ライフサイエンスコーパス: CKD

1 CKD developed in 269 (33%) patients.

2 CKD incidence varies by Hispanic/Latino heritage and thi

3 CKD induces loss of muscle proteins partly by suppressin

4 CKD is associated with abnormalities in cerebral blood f

5 CKD is associated with increased oxidative stress that c

6 CKD stage either improved or was unchanged following TAV

7 CKD suppresses muscle protein synthesis via epigenetic m

8 lts are not confirmed when excluding stage 1 CKD.

9 As an initial analysis, we analyzed 39,121 CKD outpatients (median age was 71 years, 54.7% were men

10 sleep apnea and an elevated risk of stage 3 CKD or higher, but this association was no longer signif

11 In patients with stage 3b/4 CKD, treatment with lanthanum over 96 weeks did not affe

12 domizing 278 participants with stage 3b or 4 CKD and serum phosphate >1.00 mmol/L (3.10 mg/dl) to 500

13 During 19 years (median) of follow-up, 461 CKD events occurred.

14 nary model of care for patients with stage 5 CKD who want to avoid dialysis, is guided by patient val

15 to 5 groups, ranging from stage 1 to stage 5 CKD, whereas end-stage kidney disease (ESKD) is defined

16 rial involving 756 adults with stage-3 to -5 CKD and anemia, we evaluated incidence of red blood cell

17 103 ml/min/1.73 m2), 1,192 (9%) developed a CKD after a median of eight years.

18 isk of infection has not been evaluated in a CKD population.

19 observed that the number of patients with a CKD stage G1, G2, G3a, G3b, G4 and G5 were 1,001 (2.6%),

20 st these mediators explain most of adiposity-CKD-associated risk.

21 Adjusted CKD prevalence was about 5% with repeat confirmatory tes

22 duced ejection fraction (HFrEF) and advanced CKD.

23 vational cohort of HF patients with advanced CKD (estimated glomerular filtration rate <30 mL/min per

24 inhibitor therapy in patients with advanced CKD affects outcomes.

25 flect on the care of a patient with advanced CKD and mild to moderate dementia.

26 In HFrEF patients with advanced CKD, the use of beta-blockers was associated with lower

27 ects a majority of individuals with advanced CKD.

28 4.8 versus 180.0 per 1000 person-years after CKD diagnostic date, and 109.3 versus 47.4 per 1000 pers

29 genetic background may be protected against CKD.

30 is confirmed the dominance of molecular AKI, CKD, and eGFR.

31 d fibroblast growth factor-23 (FGF23) at all CKD stages, and lower blood phosphate in CKD stages 3-5.

32 diabetes (24.7% versus 17.9%, p = 0.03), and CKD (34.2% versus 20.0%, p < 0.001); and was more likely

33 mediates the association between PM(2.5) and CKD.

34 D spectrum to these determinants in age- and CKD stage-matched patients, with causes of CKD other tha

35 d in ABMR, were related to molecular AKI and CKD and to eGFR, not rejection activity, presumably beca

36 n fewer simultaneously investigating AKI and CKD in this population.

37 l diagnostic methods in drug-induced AKI and CKD mice models, but also possesses a higher diagnostic

38 pcidin and parameters related to anaemia and CKD-MBD among haemodialysis patients.

39 3.6%] in adults) compared with the CKiD and CKD-EPI equations.

40 For HF, MI, CVD, and CKD, register-based models outperformed a reference mode

41 n the course of both periodontal disease and CKD.

42 ciation between diabetes or hypertension and CKD risk are unclear.

43 f SGLT2 inhibitors for treatment of T2DM and CKD, the National Kidney Foundation convened a scientifi

44 At baseline, CKD stage >=2 was present in 91% of patients.

45 r 1.73 m(2) and >=25% decline from baseline, CKD-related hospitalization or death, or ESKD.

46 9.3 versus 47.4 per 1000 person-years before CKD onset in those developing CKD after recruitment).

47 ymptomatic hyperuricemia alone did not cause CKD or drive the progression of aristolochic acid I-indu

48 hed signaling pathways that may characterize CKD pathology were identified from these proteins.

