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Long-term outcomes in mouse models of ischemia-reperfusion-induced acute kidney injury.
Scarfe L, Menshikh A, Newton E, Zhu Y, Delgado R, Finney C, de Caestecker MP
(2019) Am J Physiol Renal Physiol 317: F1068-F1080
MeSH Terms: Acute Kidney Injury, Animals, Diabetes Mellitus, Experimental, Diabetic Nephropathies, Disease Models, Animal, Female, Fibrosis, Kidney Function Tests, Male, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Inbred DBA, Nephrectomy, Reperfusion Injury, Sex Characteristics, Species Specificity
Show Abstract · Added May 10, 2020
Severe acute kidney injury has a high mortality and is a risk factor for progressive chronic kidney disease. None of the potential therapies that have been identified in preclinical studies have successfully improved clinical outcomes. This failure is partly because animal models rarely reflect the complexity of human disease: most preclinical studies are short term and are commonly performed in healthy, young, male mice. Therapies that are effective in preclinical models that share common clinical features seen in patients with acute kidney injury, including genetic diversity, different sexes, and comorbidities, and evaluate long-term outcomes are more likely to predict success in the clinic. Here, we evaluated susceptibility to chronic kidney disease after ischemia-reperfusion injury with delayed nephrectomy by monitoring long-term functional and histological responses to injury. We defined conditions required to induce long-term postinjury renal dysfunction and fibrosis without increased mortality in a reproducible way and evaluate effect of mouse strains, sexes, and preexisting diabetes on these responses.
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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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Malformations in the Murine Kidney Caused by Loss of CENP-F Function.
Haley CO, Waters AM, Bader DM
(2019) Anat Rec (Hoboken) 302: 163-170
MeSH Terms: Acute Kidney Injury, Animals, Centromere, Chromosomal Proteins, Non-Histone, Hydronephrosis, Kidney, Kidney Function Tests, Mice, Mice, Knockout, Microfilament Proteins, Tumor Suppressor Proteins
Show Abstract · Added January 8, 2019
Centromere-binding protein F (CENP-F) is a large and complex protein shown to play critical roles in mitosis and various other interphase functions. Previous studies have shown that the disruption of CENP-F function leads to detrimental effects on human development. Still, it is important to note the lack of studies focusing on the effects that the loss of this essential protein may have on specific adult organs. In the current study, we used a novel global knockout murine model to analyze the potential consequences deletion of CENP-F has on adult kidney structure and function. We discovered several structural abnormalities including loss of ciliary structure, tubule dilation, and disruption of the glomerulus. Along with these structural irregularities, renal dysfunction was also detected suggesting hydronephrosis and acute kidney injury in these knockout organs. Importantly, this is the first study linking CENP-F to kidney disease and hopefully these data will serve as a platform to further investigate the molecular mechanisms disrupted in the kidney by the loss of CENP-F. Anat Rec, 302:163-170, 2019. © 2018 Wiley Periodicals, Inc.
© 2018 Wiley Periodicals, Inc.
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Large-scale whole-exome sequencing association studies identify rare functional variants influencing serum urate levels.
Tin A, Li Y, Brody JA, Nutile T, Chu AY, Huffman JE, Yang Q, Chen MH, Robinson-Cohen C, Macé A, Liu J, Demirkan A, Sorice R, Sedaghat S, Swen M, Yu B, Ghasemi S, Teumer A, Vollenweider P, Ciullo M, Li M, Uitterlinden AG, Kraaij R, Amin N, van Rooij J, Kutalik Z, Dehghan A, McKnight B, van Duijn CM, Morrison A, Psaty BM, Boerwinkle E, Fox CS, Woodward OM, Köttgen A
(2018) Nat Commun 9: 4228
MeSH Terms: Exome, Genetic Predisposition to Disease, Glucose Transport Proteins, Facilitative, Humans, Kidney Function Tests, Meta-Analysis as Topic, Organic Anion Transporters, Organic Cation Transport Proteins, Protein Structure, Secondary, Uric Acid
Show Abstract · Added January 3, 2019
Elevated serum urate levels can cause gout, an excruciating disease with suboptimal treatment. Previous GWAS identified common variants with modest effects on serum urate. Here we report large-scale whole-exome sequencing association studies of serum urate and kidney function among ≤19,517 European ancestry and African-American individuals. We identify aggregate associations of low-frequency damaging variants in the urate transporters SLC22A12 (URAT1; p = 1.3 × 10) and SLC2A9 (p = 4.5 × 10). Gout risk in rare SLC22A12 variant carriers is halved (OR = 0.5, p = 4.9 × 10). Selected rare variants in SLC22A12 are validated in transport studies, confirming three as loss-of-function (R325W, R405C, and T467M) and illustrating the therapeutic potential of the new URAT1-blocker lesinurad. In SLC2A9, mapping of rare variants of large effects onto the predicted protein structure reveals new residues that may affect urate binding. These findings provide new insights into the genetic architecture of serum urate, and highlight molecular targets in SLC22A12 and SLC2A9 for lowering serum urate and preventing gout.
