Lifetime Incidence of CKD Stages 3-5 in the United States
TL;DR: In the United States, the lifetime risk of developing CKD stage 3a+ is high, emphasizing the importance of primary prevention and effective therapy to reduce CKD-related morbidity and mortality.
About: This article is published in American Journal of Kidney Diseases.The article was published on 2013-08-01 and is currently open access. It has received 249 citations till now. The article focuses on the topics: End stage renal disease & Population.
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TL;DR: Compared with matched healthy nondonors, kidney donors had an increased risk of ESRD over a median of 7.6 years; however, the magnitude of the absolute risk increase was small; these findings may help inform discussions with persons considering live kidney donation.
Abstract: Importance Risk of end-stage renal disease (ESRD) in kidney donors has been compared with risk faced by the general population, but the general population represents an unscreened, high-risk comparator. A comparison to similarly screened healthy nondonors would more properly estimate the sequelae of kidney donation. Objectives To compare the risk of ESRD in kidney donors with that of a healthy cohort of nondonors who are at equally low risk of renal disease and free of contraindications to live donation and to stratify these comparisons by patient demographics. Design, Settings, and Participants A cohort of 96 217 kidney donors in the United States between April 1994 and November 2011 and a cohort of 20 024 participants of the Third National Health and Nutrition Examination Survey (NHANES III) were linked to Centers for Medicare & Medicaid Services data to ascertain development of ESRD, which was defined as the initiation of maintenance dialysis, placement on the waiting list, or receipt of a living or deceased donor kidney transplant, whichever was identified first. Maximum follow-up was 15.0 years; median follow-up was 7.6 years (interquartile range [IQR], 3.9-11.5 years) for kidney donors and 15.0 years (IQR, 13.7-15.0 years) for matched healthy nondonors. Main Outcomes and Measures Cumulative incidence and lifetime risk of ESRD. Results Among live donors, with median follow-up of 7.6 years (maximum, 15.0), ESRD developed in 99 individuals in a mean (SD) of 8.6 (3.6) years after donation. Among matched healthy nondonors, with median follow-up of 15.0 years (maximum, 15.0), ESRD developed in 36 nondonors in 10.7 (3.2) years, drawn from 17 ESRD events in the unmatched healthy nondonor pool of 9364. Estimated risk of ESRD at 15 years after donation was 30.8 per 10 000 (95% CI, 24.3-38.5) in kidney donors and 3.9 per 10 000 (95% CI, 0.8-8.9) in their matched healthy nondonor counterparts ( P P P Conclusions and Relevance Compared with matched healthy nondonors, kidney donors had an increased risk of ESRD over a median of 7.6 years; however, the magnitude of the absolute risk increase was small. These findings may help inform discussions with persons considering live kidney donation.
774 citations
Johns Hopkins University1, University of Calgary2, The George Institute for Global Health3, University of Sydney4, Royal Prince Alfred Hospital5, University of Salerno6, Geisinger Medical Center7, Saarland University8, Tufts Medical Center9, University of Minnesota10, University of California, San Diego11, University of Tennessee Health Science Center12, Veterans Health Administration13, University of Aberdeen14, Tohoku University15, Teikyo University16, Shiga University of Medical Science17, Tel Aviv University18, Virginia Commonwealth University19, China Medical University (Taiwan)20, National Health Research Institutes21, University Medical Center Groningen22, University of Paris-Sud23
TL;DR: Declines in estimated GFR smaller than a doubling of serum creatinine concentration occurred more commonly and were strongly and consistently associated with the risk of ESRD and mortality, supporting consideration of lesser declines in Estimated GFR (such as a 30% reduction over 2 years) as an alternative end point for CKD progression.