49 ugs (D:A:D) score, which summarizes clinical CKD risk factors, and a polygenic risk score that summar

50 c Kidney Disease Epidemiology Collaboration (CKD-EPI) equation for adults are recommended serum creat

51 c Kidney Disease Epidemiology Collaboration (CKD-EPI), Modification of Diet in Renal Disease, and Coc

52 g NO66 could suggest strategies that counter CKD-induced abnormal muscle protein catabolism.

53 Nephropathic cystinosis CKD patients have mineral abnormalities that are distinc

54 The study defined CKD progression by a >=50% decline in the eGFR, initiati

55 ateralis (VL) of n=16 non-dialysis dependent CKD patient's stage 3b-5 (NDD-CKD) and n=16 healthy cont

56 dels, we compared predictions for developing CKD stage 3 and for eGFR trajectory.

57 n-years before CKD onset in those developing CKD after recruitment).

58 ronic kidney disease-cardiovascular disease (CKD-CVD) health outcomes model, a Markov state transitio

59 primary outcome was chronic kidney disease (CKD) - defined as confirmed decrease in eGFR <=60 ml/min

60 Transition to chronic kidney disease (CKD) after an episode of acute kidney injury (AKI) is kn

61 of patients develop chronic kidney disease (CKD) after liver transplantation (LT).

62 th increased risk of chronic kidney disease (CKD) and diabetes, a causal driver of CKD.

63 Associations between chronic kidney disease (CKD) and the gut microbiota have been postulated, yet qu

64 olving patients with chronic kidney disease (CKD) and type 2 diabetes.

65 Persons with chronic kidney disease (CKD) are at high risk of infection.

66 Adults with chronic kidney disease (CKD) are hospitalized more frequently than those without

67 Patients with chronic kidney disease (CKD) are often 25(OH)D(3) and 1,25(OH)(2)D(3) insufficie

68 esence or absence of chronic kidney disease (CKD) at baseline (estimated glomerular filtration rate [

69 Patients with chronic kidney disease (CKD) exhibit reduced exercise capacity, poor physical fu

70 activities change in chronic kidney disease (CKD) has not yet been elucidated.

71 Patients with chronic kidney disease (CKD) have inability to maintain the normal levels of pro

72 Chronic kidney disease (CKD) in low-resource settings poses multiple challenges,

73 is hypothesized that chronic kidney disease (CKD) induces oxidant stress which contributes to the dec

74 d antiretrovirals to chronic kidney disease (CKD) is unknown.

75 d with lower risk of chronic kidney disease (CKD) progression, implicating mechanisms beyond renal cl

76 easing prevalence of chronic kidney disease (CKD) seriously is threatening human health and overall q

77 of kidney stones and chronic kidney disease (CKD) which is characterized by 2,8-dihydroxyadenine rena

78 re (HF) and advanced chronic kidney disease (CKD), a population underrepresented in HF trials.

79 iabetes mellitus and chronic kidney disease (CKD), and they may be involved in age-related diseases.

80 Chronic kidney disease (CKD), commonly fostering nonrenal complications, themsel

81 diseases, including chronic kidney disease (CKD), epilepsy, and amyotrophic lateral sclerosis (ALS),

82 tabolic diseases and chronic kidney disease (CKD), in part via metabolism of ingested food.

83 ortant biomarker for chronic kidney disease (CKD), we tested the FOLP probe for its ability to monito

84 r filtration rate by chronic kidney disease (CKD)-EPI-CysC-creatinine <60 mL/min/1.73 m at WL inclusi

85 oration of anemia in chronic kidney disease (CKD).

86 ase in patients with chronic kidney disease (CKD).

87 y similar to that of chronic kidney disease (CKD).

88 und in patients with chronic kidney disease (CKD).

89 cipients with pre-LT chronic kidney disease (CKD).

90 moral calcinosis and chronic kidney disease (CKD).

91 million persons-have chronic kidney disease (CKD).

92 ar disease (CVD) and chronic kidney disease (CKD).

93 er-, rheumatic-, and chronic kidney disease (CKD).

94 ney injury (AKI) and chronic kidney disease (CKD).

95 ied for diabetes and chronic kidney disease (CKD, defined as estimated glomerular filtration rate <=6

96 inosis from elevations of FGF23 during early CKD stages.

97 oing TAVR, even with baseline impaired eGFR, CKD stage is more likely to stay the same or improve tha

98 d 263 ml/d in participants with normal eGFR, CKD, and kidney failure, respectively (P=0.02).

