Protein carbamylation and chronic kidney disease progression in the Chronic Renal Insufficiency Cohort (CRIC) Study

Abstract Background Protein carbamylation is a posttranslational protein modification caused, in part, by exposure to urea’s dissociation product cyanate. Carbamylation is linked to cardiovascular outcomes and mortality in dialysis dependent end stage kidney disease (ESKD), but its effects in earlier pre-dialysis stages of chronic kidney disease (CKD) are not established. Methods We conducted two nested case-control studies within the CRIC Study. First, we matched 75 cases demonstrating CKD progression (50% eGFR reduction or reaching ESKD) to 75 controls (matched on baseline eGFR, 24-hour proteinuria, age, sex, and race). In the second study, we similarly matched 75 subjects who died during follow up (cases) to 75 surviving controls. Baseline carbamylated albumin levels (C-Alb, a validated carbamylation assay) were compared between cases and controls in each study. Results At baseline, in the CKD progression study, other than blood urea nitrogen (BUN) and smoking status, there were no significant differences in any matched or other parameter. In the mortality group, the only baseline difference was smoking status. Adjusting for baseline differences, the top tertile of C-Alb was associated with an increased risk of CKD progression (odds ratio [OR], 7.9; 95% CI, 1.9-32.8; P = 0.004) and mortality (OR 3.4; 95% CI, 1.0-11.4; P = 0.05) when compared to the bottom tertile. C-Alb correlated with eGFR but was more strongly correlated with BUN. Conclusions Our data suggest protein carbamylation is a predictor of CKD progression, beyond traditional risks including eGFR and proteinuria. Carbamylation’s association with mortality was smaller in this limited sample size.

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Abstract 145: Rates of Transfusion and Progression to End-Stage Renal Disease in Chronic Kidney Disease Patients Undergoing Transradial Versus Transfemoral Cardiac Catheterization - An Analysis from the VA CART Program

Circulation Cardiovascular Quality and Outcomes ◽

10.1161/circoutcomes.7.suppl_1.145 ◽

2014 ◽

Vol 7 (suppl_1) ◽

Author(s):

Amit N Vora ◽

Maggie A Stanislawski ◽

John S Rumsfeld ◽

Thomas M Maddox ◽

Mladen Vidovich ◽

...

Keyword(s):

Chronic Kidney Disease ◽

Kidney Disease ◽

Cardiac Catheterization ◽

High Risk Population ◽

Post Procedure ◽

Increased Risk ◽

Significant Difference ◽

Independent Association ◽

Stage Renal Disease ◽

End Stage

Background: Patients with chronic kidney disease (CKD) are at increased risk of bleeding and transfusion after cardiac catheterization. Whether rates of these complications or progression to new dialysis are increased in this high-risk population undergoing transradial (TR) access compared to transfemoral (TF) access is unknown. Methods: From the Veterans Affairs Clinical Assessment, Reporting, and Tracking (CART) Program between 10/2007-09/2012 we identified 40,160 CKD patients undergoing cardiac catheterization with baseline glomerular filtration rate (GFR) ≤ 60 ml/min. We used multivariable Cox modeling to determine the independent association between TR access and post-procedure transfusion as well as progression to new dialysis using TF as the reference. Results: Overall, 3,828 (9.5%) of CKD patients underwent TR access and tended to be slightly younger but overall had similar rates of CKD severity compared with TF patients (GFR 45-60 ml/min: 77.0% vs. 77.0%; GFR 30-44 ml/min: 19.7% vs. 19.3%; GFR 15-29 ml/min: 3.3% vs. 3.7%, p=0.35). TR patients had longer fluoroscopy times (8.1 vs 6.9 minutes, p=<0.0001) but decreased contrast use (90.0 vs 100.0 ml, p=<0.0001). Among the 31,692 patients with a full year of follow-up, 42 (1.7%) of TR patients and 545 (1.9%) of TF patients progressed to new dialysis within 1 year (p=0.64). However, only 33 (0.9%) of TR patients compared with 570 TF patients (1.6%) needed post-procedure blood transfusion (p=0.0006). After multivariable adjustment, there was no significant difference in progression to ESRD between TR and TF patients but TR was associated with a significant decrease in transfusion (Figure). Conclusion: Among CKD patients undergoing cardiac catheterization in the VA health system, TR access is associated with a decreased risk for post-procedure transfusion compared with TF access. There was no significant difference between the two approaches with respect to progression to ESRD. These data suggest that TR is a reasonable option for patients with any level of CKD undergoing cardiac catheterization.

