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Timing of Recovery From Moderate to Severe AKI and the Risk for Future Loss of Kidney Function.
Siew ED, Abdel-Kader K, Perkins AM, Greevy RA, Parr SK, Horner J, Vincz AJ, Denton J, Wilson OD, Hung AM, Robinson-Cohen C, Matheny ME
(2020) Am J Kidney Dis 75: 204-213
MeSH Terms: Acute Kidney Injury, Aged, Creatinine, Disease Progression, Female, Follow-Up Studies, Glomerular Filtration Rate, Humans, Male, Prognosis, Recovery of Function, Retrospective Studies, Risk Factors, Severity of Illness Index, Time Factors, United States, Veterans
Show Abstract · Added December 15, 2020
RATIONALE & OBJECTIVE - The extent of recovery of kidney function following acute kidney injury (AKI) is known to be associated with future chronic kidney disease. Less is known about how the timing of recovery affects the rate of future loss of kidney function.
STUDY DESIGN - We performed a retrospective cohort study examining the independent association between the timing of recovery from moderate to severe AKI and future loss of kidney function.
SETTING & PARTICIPANTS - 47,903 adult US veterans with stage 2 or 3 AKI who recovered to within 120% of baseline creatinine level within 90 days of peak injury.
EXPOSURE - The timing of recovery of kidney function from peak inpatient serum creatinine level grouped into 1 to 4, 5 to 10, 11 to 30, and 31 to 90 days.
OUTCOME - A sustained 40% decline in estimated glomerular filtration rate below that calculated from the last serum creatinine level available during the 90-day recovery period or kidney failure (2 outpatient estimated glomerular filtration rates<15mL/min/1.73m, dialysis procedures > 90 days apart, kidney transplantation, or registry within the US Renal Data System).
ANALYTICAL APPROACH - Time to the primary outcome was examined using multivariable Cox proportional hazards regression.
RESULTS - Among 47,903 patients, 29,316 (61%), 10,360 (22%), 4,520 (9%), and 3,707 (8%) recovered within 1 to 4, 5 to 10, 11 to 30, and 31 to 90 days, respectively. With a median follow-up of 42 months, unadjusted incidence rates for the kidney outcome were 2.01, 3.55, 3.86, and 3.68 events/100 person-years, respectively. Compared with 1 to 4 days, recovery within 5 to 10, 11 to 30, and 31 to 90 days was associated with increased rates of the primary outcome: adjusted HRs were 1.33 (95% CI, 1.24-1.43), 1.41 (95% CI, 1.28-1.54), and 1.58 (95% CI, 1.43-1.75), respectively.
LIMITATIONS - Predominately male population, residual confounding, and inability to make causal inferences because of the retrospective observational study design.
CONCLUSIONS - The timing of recovery provides an added dimension to AKI phenotyping and prognostic information regarding the future occurrence of loss of kidney function. Studies to identify effective interventions on the timing of recovery from AKI are warranted.
Published by Elsevier Inc.
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Mapping eGFR loci to the renal transcriptome and phenome in the VA Million Veteran Program.
Hellwege JN, Velez Edwards DR, Giri A, Qiu C, Park J, Torstenson ES, Keaton JM, Wilson OD, Robinson-Cohen C, Chung CP, Roumie CL, Klarin D, Damrauer SM, DuVall SL, Siew E, Akwo EA, Wuttke M, Gorski M, Li M, Li Y, Gaziano JM, Wilson PWF, Tsao PS, O'Donnell CJ, Kovesdy CP, Pattaro C, Köttgen A, Susztak K, Edwards TL, Hung AM
(2019) Nat Commun 10: 3842
MeSH Terms: Adult, Aged, Animals, Cell Line, Chromosome Mapping, Cohort Studies, Computational Biology, Female, Genetic Loci, Genetic Predisposition to Disease, Genome-Wide Association Study, Glomerular Filtration Rate, Humans, Kidney, Male, Mice, Middle Aged, Polymorphism, Single Nucleotide, RNA-Seq, Renal Insufficiency, Chronic, Transcriptome, United States, United States Department of Veterans Affairs, Veterans
Show Abstract · Added March 3, 2020
Chronic kidney disease (CKD), defined by low estimated glomerular filtration rate (eGFR), contributes to global morbidity and mortality. Here we conduct a transethnic Genome-Wide Association Study of eGFR in 280,722 participants of the Million Veteran Program (MVP), with replication in 765,289 participants from the Chronic Kidney Disease Genetics (CKDGen) Consortium. We identify 82 previously unreported variants, confirm 54 loci, and report interesting findings including association of the sickle cell allele of betaglobin among non-Hispanic blacks. Our transcriptome-wide association study of kidney function in healthy kidney tissue identifies 36 previously unreported and nine known genes, and maps gene expression to renal cell types. In a Phenome-Wide Association Study in 192,868 MVP participants using a weighted genetic score we detect associations with CKD stages and complications and kidney stones. This investigation reinterprets the genetic architecture of kidney function to identify the gene, tissue, and anatomical context of renal homeostasis and the clinical consequences of dysregulation.