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Risk of Hypoglycemia Following Hospital Discharge in Patients With Diabetes and Acute Kidney Injury.
Hung AM, Siew ED, Wilson OD, Perkins AM, Greevy RA, Horner J, Abdel-Kader K, Parr SK, Roumie CL, Griffin MR, Ikizler TA, Speroff T, Matheny ME
(2018) Diabetes Care 41: 503-512
MeSH Terms: Acute Kidney Injury, Adult, Aged, Blood Glucose, Diabetes Mellitus, Diabetic Nephropathies, Female, Glipizide, Glyburide, Humans, Hypoglycemia, Kidney Function Tests, Male, Middle Aged, Patient Discharge, Retrospective Studies, Risk Factors
Show Abstract · Added November 29, 2018
OBJECTIVE - Hypoglycemia is common in patients with diabetes. The risk of hypoglycemia after acute kidney injury (AKI) is not well defined. The purpose of this study was to compare the risk for postdischarge hypoglycemia among hospitalized patients with diabetes who do and do not experience AKI.
RESEARCH DESIGN AND METHODS - We performed a propensity-matched analysis of patients with diabetes, with and without AKI, using a retrospective national cohort of veterans hospitalized between 2004 and 2012. AKI was defined as a 0.3 mg/dL or 50% increase in serum creatinine from baseline to peak serum creatinine during hospitalization. Hypoglycemia was defined as hospital admission or an emergency department visit for hypoglycemia or as an outpatient blood glucose <60 mg/dL. Time to incident hypoglycemia within 90 days postdischarge was examined using Cox proportional hazards models. Prespecified subgroup analyses by renal recovery, baseline chronic kidney disease, preadmission drug regimen, and HbA were performed.
RESULTS - We identified 65,151 propensity score-matched pairs with and without AKI. The incidence of hypoglycemia was 29.6 (95% CI 28.9-30.4) and 23.5 (95% CI 22.9-24.2) per 100 person-years for patients with and without AKI, respectively. After adjustment, AKI was associated with a 27% increased risk of hypoglycemia (hazard ratio [HR] 1.27 [95% CI 1.22-1.33]). For patients with full recovery, the HR was 1.18 (95% CI 1.12-1.25); for partial recovery, the HR was 1.30 (95% CI 1.23-1.37); and for no recovery, the HR was 1.48 (95% CI 1.36-1.60) compared with patients without AKI. Across all antidiabetes drug regimens, patients with AKI experienced hypoglycemia more frequently than patients without AKI, though the incidence of hypoglycemia was highest among insulin users, followed by glyburide and glipizide users, respectively.
CONCLUSIONS - AKI is a risk factor for hypoglycemia in the postdischarge period. Studies to identify risk-reduction strategies in this population are warranted.
© 2018 by the American Diabetes Association.
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High-Density Lipoprotein Cholesterol Concentration and Acute Kidney Injury After Cardiac Surgery.
Smith LE, Smith DK, Blume JD, Linton MF, Billings FT
(2017) J Am Heart Assoc 6:
MeSH Terms: Acute Kidney Injury, Aged, Aged, 80 and over, Atorvastatin, Cardiac Surgical Procedures, Cholesterol, HDL, Coronary Artery Disease, Dose-Response Relationship, Drug, Double-Blind Method, Female, Follow-Up Studies, Humans, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Kidney Function Tests, Male, Middle Aged, Postoperative Complications, Postoperative Period, Preoperative Period, Risk Factors, Treatment Outcome
Show Abstract · Added April 10, 2018
BACKGROUND - Acute kidney injury (AKI) after cardiac surgery is associated with increased short- and long-term mortality. Inflammation, oxidative stress, and endothelial dysfunction and damage play important roles in the development of AKI. High-density lipoproteins (HDLs) have anti-inflammatory and antioxidant properties and improve endothelial function and repair. Statins enhance HDL's anti-inflammatory and antioxidant capacities. We hypothesized that a higher preoperative HDL cholesterol concentration is associated with decreased AKI after cardiac surgery and that perioperative statin exposure potentiates this association.
METHODS AND RESULTS - We tested our hypothesis in 391 subjects from a randomized clinical trial of perioperative atorvastatin to reduce AKI after cardiac surgery. A 2-component latent variable mixture model was used to assess the association between preoperative HDL cholesterol concentration and postoperative change in serum creatinine, adjusted for known AKI risk factors and suspected confounders. Interaction terms were used to examine the effects of preoperative statin use, preoperative statin dose, and perioperative atorvastatin treatment on the association between preoperative HDL and AKI. A higher preoperative HDL cholesterol concentration was independently associated with a decreased postoperative serum creatinine change (=0.02). The association between a high HDL concentration and an attenuated increase in serum creatinine was strongest in long-term statin-using patients (=0.008) and was further enhanced with perioperative atorvastatin treatment (=0.004) and increasing long-term statin dose (=0.003).
