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Little is known regarding chronic kidney disease (CKD) in Hispanics. We compared baseline characteristics of Hispanic participants in the Chronic Renal Insufficiency Cohort (CRIC) and Hispanic-CRIC (H-CRIC) Studies with non-Hispanic CRIC participants.
Participants were aged 21–74 years with CKD using age-based glomerular filtration rate (eGFR) at enrollment into the CRIC/H-CRIC Studies. H-CRIC included Hispanics recruited at the University of Illinois from 2005–2008 while CRIC included Hispanics and non-Hispanics recruited at seven clinical centers from 2003–2007.
Blood pressure, angiotensin-converting enzyme (ACE) inhibitor/angiotensin receptor blocker (ARB) use, CKD-associated complications
Demographic characteristics, laboratory data, blood pressure, and medications were assessed using standard techniques and protocols
Among H-CRIC/ CRIC participants, 497 were Hispanic, 1650 non-Hispanic Black, and 1638 non-Hispanic White. Low income and educational attainment were nearly twice as prevalent in Hispanics compared with non-Hispanics (p<0.01). Hispanics had self-reported diabetes (67%) more frequently than non-Hispanic Blacks (51%) and Whites (40%) (p<0.01). Blood pressure > 130/80 mmHg was more common in Hispanics (62%) compared with Blacks (57%) and Whites (35%) (p<0.05), and abnormalities in hematologic, metabolic, and bone metabolism parameters were more prevalent in Hispanics (p<0.05), even after stratifying by entry eGFR. Hispanics had the lowest receipt of ACE inhibitor/ARB among high-risk subgroups, including participants with diabetes, proteinuria, and blood pressure > 130/80 mmHg. Mean eGFR (ml/min/m2) was lower in Hispanics (39.6) than in Blacks (43.7) and Whites (46.2), while median proteinuria was higher in Hispanics (0.72 g/d) than in Blacks (0.24 g/d) and Whites (0.12 g/d) (p<0.01).
Generalizability; observed associations limited by residual bias and confounding
Hispanics with CKD in CRIC/H-CRIC Studies are disproportionately burdened with lower socioeconomic status, more frequent diabetes mellitus, less ACE inhibitor/ARB use, worse blood pressure control, and more severe CKD and associated complications than their non-Hispanic counterparts.
Hispanics are now the largest minority group in the United States (U.S.) (1). Of interest, there has also been a particularly rapid concomitant increase in the incidence and prevalence of end-stage renal disease (ESRD) in Hispanics observed in the United States over the last two decades (2). Compared with non-Hispanic Whites, the incidence of ESRD in Hispanics is nearly two fold higher (2). Because of the high frequency of risk factors for ESRD among U.S. Hispanics (e.g., diabetes mellitus), it is anticipated that Hispanic ESRD population will continue to undergo substantial growth (3–4).
Despite the magnitude of this public health problem, little is known regarding earlier stages of chronic kidney disease (CKD) in Hispanics (5). A few prior reports have noted that although the prevalence of eGFR < 60 ml/min/1.73m2 is similar among Hispanics and non-Hispanics, Hispanic ethnicity is associated with higher levels of microalbuminuria and proteinuria, and almost a two-fold higher risk of ESRD in comparison with non-Hispanic Whites and Blacks (6–10). Hispanics have not been well represented in most large prospective studies and clinical trials of CKD; therefore, our understanding of the risk factors, complications, and outcomes associated with CKD among Hispanics is limited (11–15). One exception was a post-hoc analysis of the RENAAL (Reduction in End Points in Non-Insulin-Dependent Diabetes With the Angiotensin II Antagonist Losartan) trial, which focused on the role of ethnicity and found that while baseline proteinuria and the risk of ESRD were higher in Hispanics compared with non-Hispanic Whites and Blacks, all ethnic groups achieved renoprotection from losartan after baseline differences in albuminuria where taken into account (16).
The Hispanic Chronic Renal Insufficiency Cohort (H-CRIC) Study, an ancillary study to the multi-center National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)-sponsored Chronic Renal Insufficiency Cohort (CRIC) Study, is the first prospective longitudinal study examining risk factors for the progression of CKD and cardiovascular disease in a sizable cohort of U.S. Hispanics with a broad range of kidney dysfunction (17–18). The H-CRIC Study was initiated because of less-than-anticipated recruitment of Hispanics in the CRIC Study, and it was conducted at the University of Illinois at Chicago because of disproportionately successful Hispanic recruitment into the CRIC Study at this clinical site (18). In this article, we compare baseline characteristics among Hispanic and non-Hispanic participants in the CRIC and H-CRIC studies, especially as they pertain to risk factors, complications, and management of CKD.
