Abstract P147: Association Of Rosuvastatin Use With Risk Of Rhabdomyolysis Across Chronic Kidney Disease Status

Introduction: Statin-induced rhabdomyolysis is a rare, but potentially life-threatening condition. It is unknown whether specific statins carry a greater risk of rhabdomyolysis and whether the risk differs between patients with and without chronic kidney disease (CKD). The objective of this study was to investigate the association of rosuvastatin use vs. atorvastatin use with the risk of rhabdomyolysis across CKD status. Hypothesis: Rosuvastatin use is associated with a higher risk of rhabdomyolysis as compared to atorvastatin use and the risk is greater among those with CKD than those without CKD. Methods: We identified adult patients who initiated rosuvastatin or atorvastatin between January 1, 2004 and December 31, 2018 and were free of end-stage kidney disease at the time of prescription in the Geisinger Health System. The association between rosuvastatin use and rhabdomyolysis was assessed using Cox proportional hazards regression models with an interaction between rosuvastatin use and CKD (i.e., estimated glomerular filtration rate <60 ml/min/1.73 m 2 ) in an inverse probability of treatment weighted (IPTW) sample. Results: Of 8,748 rosuvastatin users (mean [SD] age, 59.7 [12.6] years; 49.8% female; 11.8% CKD) and 31,770 atorvastatin users (mean [SD] age, 59.1 [12.6] years; 48.2% female; 11.9% CKD), 0.7% and 0.4% patients developed rhabdomyolysis, respectively, during a median follow-up of 5.1 years. Rosuvastatin use was associated with a higher risk of rhabdomyolysis in patients with CKD (hazard ratio [HR], 3.29; 95% CI, 1.53-7.09), but not in those without CKD (HR, 1.29; 95% CI, 0.82-2.03; p-interaction=0.04). A higher risk of rhabdomyolysis associated with rosuvastatin use in lower eGFR was also observed in the analysis with continuous eGFR ( Figure ). Conclusions: The findings suggest that rosuvastatin use in patients with CKD may be associated with excess risk of rhabdomyolysis as compared to atorvastatin.

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Abstract P037: Progression Of Coronary Artery Calcification And Risk Of Clinical Events In Chronic Kidney Disease

Circulation ◽

10.1161/circ.143.suppl_1.p037 ◽

2021 ◽

Vol 143 (Suppl_1) ◽

Author(s):

Joshua D Bundy ◽

Ling Tian ◽

Matthew J Budoff ◽

Julia J Scialla ◽

Rupal Mehta ◽

...

Keyword(s):

Myocardial Infarction ◽

Chronic Kidney Disease ◽

Coronary Artery ◽

Kidney Disease ◽

Coronary Artery Calcification ◽

Proportional Hazards ◽

Cox Proportional Hazards ◽

Clinical Events ◽

Prospective Longitudinal

Introduction: Patients with chronic kidney disease (CKD) are at high risk for cardiovascular disease (CVD) events. Coronary artery calcification (CAC) and progression of CAC are associated with higher risk of clinical events in the general population, but this has not been quantified among patients with CKD. Hypothesis: Progression of CAC is independently associated with CVD events and mortality among patients with CKD stages 2-4. Methods: We pooled individual-level data from 2 prospective longitudinal cohort studies (the Chronic Renal Insufficiency Cohort [CRIC] Study and the Multi-Ethnic Study of Atherosclerosis [MESA]). We included participants with CKD, defined as an estimated glomerular filtration rate <60 mL/min/1.73m 2 or urinary albumin-to-creatine ratio ≥30 mg/g. In both cohorts, CAC was measured at baseline and a follow-up visit using electron beam or multidetector computed tomography. Multivariable-adjusted Cox proportional hazards regression models were used to assess the associations of CAC progression between visits with risks of adjudicated atherosclerotic CVD events (myocardial infarction, stroke) and all-cause mortality. Analyses were stratified by presence or absence of CAC at baseline. Results: 2111 participants with CKD were included (1314 with and 797 without CAC at baseline). Over an average of 3 years between CAC scans, 192 (24%) participants without baseline CAC developed CAC while 222 participants (17%) with baseline CAC increased ≥100 Agatston units per year. Over an average 9.4-year follow-up after the second CAC scan, we observed 272 atherosclerotic CVD events (178 myocardial infarction, 94 stroke) and 570 deaths. After multivariable adjustment, CAC progression was significantly associated with higher risk of atherosclerotic CVD and mortality, particularly among those with CAC at baseline (Table). Conclusions: Among adults with CKD stages 2-4, progression of CAC over approximately 3 years is significantly associated with atherosclerotic CVD and mortality.