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Abstract MP08: Whole Exome Sequencing Study Identified A Novel Variant For Kidney Function And Progression Of Chronic Kidney Disease

Circulation ◽

10.1161/circ.143.suppl_1.mp08 ◽

2021 ◽

Vol 143 (Suppl_1) ◽

Author(s):

Changwei Li ◽

Michael Francis ◽

Adrianna Westbrook ◽

Ruiyuan Zhang ◽

Ye Shen ◽

...

Keyword(s):

Chronic Kidney Disease ◽

Kidney Disease ◽

Exome Sequencing ◽

Whole Exome Sequencing ◽

Kidney Function ◽

Cystatin C ◽

Smoking Status ◽

Missense Variant ◽

Ckd Progression ◽

Whole Exome

Introduction: Most genetic variants for chronic kidney disease (CKD) have been identified in non-coding regions, with functional roles that are difficult to interpret. Hypothesis: A whole exome sequencing study focusing on coding variants will reveal novel mechanisms of kidney function and CKD. Methods: We performed whole exome sequencing analyses of cystatin C among 29,789 UK Biobank (UKB) participants with further confirmation among 4,297 white and 607 African American participants of the Health and Retirement Study (HRS). Conditional analyses for loci achieving exome-wide significance ( P <3.5х10 -7 ) were conducted in UKB using both the exome (n=29,789) and imputed GWAS data (n=295,122). Genomic findings were tested for relevance to baseline estimated glomerular filtration rate (eGFR) and stringently adjudicated CKD progression events among participants of the Chronic Renal Insufficiency Cohort (CRIC) by race and smoking status, using a base model and a full model ( Table ). Results: We identified a common missense variant, CST9 rs2983640, in a previously reported locus ( CST3 intron rs13038305), of which the minor G allele was associated with lower serum cystatin C level (UKB: beta=-0.03 mg/L, P =7.64х10 -92 ; HRS whites: beta=-0.05 mg/L, P =4.71х10 -6 ; HRS African Americans: beta=-0.03 mg/L, P =0.64; and multi-ethnic meta-analysis beta=-0.03 mg/L, P =2.46х10 -91 ). After controlling for the CST3 variant, the G allele was associated with higher cystatin C level (UKB exome: beta=0.003 mg/L, P =0.04; UKB GWAS: beta=0.003 mg/L, P =1.47х10 -10 ). Similar associations were identified in white CRIC participants (direct effect: beta=-0.05 mg/L, P =0.005; conditional effect: beta=0.004 mg/L, P =0.86). The CST9 rs2983640 G allele was associated with lower baseline eGFR (base model beta=-0.33 ml/min/1.73 m 2 , P =1.98х10 -6 ) and higher hazard of developing CKD progression independent of the reported CST3 variant ( Table ). Conclusions: We identified a novel missense variant influencing cystatin C level and CKD progression.