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Cell-free hemoglobin augments acute kidney injury during experimental sepsis.
Shaver CM, Paul MG, Putz ND, Landstreet SR, Kuck JL, Scarfe L, Skrypnyk N, Yang H, Harrison FE, de Caestecker MP, Bastarache JA, Ware LB
(2019) Am J Physiol Renal Physiol 317: F922-F929
MeSH Terms: Acute Kidney Injury, Animals, Cell Line, Cell Survival, Cell-Free System, Cytokines, Female, Glomerular Filtration Rate, Hemoglobins, Hepatitis A Virus Cellular Receptor 1, Kidney Tubules, Lipocalin-2, Male, Mice, Mice, Inbred C57BL, Sepsis, Survival Analysis
Show Abstract · Added May 10, 2020
Acute kidney injury is a common complication of severe sepsis and contributes to high mortality. The molecular mechanisms of acute kidney injury during sepsis are not fully understood. Because hemoproteins, including myoglobin and hemoglobin, are known to mediate kidney injury during rhabdomyolysis, we hypothesized that cell-free hemoglobin (CFH) would exacerbate acute kidney injury during sepsis. Sepsis was induced in mice by intraperitoneal injection of cecal slurry (CS). To mimic elevated levels of CFH observed during human sepsis, mice also received a retroorbital injection of CFH or dextrose control. Four groups of mice were analyzed: sham treated (sham), CFH alone, CS alone, and CS + CFH. The addition of CFH to CS reduced 48-h survival compared with CS alone (67% vs. 97%, = 0.001) and increased the severity of illness. After 24 and 48 h, CS + CFH mice had a reduced glomerular filtration rate from baseline, whereas sham, CFH, and CS mice maintained baseline glomerular filtration rate. Biomarkers of acute kidney injury, neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1), were markedly elevated in CS+CFH compared with CS (8-fold for NGAL and 2.4-fold for KIM-1, < 0.002 for each) after 48 h. Histological examination showed a trend toward increased tubular injury in CS + CFH-exposed kidneys compared with CS-exposed kidneys. However, there were similar levels of renal oxidative injury and apoptosis in the CS + CFH group compared with the CS group. Kidney levels of multiple proinflammatory cytokines were similar between CS and CS + CFH groups. Human renal tubule cells (HK-2) exposed to CFH demonstrated increased cytotoxicity. Together, these results show that CFH exacerbates acute kidney injury in a mouse model of experimental sepsis, potentially through increased renal tubular injury.
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A catalog of genetic loci associated with kidney function from analyses of a million individuals.