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Taking Sleeping Pills and the Risk of Chronic Kidney Disease: A Nationwide Population-Based Retrospective Cohort Study

Frontiers in Pharmacology ◽

10.3389/fphar.2020.524113 ◽

2021 ◽

Vol 11 ◽

Author(s):

Chen-Yi Liao ◽

Chi-Hsiang Chung ◽

Kuo-Cheng Lu ◽

Cheng-Yi Cheng ◽

Sung-Sen Yang ◽

...

Keyword(s):

Chronic Kidney Disease ◽

Kidney Disease ◽

Proportional Hazards ◽

Population Based ◽

Cox Proportional Hazards ◽

Sleeping Pills ◽

Potential Association ◽

Increased Risk ◽

Stage Renal Disease ◽

End Stage

Background: Sleeping disorder has been associated with chronic kidney disease (CKD); however, the correlation between sleeping pills use and CKD has not been investigated in-depth yet. This study elucidated the potential association of sleeping pill use with the risk of CKD and CKD progression to end-stage renal disease (ESRD) requiring dialysis.Methods: This study was based on a population-based cohort that included 209,755 sleeping pill users among 989,753 individuals. After applying the exclusion criteria, 186,654 sleeping pill users and 373,308 nonusers were enrolled to monitor the occurrence of CKD. Using a cumulative daily dose, we analyzed the types of sleeping pills related to the risk of CKD and ESRD. Propensity score matching and analysis using Cox proportional hazards regression were performed with adjustments for sex, age, and comorbidities.Results: Sleeping pill use was related to increased CKD risk after adjusting for underlying comorbidities (adjusted hazard ratio [aHR] = 1.806, 95% confidence interval [CI]: 1.617–2.105, p < 0.001). With the exception of hyperlipidemia, most comorbidities correlated with an increased risk of CKD. Persistent use of sleeping pills after CKD diagnosis increased the risk of concurrent ESRD (aHR = 7.542; 95% CI: 4.267–10.156; p < 0.001). After the subgroup analysis for sleeping pill use, brotizolam (p = 0.046), chlordiazepoxide (p < 0.001), clonazepam (p < 0.001), diazepam (p < 0.001), dormicum (p < 0.001), estazolam (p < 0.001), fludiazepam (p < 0.001), flunitrazepam (p < 0.001), nitrazepam (p < 0.001), trazodone (p < 0.001), zolpidem (p < 0.001), and zopiclone (p < 0.001) were found to have significant correlation with increased CKD risk.Conclusion: Sleeping pill use was related to an increased risk of CKD and ESRD. Further studies are necessary to corroborate these findings.

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MO051EFFECTS OF SEMAGLUTIDE ON CHRONIC KIDNEY DISEASE OUTCOMES: A POST HOC POOLED ANALYSIS FROM THE SUSTAIN 6 AND PIONEER 6 TRIALS

Nephrology Dialysis Transplantation ◽

10.1093/ndt/gfaa140.mo051 ◽

2020 ◽

Vol 35 (Supplement_3) ◽

Author(s):

Katherine Tuttle ◽

David Cherney ◽

Samy Hadjadj ◽

Thomas Idorn ◽

Ofri Mosenzon ◽

...