99 r are also at increased risk for established CKD risk factors, including obesity, hypertension, and t

100 isorder that can also initiate or exacerbate CKD, is merely supportive.

101 ntributed to the progression of pre-existing CKD.

102 stal granulomas may form due to pre-existing CKD; and (3) proinflammatory granuloma-related M1-like m

103 were identified as baseline risk factors for CKD development.

104 s was performed to identify risk factors for CKD development.

105 ible by people with T2DM to reduce risks for CKD and CVD in alignment with the clinical trial entry c

106 e benefits of population-based screening for CKD are uncertain; that there is potential for harms; th

107 ntially increase the appeal of searching for CKD in people with known kidney risk factors (case findi

108 t (10%), and test set (10%) - stratified for CKD status and follow-up length.

109 Formal CKD surveillance programs in Nicaragua are needed to ass

110 HDL from CKD rabbits and patients on hemodialysis had HNE adducts

111 gative phenotype in the presence of HDL from CKD rabbits, patients on hemodialysis and peritoneal dia

112 Absolute risks of stage 3b or higher CKD were <2%, 3% to 14%, 21% to 26%, and 46% to 69% acro

113 In CKD mice, cardiac fibrosis was associated with upregulat

114 In CKD rats, we found cognitive impairment in the novel obj

115 In CKD stages 2, 3, 4, and 5, five proteins showed signific

116 production is the major driver of anemia in CKD, iron deficiency stands out among the mechanisms con

117 ciency plays a significant role in anemia in CKD.

118 otential of 'food as medicine' approaches in CKD beyond the current strategies of protein, sodium and

119 In contrast, in CKD kidneys higher levels of Ang II were recorded, which

120 hyperuricemia or uric acid (UA) crystals in CKD progression are unknown.

121 o absolute and functional iron deficiency in CKD, including blood losses, impaired iron absorption, a

122 idered less effective than loop diuretics in CKD.

123 SCFAs) through gut fermentation of fiber, in CKD and diabetes.

124 e (NaHCO(3)) may preserve kidney function in CKD, even if initiated when serum bicarbonate concentrat

125 ctice guidelines for the treatment of IDA in CKD, and we summarize the available oral and intravenous

126 gy and available diagnostic tests for IDA in CKD, we discuss the literature that has informed the cur

127 ron formulations for the treatment of IDA in CKD.

128 E), and found both were sharply increased in CKD heart; DMTU treatment and UT-KO significantly abolis

129 d G2) are associated with large increases in CKD rates among populations of recent African descent, b

130 However, pathogenic mechanisms involved in CKD such as renal hypoxia result in loss of kidney funct

131 ications of disordered mineral metabolism in CKD.

132 with decreased inflammation and mortality in CKD, and SCFAs have been proposed to mediate this effect

133 nes in adipose tissue and skeletal muscle in CKD mice.

134 ern distinct from that typically observed in CKD-mineral and bone disorder.

135 hological step along the fibrotic pathway in CKD.

136 ht improve arterial stiffness in patients in CKD, we conducted a parallel-group, double-blind, random

137 rast to the detrimental role of periostin in CKD, we discovered a protective role of periostin in AKI

138 all CKD stages, and lower blood phosphate in CKD stages 3-5.

139 Severe RAS dysregulation is present in CKD dictated by high chymase-mediated Ang II formation.

140 es to answer important clinical questions in CKD care.

141 we show that 25(OH)D clearance is reduced in CKD and may differ by race.

142 athways related to muscle mass regulation in CKD mice.

143 striction, may reduce cardiovascular risk in CKD, but this requires testing in prospective randomised

144 Diuretic sensitivity in CKD is maintained despite lower diuretic clearance.

145 Low sKlotho in CKD is associated with disease progression, and sKlotho

146 bnormalities that are distinct from those in CKD stemming from other causes.

147 n in reducing BP and extracellular volume in CKD.

148 ard ratio:1.20, 95% CI: 1.13-1.29), incident CKD (1.28, 1.18-1.39), >=30% decline in eGFR (1.23, 1.15

149 .9; and severe, >=30.0) and defined incident CKD (stage 3 or higher) as eGFR<60 ml/min per 1.73 m(2)

150 sleep characteristics, and risk of incident CKD (stage 3 or higher) in 1525 participants (mean age,

151 regression analysis, predictors of incident CKD included BP >140/90 mm Hg, higher glycated hemoglobi

152 e sleep apnea severity with risk of incident CKD, adjusting for demographics, lifestyle behaviors, an

153 eep characteristics associated with incident CKD.

