measured in LT recipients by iothalamate clearan

273 The GFR was then used for reverse calculation of CrC conside

274 y size increased by a mean of 29.3%, and the GFR by 35.6%.

275 ean single-nephron GFR was calculated as the GFR divided by the number of nephrons (calculated as the

276 ring the first week was used to estimate the GFR.

277 ion of synthetic NPs similarly increased the GFR and renal perfusion in both genotypes.

278 and an iothalamate-based measurement of the GFR during donor evaluation and who underwent a kidney b

279 alpha-like (GFRAL), an orphan member of the GFR-alpha family, is a high-affinity receptor for GDF15.

280 level distributions and the strength of the GFR-birth weight association.

281 made on the basis of factors in addition to GFR.

282 idemiologic studies might be attributable to GFR.

283 between PFAS levels and birth weight due to GFR.

284 d body size, aortic stiffness was related to GFR (Slope of regression B=-2.28+/-0.85 ml/min per SD, P

285 for important clinical variables for time to GFR event (change in GFR of 50% or 25-ml/min per 1.73 m(

286 ts with severe kidney disease at transplant (GFR < 30) are the group most likely to experience improv

287 (2) Two GFR thresholds are used for decision-making: a high thre

288 rtality prediction, in comparison to various GFR-estimating equations.

289 The predicted equation (r(2) = 74.6%) was GFR = 45.9 x (creatinine(-0.836) ) x (urea(-0.229) ) x (

290 The predicted equation (r(2) = 74.6%) was GFR = 45.9 x (creatinine(-0.836) ) x (urea(-0.229) ) x (

291 ress (FSS); however, it is not known whether GFR modulates PT endocytosis to enable maximally efficie

292 aluated in light of long-term risk, in which GFR is one of many factors.

293 We also report associations with GFR and albumin, which were strongly related to PFAS con

294 The associations of these molecules with GFR estimated on the basis of creatinine (eGFRcr) and cy

295 Mortality with GFR >95.3 was 28/457 (6.1%), and 131/432 (30.3%) was wit

296 Relative to the 861 (68%) patients with GFR >/=60 (mean, 79.6+/-16.0) mL/min per 1.73 m(2), low-

297 firm or exclude the diagnosis in people with GFR 45-59 ml/min/1.73 m2 and no albuminuria (CKD G3aA1).

298 care, the setting in which most people with GFR in this range are managed.

299 nch block patients, 413 (32%) presented with GFR <60 (mean, 48.1+/-8.3) mL/min per 1.73 m(2).

300 28/457 (6.1%), and 131/432 (30.3%) was with GFR < 48.3 (P < 0.0001).