ライフサイエンスコーパス: CKD

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

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

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

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

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

6 moral calcinosis and chronic kidney disease (CKD).

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

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

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

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

11 ects a majority of individuals with advanced CKD.

12 ron formulations for the treatment of IDA in CKD.

13 ve been proposed as an approach for treating CKD.

14 slopes in clinical assessment of adults with CKD.

15 ications of disordered mineral metabolism in CKD.

16 ts along the genotype-phenotype continuum of CKD.

17 potential therapeutic strategy for managing CKD.

18 atly increased in the intestine of mice with CKD.

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

20 erapies to improve the care of patients with CKD.

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

22 n the course of both periodontal disease and CKD.

23 lts are not confirmed when excluding stage 1 CKD.

24 ciency plays a significant role in anemia in CKD.

25 e progression of aristolochic acid I-induced CKD.

26 idered less effective than loop diuretics in CKD.

27 ategory was 98.9% for clinically significant CKD.

28 lth in this trial involving individuals with CKD.

29 ction and blood pressure among children with CKD.

30 gnitive impairment found among patients with CKD.

31 hological step along the fibrotic pathway in CKD.

32 3 m(2)), 195 (30%) had a glomerular cause of CKD.

33 duced ejection fraction (HFrEF) and advanced CKD.

34 eep characteristics associated with incident CKD.

35 p pattern commonly observed in patients with CKD.

36 tic glomeruli or IF/TA predicted progressive CKD.

37 n in reducing BP and extracellular volume in CKD.

38 ntributed to the progression of pre-existing CKD.

39 evaluation of hypertension in patients with CKD.

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

41 genetic background may be protected against CKD.

42 tibility to infection among individuals with CKD.

43 h these two approaches to early detection of CKD.

44 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

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

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

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

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

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

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

51 inhibitor therapy in patients with advanced CKD affects outcomes.

52 103 ml/min/1.73 m2), 1,192 (9%) developed a CKD after a median of eight years.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

68 rosclerosis may be important determinants of CKD and mortality.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

112 es to answer important clinical questions in CKD care.

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

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

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

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

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

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

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

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

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

122 CKD developed in 269 (33%) patients.

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

124 were identified as baseline risk factors for CKD development.

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

126 4.8 versus 180.0 per 1000 person-years after CKD diagnostic date, and 109.3 versus 47.4 per 1000 pers

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

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

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

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

131 3.6%] in adults) compared with the CKiD and CKD-EPI equations.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

166 CKD incidence varies by Hispanic/Latino heritage and thi

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

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

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

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

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

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

173 CKD induces loss of muscle proteins partly by suppressin

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

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

176 CKD is associated with abnormalities in cerebral blood f

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

178 CKD is associated with increased oxidative stress that c

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

180 gression of atherosclerosis in patients with CKD is unknown.

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

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

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

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

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

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

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

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

189 In CKD mice, cardiac fibrosis was associated with upregulat

190 athways related to muscle mass regulation in CKD mice.

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

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

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

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

195 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]).

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

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

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

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

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

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

202 9.3 versus 47.4 per 1000 person-years before CKD onset in those developing CKD after recruitment).

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

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

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

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

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

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

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

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

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

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

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

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

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

216 NDD-CKD patients exhibit reduced skeletal muscle mitochondri

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

218 Nephropathic cystinosis CKD patients have mineral abnormalities that are distinc

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

257 CKD stage either improved or was unchanged following TAV

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

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

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

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

262 .9; and severe, >=30.0) and defined incident CKD (stage 3 or higher) as eGFR<60 ml/min per 1.73 m(2)

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

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

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

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

267 inosis from elevations of FGF23 during early CKD stages.

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

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

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

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

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

273 CKD suppresses muscle protein synthesis via epigenetic m

274 Formal CKD surveillance programs in Nicaragua are needed to ass

275 %, respectively) and have preexisting CKD or CKD that developed during follow-up (46.3% versus 17.2%,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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