Keyword(s):

Chronic Kidney Disease ◽

Kidney Disease ◽

Proportional Hazards ◽

Proportional Hazards Model ◽

Statistical Significance ◽

Cox Proportional Hazards ◽

Cox Proportional Hazards Model ◽

Post Hoc ◽

Time To Onset

Abstract Background and Aims The SUSTAIN 6 cardiovascular outcomes trial (CVOT) indicated a renal benefit with subcutaneous (s.c.) once-weekly (OW) semaglutide vs placebo. The PIONEER 6 CVOT reported cardiovascular safety with oral semaglutide in a similar cohort using a similar trial design. In the present post hoc study, eGFR data from the SUSTAIN 6 and PIONEER 6 trials were pooled to evaluate the potential benefit of semaglutide (s.c. or oral) vs placebo on chronic kidney disease (CKD) outcomes. Method Data from 6,480 subjects from SUSTAIN 6 (N=3,297; median follow-up, 2.1 years; mean baseline eGFR, 76 mL/min/1.73 m2) and PIONEER 6 (N=3,183; median follow-up, 1.3 years; mean baseline eGFR, 74 mL/min/1.73 m2) were pooled for semaglutide (0.5 mg s.c. OW, 1.0 mg s.c. OW or 14 mg oral once daily) or placebo. We evaluated time to onset of persistent eGFR reduction (thresholds of ≥30%, ≥40%, ≥50% and ≥57% [57% corresponds to a doubling of serum creatinine]) from baseline in the overall pooled population and by baseline CKD subgroups (≥30–<60 mL/min/1.73 m2, n=1,699; ≥60 mL/min/1.73 m2, n=4,762; data were missing for 19 subjects). Analyses were performed using a Cox proportional-hazards model with treatment group (semaglutide vs placebo) and CKD subgroup as fixed factors and the interaction between both stratified by trial. Results In the overall population, the hazard ratios (HRs) for time to onset of persistent eGFR reductions with semaglutide vs placebo were <1.0, but did not achieve statistical significance. In subjects with baseline eGFR ≥30–<60 mL/min/1.73 m2, HRs for semaglutide vs placebo were consistently lower compared with the overall population and, in this subgroup, semaglutide significantly reduced the risk of developing a persistent 30% eGFR reduction vs placebo (Figure; p=0.03). Numerically larger effects were seen with increasing eGFR reduction thresholds in this subgroup, with the exception of the 57% eGFR reduction threshold. No statistically different interactions between treatment and CKD subgroup were observed. Conclusion The findings of this post hoc analysis of pooled data from SUSTAIN 6 and PIONEER 6 on clinically relevant outcomes for CKD support a smaller magnitude of eGFR decline with semaglutide vs placebo, despite relatively short follow-up times. The small number of events at both the 50% and 57% thresholds, and the associated broad confidence intervals, limit the interpretability of the results. In line with previous findings, the data suggest a renal benefit of semaglutide vs placebo in subjects with established CKD. The FLOW trial (ClinicalTrials.gov Identifier: NCT03819153), which is dedicated to exploring CKD outcomes with semaglutide treatment, is ongoing to test this hypothesis in patients with CKD at baseline.

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Plasma Oxalate as a Predictor of Kidney Function Decline in a Primary Hyperoxaluria Cohort

International Journal of Molecular Sciences ◽

10.3390/ijms21103608 ◽

2020 ◽

Vol 21 (10) ◽

pp. 3608 ◽

Cited By ~ 2

Author(s):

Ronak Jagdeep Shah ◽

Lisa E. Vaughan ◽

Felicity T. Enders ◽

Dawn S. Milliner ◽

John C. Lieske

Keyword(s):