Abstract: IMPORTANCE: The established chronic kidney disease (CKD) progression end point of end-stage renal disease (ESRD) or a doubling of serum creatinine concentration (corresponding to a change in estimated glomerular filtration rate [GFR] of −57% or greater) is a late event.OBJECTIVE: To characterize the association of decline in estimated GFR with subsequent progression to ESRD with implications for using lesser declines in estimated GFR as potential alternative end points for CKD progression. Because most people with CKD die before reaching ESRD, mortality risk also was investigated.DATA SOURCES AND STUDY SELECTION: Individual meta-analysis of 1.7 million participants with 12,344 ESRD events and 223,944 deaths from 35 cohorts in the CKD Prognosis Consortium with a repeated measure of serum creatinine concentration over 1 to 3 years and outcome data.DATA EXTRACTION AND SYNTHESIS: Transfer of individual participant data or standardized analysis of outputs for random-effects meta-analysis conducted between July 2012 and September 2013, with baseline estimated GFR values collected from 1975 through 2012.MAIN OUTCOMES AND MEASURES: End-stage renal disease (initiation of dialysis or transplantation) or all-cause mortality risk related to percentage change in estimated GFR over 2 years, adjusted for potential confounders and first estimated GFR.RESULTS: The adjusted hazard ratios (HRs) of ESRD and mortality were higher with larger estimated GFR decline. Among participants with baseline estimated GFR of less than 60 mL/min/1.73 m2, the adjusted HRs for ESRD were 32.1 (95% CI, 22.3-46.3) for changes of −57% in estimated GFR and 5.4 (95% CI, 4.5-6.4) for changes of −30%. However, changes of −30% or greater (6.9% [95% CI, 6.4%-7.4%] of the entire consortium) were more common than changes of −57% (0.79% [95% CI, 0.52%-1.06%]). This association was strong and consistent across the length of the baseline period (1 to 3 years), baseline estimated GFR, age, diabetes status, or albuminuria. Average adjusted 10-year risk of ESRD (in patients with a baseline estimated GFR of 35 mL/min/1.73 m2) was 99% (95% CI, 95%-100%) for estimated GFR change of −57%, was 83% (95% CI, 71%-93%) for estimated GFR change of −40%, and was 64% (95% CI, 52%-77%) for estimated GFR change of −30% vs 18% (95% CI, 15%-22%) for estimated GFR change of 0%. Corresponding mortality risks were 77% (95% CI, 71%-82%), 60% (95% CI, 56%-63%), and 50% (95% CI, 47%-52%) vs 32% (95% CI, 31%-33%), showing a similar but weaker pattern.CONCLUSIONS AND RELEVANCE: Declines in estimated GFR smaller than a doubling of serum creatinine concentration occurred more commonly and were strongly and consistently associated with the risk of ESRD and mortality, supporting consideration of lesser declines in estimated GFR (such as a 30% reduction over 2 years) as an alternative end point for CKD progression.
742 citations
Additional excerpts
...6) 21 (20-21) 28 (27-29) 32 (30-34) 35 (33-37) 41 (33-47) 3-y Baseline period Adjusted HR (95% CI) 60....
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...9) 13 (12-13) 20 (19-21) 25 (23-26) 30 (27-31) 37 (31-42) 2-y Baseline period Adjusted HR (95% CI) 57....
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...73 m2 Total Cholesterol, mmol/L SBP, mm Hg Female Black DM History of CVD Albuminuriab Current Cigarette Smoking AASK 55 (10) 67 (6) 5 (1) 150 (24) 38 100 0 45 38 41 ADVANCE 66 (6) 83 (13) 5 (1) 144 (21) 40 0 100 24 28 16 Aichi 49 (6) 92 (14) 5 (1) 126 (15) 18 0 0....
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...3) 13 (13-14) 20 (19-21) 23 (22-24) 27 (25-29) 34 (28-38)...