We conducted a cross-sectional comparative analysis of Hispanic and non-Hispanic participants at enrollment into the Chronic Renal Insufficiency Cohort (CRIC) and Hispanic-CRIC (H-CRIC) Studies. The CRIC study is a prospective multicenter cohort study of adult individuals with chronic kidney disease (CKD). Details of the design and methods of the CRIC study have been previously published (17–18). Major eligibility criteria for the CRIC study included adults aged 21 to 74 years with mild to moderate CKD using age-based estimated glomerular filtration rate (eGFR). Exclusion criteria included inability to consent, New York Heart Association Class III or IV heart failure, cirrhosis, HIV/AIDS, polycystic kidney disease, prior dialysis or transplant, immunosuppressive therapy within 6 months, or chemotherapy for cancer within 2 years. The H-CRIC Study adopted identical eligibility and exclusion criteria as the parent CRIC Study. However, while CRIC included 169 Hispanics and 3289 non-Hispanics recruited at seven clinical centers from May 2003 through March 2007, H-CRIC included 327 Hispanics recruited at the University of Illinois at Chicago and Chicago metropolitan area from October 2005 through June 2008. Recruitment sites included university-, community-, and private-based health clinics. Both studies were approved by the Institutional Review Boards of the participating centers and the research was conducted in accordance with the principles of the Declaration of Helsinki. All study participants provided written informed consent.
H-CRIC Study participants underwent the same evaluation and test strategy as CRIC Study participants, which have been fully described previously (17–18), as well as additional evaluations (only for H-CRIC participants) focusing on primary language (19). Sociodemographic characteristics (e.g., age, gender, race/ethnicity, education, annual household income, smoking, health insurance) were self-reported and recorded at the baseline visit. Medical conditions (e.g., hypertension, high cholesterol, chronic heart failure, peripheral arterial disease, diabetes, myocardial infarction or coronary revascularization) were also self-reported at baseline. Anthropometric measures (height, weight, body mass index, waist circumference) were measured by trained study personnel and recorded. Current medications were reviewed and documented. As previously noted, blood pressure measurements and ankle brachial indices were obtained using standard and validated protocols (17–18). For each participant at baseline, the urine creatinine and protein was determined from a 24 hour urine collection and an eGFR was calculated by the CKD-EPI estimating equation, using a locally measured serum creatinine calibrated to the Roche Enzymatic Method (20). GFR was assessed by the renal clearance of 125-iodine iothalamate (measured GFR [mGFR]) in a select subcohort (17–18).
Baseline participant characteristics were summarized using means with standard deviations, or medians (25th–75th percentile) for continuous variables; and frequency distribution with percentages for categorical variables. Missing values occurred very infrequently and generally under the following circumstances: i) when a participant failed to answer a question on a reporting form, ii) when a physical measure was not obtained, iii) when a laboratory test was not performed. The only variables with > 3% missing values were: primary language spoken (17%) [percentage missing in Hispanics since language only assessed in this group], health insurance (12%), and urine studies (6%). Analyses for each variable included only the observed values. Baseline participant characteristics were compared between groups using t-tests, chi-squared tests, or analysis of variance, as appropriate. Two-sided p-values less than 0.05 were considered statistically significant. All statistical analyses were conducted using SAS, version 9.1 (Cary, NC).
Among a total of 497 H-CRIC and CRIC Hispanic participants, 69% were Mexican American, 16% were Puerto Rican, and 25% had other Latin American ancestry (Table 1). The proportion of participants with low annual household income (<$20,000/year), low educational attainment (< high school diploma), and lack of health insurance was significantly higher among Mexican Americans than among Puerto Rican Americans and other Latin Americans (p<0.02). Mexican Americans more often spoke primarily Spanish (76%) relative to other Hispanic groups (≈43%) (p<0.001). Compared with other Hispanic subgroups, the prevalence of diabetes and blood pressure > 130/80 mmHg was more frequent in Mexican Americans. Mean eGFR was significantly lower in Mexican Americans (37.4 ml/min/1.73m2) compared with Puerto Rican Americans (43.3 ml/min/1.73m2) and other Latin Americans (45.6 ml/min/1.73m2) (p<0.001), and mGFR results on select participants were consistent with these findings. Median 24 hour urine protein and spot urine albumin-creatinine ratios were substantially higher in Mexican Americans compared to Puerto Rican Americans and other Latin Americans, and these trends persisted in both diabetic and non-diabetic subgroups. Compared with other Hispanic subgroups, Mexican Americans had significantly lower serum hemoglobin and calcium and higher serum phosphorus and total parathyroid hormone values (p<0.05).