154 ient-level risk factors for AKI-RRT included CKD, men, non-White race, hypertension, diabetes mellitu

155 irst genetic score quartile had no increased CKD risk, even if they were in the fourth D:A:D score qu

156 Genetic score increased CKD risk similar to clinical D:A:D score and potentially

157 ekly injections of aristolochic acid induced CKD in age- and sex-matched wild-type and Slc26a6 (-/-)

158 ike macrophages may drive UA crystal-induced CKD progression.

159 e progression of aristolochic acid I-induced CKD.

160 ities in three rat models of CKD, we induced CKD in rats by an adenine-rich diet or by 5/6 nephrectom

161 ized exchangeable information storage, the J-CKD-DB succeeded to efficiently collect clinical data of

162 updated with an anonymized patient ID, the J-CKD-DB will be a dynamic registry of Japanese CKD patien

163 KD-DB will be a dynamic registry of Japanese CKD patients by expanding and linking with other existin

164 potential therapeutic strategy for managing CKD.

165 glomerular filtration rate (GFR) not meeting CKD criteria was observed in 66% of patients with cirrho

166 t of 15 346 patients with HFrEF and moderate CKD (estimated glomerular filtration rate <60-30 mL/min

167 Univariable and multivariable CKD odds ratios (ORs) were calculated based on the Data

168 reasing the body burden of oxalate in murine CKD models.

169 NDD-CKD patients exhibit reduced skeletal muscle mitochondri

170 ysis dependent CKD patient's stage 3b-5 (NDD-CKD) and n=16 healthy controls matched for age, gender a

171 spects of mitochondrial dysfunction in a NDD-CKD cohort.For the comparison between NDD-CKD and HC pop

172 DD-CKD cohort.For the comparison between NDD-CKD and HC populations, skeletal muscle biopsies were co

173 the dysregulation of these processes in NDD-CKD may provide a therapeutic opportunity to improve mus

174 In addition, non-CKD AhR(-/-) knockout mice were protected against indoxy

175 s clinical tool's quantitative assessment of CKD risk may be weighed against other considerations whe

176 a are needed to assess the overall burden of CKD nationally, with a focus on agricultural workers.

177 ar pressure (Pglom) is an important cause of CKD, but there is no feasible method to directly assess

178 Glomerular injury is a major cause of CKD, which is epidemic and without therapeutic options.

179 3 m(2)), 195 (30%) had a glomerular cause of CKD.

180 d CKD stage-matched patients, with causes of CKD other than nephropathic cystinosis.

181 iochemical abnormalities in common causes of CKD-mineral and bone disorder have been defined, it is u

182 ts along the genotype-phenotype continuum of CKD.

183 autophagy, but its effects on the course of CKD have been demonstrated only in the experimental sett

184 eded to efficiently collect clinical data of CKD patients across hospitals despite their different EH

185 h these two approaches to early detection of CKD.

186 rosclerosis may be important determinants of CKD and mortality.

187 apnea may be associated with development of CKD through hypoxia, inflammation, and oxidative stress.

188 sease (CKD) and diabetes, a causal driver of CKD.

189 glomerular versus nonglomerular etiology of CKD, effect estimates did not differ significantly.

190 Evidence of CKD was found in 18,034 (6.4%) participants.

191 e meaningfully to seemingly complex forms of CKD across different clinically defined subgroups and ar

192 Rare inherited forms of CKD frequently span diverse phenotypes, reflecting genet

193 ch technique to evaluate the hemodynamics of CKD on the basis of direct pressure and flow measurement

194 pt, bolstered by extensive investigations of CKD as a risk factor of cardiovascular disease.

195 invasive and convenient diagnosis methods of CKD and its complications through urine testing in the f

196 ubtotal nephrectomy created a mouse model of CKD with BUN >80 mg/dl.

197 In a mouse model of CKD, we found that a high sulfur amino acid-containing d

198 ue and muscle metabolism in a mouse model of CKD-associated cachexia.