Wuttke M, Li Y, Li M, Sieber KB, Feitosa MF, Gorski M, Tin A, Wang L, Chu AY, Hoppmann A, Kirsten H, Giri A, Chai JF, Sveinbjornsson G, Tayo BO, Nutile T, Fuchsberger C, Marten J, Cocca M, Ghasemi S, Xu Y, Horn K, Noce D, van der Most PJ, Sedaghat S, Yu Z, Akiyama M, Afaq S, Ahluwalia TS, Almgren P, Amin N, Ärnlöv J, Bakker SJL, Bansal N, Baptista D, Bergmann S, Biggs ML, Biino G, Boehnke M, Boerwinkle E, Boissel M, Bottinger EP, Boutin TS, Brenner H, Brumat M, Burkhardt R, Butterworth AS, Campana E, Campbell A, Campbell H, Canouil M, Carroll RJ, Catamo E, Chambers JC, Chee ML, Chee ML, Chen X, Cheng CY, Cheng Y, Christensen K, Cifkova R, Ciullo M, Concas MP, Cook JP, Coresh J, Corre T, Sala CF, Cusi D, Danesh J, Daw EW, de Borst MH, De Grandi A, de Mutsert R, de Vries APJ, Degenhardt F, Delgado G, Demirkan A, Di Angelantonio E, Dittrich K, Divers J, Dorajoo R, Eckardt KU, Ehret G, Elliott P, Endlich K, Evans MK, Felix JF, Foo VHX, Franco OH, Franke A, Freedman BI, Freitag-Wolf S, Friedlander Y, Froguel P, Gansevoort RT, Gao H, Gasparini P, Gaziano JM, Giedraitis V, Gieger C, Girotto G, Giulianini F, Gögele M, Gordon SD, Gudbjartsson DF, Gudnason V, Haller T, Hamet P, Harris TB, Hartman CA, Hayward C, Hellwege JN, Heng CK, Hicks AA, Hofer E, Huang W, Hutri-Kähönen N, Hwang SJ, Ikram MA, Indridason OS, Ingelsson E, Ising M, Jaddoe VWV, Jakobsdottir J, Jonas JB, Joshi PK, Josyula NS, Jung B, Kähönen M, Kamatani Y, Kammerer CM, Kanai M, Kastarinen M, Kerr SM, Khor CC, Kiess W, Kleber ME, Koenig W, Kooner JS, Körner A, Kovacs P, Kraja AT, Krajcoviechova A, Kramer H, Krämer BK, Kronenberg F, Kubo M, Kühnel B, Kuokkanen M, Kuusisto J, La Bianca M, Laakso M, Lange LA, Langefeld CD, Lee JJ, Lehne B, Lehtimäki T, Lieb W, Lifelines Cohort Study, Lim SC, Lind L, Lindgren CM, Liu J, Liu J, Loeffler M, Loos RJF, Lucae S, Lukas MA, Lyytikäinen LP, Mägi R, Magnusson PKE, Mahajan A, Martin NG, Martins J, März W, Mascalzoni D, Matsuda K, Meisinger C, Meitinger T, Melander O, Metspalu A, Mikaelsdottir EK, Milaneschi Y, Miliku K, Mishra PP, V. A. Million Veteran Program, Mohlke KL, Mononen N, Montgomery GW, Mook-Kanamori DO, Mychaleckyj JC, Nadkarni GN, Nalls MA, Nauck M, Nikus K, Ning B, Nolte IM, Noordam R, O'Connell J, O'Donoghue ML, Olafsson I, Oldehinkel AJ, Orho-Melander M, Ouwehand WH, Padmanabhan S, Palmer ND, Palsson R, Penninx BWJH, Perls T, Perola M, Pirastu M, Pirastu N, Pistis G, Podgornaia AI, Polasek O, Ponte B, Porteous DJ, Poulain T, Pramstaller PP, Preuss MH, Prins BP, Province MA, Rabelink TJ, Raffield LM, Raitakari OT, Reilly DF, Rettig R, Rheinberger M, Rice KM, Ridker PM, Rivadeneira F, Rizzi F, Roberts DJ, Robino A, Rossing P, Rudan I, Rueedi R, Ruggiero D, Ryan KA, Saba Y, Sabanayagam C, Salomaa V, Salvi E, Saum KU, Schmidt H, Schmidt R, Schöttker B, Schulz CA, Schupf N, Shaffer CM, Shi Y, Smith AV, Smith BH, Soranzo N, Spracklen CN, Strauch K, Stringham HM, Stumvoll M, Svensson PO, Szymczak S, Tai ES, Tajuddin SM, Tan NYQ, Taylor KD, Teren A, Tham YC, Thiery J, Thio CHL, Thomsen H, Thorleifsson G, Toniolo D, Tönjes A, Tremblay J, Tzoulaki I, Uitterlinden AG, Vaccargiu S, van Dam RM, van der Harst P, van Duijn CM, Velez Edward DR, Verweij N, Vogelezang S, Völker U, Vollenweider P, Waeber G, Waldenberger M, Wallentin L, Wang YX, Wang C, Waterworth DM, Bin Wei W, White H, Whitfield JB, Wild SH, Wilson JF, Wojczynski MK, Wong C, Wong TY, Xu L, Yang Q, Yasuda M, Yerges-Armstrong LM, Zhang W, Zonderman AB, Rotter JI, Bochud M, Psaty BM, Vitart V, Wilson JG, Dehghan A, Parsa A, Chasman DI, Ho K, Morris AP, Devuyst O, Akilesh S, Pendergrass SA, Sim X, Böger CA, Okada Y, Edwards TL, Snieder H, Stefansson K, Hung AM, Heid IM, Scholz M, Teumer A, Köttgen A, Pattaro C
(2019) Nat Genet 51: 957-972