Mean age was approximately 2 years lower in the 497 Hispanic H-CRIC/CRIC participants than in the 1638 Non-Hispanic White and 1650 Non-Hispanic Black CRIC participants (Table 2). Compared with non-Hispanic Whites and Blacks, Hispanics more often had low annual household income, low educational attainment, lack of health insurance, and less current and former tobacco use (p<0.05). The prevalence of diabetes was highest among Hispanics (67%), while the self-reported history of myocardial infarction/prior revascularization was least prevalent among Hispanics (18%). The prevalence of self-reported hypertension for Hispanics (89%) was between that for non-Hispanic Whites (79%) and Blacks (93%), while blood pressure > 130/80 mmHg at cohort entry was more common among Hispanics (62%) than among non-Hispanic Whites (35%) and non-Hispanic Blacks (57%) (p<0.05). Mean glycosylated hemoglobin in Hispanics (7.0%) was significantly higher than in non-Hispanic Whites (6.3%) (p<0.05) and similar to non-Hispanic Blacks (6.9%) (p>0.05). Mean eGFR was significantly lower in Hispanics (39.6 ml/min/1.73m2) compared with non-Hispanic Whites (46.2 ml/min/1.73m2) and Blacks (43.7 ml/min/1.73m2) (p<0.001), and mGFR results on select participants were consistent with these findings. Median 24 hour urine protein and spot urine albumin-creatinine ratios were substantially higher in Hispanics compared to Non-Hispanic Whites and Blacks, and these trends persisted in both diabetic and non-diabetic subgroups (p<0.001). Lipoprotein levels, hemoglobin concentration, and bone metabolism parameters were less favorable in Hispanics compared with non-Hispanic Whites and similar to those in non-Hispanic Blacks.
Overall, use of angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) medications was not significantly different among H-CRIC/CRIC participants (Table 3). However, among important subgroups, including those with blood pressure > 130/80 mmHg, diabetes, or urine protein > 0.3 g/d, Hispanics consistently had the lowest receipt of ACE inhibitor/ARB compared with Non-Hispanic Whites and Blacks (p<0.05)
Across all eGFR categories and albuminuria strata, the proportion of participants with blood pressure > 130/80 mmHg was significantly higher for Hispanics compared with non-Hispanic White participants (p<0.05) (Table 4). However, only in the eGFR < 30 ml/min/m2 strata was the percentage of Hispanics with blood pressure > 130/80 mmHg significantly higher than that of non-Hispanic Blacks (p<0.05), whereas this percentage was not significantly different between these two groups for all other eGFR strata. No significant differences were found between proportions of Hispanic and non-Hispanic Blacks with blood pressure > 130/80 mmHg across strata of albuminuria.
Across all eGFR categories and albuminuria strata, Hispanic participants had significantly lower serum sodium and bicarbonate levels compared with non-Hispanic Whites and Blacks (p<0.05), while less pronounced differences existed for serum potassium levels among these groups (Table 5). There were no significant differences in hemoglobin levels between Hispanics and non-Hispanic Blacks, but levels were significantly lower in Hispanics compared with non-Hispanic Whites across eGFR and albuminuria (p<0.05). Calcium levels were lower and serum phosphorus levels higher in Hispanics versus non-Hispanics with eGFR < 45 ml/min/1.73m2 or albumin-creatinine ratio > = 30 (mg/g) (p<0.05). Total intact parathyroid hormone (PTH) levels for Hispanics were generally significantly higher than non-Hispanic Whites but lower than those in non-Hispanic Blacks across eGFR and albuminuria levels. Serum albumin was consistently the lowest in Hispanics compared with non-Hispanics, regardless of eGFR or albuminuria group.
We found that among participants with CKD in the CRIC and H-CRIC Studies, Hispanics were disproportionately burdened with lower socioeconomic status, more frequent diabetes mellitus, worse blood pressure control, lower receipt of ACE inhibitor/ARB medications, and more severe CKD compared with non-Hispanic Whites and Blacks. In particular, in the setting of CKD, Mexican Americans had especially unfavorable sociodemographic and clinical parameters relative to Puerto Rican Americans and other Latin Americans. Even when level of eGFR was taken into account, Hispanics with CKD more often had uncontrolled blood pressure, lower serum hemoglobin levels, and worse metabolic and bone metabolism parameters than non-Hispanic Whites and Blacks.