Kidney Disease ◽

Proportional Hazards ◽

Proportional Hazards Model ◽

Primary Hyperoxaluria ◽

Cox Proportional Hazards ◽

Cox Proportional Hazards Model ◽

Hazards Model ◽

Hazard Ratios ◽

End Stage

This retrospective analysis investigated plasma oxalate (POx) as a potential predictor of end-stage kidney disease (ESKD) among primary hyperoxaluria (PH) patients. PH patients with type 1, 2, and 3, age 2 or older, were identified in the Rare Kidney Stone Consortium (RKSC) PH Registry. Since POx increased with falling estimated glomerular filtration rate (eGFR), patients were stratified by chronic kidney disease (CKD) subgroups (stages 1, 2, 3a, and 3b). POx values were categorized into quartiles for analysis. Hazard ratios (HRs) and 95% confidence intervals (95% CIs) for risk of ESKD were estimated using the Cox proportional hazards model with a time-dependent covariate. There were 118 patients in the CKD1 group (nine ESKD events during follow-up), 135 in the CKD 2 (29 events), 72 in CKD3a (34 events), and 45 patients in CKD 3b (31 events). During follow-up, POx Q4 was a significant predictor of ESKD compared to Q1 across CKD2 (HR 14.2, 95% CI 1.8–115), 3a (HR 13.7, 95% CI 3.0–62), and 3b stages (HR 5.2, 95% CI 1.1–25), p < 0.05 for all. Within each POx quartile, the ESKD rate was higher in Q4 compared to Q1–Q3. In conclusion, among patients with PH, higher POx concentration was a risk factor for ESKD, particularly in advanced CKD stages.

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Plasma potassium ranges associated with mortality across stages of chronic kidney disease: the Stockholm CREAtinine Measurements (SCREAM) project

Nephrology Dialysis Transplantation ◽

10.1093/ndt/gfy249 ◽

2018 ◽

Vol 34 (9) ◽

pp. 1534-1541 ◽

Cited By ~ 11

Author(s):

Alessandro Gasparini ◽

Marie Evans ◽

Peter Barany ◽

Hairong Xu ◽

Tomas Jernberg ◽

...

Keyword(s):

Chronic Kidney Disease ◽

Kidney Disease ◽

Estimated Glomerular Filtration Rate ◽

Plasma Potassium ◽

Small Scale ◽

Cross Sectional ◽

Ckd Stage ◽

Lower Egfr ◽

Threatening Condition

Abstract Background Small-scale studies suggest that hyperkalaemia is a less threatening condition in chronic kidney disease (CKD), arguing adaptation/tolerance to potassium (K+) retention. This study formally evaluates this hypothesis by estimating the distribution of plasma K+ and its association with mortality across CKD stages. Methods This observational study included all patients undergoing plasma K+ testing in Stockholm during 2006–11. We randomly selected one K+ measurement per patient and constructed a cross-sectional cohort with mortality follow-up. Covariates included demographics, comorbidities, medications and estimated glomerular filtration rate (eGFR). We estimated K+ distribution and defined K+ ranges associated with 90-, 180- and 365-day mortality. Results Included were 831 760 participants, of which 70 403 (8.5%) had CKD G3 (eGFR <60–30 mL/min) and 8594 (1.1%) had CKD G4–G5 (eGFR <30 mL/min). About 66 317 deaths occurred within a year. Adjusted plasma K+ increased across worse CKD stages: from median 3.98 (95% confidence interval 3.49–4.59) for eGFR >90 to 4.43 (3.22–5.65) mmol/L for eGFR ≤15 mL/min/1.73 m2. The association between K+ and mortality was U-shaped, but it flattened at lower eGFR strata and shifted upwards. For instance, the range where the 90-day mortality risk increased by no more than 100% was 3.45–4.94 mmol/L in eGFR >60 mL/min, but was 3.36–5.18 in G3 and 3.26–5.53 mmol/L in G4–G5. In conclusion, CKD stage modifies K+ distribution and the ranges that predict mortality in the community. Conclusion Although this study supports the view that hyperkalaemia is better tolerated with worse CKD, it challenges the current use of a single optimal K+ range for all patients.

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Abstract P295: Exercise Capacity and Rate of Progression to Chronic Kidney Disease

Circulation ◽

10.1161/circ.129.suppl_1.p295 ◽

2014 ◽

Vol 129 (suppl_1) ◽

Author(s):

Peter Kokkinos ◽

Apostolos Tsimploulis ◽

Charles Faselis ◽

Jonathan Myers ◽

Jiajia Zhang ◽

...