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...73 m2 Total Cholesterol, mmol/L SBP, mm Hg Female Black DM History of CVD Albuminuriab Current Cigarette Smoking AASK 54 (11) 42 (11) 5 (1) 150 (24) 39 100 0 53 64 44 ADVANCE 69 (6) 51 (8) 5 (1) 147 (23) 54 0 100 31 39 9 Aichic NA NA NA NA NA NA NA NA NA NA AKDNc 73 (11) 48 (10) NA NA 60 0 18 17 12 NA BC CKD 70 (13) 33 (10) 5 (1) 134 (22) 46 0 42 4 69 6 CARE 66 (7) 52 (7) 5 (0) 134 (20) 21 2 18 100 19 8 CCF 72 (11) 47 (10) 5 (1) 131 (19) 55 12 26 22 27 8 CIRCS 63 (6) 54 (6) 5 (1) 135 (19) 70 0 6 4 7 14 CRIB 61 (15) 28 (9) 6 (1) 150 (23) 34 6 16 44 81 12 Framinghamc 70 (6) 51 (8) 5 (1) 139 (16) 52 0 20 13 NA 13 Geisinger 70 (10) 52 (8) 5 (1) 131 (19) 59 1 31 15 44 7 GLOMMS 1c 70 (13) 33 (7) NA NA 50 0 61 48 72 11 IPHS 70 (6) 54 (6) 5 (1) 139 (17) 68 0 9 16 9 9 KP Hawaii 71 (11) 47 (10) 5 (1) 137 (22) 53 0 52 35 66 7 KPNWc 71 (10) 47 (11) NA 142 (23) 48 2 40 24 8 13 KSHSc NA NA NA NA NA NA NA NA NA NA Maccabi 72 (11) 50 (9) 5 (1) 134 (19) 58 0 30 9 40 1 MASTERPLAN 61 (12) 36 (11) 5 (1) 136 (20) 31 0 24 30 37 21 MDRD 52 (12) 35 (11) 6 (1) 132 (18) 38 7 4 13 83 10 MRFIT 52 (5) 55 (5) 6 (1) 130 (17) 0 5 10 3 13 34 NephroTest 60 (14) 37 (12) 5 (1) 137 (20) 32 10 24 19 96 15 NZDCS 71 (9) 48 (10) 5 (1) 142 (21) 57 0 100 2 14 8 Ohasamac NA NA NA NA NA NA NA NA NA NA Pimac NA NA NA NA NA NA NA NA NA NA PREVEND 67 (9) 53 (7) 5 (1) 137 (21) 53 0 16 16 27 22 Rancho Bernardoc NA NA NA NA NA NA NA NA NA NA RENAAL 61 (7) 40 (11) 6 (1) 152 (19) 38 13 100 44 100 18 Severancec NA NA NA NA NA NA NA NA NA NA Sunnybrookc 69 (14) 38 (12) NA NA 40 0 37 48 81 5 Taiwan 63 (10) 52 (8) 5 (1) 139 (24) 40 0 9 9 12 21 VA CKDc 75 (9) 48 (9) 4 (1) NA 3 8 43 45 41 NA ZODIAC 74 (8) 50 (8) 6 (1) 159 (24) 72 0 100 43 43 13 Total 74 (10) 48 (10) 4 (1) 135 (20) 20 7 38 35 38 6...
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TL;DR: In mouse models of experimentally induced renal fibrosis, conditional deletion of Twist1 or Snai1 in proximal TECs resulted in inhibition of the EMT program and the maintenance of TEC integrity, while also restoring cell proliferation, dedifferentiation-associated repair and regeneration of the kidney parenchyma and attenuating interstitial fibrosis.
Abstract: Kidney fibrosis is marked by an epithelial-to-mesenchymal transition (EMT) of tubular epithelial cells (TECs). Here we find that, during renal fibrosis, TECs acquire a partial EMT program during which they remain associated with their basement membrane and express markers of both epithelial and mesenchymal cells. The functional consequence of the EMT program during fibrotic injury is an arrest in the G2 phase of the cell cycle and lower expression of several solute and solvent transporters in TECs. We also found that transgenic expression of either Twist1 (encoding twist family bHLH transcription factor 1, known as Twist) or Snai1 (encoding snail family zinc finger 1, known as Snail) expression is sufficient to promote prolonged TGF-β1-induced G2 arrest of TECs, limiting the cells' potential for repair and regeneration. In mouse models of experimentally induced renal fibrosis, conditional deletion of Twist1 or Snai1 in proximal TECs resulted in inhibition of the EMT program and the maintenance of TEC integrity, while also restoring cell proliferation, dedifferentiation-associated repair and regeneration of the kidney parenchyma and attenuating interstitial fibrosis. Thus, inhibition of the EMT program in TECs during chronic renal injury represents a potential anti-fibrosis therapy.