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Abstract MP30: Chronic Kidney Disease Progression and Risk of End-Stage Renal Disease: The Use of Change in Novel Kidney Filtration Markers

Circulation ◽

10.1161/circ.129.suppl_1.mp30 ◽

2014 ◽

Vol 129 (suppl_1) ◽

Author(s):

Casey M Rebholz ◽

Kunihiro Matsushita ◽

Elizabeth Selvin ◽

Morgan E Grams ◽

Josef Coresh

Keyword(s):

Chronic Kidney Disease ◽

Clinical Trials ◽

Kidney Disease ◽

Cystatin C ◽

End Stage Renal Disease ◽

Ckd Progression ◽

Percent Change ◽

Stage Renal Disease ◽

End Stage

Introduction: Chronic kidney disease (CKD) progression assessed by estimated GFR from creatinine (eGFR-Cr) is a risk factor for cardiovascular disease and end-stage renal disease (ESRD) and has been proposed as a surrogate endpoint for clinical trials. It is unclear if CKD progression assessed by change in different filtration markers has similar risk associations with ESRD. Hypothesis: We hypothesized that percent change in novel kidney filtration markers (β 2 -microglobulin and cystatin C) over a 6-year period would be independently associated with increased risk of ESRD during 15 years of follow-up, similar to the risk seen with change in eGFR-Cr. Methods: We conducted prospective analyses of the ARIC study (N=9,703). β 2 -microglobulin, cystatin C, and creatinine were measured at study visits 1 (1990-92) and 2 (1996-98). Incident ESRD (kidney dialysis or transplant) was defined as entry into the U.S. Renal Data System registry between study visit 2 and September 30, 2011. Cox proportional hazards regression was used to estimate the association between percent change in filtration marker and incident ESRD, adjusting for demographics, kidney disease risk factors, and 1 st measurement of the filtration marker. Results: During a median follow-up of 13.1 years, there were 142 incident ESRD cases. Median eGFR-Cr was 97.3 mL/min/1.73 m 2 at 1 st measurement and 89.0 mL/min/1.73 m 2 at 2 nd measurement. Percent change in eGFR-Cr was moderately correlated with percent change in the inverse of β 2 -microglobulin (r = 0.34) and the inverse of cystatin C (r = 0.36). Progression of CKD (10-25% and >25% decline in filtration function) was associated with increased ESRD risk, with novel markers (β 2 -microglobulin, cystatin C) showing an association at least as strong as the creatinine and eGFR-Cr estimates (Table). Conclusions: CKD progression assessed using novel filtration markers is independently associated with ESRD risk, suggesting the potential utility of measuring change in β 2 -microglobulin and cystatin C in clinical trials.

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Types of erythropoiesis-stimulating agents and risk of end-stage kidney disease and death in patients with non-dialysis chronic kidney disease

Nephrology Dialysis Transplantation ◽

10.1093/ndt/gfaa088 ◽

2020 ◽

Author(s):

Roberto Minutolo ◽

Carlo Garofalo ◽

Paolo Chiodini ◽

Filippo Aucella ◽

Lucia Del Vecchio ◽

...

Keyword(s):

Chronic Kidney Disease ◽

Kidney Disease ◽

Primary Endpoint ◽

End Stage Kidney Disease ◽

Short Acting ◽

Erythropoiesis Stimulating Agents ◽

Increased Risk ◽

Significant Difference ◽

Long Acting ◽

End Stage

Abstract Background Despite the widespread use of erythropoiesis-stimulating agents (ESAs) to treat anaemia, the risk of adverse outcomes associated with the use of different types of ESAs in non-dialysis chronic kidney disease (CKD) is poorly investigated. Methods From a pooled cohort of four observational studies, we selected CKD patients receiving short-acting (epoetin α/β; n = 299) or long-acting ESAs (darbepoetin and methoxy polyethylene glycol-epoetin β; n = 403). The primary composite endpoint was end-stage kidney disease (ESKD; dialysis or transplantation) or all-cause death. Multivariable Cox models were used to estimate the relative risk of the primary endpoint between short- and long-acting ESA users. Results During follow-up [median 3.6 years (interquartile range 2.1–6.3)], the primary endpoint was registered in 401 patients [166 (72%) in the short-acting ESA group and 235 (58%) in the long-acting ESA group]. In the highest tertile of short-acting ESA dose, the adjusted risk of primary endpoint was 2-fold higher {hazard ratio [HR] 2.07 [95% confidence interval (CI) 1.37–3.12]} than in the lowest tertile, whereas it did not change across tertiles of dose for long-acting ESA patients. Furthermore, the comparison of ESA type in each tertile of ESA dose disclosed a significant difference only in the highest tertile, where the risk of the primary endpoint was significantly higher in patients receiving short-acting ESAs [HR 1.56 (95% CI 1.09–2.24); P = 0.016]. Results were confirmed when ESA dose was analysed as continuous variable with a significant difference in the primary endpoint between short- and long-acting ESAs for doses >105 IU/kg/week. Conclusions Among non-dialysis CKD patients, the use of a short-acting ESA may be associated with an increased risk of ESKD or death versus long-acting ESAs when higher ESA doses are prescribed.