MeSH Terms: Chromosome Mapping, European Continental Ancestry Group, Genetic Association Studies, Genetic Predisposition to Disease, Genome-Wide Association Study, Glomerular Filtration Rate, Humans, Inheritance Patterns, Kidney Function Tests, Phenotype, Polymorphism, Single Nucleotide, Quantitative Trait Loci, Quantitative Trait, Heritable, Renal Insufficiency, Chronic, Uromodulin
Show Abstract · Added March 3, 2020
Chronic kidney disease (CKD) is responsible for a public health burden with multi-systemic complications. Through trans-ancestry meta-analysis of genome-wide association studies of estimated glomerular filtration rate (eGFR) and independent replication (n = 1,046,070), we identified 264 associated loci (166 new). Of these, 147 were likely to be relevant for kidney function on the basis of associations with the alternative kidney function marker blood urea nitrogen (n = 416,178). Pathway and enrichment analyses, including mouse models with renal phenotypes, support the kidney as the main target organ. A genetic risk score for lower eGFR was associated with clinically diagnosed CKD in 452,264 independent individuals. Colocalization analyses of associations with eGFR among 783,978 European-ancestry individuals and gene expression across 46 human tissues, including tubulo-interstitial and glomerular kidney compartments, identified 17 genes differentially expressed in kidney. Fine-mapping highlighted missense driver variants in 11 genes and kidney-specific regulatory variants. These results provide a comprehensive priority list of molecular targets for translational research.
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Transdermal Measurement of Glomerular Filtration Rate in Mice.
Scarfe L, Schock-Kusch D, Ressel L, Friedemann J, Shulhevich Y, Murray P, Wilm B, de Caestecker M
(2018) J Vis Exp :
MeSH Terms: Administration, Cutaneous, Animals, Glomerular Filtration Rate, Male, Mice
Show Abstract · Added May 10, 2020
Transdermal analysis of glomerular filtration rate (GFR) is an established technique that is used to assess renal function in mouse and rat models of acute kidney injury and chronic kidney disease. The measurement system consists of a miniaturized fluorescence detector that is directly attached to the skin on the back of conscious, freely moving animals, and measures the excretion kinetics of the exogenous GFR tracer, fluorescein-isothiocyanate (FITC) conjugated sinistrin (an inulin analog). This system has been described in detail in rats. However, because of their smaller size, measurement of transcutaneous GFR in mice presents additional technical challenges. In this paper we therefore provide the first detailed practical guide to the use of transdermal GFR monitors in mice based on the combined experience of three different investigators who have been performing this assay in mice over a number of years.
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Clinical Outcomes for Cystinuria Patients with Unilateral Versus Bilateral Cystine Stone Disease.
Usawachintachit M, Sherer B, Hudnall M, Tzou DT, Taguchi K, Hsi RS, Stoller M, Chi T
(2018) J Endourol 32: 148-153
MeSH Terms: Adult, Aged, Case-Control Studies, Cystine, Cystinuria, Female, Glomerular Filtration Rate, Humans, Kidney, Kidney Calculi, Male, Middle Aged, Retrospective Studies, San Francisco
Show Abstract · Added January 16, 2018
INTRODUCTION - Cystinuria is a genetic disorder marked by elevated urinary cystine excretion and recurrent cystine nephrolithiasis. Interestingly, despite seemingly similar contralateral renal anatomy, a subset of cystinuric patients consistently form stones in only one kidney. The aim of this study is to evaluate clinical outcomes in unilateral vs bilateral cystine stone formers.