Keyword(s):

Chronic Kidney Disease ◽

Kidney Disease ◽

Exercise Capacity ◽

Proportional Hazards ◽

Reference Group ◽

Cox Proportional Hazards ◽

Cox Proportional Hazards Model ◽

Exercise Stress ◽

Rate Of Progression

Introduction: Increased exercise capacity is associated with better health outcomes. It is not known if increased fitness can attenuate the progression to chronic kidney disease (CKD). Hypothesis: We assessed the hypothesis that increased exercise capacity is associated inversely with the rate of progression to CKD. Methods: A routine exercise stress was performed on 6,452 veterans (mean age: 58±12) with normal kidney function at VA Medical Centers in Washington DC. We used Cox proportional hazards model with spline function of MET to define the MET level associated with no increase in rate of progression to CKD (hazard ratio (HR)=1.0). We used this MET level to guide the formation of the following four fitness categories based on intervals of 2 METs achieved above and below this threshold: Least-Fit (<5.5 METs; n=1,392); Low-Fit (5.5-7.5 METs; n=2,270); Moderate-Fit (7.6-9.5 METs; n=2,192) and High-Fit (>9.5 METs; n=714). We then performed Cox proportional hazards analysis adjusted for age, BMI, cardiac risk factors, sleep apnea, alcohol dependence and medications. We used the Least-fit category as the reference group. Results: The MET threshold for the entire cohort was defined at 7.5 METs. During the follow-up period (median 8.8 years; 50,371 person-years of follow-up), 925 individuals developed CKD based on an estimated glomerular filtration rate <60 ml/min/1.73m 2 . Cox proportional hazards analysis revealed that exercise capacity was inversely associated with the rate of progression to CKD. More specifically, the rate of progression was lower by 25% (HR=0.75; CI: 0.64-0.87; p<0.001) for Low-Fit individuals, 40% (HR=0.60; CI: 0.48-0.73; p<0.001) for the Moderate-Fit and 68% (HR=0.42; CI: 0.28-0.64; p<0.001) for High-Fit individuals. Conclusions: Exercise capacity is inversely associated with the rate of progression to CKD.

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Effect of zinc deficiency on chronic kidney disease progression and effect modification by hypoalbuminemia

PLoS ONE ◽

10.1371/journal.pone.0251554 ◽

2021 ◽

Vol 16 (5) ◽

pp. e0251554

Author(s):

Atsuyuki Tokuyama ◽

Eiichiro Kanda ◽

Seiji Itano ◽

Megumi Kondo ◽

Yoshihisa Wada ◽

...

Keyword(s):

Chronic Kidney Disease ◽

Kidney Disease ◽

Zinc Deficiency ◽

Primary Outcome ◽

Proportional Hazards ◽

Serum Zinc ◽

Cox Proportional Hazards ◽

Ckd Progression ◽

Cox Proportional Hazards Models ◽

End Stage

Serum zinc (Zn) levels tend to be low in chronic kidney disease (CKD) patients. This cohort study was conducted to investigate the relationship between zinc deficiency and CKD progression. Patients were classified into two groups based on Zn levels < 60 μg/dl (low-Zn group, n = 160) and ≥ 60 μg/dl (high-Zn group, n = 152). The primary outcome was defined as end-stage kidney disease (ESKD) or death and was examined over a 1-year observation period. Overall, the mean Zn level was 59.6 μg/dl and the median eGFR was 20.3 ml/min/1.73 m2. The incidence of the primary outcome was higher in the low-Zn group (p<0.001). Various Cox proportional hazards models adjusted for baseline characteristics showed higher risks of the primary outcome in the low-Zn group than in the high-Zn group. Competing risks analysis showed that low Zn levels were associated with ESKD but not with death. Moreover, in propensity score-matched analysis, the low-Zn group showed a higher risk of the primary outcome [adjusted hazard ratio 1.81 (95% confidence interval 1.02, 3.24)]. Furthermore, an interaction was observed between Zn and serum albumin levels (interaction p = 0.026). The results of this study indicate that zinc deficiency is a risk factor for CKD progression.

