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

Circulation ◽  
2012 ◽  
Vol 125 (suppl_10) ◽  
Author(s):  
Baback Roshanravan ◽  
Cassiane Robinson-Cohen ◽  
Kushang V Patel ◽  
Greg Levin ◽  
Ian H de Boer ◽  
...  

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.

2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Marcelo Arruda Nakazone ◽  
Maurício Nassau Machado ◽  
Ana Paula Otaviano ◽  
Ana Maria Silveira Rodrigues ◽  
Augusto Cardinalli-Neto ◽  
...  

Background. Few studies regarding chronic kidney disease (CKD) and anemia have been conducted in patients with Chagas cardiomyopathy (CC). We evaluated the risk prediction performance of the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation and anemia in CC patients. Methods. From 2000 to 2010, a total of 232 patients were studied in a single-center retrospective study. CKD was defined as creatinine clearance <60 mL/min/1.73 m2 according to CKD-EPI equation. Anemia was defined as hemoglobin <12 g/dL (women) and <13 g/dL (men). Cox proportional hazards models were used to establish predictors for death. Results. At baseline, 98 individuals (42.2%) had criteria for CKD and 41 (17.7%) for anemia. During follow-up, 136 patients (58.6%) died. Independently, CKD and anemia were not associated with all-cause mortality. However, when they coexisted, an additional risk was attributed for these patients. Cox proportional hazard models analysis identified systolic blood pressure (hazard ratio, 0.99; 95% confidence interval (CI), 0.98 to 1.00; P=0.015), implantable cardioverter-defibrillator (hazard ratio, 0.48; 95% CI, 0.27 to 0.85; P=0.012), left anterior fascicular block (hazard ratio, 1.52; 95% CI, 1.08 to 2.13; P=0.017), left ventricular end-diastolic diameter (hazard ratio, 1.04; 95% CI, 1.02 to 1.06; P<0.001), and serum sodium (hazard ratio, 0.95; 95% CI, 0.92 to 0.99; P=0.020) as independent predictors for death. Conclusions. CKD and anemia are not independent predictors for long-term mortality in CC patients. However, the prognosis is poorer in individuals with both comorbidities.


Circulation ◽  
2021 ◽  
Vol 143 (Suppl_1) ◽  
Author(s):  
Jung-Im Shin ◽  
Yao Qiao ◽  
Aditya Surapaneni ◽  
Lesley Inker ◽  
Derek Fine ◽  
...  

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.


BMJ ◽  
2019 ◽  
pp. l1516 ◽  
Author(s):  
Jonas H Kristensen ◽  
Saima Basit ◽  
Jan Wohlfahrt ◽  
Mette Brimnes Damholt ◽  
Heather A Boyd

ABSTRACTObjectiveTo investigate associations between pre-eclampsia and later risk of kidney disease.DesignNationwide register based cohort study.SettingDenmark.PopulationAll women with at least one pregnancy lasting at least 20 weeks between 1978 and 2015.Main outcome measureHazard ratios comparing rates of kidney disease between women with and without a history of pre-eclampsia, stratified by gestational age at delivery and estimated using Cox regression.ResultsThe cohort consisted of 1 072 330 women followed for 19 994 470 person years (average 18.6 years/woman). Compared with women with no previous pre-eclampsia, those with a history of pre-eclampsia were more likely to develop chronic renal conditions: hazard ratio 3.93 (95% confidence interval 2.90 to 5.33, for early preterm pre-eclampsia (delivery <34 weeks); 2.81 (2.13 to 3.71) for late preterm pre-eclampsia (delivery 34-36 weeks); 2.27 (2.02 to 2.55) for term pre-eclampsia (delivery ≥37 weeks). In particular, strong associations were observed for chronic kidney disease, hypertensive kidney disease, and glomerular/proteinuric disease. Adjustment for cardiovascular disease and hypertension only partially attenuated the observed associations. Stratifying the analyses on time since pregnancy showed that associations between pre-eclampsia and chronic kidney disease and glomerular/proteinuric disease were much stronger within five years of the latest pregnancy (hazard ratio 6.11 (3.84 to 9.72) and 4.77 (3.88 to 5.86), respectively) than five years or longer after the latest pregnancy (2.06 (1.69 to 2.50) and 1.50 (1.19 to 1.88). By contrast, associations between pre-eclampsia and acute renal conditions were modest.Conclusions Pre-eclampsia, particularly early preterm pre-eclampsia, was strongly associated with several chronic renal disorders later in life. More research is needed to determine which women are most likely to develop kidney disease after pre-eclampsia, what mechanisms underlie the association, and what clinical follow-up and interventions (and in what timeframe post-pregnancy) would be most appropriate and effective.