199 avioral abnormalities in three rat models of CKD, we induced CKD in rats by an adenine-rich diet or b

200 a 29% (1.29; 1.20 to 1.38) increased odds of CKD, and each 5-kg/m(2) genetically-predicted higher BMI

201 ening (such as markedly higher prevalence of CKD in people with diabetes, hypertension, and cardiovas

202 O for only 4 weeks attenuates progression of CKD beyond MRE therapy in mice with type 2 diabetes.

203 Progression of CKD in type 2 diabetes, despite dual inhibition of sodiu

204 nks between UA deposition and progression of CKD include that (1) asymptomatic hyperuricemia does not

205 leep apnea associated with increased risk of CKD (hazard ratio [HR], 1.51; 95% confidence interval [9

206 lop a tool for stratifying patients' risk of CKD arising after surgery for kidney cancer, we tested m

207 t with finerenone resulted in lower risks of CKD progression and cardiovascular events than placebo.

208 sociated with significantly greater risks of CKD progression, with clearance of kynurenic acid, a hig

209 We looked at the severity of CKD at the time of waitlisting on posttransplant ESRD an

210 ion and fibrosis that may lead to slowing of CKD progression.

211 More detailed study of CKD-associated MCI is needed to fully understand its cli

212 d the protein concentrations in the urine of CKD patients and extracted abnormal protein signals comp

213 statins) seem to have little or no effect on CKD-associated MCI, suggesting that the accumulation of

214 n evaluating the impact of oxidant stress on CKD progression in children.

215 examined rates and risk factors of new-onset CKD using data from 8774 adults in the Hispanic Communit

216 96 events; HR, 0.91 [95% CI, 0.76-1.09]), or CKD (n = 2433 events; HR, 0.98 [95% CI, 0.65-1.11]).

217 %, respectively) and have preexisting CKD or CKD that developed during follow-up (46.3% versus 17.2%,

218 , an observational cohort study of pediatric CKD patients from the US and Canada.

219 phropathic cystinosis across the predialysis CKD spectrum to these determinants in age- and CKD stage

220 ), and CysC (SHR, 1.38; 1.01-1.89) predicted CKD development.

221 us 17.2%, respectively) and have preexisting CKD or CKD that developed during follow-up (46.3% versus

222 TNFR-2, and KIM-1 in patients with prevalent CKD and provide new insights into the influence of suPAR

223 R, 48 ml/min per 1.73 m(2)), 117 progressive CKD events, 183 noncancer deaths, and 116 cancer deaths

224 mined which patients experienced progressive CKD (defined as dialysis, kidney transplantation, or a 4

225 tic glomeruli or IF/TA predicted progressive CKD.

226 asymptomatic hyperuricemia does not promote CKD progression unless UA crystallizes in the kidney; (2

227 sk are needed to benefit patients and reduce CKD's economic burden.

228 Additional therapies to reduce CKD incidence, slow CKD progression, and lower hospitali

229 o CKD; however, the mechanism of HIV-related CKD has not been thoroughly investigated.

230 ied 2738 individuals with moderate to severe CKD participating in the multicenter Chronic Renal Insuf

231 ohort of individuals with moderate to severe CKD, we observed steep declines of eGFR were associated

232 to degree of risk of clinically significant CKD (negligible, low, moderate, or high risk).

233 s to stratify risk of clinically significant CKD after nephrectomy are needed.

234 ategory was 98.9% for clinically significant CKD.

235 onal therapies to reduce CKD incidence, slow CKD progression, and lower hospitalization risk are need

236 This treatment suppressed CKD-induced hypertension and cardiac hypertrophy.

237 al area stained with oil red O revealed that CKD-bMPOKO mice had significantly decreased aortic plaqu

238 non-Hispanics, but little is known about the CKD incidence in this population.

239 (uCrCl) versus GFR estimation (eGFR) by the CKD-EPI formula versus both] is unclear.

240 ml/min per 1.73 m(2) (IQR, 74-100) using the CKD-EPI formula, 30% had microalbuminuria, and 32% had d

241 ribution of central and general adiposity to CKD risk and the underlying mechanism of mediation are u

242 st-to-hip ratio and body mass index (BMI) to CKD prevalence.

243 cing activity and ameliorated progression to CKD in the mice.

244 Progression to CKD stage 5 occurred in 1 (0.035%) of 2,892 patients wit

245 ave implicated epigenetic changes related to CKD; however, the mechanism of HIV-related CKD has not b

246 l methods to determine their relationship to CKD status and further renal function decline.