CONCLUSIONS - A higher preoperative HDL cholesterol concentration was associated with decreased AKI after cardiac surgery. Preoperative and perioperative statin treatment enhanced this association, demonstrating that pharmacological potentiation is possible during the perioperative period.
CLINICAL TRIAL REGISTRATION - URL: http://www.clinicaltrials.gov. Unique Identifier: NCT00791648.
© 2017 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.
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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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Risk Factors for Rapid Kidney Function Decline Among African Americans: The Jackson Heart Study (JHS).
Young BA, Katz R, Boulware LE, Kestenbaum B, de Boer IH, Wang W, Fülöp T, Bansal N, Robinson-Cohen C, Griswold M, Powe NR, Himmelfarb J, Correa A
(2016) Am J Kidney Dis 68: 229-239
MeSH Terms: African Americans, Female, Humans, Kidney, Kidney Function Tests, Male, Middle Aged, Prospective Studies, Renal Insufficiency, Risk Factors, Time Factors
Show Abstract · Added September 19, 2017
BACKGROUND - Racial differences in rapid kidney function decline exist, but less is known regarding factors associated with rapid decline among African Americans. Greater understanding of potentially modifiable risk factors for early kidney function loss may help reduce the burden of kidney failure in this high-risk population.
STUDY DESIGN - Prospective cohort study.
SETTING & PARTICIPANTS - 3,653 African American participants enrolled in the Jackson Heart Study (JHS) with kidney function data from 2 of 3 examinations (2000-2004 and 2009-2013). Estimated glomerular filtration rate (eGFR) was calculated from serum creatinine using the CKD-EPI creatinine equation.
PREDICTORS - Demographics, socioeconomic status, lifestyle, and clinical risk factors for kidney failure.
OUTCOMES - Rapid decline was defined as a ≥30% decline in eGFR during follow-up. We quantified the association of risk factors with rapid decline in multivariable models.
MEASUREMENTS - Clinical (systolic blood pressure and albuminuria [albumin-creatinine ratio]) and modifiable risk factors.
RESULTS - Mean age was 54±12 (SD) years, 37% were men, average body mass index was 31.8±7.1kg/m(2), 19% had diabetes mellitus (DM), and mean eGFR was 96.0±20mL/min/1.73m(2) with an annual rate of decline of 1.27mL/min/1.73m(2). Those with rapid decline (11.5%) were older, were more likely to be of low/middle income, and had higher systolic blood pressures and greater DM than those with nonrapid decline. Factors associated with ≥30% decline were older age (adjusted OR per 10 years older, 1.51; 95% CI, 1.34-1.71), cardiovascular disease (adjusted OR, 1.53; 95% CI, 1.12-2.10), higher systolic blood pressure (adjusted OR per 17mmHg greater, 1.22; 95% CI, 1.06-1.41), DM (adjusted OR, 2.63; 95% CI, 2.02-3.41), smoking (adjusted OR, 1.60; 95% CI, 1.10-2.31), and albumin-creatinine ratio > 30mg/g (adjusted OR, 1.55; 95% CI, 1.08-1.21). Conversely, results did not support associations of waist circumference, C-reactive protein level, and physical activity with rapid decline.
LIMITATIONS - No midstudy creatinine measurement at examination 2 (2005-2008).
CONCLUSIONS - Rapid decline heterogeneity exists among African Americans in JHS. Interventions targeting potentially modifiable factors may help reduce the incidence of kidney failure.
Published by Elsevier Inc.
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Plasma FGF23 and Calcified Atherosclerotic Plaque in African Americans with Type 2 Diabetes Mellitus.
Freedman BI, Divers J, Russell GB, Palmer ND, Bowden DW, Carr JJ, Wagenknecht LE, Hightower RC, Xu J, Smith SC, Langefeld CD, Hruska KA, Register TC
(2015) Am J Nephrol 42: 391-401
MeSH Terms: Adult, African Americans, Aged, Albuminuria, Blood Pressure, Bone Density, Carotid Arteries, Coronary Vessels, Cross-Sectional Studies, Diabetes Mellitus, Type 2, Female, Fibroblast Growth Factors, Follow-Up Studies, Glomerular Filtration Rate, Glycated Hemoglobin A, Humans, Iliac Artery, Kidney Function Tests, Male, Middle Aged, Phosphates, Plaque, Atherosclerotic, Renin-Angiotensin System, Risk Factors, Tomography, X-Ray Computed, Vitamin D
Show Abstract · Added September 29, 2016
BACKGROUND - Fibroblast growth factor 23 (FGF23) is a phosphaturic hormone implicated in disorders of serum phosphorus concentration and vitamin D. The role of FGF23 in vascular calcification remains controversial.