2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Yooju Nam ◽  
Seonyeong Lee ◽  
Hyung Woo Kim ◽  
Jae Hyun Chang ◽  
Tae-Hyun Yoo

Abstract Background and Aims Osteoprotegerin (OPG), which is an osteoclastic inhibitory factor, have been shown associated with adverse renal outcomes and progression of vascular calcification in chronic kidney disease (CKD) patients. Anemia and CKD-bone mineral disorders (CKD-MBD) are also frequently observed in these patients. Since CKD-MBD and anemia might be closely linked, therefore, we further examined whether OPG level as a marker for bone turnover can predict the future development of anemia in a large-scale prospective cohort. Method Among 2,238 patients with non-dialysis CKD enrolled in the KoreaN cohort study for Outcome in patients With Chronic Kidney Disease (KNOW-CKD), 2,086 patients who measured hemoglobin, hepcidin, iron profiles and OPG level were included in the analysis. Anemia was defined as a hemoglobin level of &lt; 13.0 g/dL and 12.0 g/dL for male and female, respectively. Results The mean age was 53.6 ± 12.2 years and 1,270 (60.9%) patients were males. At baseline, anemia was found in 941 (45.1%) patients. Log transformed OPG levels significantly correlated with FGF23 levels, but inversely with iron profiles and hemoglobin levels at baseline. A multivariate logistic regression model showed that log OPG level was independently associated with the prevalence of anemia (odds ratio [OR], 2.22; 95% confidence interval [CI], 1.41-3.48, P=0.001). Among 1110 patients without baseline anemia, 258 (25.3%) patients developed anemia during a median follow-up duration of 34.6 (interquartile range, 23-48) months. In the fully adjusted multivariable Cox models, risk of developing anemia was significantly higher in the fourth (hazard ratio [HR], 1.99; 95% CI, 1.08-3.67; P =0.028) than in the first OPG quartile. Similar association was observed in a model when OPG was treated as a continuous variable. Conclusion We showed that high serum OPG levels are associated with an increased risk of developing anemia in patients with non-dialysis CKD.


Circulation ◽  
2021 ◽  
Vol 143 (Suppl_1) ◽  
Author(s):  
Joshua D Bundy ◽  
Ling Tian ◽  
Matthew J Budoff ◽  
Julia J Scialla ◽  
Rupal Mehta ◽  
...  

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.


2015 ◽  
Vol 16 (1) ◽  
Author(s):  
Simon D. S. Fraser ◽  
Paul J. Roderick ◽  
Carl R. May ◽  
Natasha McIntyre ◽  
Christopher McIntyre ◽  
...  