247 vitro and in vivo and the susceptibility to CKD in rats with wild-type or mutated Add3 and in geneti

248 ve been proposed as an approach for treating CKD.

249 .01) were more often seen in men, and so was CKD (P=0.03).

250 s between central and general adiposity with CKD are largely causal.

251 In this study, we observed that adults with CKD had a higher hospitalization rate than the general p

252 slopes in clinical assessment of adults with CKD.

253 nous secretory solutes to be associated with CKD progression and all-cause mortality, independent of

254 r protein periostin has been associated with CKD progression in animal models and human biopsy specim

255 e 6-bromotryptophan and its association with CKD risk factors and incident end-stage kidney disease (

256 R-1], and TNFR-2) may identify children with CKD at risk for GFR decline.

257 ction and blood pressure among children with CKD.

258 tress over time in a cohort of children with CKD.

259 ciations of secretory-solute clearances with CKD progression and mortality, adjusting for eGFR, album

260 ecreased aortic plaque area as compared with CKD-bMPOWT mice.

261 om 3 prospective cohorts of individuals with CKD (not on dialysis or with a kidney transplant): (1) R

262 lth in this trial involving individuals with CKD.

263 tibility to infection among individuals with CKD.

264 dividuals with diabetes and individuals with CKD: 1 SD higher daily CML intake was associated with a

265 Muscles of mice with CKD have increased expression of nucleolar protein 66 (N

266 atly increased in the intestine of mice with CKD.

267 trial in participants aged 18 or older with CKD stage 3b or 4 (eGFR 15-45 ml/min per 1.73 m(2)).

268 Results Fifty-nine participants with CKD (mean age, 59 years +/- 13 [standard deviation]; 30

269 Among participants with CKD, AKI rate in people with diabetes was more than twic

270 In this cohort of participants with CKD, BP metrics derived from ambulatory BP monitoring ar

271 orbidities but up to 55% among patients with CKD and heart failure.

272 Among 596 patients with CKD and MG from 2017 to 2018, 62 (10.4%) underwent a kid

273 ial, we randomly assigned 5734 patients with CKD and type 2 diabetes in a 1:1 ratio to receive finere

274 In patients with CKD and type 2 diabetes, treatment with finerenone resul

275 Patients with CKD are at an increased risk (compared with the general

276 Patients with CKD are uniquely poised to benefit from these integrativ

277 and detecting herpesviruses in patients with CKD as the inflammatory process observed in these clinic

278 ron-deficiency anemia (IDA) in patients with CKD have limitations, leading to persistent challenges i

279 gression of atherosclerosis in patients with CKD is unknown.

280 o muscle biopsy specimens from patients with CKD or those undergoing hemodialysis.

281 ation patterns of kidneys from patients with CKD showed defects similar to those in mice with Dnmt3a

282 restriction in reducing BP in patients with CKD stage G3 or G4 and hypertension, we conducted a 6-we

283 ere differentially effected in patients with CKD stemming from nephropathic cystinosis versus other c

284 Patients with CKD who are on hemodialysis are hyporesponsive to erythr

285 reduce cardiovascular risk in patients with CKD who have normophosphatemia.

286 ape of therapeutic options for patients with CKD with T2D, with demonstration of significant reductio

287 total health care costs among patients with CKD without comorbidities were 31% higher than among pat

288 In patients with CKD, the kidney and CVD benefits of canagliflozin were e

289 In patients with CKD, untreated chronic metabolic acidosis often leads to

290 erapies to improve the care of patients with CKD.

291 gnitive impairment found among patients with CKD.

292 p pattern commonly observed in patients with CKD.

293 evaluation of hypertension in patients with CKD.

294 phosphate levels in WT mice and in rats with CKD due to subtotal nephrectomy.

295 Among 3146 SLK recipients with CKD, nearly two-thirds were 50-64 years of age, while 46

296 nted for 35% of total costs among those with CKD and no comorbidities but up to 55% among patients wi

297 unction decline in patients with and without CKD, and regardless of the severity of kidney impairment

298 duced similarly in patients with and without CKD: HR=0.53 (95% CI, 0.31-0.91) and HR=0.46 (95% CI, 0.

299 were 31% higher than among patients without CKD ($7374 versus $5631, respectively).

300 pitalized more frequently than those without CKD, but the magnitude of this excess morbidity and the