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Cardiac and Stress Biomarkers and Chronic Kidney Disease Progression: The CRIC Study

Clinical Chemistry ◽

10.1373/clinchem.2019.305797 ◽

2019 ◽

Vol 65 (11) ◽

pp. 1448-1457 ◽

Cited By ~ 6

Author(s):

Nisha Bansal ◽

Leila Zelnick ◽

Michael G Shlipak ◽

Amanda Anderson ◽

Robert Christenson ◽

...

Keyword(s):

Chronic Kidney Disease ◽

Kidney Disease ◽

Troponin T ◽

Mineral Metabolism ◽

Kidney Injury ◽

High Sensitivity ◽

Ckd Progression ◽

Cox Models ◽

Stress Biomarkers ◽

Increased Risk

Abstract BACKGROUND Increases in cardiac and stress biomarkers may be associated with loss of kidney function through shared mechanisms involving cardiac and kidney injury. We evaluated the associations of cardiac and stress biomarkers [N-terminal pro-B-type natriuretic peptide (NT-proBNP), high-sensitivity troponin T (hsTnT), growth differentiation factor 15 (GDF-15), soluble ST-2 (sST-2)] with progression of chronic kidney disease (CKD). METHODS We included 3664 participants with CKD from the Chronic Renal Insufficiency Cohort study. All biomarkers were measured at entry. The primary outcome was CKD progression, defined as progression to end-stage renal disease (ESRD) or 50% decline in estimated glomerular filtration rate (eGFR). Cox models tested the association of each biomarker with CKD progression, adjusting for demographics, site, diabetes, cardiovascular disease, eGFR, urine proteinuria, blood pressure, body mass index, cholesterol, medication use, and mineral metabolism. RESULTS There were 1221 participants who had CKD progression over a median (interquartile range) follow-up of 5.8 (2.4–8.6) years. GDF-15, but not sST2, was significantly associated with an increased risk of CKD progression [hazard ratios (HRs) are per SD increase in log-transformed biomarker]: GDF-15 (HR, 1.50; 95% CI, 1.35–1.67) and sST2 (HR, 1.07; 95% CI, 0.99–1.14). NT-proBNP and hsTnT were also associated with increased risk of CKD progression, but weaker than GDF-15: NT-proBNP (HR, 1.24; 95% CI, 1.13–1.36) and hsTnT (HR, 1.11; 95% CI, 1.01–1.22). CONCLUSIONS Increases in GDF-15, NT-proBNP, and hsTnT are associated with greater risk for CKD progression. These biomarkers may inform mechanisms underlying kidney injury.

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Effect of intensive blood pressure on the progression of non-diabetic chronic kidney disease at varying degrees of proteinuria

Journal of Investigative Medicine ◽

10.1136/jim-2020-001702 ◽

2021 ◽

pp. jim-2020-001702

Author(s):

Paul J Der Mesropian ◽

Gulvahid Shaikh ◽

Kelly H Beers ◽

Swati Mehta ◽

Mauricio R Monrroy Prado ◽

...