691 citations
University of Maryland, Baltimore1, Johns Hopkins University2, University of Pennsylvania3, University of Wisconsin-Madison4, Kaiser Permanente5, University of California, San Francisco6, University of Toronto7, National Institutes of Health8, University of Utah9, Case Western Reserve University10, University of Illinois at Chicago11, Wake Forest University12, University of Michigan13, Science Applications International Corporation14, George Washington University15, Tulane University16, Georgetown University17
TL;DR: Renal risk variants in APOL1 were associated with the higher rates of end-stage renal disease and progression of chronic kidney disease that were observed in black patients as compared with white patients, regardless of diabetes status.
Abstract: Methods In two studies, we examined the effects of variants in the gene encoding apolipoprotein L1 (APOL1) on the progression of chronic kidney disease. In the African American Study of Kidney Disease and Hypertension (AASK), we evaluated 693 black patients with chronic kidney disease attributed to hypertension. In the Chronic Renal Insufficiency Cohort (CRIC) study, we evaluated 2955 white patients and black patients with chronic kidney disease (46% of whom had diabetes) according to whether they had 2 copies of high-risk APOL1 variants (APOL1 high-risk group) or 0 or 1 copy (APOL1 low-risk group). In the AASK study, the primary outcome was a composite of end-stage renal disease or a doubling of the serum creatinine level. In the CRIC study, the primary outcomes were the slope in the estimated glomerular filtration rate (eGFR) and the composite of end-stage renal disease or a reduction of 50% in the eGFR from baseline. Results In the AASK study, the primary outcome occurred in 58.1% of the patients in the APOL1 high-risk group and in 36.6% of those in the APOL1 low-risk group (hazard ratio in the high-risk group, 1.88; P<0.001). There was no interaction between APOL1 status and trial interventions or the presence of baseline proteinuria. In the CRIC study, black patients in the APOL1 high-risk group had a more rapid decline in the eGFR and a higher risk of the composite renal outcome than did white patients, among those with diabetes and those without diabetes (P<0.001 for all comparisons). Conclusions Renal risk variants in APOL1 were associated with the higher rates of end-stage renal disease and progression of chronic kidney disease that were observed in black patients as compared with white patients, regardless of diabetes status. (Funded by the National Institute of Diabetes and Digestive and Kidney Diseases and others.)
630 citations
TL;DR: Optimal management of CKD includes cardiovascular risk reduction, treatment of albuminuria, avoidance of potential nephrotoxins, and adjustments to drug dosing (eg, many antibiotics and oral hypoglycemic agents).
Abstract: Importance Chronic kidney disease (CKD) is the 16th leading cause of years of life lost worldwide. Appropriate screening, diagnosis, and management by primary care clinicians are necessary to prevent adverse CKD-associated outcomes, including cardiovascular disease, end-stage kidney disease, and death. Observations Defined as a persistent abnormality in kidney structure or function (eg, glomerular filtration rate [GFR] Conclusions and Relevance Diagnosis, staging, and appropriate referral of CKD by primary care clinicians are important in reducing the burden of CKD worldwide.
594 citations
References
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TL;DR: Dairy therapy remains the first line of treatment of high blood cholesterol, and drug therapy is reserved for patients who are considered to be at high risk for CHD, and the fundamental approach to treatment is comparable.