METHODS - Relationships between FGF23 and coronary artery calcified atherosclerotic plaque (CAC), aortoiliac calcified plaque (CP), carotid artery CP, volumetric bone mineral density (vBMD), albuminuria, and estimated glomerular filtration rate (eGFR) were determined in 545 African Americans with type 2 diabetes (T2D) and preserved kidney function in African American-Diabetes Heart Study participants. Generalized linear models were fitted to test associations between FGF23 and cardiovascular, bone, and renal phenotypes, and change in measurements over time, adjusting for age, gender, African ancestry proportion, body mass index, diabetes duration, hemoglobin A1c, blood pressure, renin-angiotensin-system inhibitors, statins, calcium supplements, serum calcium, and serum phosphate.
RESULTS - The sample was 56.7% female with a mean (SD) age of 55.6 (9.6) years, diabetes duration of 10.3 (8.2) years, eGFR 90.9 (22.1) ml/min/1.73 m2, urine albumin:creatinine ratio (UACR) 151 (588) (median 13) mg/g, plasma FGF23 161 (157) RU/ml, and CAC 637 (1,179) mg. In fully adjusted models, FGF23 was negatively associated with eGFR (p < 0.0001) and positively associated with UACR (p < 0.0001) and CAC (p = 0.0006), but not with carotid CP or aortic CP. Baseline FGF23 concentration did not associate with changes in vBMD or CAC after a mean of 5.1 years follow-up.
CONCLUSIONS - Plasma FGF23 concentrations were independently associated with subclinical coronary artery disease, albuminuria, and kidney function in the understudied African American population with T2D. Findings support relationships between FGF23 and vascular calcification, but not between FGF23 and bone mineral density, in African Americans lacking advanced nephropathy.
© 2016 S. Karger AG, Basel.
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Acute Kidney Injury Incidence in Noncritically Ill Hospitalized Children, Adolescents, and Young Adults: A Retrospective Observational Study.
McGregor TL, Jones DP, Wang L, Danciu I, Bridges BC, Fleming GM, Shirey-Rice J, Chen L, Byrne DW, Van Driest SL
(2016) Am J Kidney Dis 67: 384-90
MeSH Terms: Acute Kidney Injury, Adolescent, Child, Child, Preschool, Cohort Studies, Creatinine, Female, Hospital Mortality, Humans, Incidence, Infant, Inpatients, Kidney Function Tests, Length of Stay, Male, Retrospective Studies, Risk Factors, Severity of Illness Index, Tertiary Care Centers, Time Factors, United States, Young Adult
Show Abstract · Added April 11, 2017
BACKGROUND - Acute kidney injury (AKI) has been characterized in high-risk pediatric hospital inpatients, in whom AKI is frequent and associated with increased mortality, morbidity, and length of stay. The incidence of AKI among patients not requiring intensive care is unknown.
STUDY DESIGN - Retrospective cohort study.
SETTING & PARTICIPANTS - 13,914 noncritical admissions during 2011 and 2012 at our tertiary referral pediatric hospital were evaluated. Patients younger than 28 days or older than 21 years of age or with chronic kidney disease (CKD) were excluded. Admissions with 2 or more serum creatinine measurements were evaluated.
FACTORS - Demographic features, laboratory measurements, medication exposures, and length of stay.
OUTCOME - AKI defined as increased serum creatinine level in accordance with KDIGO (Kidney Disease: Improving Global Outcomes) criteria. Based on time of admission, time interval requirements were met in 97% of cases, but KDIGO time window criteria were not strictly enforced to allow implementation using clinically obtained data.
RESULTS - 2 or more creatinine measurements (one baseline before or during admission and a second during admission) in 2,374 of 13,914 (17%) patients allowed for AKI evaluation. A serum creatinine difference ≥0.3mg/dL or ≥1.5 times baseline was seen in 722 of 2,374 (30%) patients. A minimum of 5% of all noncritical inpatients without CKD in pediatric wards have an episode of AKI during routine hospital admission.
LIMITATIONS - Urine output, glomerular filtration rate, and time interval criteria for AKI were not applied secondary to study design and available data. The evaluated cohort was restricted to patients with 2 or more clinically obtained serum creatinine measurements, and baseline creatinine level may have been measured after the AKI episode.
CONCLUSIONS - AKI occurs in at least 5% of all noncritically ill hospitalized children, adolescents, and young adults without known CKD. Physicians should increase their awareness of AKI and improve surveillance strategies with serum creatinine measurements in this population so that exacerbating factors such as nephrotoxic medication exposures may be modified as indicated.
Copyright © 2016 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.
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