Keyword(s):

Blood Pressure ◽

Chronic Kidney Disease ◽

Kidney Disease ◽

Pooled Analysis ◽

Ckd Progression ◽

Glomerular Filtration Rate Decline ◽

Multivariable Regression ◽

Stage Renal Disease ◽

End Stage

The ideal blood pressure (BP) target for renoprotection is uncertain in patients with non-diabetic chronic kidney disease (CKD), especially considering the influence exerted by pre-existing proteinuria. In this pooled analysis of landmark trials, we coalesced individual data from 5001 such subjects randomized to intensive versus standard BP targets. We employed multivariable regression to evaluate the relationship between follow-up systolic blood pressure (SBP) and diastolic blood pressure (DBP) on CKD progression (defined as glomerular filtration rate decline by 50% or end-stage renal disease), focusing on the potential for effect modification by baseline proteinuria or albuminuria. The median follow-up was 3.2 years. We found that SBP rather than DBP was the primary predictor of renal outcomes. The optimal SBP target was 110–129 mm Hg. We observed a strong interaction between SBP and proteinuria such that lower SBP ranges were significantly linked with progressively lower CKD risk in grade A3 albuminuria or ≥0.5–1 g/day proteinuria (relative to SBP 110–119 mm Hg, the adjusted HR for SBP 120–129 mm Hg, 130–139 mm Hg, and 140–149 mm Hg was 1.5, 2.3, and 3.3, respectively; all p<0.05). In grade A2 microalbuminuria or proteinuria near 0.5 g/day, a non-significant but possible connection was seen between tighter BP and decreased CKD (aforementioned HRs all <2; all p>0.05), while in grade A1 albuminuria or proteinuria <0.2 g/day no significant association was apparent (HRs all <1.5; all p>0.1). We conclude that in non-diabetic CKD, stricter BP targets <130 mm Hg may help limit CKD progression as proteinuria rises.

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MO465PROGNOSTIC IMPLICATION OF URINARY POTASSIUM EXCRETION IN PATIENTS WITH CHRONIC KIDNEY DISEASE

Nephrology Dialysis Transplantation ◽

10.1093/ndt/gfab090.0027 ◽

2021 ◽

Vol 36 (Supplement_1) ◽

Author(s):

Daisuke Mori ◽

Shinjiro Tamai ◽

Maho Tokuchi ◽

Natsumi Inoue ◽

Hideaki Kawai ◽

...

Keyword(s):

Chronic Kidney Disease ◽

Kidney Disease ◽

Serum Potassium ◽

Cardiovascular Events ◽

Renal Outcome ◽

Potassium Excretion ◽

Ckd Progression ◽

Increased Risk ◽

Urinary Potassium ◽

All Cause Mortality

Abstract Background and Aims Plasma potassium levels are impacted by decreased kidney function and are known to be associated with increased mortality, adverse cardiovascular events and adverse kidney events. However, the prognostic implication of urinary potassium is unclear. Method We conducted an observational study of 1102 patients with chronic kidney disease (CKD) who were hospitalized between 2010 and 2018. The expected primary outcomes were all-cause mortality, adverse cardiovascular events and CKD progression. CKD progression was defined as a 30% increase in serum creatinine, the initiation of maintenance dialysis or the need for kidney transplantation. The Cox proportional hazards model was used to analyse the association between urinary potassium excretion and adverse clinical outcomes after adjustment for potential confounders. Results At baseline, 66% of the patients were men, with a median age of 72 years (interquartile range or IQR, 64–79 years); 61% of the patients were diabetic, and 54% of them were hypertensive. The median values for estimated glomerular filtration rate (eGFR) was 12 mL/min/1.73m2 (IQR, 8–18), serum potassium 4.5 mmol/L (IQR, 4.1–5.1) and urinary potassium/creatinine ratio (UK/Cr) 27 mmol/gCr (IQR, 20–38). Over a median follow-up period of 2.6 years (IQR 0.2–4.5), the number of all-cause deaths was 87. There were 171 cases of cardiovascular events and 860 cases of CKD progression. After adjusting for the eGFR, serum potassium level, proteinuria, renin–angiotensin system inhibitors, diuretics and other potential confounders, UK/Cr was found to be neither significantly associated with all-cause mortality nor with adverse cardiovascular events. However, a low UK/Cr was associated with an increased risk of CKD progression (adjusted hazard ratio [95% confidence interval] for the first, second and third quartiles, compared with the fourth quartile, were as follows: 2.09 [1.43-3.06], 1.33 [0.96-1.86] and 1.05 [0.75-1.46]) Conclusion A low UK/Cr might be an independent risk factor for poor renal outcome.