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Low hemoglobin levels and an increased risk of psoriasis in patients with chronic kidney disease

Scientific Reports ◽

10.1038/s41598-021-94165-w ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Si-Hyung Lee ◽

Miri Kim ◽

Kyung-Do Han ◽

Ji Hyun Lee

Keyword(s):

Chronic Kidney Disease ◽

Kidney Disease ◽

Regression Models ◽

Proportional Hazards ◽

Surrogate Marker ◽

Cox Proportional Hazards ◽

Proportional Hazards Regression ◽

Increased Risk ◽

Using Data

AbstractChronic diseases, such as chronic kidney disease (CKD), are frequently accompanied by various comorbidities, including anemia, which is considered a surrogate marker of systemic inflammation. Psoriasis is a chronic inflammatory skin disease prevalent in patients with chronic disease. Psoriasis risk in patients with CKD, however, especially in patients with low hemoglobin levels, has never been investigated. In this study, we investigated associations between low hemoglobin levels and psoriasis in patients with CKD using data from the National Health Insurance Service of Korea. During a mean follow-up period of 6.16 ± 1.02 years, psoriasis was recorded in 13,803 patients with CKD (2.39% of CKD patients). The cumulative incidence of psoriasis was significantly higher in CKD patients with anemia (hemoglobin levels < 13 g/dL in men and < 12 g/dL in women) than those without. In multivariate-adjusted Cox proportional hazards regression models, the risk of psoriasis was significantly higher in anemic CKD patients than nonanemic CKD patients (hazard ratio [HR] 1.136, 95% CI 1.089–1.185, p < 0.001). Additionally, we noted that the incidence of psoriasis decreased with increasing hemoglobin levels in CKD patients (HR 0.953, 95% CI 0.942–0.965, p < 0.001). Altogether, our findings indicate that low hemoglobin levels are significantly related to psoriasis risk in patients with CKD. Further study is required to elucidate whether low hemoglobin levels have an impact on the development of psoriasis or are merely a surrogate marker of psoriasis risk in patients with CKD.

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Serum Sodium Levels and Patient Outcomes in an Ambulatory Clinic-Based Chronic Kidney Disease Cohort

American Journal of Nephrology ◽

10.1159/000381193 ◽

2015 ◽

Vol 41 (3) ◽

pp. 200-209 ◽

Cited By ~ 10

Author(s):

Sang-Woong Han ◽

Anca Tilea ◽

Brenda W. Gillespie ◽

Fredric O. Finkelstein ◽

Margaret A. Kiser ◽

...

Keyword(s):

Chronic Kidney Disease ◽

Kidney Disease ◽

Patient Outcomes ◽

Serum Sodium ◽

Risk Of Mortality ◽

Ambulatory Patients ◽

Lower Egfr ◽

Stage Renal Disease ◽

End Stage ◽

Improve Patient

Background: Chronic kidney disease (CKD) patients are prone to both hypo- and hypernatremia. Little has been published on the epidemiology of hypo- and hypernatremia in ambulatory patients with non-dialysis CKD. Methods: Data collected in two contemporaneous CKD cohort studies, the Renal Research Institute (RRI)-CKD study (n = 834) and the Study of Treatment of Renal Insufficiency: Data and Evaluation (STRIDE) (n = 1,348) were combined and analyzed to study the association between serum sodium (Na+) and clinical outcomes. Results: Baseline estimated glomerular filtration rate (eGFR) and Na+ were 26 ± 11 ml/min/1.73 m2 and 140.2 ± 3.4 mEq/l, respectively. The prevalence of Na+ ≤135 mEq/l and ≥144 mEq/l was 6 and 16%, respectively. Higher baseline Na+ was significantly associated with male sex, older age, systolic blood pressure, BMI, serum albumin, presence of heart failure, and lower eGFR. The risk of end-stage renal disease (ESRD) was marginally significantly higher among patients with Na+ ≤135 mEq/l, compared with 140< Na+ <144 mEq/l (referent), in time-dependent models (adjusted hazard ratio, HR = 1.52, p = 0.06). Mortality risk was significantly greater at 135< Na+ ≤140 mEq/l (adjusted HR = 1.68, p = 0.02) and Na+ ≥144 mEq/l (adjusted HR = 2.01, p = 0.01). Conclusion: CKD patients with Na+ ≤135 mEq/l were at a higher risk for progression to ESRD, whereas both lower and higher Na+ levels were associated with a higher risk of mortality. While caring for CKD patients, greater attention to serum sodium levels by clinicians is warranted and could potentially help improve patient outcomes.