PATIENTS AND METHODS - We performed a retrospective case-control study of cystinuric patients evaluated and treated at the University of California, San Francisco between 1994 and 2015 and categorized patients as either unilateral or bilateral stone formers. Clinical presentation, baseline patient demographics, stone procedures, medical therapy regimens, and long-term renal function were compared between the two groups.
RESULTS - A total of 42 cystine stone patients (22 female, 20 male) were included in the analysis. The median age at first presentation was 18.5 years and median age at study conclusion was 45.5 years. Two-thirds of patients (n = 28) had a history of bilateral stones, whereas one-third (n = 14) had unilateral stones. Medical therapy regimens were similar between groups. Despite an increased average number of lifetime surgeries (7.5 sessions for bilateral vs 3.7 sessions for unilateral, p < 0.05), there was no significant difference in medians of the most recent glomerular filtration rate when compared with unilateral stone formers (81.5 vs 95 mL/min, respectively; p = 0.28).
CONCLUSIONS - The majority of cystinuric patients within our cohort form stones bilaterally during their lifetime, and require more surgical interventions than unilateral stone formers. Despite this, overall renal function is well preserved in unilateral and bilateral cystinuric stone formers treated with minimally invasive stone extraction procedures.
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Acute Kidney Injury and Risk of Incident Heart Failure Among US Veterans.
Bansal N, Matheny ME, Greevy RA, Eden SK, Perkins AM, Parr SK, Fly J, Abdel-Kader K, Himmelfarb J, Hung AM, Speroff T, Ikizler TA, Siew ED
(2018) Am J Kidney Dis 71: 236-245
MeSH Terms: Acute Kidney Injury, Aged, Cardiovascular Diseases, Cohort Studies, Creatinine, Disease Progression, Female, Glomerular Filtration Rate, Heart Failure, Hospitalization, Humans, Incidence, Kidney, Male, Middle Aged, Renal Insufficiency, Chronic, Retrospective Studies, Risk Factors, United States, Veterans
Show Abstract · Added November 29, 2018
BACKGROUND - Acute kidney injury (AKI) is common and associated with poor outcomes. Heart failure is a leading cause of cardiovascular disease among patients with chronic kidney disease. The relationship between AKI and heart failure remains unknown and may identify a novel mechanistic link between kidney and cardiovascular disease.
STUDY DESIGN - Observational study.
SETTING & PARTICIPANTS - We studied a national cohort of 300,868 hospitalized US veterans (2004-2011) without a history of heart failure.
PREDICTOR - AKI was the predictor and was defined as a 0.3-mg/dL or 50% increase in serum creatinine concentration from baseline to the peak hospital value. Patients with and without AKI were matched (1:1) on 28 in- and outpatient covariates using optimal Mahalanobis distance matching.
OUTCOMES - Incident heart failure was defined as 1 or more hospitalization or 2 or more outpatient visits with a diagnosis of heart failure within 2 years through 2013.
RESULTS - There were 150,434 matched pairs in the study. Patients with and without AKI during the index hospitalization were well matched, with a median preadmission estimated glomerular filtration rate of 69mL/min/1.73m. The overall incidence rate of heart failure was 27.8 (95% CI, 19.3-39.9) per 1,000 person-years. The incidence rate was higher in those with compared with those without AKI: 30.8 (95% CI, 21.8-43.5) and 24.9 (95% CI, 16.9-36.5) per 1,000 person-years, respectively. In multivariable models, AKI was associated with 23% increased risk for incident heart failure (HR, 1.23; 95% CI, 1.19-1.27).
LIMITATIONS - Study population was primarily men, reflecting patients seen at Veterans Affairs hospitals.
CONCLUSIONS - AKI is an independent risk factor for incident heart failure. Future studies to identify underlying mechanisms and modifiable risk factors are needed.
Copyright © 2017 National Kidney Foundation, Inc. All rights reserved.