Abstract Background Multimorbidity is a growing concern for healthcare systems, with many countries experiencing demographic transition to older population profiles. Chronic kidney disease (CKD) is common but often considered in isolation. The extent and prognostic significance of its comorbidities is not well understood. This study aimed to assess the extent and prognostic significance of 11 comorbidities in people with CKD stage 3. Methods A prospective cohort of 1741 people with CKD stage 3 was recruited from primary care between August 2008 and March 2010. Participants underwent medical history, clinical assessment, blood and urine sampling. Comorbidity was defined by self-reported doctor-diagnosed condition, disease-specific medication or blood results (hemoglobin), and treatment burden as number of ongoing medications. Logistic regression was used to identify associations with greater treatment burden (taking >5 medications) and greater multimorbidity (3 or more comorbidities). Kaplan Meier plots and multivariate Cox proportional hazards models were used to investigate associations between multimorbidity and all-cause mortality. Results One thousand seven hundred forty-one people were recruited, mean age 72.9 +/−9 years. Mean baseline eGFR was 52 ml/min/1.73 m2. Only 78/1741 (4 %) had no comorbidities, 453/1741 (26 %) had one, 508/1741 (29 %) had two and 702/1741 (40 %) had >2. Hypertension was common (88 %), 30 % had ‘painful condition’, 24 % anemia, 23 %, ischaemic heart disease, 17 % diabetes and 12 % thyroid disorders. Median medication use was 5 medications (interquartile range 3–8) and increased with degree of comorbidity. Greater treatment burden and multimorbidity were independently associated with age, smoking, increasing body mass index and decreasing eGFR. Treatment burden was also independently associated with lower education status. After median 3.6 years follow-up, 175/1741 (10 %) died. Greater multimorbidity was independently associated with mortality (hazard ratio 2.81 (95 % confidence intervals 1.72–4.58), p < 0.001) for 3 or more comorbidities vs 0 or 1). Conclusions Isolated CKD was rare and multimorbidity the norm in this cohort of people with moderate CKD. Increasing multimorbidity was associated with greater medication burden and poorer survival. CKD management should include consideration of comorbidities.


2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Katherine Tuttle ◽  
David Cherney ◽  
Samy Hadjadj ◽  
Thomas Idorn ◽  
Ofri Mosenzon ◽  
...  

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–&lt;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 &lt;1.0, but did not achieve statistical significance. In subjects with baseline eGFR ≥30–&lt;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.


Author(s):  
Marco Trevisan ◽  
Catherine M Clase ◽  
Marie Evans ◽  
Tamara Popov ◽  
Jonas F Ludvigsson ◽  
...  

Abstract Background Whether hyperkalaemia in CKD is chronic or transient, and whether this has different outcome implications, is not known. Methods This was an observational study of adults with CKD G3–5 from Stockholm, Sweden 2006–11. We examined individual trajectories of potassium from all measurements obtained through routine outpatient care. For each month of follow-up, we created a rolling assessment of the proportion of time in which potassium was abnormal during the previous 12 months. We defined patterns of hyperkalaemia as transient (≤50% of time during the previous year with potassium &gt;5.0 mmol/L) and chronic (&gt;50% of time with potassium &gt;5.0 mmol/L), and examined whether previous hyperkalaemia pattern offers additional predictive value beyond that provided by the most recent (current) potassium value. Results We included 36 511 participants (56% women) with CKD G3–5 and median estimated glomerular filtration rate 46 mL/min/1.73 m2. Transient and chronic hyperkalaemia, respectively, were observed in 15% and 4% of patients with CKD G3a, and in 50% and 17% of patients with CKD G5. In fully adjusted models, transient (hazard ratio 1.36, 95% confidence interval 1.29–1.46) or chronic (1.16, 1.04–1.32) hyperkalaemia patterns, but not current hyperkalaemia, were associated with major adverse cardiovascular events (MACE), compared with normokalaemia. Transient hyperkalaemia (1.43, 1.35–1.52) and current potassium values, but not chronic hyperkalaemia, were associated with the risk of death. Conclusions Between 4% and 17% of patients with CKD G3–5 develop chronic hyperkalaemia. In general, hyperkalaemia predicted MACE and death; however, the lack of effect of current potassium on MACE when adjusted for the previous pattern, and the stronger effects on death than on MACE, lead us to question whether hyperkalaemia is causal in these relationships.