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Elevated lipoxygenase and cytochrome P450 products predict progression of chronic kidney disease

Nephrology Dialysis Transplantation ◽

10.1093/ndt/gfy232 ◽

2018 ◽

Vol 35 (2) ◽

pp. 303-312 ◽

Cited By ~ 2

Author(s):

Farsad Afshinnia ◽

Lixia Zeng ◽

Jaeman Byun ◽

Stefanie Wernisch ◽

Rajat Deo ◽

...

Keyword(s):

Chronic Kidney Disease ◽

Cytochrome P450 ◽

Kidney Disease ◽

Metabolic Pathways ◽

Risk Estimation ◽

Ckd Progression ◽

Standard Deviation Increase ◽

Logistic Regression Models ◽

Major Cardiovascular Events ◽

End Stage

Abstract Background The clinical relevance of arachidonic acid (AA) metabolites in chronic kidney disease (CKD) progression is poorly understood. We aimed to compare the concentrations of 85 enzymatic pathway products of AA metabolism in patients with CKD who progressed to end-stage kidney disease (ESKD) versus patients who did not in a subcohort of Chronic Renal Insufficiency Cohort (CRIC) and to estimate the risk of CKD progression and major cardiovascular events by levels of AA metabolites and their link to enzymatic metabolic pathways. Methods A total 123 patients in the CRIC study who progressed to ESKD were frequency matched with 177 nonprogressors and serum eicosanoids were quantified by mass spectrometry. We applied serum collected at patients’ Year 1 visit and outcome of progression to ESKD was ascertained over the next 10 years. We used logistic regression models for risk estimation. Results Baseline 15-hydroxyeicosatetraenoate (HETE) and 20-HETE levels were significantly elevated in progressors (false discovery rate Q ≤ 0.026). The median 20-HETE level was 7.6 pmol/mL [interquartile range (IQR) 4.2–14.5] in progressors and 5.4 pmol/mL (IQR 2.8–9.4) in nonprogressors (P < 0.001). In an adjusted model, only 20-HETE independently predicted CKD progression. Each 1 standard deviation increase in 20-HETE was independently associated with 1.45-fold higher odds of progression (95% confidence interval 1.07–1.95; P = 0.017). Principal components of lipoxygenase (LOX) and cytochrome P450 (CYP450) pathways were independently associated with CKD progression. Conclusions We found higher odds of CKD progression associated with higher 20-HETE, LOX and CYP450 metabolic pathways. These alterations precede CKD progression and may serve as targets for interventions aimed at halting progression.

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Smoking, Smoking Cessation, and Progression of Chronic Kidney Disease: Results From KNOW-CKD Study

Nicotine & Tobacco Research ◽

10.1093/ntr/ntaa071 ◽

2020 ◽

Author(s):

Sangmi Lee ◽

Shinchan Kang ◽

Young Su Joo ◽

Changhyun Lee ◽

Ki Heon Nam ◽

...

Keyword(s):