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FGF23 Concentration and Genotype Are Novel Predictors of Mortality in African Americans With Type 2 Diabetes.
Chan GC, Divers J, Russell GB, Langefeld CD, Wagenknecht LE, Hsu FC, Xu J, Smith SC, Palmer ND, Hicks PJ, Bowden DW, Register TC, Ma L, Carr JJ, Freedman BI
(2018) Diabetes Care 41: 178-186
MeSH Terms: African Americans, Albuminuria, Apolipoprotein L1, Atherosclerosis, Cohort Studies, Creatinine, Diabetes Mellitus, Type 2, Female, Fibroblast Growth Factors, Follow-Up Studies, Genotyping Techniques, Glomerular Filtration Rate, Glycated Hemoglobin A, Humans, Kidney Function Tests, Male, Middle Aged, Proportional Hazards Models, Risk Factors
Show Abstract · Added January 10, 2020
OBJECTIVE - Cardiovascular and renal complications contribute to higher mortality in patients with diabetes. We assessed novel and conventional predictors of mortality in African American-Diabetes Heart Study (AA-DHS) participants.
RESEARCH DESIGN AND METHODS - Associations between mortality and subclinical atherosclerosis, urine albumin-to-creatinine ratio (UACR), estimated glomerular filtration rate (eGFR), plasma fibroblast growth factor 23 (FGF23) concentration, African ancestry proportion, and apolipoprotein L1 genotypes () were assessed in 513 African Americans with type 2 diabetes; analyses were performed using Cox proportional hazards models.
RESULTS - At baseline, participants were 55.6% female with median (25th, 75th percentile) age 55 years (49.0, 62.0), diabetes duration 8 years (5.0, 13.0), glycosylated hemoglobin 60.7 mmol/mol (48.6, 76.0), eGFR 91.3 mL/min/1.73 m (76.4, 111.3), UACR 12.5 mg/mmol (4.2, 51.2), and coronary artery calcium 28.5 mg Ca (1.0, 348.6); 11.5% had two renal-risk variants. After 6.6-year follow-up (5.8, 7.5), 54 deaths were recorded. Higher levels of coronary artery calcified plaque, carotid artery calcified plaque, albuminuria, and FGF23 were associated with higher mortality after adjustment for age, sex, and African ancestry proportion. A penalized Cox regression that included all covariates and predictors associated with mortality identified male sex (hazard ratio [HR] 4.17 [95% CI 1.96-9.09]), higher FGF23 (HR 2.10 [95% CI 1.59-2.78]), and absence of renal-risk genotypes (HR 0.07 [95% CI 0.01-0.69]) as the strongest predictors of mortality.
CONCLUSIONS - Accounting for conventional risk factors, higher FGF23 concentrations and non-renal-risk genotypes associated with higher mortality in African Americans with diabetes. These data add to growing evidence supporting FGF23 association with mortality; mechanisms whereby these novel predictors impact survival remain to be determined.
© 2017 by the American Diabetes Association.
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Diabetes and CKD in the United States Population, 2009-2014.
Zelnick LR, Weiss NS, Kestenbaum BR, Robinson-Cohen C, Heagerty PJ, Tuttle K, Hall YN, Hirsch IB, de Boer IH
(2017) Clin J Am Soc Nephrol 12: 1984-1990
MeSH Terms: Albuminuria, Creatinine, Cross-Sectional Studies, Diabetes Mellitus, Female, Glomerular Filtration Rate, Humans, Male, Middle Aged, Nutrition Surveys, Prevalence, Renal Insufficiency, Chronic, United States
Show Abstract · Added October 24, 2017
BACKGROUND AND OBJECTIVES - Diabetes is an important cause of CKD. However, among people with diabetes, it is unclear to what extent CKD is attributable to diabetes itself versus comorbid conditions, such as advanced age and hypertension. We examined associations of diabetes with clinical manifestations of CKD independent of age and BP and the extent to which diabetes contributes to the overall prevalence of CKD in the United States.
DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS - We performed a cross-sectional study of 15,675 participants in the National Health and Nutrition Examination Surveys from 2009 to 2014. Diabetes was defined by use of glucose-lowering medications or hemoglobin A ≥6.5%. eGFR was calculated using the CKD Epidemiology Collaboration formula, and albumin-to-creatinine ratio was measured in single-void urine samples. We calculated the prevalence of CKD manifestations by diabetes status as well as prevalence ratios, differences in prevalence, and prevalence attributable to diabetes using binomial and linear regression, incorporating data from repeat eGFR and urine albumin-to-creatinine ratio measurements to estimate persistent disease.
RESULTS - For participants with diabetes (=2279) versus those without diabetes (=13,396), the estimated prevalence of any CKD (eGFR<60 ml/min per 1.73 m; albumin-to-creatinine ratio ≥30 mg/g, or both) was 25% versus 5.3%, respectively; albumin-to-creatinine ratio ≥30 mg/g was 16% versus 3.0%, respectively; albumin-to-creatinine ratio ≥300 mg/g was 4.6% versus 0.3%, respectively; eGFR<60 ml/min per 1.73 m was 12% versus 2.5%, respectively; and eGFR<30 ml/min per 1.73 m was 2.4% versus 0.4%, respectively (each <0.001). Adjusting for demographics and several aspects of BP, prevalence differences were 14.6% (<0.001), 10.8% (<0.001), 4.5% (<0.001), 6.5% (<0.001), and 1.8% (=0.004), respectively. Approximately 24% (95% confidence interval, 19% to 29%) of CKD among all United States adults was attributable to diabetes after adjusting for demographics.
CONCLUSIONS - Diabetes is strongly associated with both albuminuria and reduced GFR independent of demographics and hypertension, contributing substantially to the burden of CKD in the United States.
Copyright © 2017 by the American Society of Nephrology.
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APOL1 nephropathy risk variants do not associate with subclinical atherosclerosis or left ventricular mass in middle-aged black adults.
Gutiérrez OM, Limou S, Lin F, Peralta CA, Kramer HJ, Carr JJ, Bibbins-Domingo K, Winkler CA, Lewis CE, Kopp JB
(2018) Kidney Int 93: 727-732
MeSH Terms: Adult, African Americans, Age of Onset, Apolipoprotein L1, Asymptomatic Diseases, Carotid Artery Diseases, Coronary Artery Disease, Female, Genetic Association Studies, Genetic Predisposition to Disease, Genetic Variation, Glomerular Filtration Rate, Humans, Hypertrophy, Left Ventricular, Incidence, Kidney, Kidney Diseases, Male, Middle Aged, Phenotype, Prevalence, Prospective Studies, Risk Assessment, Risk Factors, United States
Show Abstract · Added January 10, 2020
Prior studies reported associations of APOL1 nephropathy risk variants with subclinical atherosclerosis. However, these findings were limited to older individuals with high comorbidities. To evaluate this in younger individuals, we calculated associations of APOL1 risk variants (high risk [2 risk variants] vs. low risk [0-1 risk variant]) with prevalent, incident, or progressive coronary artery calcification, a carotid intima media thickness over the 90th percentile, and left ventricular hypertrophy in 1315 black participants of the Coronary Artery Risk Development in Young Adults (CARDIA) study. The mean age of this cohort was 44.6 years and their mean estimated glomerular filtration rate was 102.5 ml/min/1.73m. High-risk participants were found to be younger and have a higher prevalence of albuminuria than low-risk participants. In Poisson regression models adjusted for comorbidities and kidney function, the risk of prevalent coronary artery calcification (relative risk [95% confidence interval] 1.12 [0.72,1.71]), the incident coronary artery calcification (1.50 [0.87,2.59]), and the progression of coronary artery calcification (1.40 [0.88,2.23]) did not significantly differ in high vs. low-risk participants. Furthermore, the risk of carotid intima media thickness over the 90th percentile (1.28 [0.78,2.10]) and left ventricular hypertrophy (1.02[0.73,1.43]) did not significantly differ in high vs. low-risk participants in fully-adjusted models. Thus, APOL1 risk variants did not associate with subclinical markers of atherosclerosis or left ventricular hypertrophy in middle-aged black adults with preserved kidney function.
Copyright © 2017 International Society of Nephrology. All rights reserved.
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