2019 ◽  
Vol 104 (9) ◽  
pp. 4024-4032 ◽  
Author(s):  
Miguel Bigotte Vieira ◽  
João Sérgio Neves ◽  
Lia Leitão ◽  
Rute Baeta Baptista ◽  
Rita Magriço ◽  
...  

Abstract Purpose Diabetes mellitus is a risk factor for the development and progression of chronic kidney disease (CKD). However, the association of prediabetes with adverse kidney outcomes is uncertain. Methods We performed a secondary analysis of the Systolic Blood Pressure Intervention Trial (SPRINT), including 9361 participants without diabetes at baseline. We categorized participants according to fasting glucose level as having impaired fasting glucose [≥100 mg/dL (≥5.6 mmol/L)] or normoglycemia [&lt;100 mg/dL (&lt;5.6 mmol/L)]. Unadjusted and adjusted proportional hazards models were fitted to estimate the association of impaired fasting glucose (vs normoglycemia) with a composite outcome of worsening kidney function [≥30% decrease in estimated glomerular filtration rate (eGFR) to &lt;60 mL/min/1.73 m2 in participants without baseline CKD; ≥50% decrease in eGFR or need for long-term dialysis/kidney transplantation in participants with CKD] or incident albuminuria (doubling of urinary albumin/creatinine ratio from &lt;10 mg/g to &gt;10 mg/g). These outcomes were also evaluated separately and according to CKD status at baseline. Results Participants’ mean age was 67.9 ± 9.4 years, 35.5% were female, and 31.4% were black. The median follow-up was 3.3 years, and 41.8% had impaired fasting glucose. Impaired fasting glucose was not associated with higher rates of the composite outcome [hazard ratio (HR): 0.97; 95% CI: 0.8 to 1.16], worsening kidney function (HR: 1.02; 95% CI: 0.75 to 1.37), or albuminuria (HR: 0.98; 95% CI: 0.78 to 1.23). Similarly, there was no association of impaired fasting glucose with outcomes according to baseline CKD status. Conclusions Impaired fasting glucose at baseline was not associated with the development of worsening kidney function or albuminuria in participants of SPRINT.


2020 ◽  
Vol 35 (5) ◽  
pp. 803-810 ◽  
Author(s):  
Helmut Reichel ◽  
Jarcy Zee ◽  
Charlotte Tu ◽  
Eric Young ◽  
Ronald L Pisoni ◽  
...  

Abstract Background Chronic kidney disease (CKD) progression among German patients in a representative setting has not been described previously. The Verband Deutsche Nierenzentren and Chronic Kidney Disease Outcomes and Practice Patterns Study established a longitudinal observational cohort among German CKD patients to research variations in patient care and outcomes in real-world nephrology practices. Methods A cohort of CKD Stages 3 (25%) and 4 (75%) patients was established from German nephrologist-run CKD clinics in 2013–16. Linear models were used to determine the estimated glomerular filtration rate (eGFR) slope during follow-up and Cox models were used to assess outcomes of end-stage kidney disease (ESKD) and death. Results A total of 1834 patients (median age 75 years, 58% male, 42% diabetics, median baseline eGFR 25 mL/min/1.73 m2) were followed for a median of 29 months. More than 50% had slow or no decline and 17% declined ≥5 mL/min/1.73 m2/year. After 4.5 years, the incidence of ESKD was 8% and of deaths without ESKD 16% among patients with eGFR ≥30 mL/min/1.73 m2 and 37% and 19% for eGFR &lt;30 mL/min/1.73 m2. Adjusted models showed higher risks of ESKD or death for patients with worse kidney function at baseline, male sex, diabetes and higher blood pressure; a higher risk of ESKD with higher albuminuria; and a higher risk of death with older age or cardiovascular comorbidity. Conclusions Routine nephrology care of patients in Germany comprises mostly elderly patients, many with slow CKD progression. Identification of risk factors for CKD progression and mortality may help guide resources by closer follow-up of high-risk patients.


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