Chronic Kidney Disease ◽

Smoking Cessation ◽

Cohort Study ◽

Kidney Disease ◽

Kidney Function ◽

Primary Outcome ◽

Incidence Rates ◽

Ckd Progression ◽

Increased Risk ◽

Never Smokers

Abstract Introduction In patients with chronic kidney disease (CKD), studies investigating the association between smoking and deterioration of kidney function are scarce. Aims and Methods We analyzed data for 1,951 patients with an estimated glomerular filtration rate (eGFR) ≥15 mL/min/1.73 m2 enrolled in the KoreaN cohort study for Outcome in patients With Chronic Kidney Disease (KNOW-CKD) from 2011 to 2016. Patients were categorized by smoking load. Primary outcome was a composite of a ≥50% reduction in eGFR, initiation of dialysis, or kidney transplantation. Results There were 967 never-smokers and 369, 276, and 339 smokers who smoked <15, 15 to 29, ≥30 pack-years, respectively. During a mean follow-up of 3.0 years, the incidence rates (95% confidence interval [CI]) of the primary outcome were 54.3 (46.4–63.5), 46.9 (35.9–61.4), 69.2 (52.9–90.6), and 76.3 (60.7–96.0) events per 1,000 person-yr in never-, <15, 15 to 29, and ≥30 pack-year smokers. In cause-specific hazard model after adjustment of confounding factors, smokers were associated with 1.09 (0.73–1.63), 1.48 (1.00–2.18), and 1.94 (1.35–2.77) fold increased risk (95% CI) of primary outcome in <15, 15–29, and ≥30 pack-year smokers compared with never-smokers. The association of longer smoking duration with higher risk of CKD progression was evident particularly in patients with eGFR < 45 mL/min/1.73 m2 and proteinuria ≥ 1.0 g/g. In contrast, the risk of adverse kidney outcome decreased with longer smoking-free periods among former-smokers. Conclusions These findings suggest potentially harmful effects of the degree of exposure to smoking on the progression of CKD. Implications Among patients with CKD, there has been lack of studies on the association between smoking and CKD progression and studies to date have yielded conflicting results. In this prospective cohort study involving Korean CKD patients, smoking was associated with significantly higher risk of worsening kidney function. Furthermore, the risk of adverse kidney outcome was incrementally higher as smoking pack-years were higher. As the duration of smoking cessation increased, the hazard ratios for adverse kidney outcome were attenuated, suggesting that quitting smoking may be a modifiable factor to delay CKD progression.

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High Unawareness of Chronic Kidney Disease in Germany

International Journal of Environmental Research and Public Health ◽

10.3390/ijerph182211752 ◽

2021 ◽

Vol 18 (22) ◽

pp. 11752

Author(s):

Susanne Stolpe ◽

Bernd Kowall ◽

Christian Scholz ◽

Andreas Stang ◽

Cornelia Blume

Keyword(s):

Risk Factors ◽

Chronic Kidney Disease ◽

Kidney Disease ◽

Cardiovascular Comorbidities ◽

Increased Risk ◽

Binomial Regression ◽

Ckd Stage ◽

Stage Renal Disease ◽

End Stage ◽

Prevalence Ratios

Chronic kidney disease (CKD) is associated with an increased risk for cardiovascular events, hospitalizations, end stage renal disease and mortality. Main risk factors for CKD are diabetes, hypertension, and older age. Although CKD prevalence is about 10%, awareness for CKD is generally low in patients and physicians, hindering early diagnosis and treatment. We analyzed baseline data of 3305 participants with CKD Stages 1–4 from German cohorts and registries collected in 2010. Prevalence of CKD unawareness and prevalence ratios (PR) (each with 95%-confidence intervals) were estimated in categories of age, sex, CKD stages, BMI, hypertension, diabetes and other relevant comorbidities. We used a log-binomial regression model to estimate the PR for CKD unawareness for females compared to males adjusting for CKD stage and CKD risk factors. CKD unawareness was high, reaching 71% (68–73%) in CKD 3a, 49% (45–54%) in CKD 3b and still 30% (24–36%) in CKD4. Prevalence of hypertension, diabetes or cardiovascular comorbidities was not associated with lower CKD unawareness. Independent of CKD stage and other risk factors unawareness was higher in female patients (PR = 1.06 (1.01; 1.10)). Even in patients with CKD related comorbidities, CKD unawareness was high. Female sex was strongly associated with CKD unawareness. Guideline oriented treatment of patients at higher risk for CKD could increase CKD awareness. Patient–physician communication about CKD might be amendable.

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