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Abstract P098: Slower Gait Speed is Associated with Increased Mortality Risk in Chronic Kidney Disease.

Circulation ◽

10.1161/circ.125.suppl_10.ap098 ◽

2012 ◽

Vol 125 (suppl_10) ◽

Author(s):

Baback Roshanravan ◽

Cassiane Robinson-Cohen ◽

Kushang V Patel ◽

Greg Levin ◽

Ian H de Boer ◽

...

Keyword(s):

Chronic Kidney Disease ◽

Kidney Disease ◽

Gait Speed ◽

Proportional Hazards ◽

Prognostic Significance ◽

Continuous Variable ◽

Hazard Ratio ◽

Risk Of Death ◽

Social Security Death Index

Objective: Skeletal muscle dysfunction (sarcopenia) is an under-recognized complication of chronic kidney disease (CKD) that may have important clinical consequences. Gait speed is associated with sarcopenia and comorbid disease burden among older adults; however, little is known about the prognostic significance of gait speed in CKD. We determined the association of gait speed with all-cause mortality in a prospective cohort of non-dialysis CKD patients. Methods: We measured usual gait speed over 4-meters in 309 participants from a prospective study of non-dialysis CKD. Included subjects had an estimated glomerular filtration rate (eGFR ckdepi ) <90mL/min/1.73m 2 , were stroke-free and did not require a wheelchair for ambulation. Study coordinators assessed mortality during follow-up by phone contacts, medical record review, and the social security death index. We evaluated gait speed continuously, and using a cut point of 0.8 m/s, consistent with previous studies. We used Cox's proportional hazards to estimate the association of gait speed with mortality after adjustment for age, sex, race, smoking, diabetes, pre-existing CAD, BMI, eGFR and hemoglobin. Results: Median follow-up time was 2.7 years; range 27 days to 4.8 years. The mean age was 58.9 ± 13 years and mean eGFR by cystatin C (eGFR cysc ) was 48.5 ± 23mL/min/1.73m 2 . There were a total of 31 deaths (10.4%) during follow-up. Unadjusted mortality rates were 23 and 80 deaths per 1,000 person-years among participants who had a gait speed of >0.8m/s versus ≤0.8m/s, respectively. After full adjustment, gait speed ≤0.8m/s was associated with a 2.8-fold greater risk of death compared to a gait speed >0.8 m/s. Gait speed was also strongly associated with mortality when analyzed as a continuous variable ( Table ) and a stronger predictor of death than age, history of CAD, or diabetes. No. Deaths (%) Model 1 + Model 2 # Hazard Ratio 95% CI Hazard Ratio 95% CI Gait speed * 32(10) 0.74 (0.64-0.86) 0.75 (0.64-0.87) >0.8m/s 13 (6) Reference Reference ≤0.8m/s 19(19) 3.49 (1.54-7.95) 2.84 (1.25-6.48) * Gait speed analyzed continuously per 10cm/s increase in speed. +Model 1: Adjusted for age, sex, race, study site #Model 2: adds smoking, BMI, eGFR cysc , diabetes, prevalent coronary disease. Conclusion: Gait speed is strongly associated with death in a cohort of middle-aged CKD patients.

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