Abstract: THE SECOND report of the Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel II, or ATP II) presents the National Cholesterol Education Program's updated recommendations for cholesterol management. It is similar to the first in general outline, and the fundamental approach to treatment of high blood cholesterol is comparable. This report continues to identify low-density lipoproteins (LDL) as the primary target of cholesterol-lowering therapy. As in the first report, the second report emphasizes the role of the clinical approach in primary prevention of coronary heart disease (CHD). Dietary therapy remains the first line of treatment of high blood cholesterol, and drug therapy is reserved for patients who are considered to be at high risk for CHD. However, the second report contains new features that distinguish it from the first. These include the following: Increased emphasis on See also pp 3002 and 3009.
28,495 citations
TL;DR: The CKD-EPI creatinine equation is more accurate than the Modification of Diet in Renal Disease Study equation and could replace it for routine clinical use.
Abstract: The Modification of Diet in Renal Disease (MDRD) Study equation underestimates glomerular filtration rate (GFR) in patients with mild kidney disease. Levey and associates therefore developed and va...
18,691 citations
01 Jan 2009
15,111 citations
TL;DR: The prevalence of CKD in the United States in 1999-2004 is higher than it was in 1988-1994 and this increase is partly explained by the increasing prevalence of diabetes and hypertension and raises concerns about future increased incidence of kidney failure and other complications.
Abstract: ContextThe prevalence and incidence of kidney failure treated by dialysis and transplantation in the United States have increased from 1988 to 2004. Whether there have been changes in the prevalence of earlier stages of chronic kidney disease (CKD) during this period is uncertain.ObjectiveTo update the estimated prevalence of CKD in the United States.Design, Setting, and ParticipantsCross-sectional analysis of the most recent National Health and Nutrition Examination Surveys (NHANES 1988-1994 and NHANES 1999-2004), a nationally representative sample of noninstitutionalized adults aged 20 years or older in 1988-1994 (n = 15 488) and 1999-2004 (n = 13 233).Main Outcome MeasuresChronic kidney disease prevalence was determined based on persistent albuminuria and decreased estimated glomerular filtration rate (GFR). Persistence of microalbuminuria (>30 mg/g) was estimated from repeat visit data in NHANES 1988-1994. The GFR was estimated using the abbreviated Modification of Diet in Renal Disease Study equation reexpressed to standard serum creatinine.ResultsThe prevalence of both albuminuria and decreased GFR increased from 1988-1994 to 1999-2004. The prevalence of CKD stages 1 to 4 increased from 10.0% (95% confidence interval [CI], 9.2%-10.9%) in 1988-1994 to 13.1% (95% CI, 12.0%-14.1%) in 1999-2004 with a prevalence ratio of 1.3 (95% CI, 1.2-1.4). The prevalence estimates of CKD stages in 1988-1994 and 1999-2004, respectively, were 1.7% (95% CI, 1.3%-2.2%) and 1.8% (95% CI, 1.4%-2.3%) for stage 1; 2.7% (95% CI, 2.2%-3.2%) and 3.2% (95% CI, 2.6%-3.9%) for stage 2; 5.4% (95% CI, 4.9%-6.0%) and 7.7% (95% CI, 7.0%-8.4%) for stage 3; and 0.21% (95% CI, 0.15%-0.27%) and 0.35% (0.25%-0.45%) for stage 4. A higher prevalence of diagnosed diabetes and hypertension and higher body mass index explained the entire increase in prevalence of albuminuria but only part of the increase in the prevalence of decreased GFR. Estimation of GFR from serum creatinine has limited precision and a change in mean serum creatinine accounted for some of the increased prevalence of CKD.ConclusionsThe prevalence of CKD in the United States in 1999-2004 is higher than it was in 1988-1994. This increase is partly explained by the increasing prevalence of diabetes and hypertension and raises concerns about future increased incidence of kidney failure and other complications of CKD.
4,567 citations
TL;DR: In this article, a meta-analysis of general population cohorts was conducted to assess the independent and combined associations of estimated glomerular filtration rate (eGFR) and albuminuria with mortality.
3,087 citations