In contrast to prior reports and studies that focused chiefly on populations with ESRD (2–4), this work is one of the few systematic evaluations of CKD in Hispanics, who constitute a growing high-risk population well-known to be affected by health disparities (21–27). The CRIC and H-CRIC studies were designed to examine prospectively risk factors for CKD progression and CVD incidence and progression among a large diverse representative cohort of individuals with CKD (17–18). By capturing a wide array of data on a broad range of demographic factors and clinical exposures, the H-CRIC and CRIC studies will further elucidate the reasons for health disparities in Hispanics with CKD and will inform clinical trials of therapeutic interventions that may potential lead to improvements in clinical outcomes (28).
A few prior studies examined differences in the burden of CKD among Hispanics and non-Hispanics. Although analyses from NHANES have found the prevalence of eGFR < 60 ml/min/m2 to be similar among Mexican Americans and non-Hispanic Whites, they have generally noted a higher prevalence of micro- and macroalbuminuria (6, 9–10). In a large cohort of adults with stage 3–4 CKD from Kaiser Permanente of Northern California, higher levels of proteinuria were also observed among Hispanics compared with non-Hispanic Whites, which is consistent with our observations in the H-CRIC/CRIC Studies (7). Less is known about complications of CKD. Similar to our findings, a recent analysis from NHANES found that several metabolic abnormalities, including those involving hemoglobin, phosphorus, potassium, and bicarbonate, were more common in Hispanic than White adults with an eGFR < 60 ml/min/m2 (29). Differences in socioeconomic status may explain some of these observed differences. For example, two recent studies found that low socioeconomic status was strongly associated with higher serum phosphorus in adults with CKD regardless of race/ethnicity (30–31). The impact of these complications on health outcomes will be assessed in future longitudinal analyses.
Optimal control of blood pressure and use of renoprotective medications was also found to be inferior in Hispanics compared with non-Hispanic Whites in H-CRIC/CRIC, despite evidence supporting these measures to attenuate CKD progression (16). Similar patterns of greater uncontrolled blood pressure in Hispanics with and without CKD have also been observed in samples from NHANES (29, 32) and MESA (the Multi-Ethnic Study of Atherosclerosis) (33), which appear in part due to socioeconomic differences. Only one prior study has examined the relationship between race/ethnicity and ACE inhibitor/ARB use among individuals at high risk for progressive CKD. Among near 40,000 diabetic adults in the Kaiser Permanente of Northern California Diabetes Registry, 59% of Latinos received an ACE inhibitor/ARB, including 54% with albuminuria, and this proportion was not significantly different from that observed among Whites (34). Although we observed a similar proportion of Hispanics receiving ACE inhibitor/ARB in H-CRIC/CRIC overall, we found that Hispanics had a significantly lower receipt of these medications in high risk groups (e.g., diabetes, proteinuria, and blood pressure > 130/80 mmHg) compared with non-Hispanic Whites and Blacks. In addition to local clinical practice patterns, the lower prevalence of health insurance among Hispanics in H-CRIC/CRIC likely contributes to these observed differences. Although not specifically evaluated in regard to categories of race and ethnicity, lack of health insurance has been associated with decreased access to regular care, worse control of hypertension, and lesser receipt of ACE inhibitor/ARB among adults with diabetes and CKD (35–36). Because of its robust data collection, future H-CRIC/ CRIC analyses will delineate the relationships between race/ethnicity, socioeconomic status (e.g., income, health insurance, access to healthcare), risk factors for CKD, and CKD progression.
There is notable heterogeneity among Hispanics in the U.S. with regard to race, country of origin, language, health beliefs, and social customs (37). The H-CRIC and CRIC Studies also afford an initial examination of differences among subgroups of Hispanics with CKD, finding that Mexican Americans had more severe CKD (i.e., lower eGFR, higher proteinuria), a disproportionate burden of unfavorable CKD risk factors, and a higher prevalence of CKD-related metabolic complications compared with Puerto Rican Americans and other Latin Americans. Only a few prior studies have investigated differences in CKD parameters and outcomes among Hispanic subgroups. In a prospective observational study of nearly 5,000 Hispanics receiving long-term dialysis, Mexican Americans were found to have significantly lower mortality than their Puerto Rican Americans counterparts over two years (38). An analysis of NHANES data revealed that Cuban Americans were more likely to have an estimated creatinine clearance < 60 ml/min/1.73m2 compared with Mexican Americans or Puerto Ricans (39). Recently, findings from the MESA demonstrated the while Puerto Ricans had levels of albuminuria similar to non-Hispanic Whites, Mexicans and Dominicans had much higher albuminuria than Whites, which appeared to be related to the heterogeneity in genetic admixture between European, African, and Native American ancestry among these groups (40). Further analyses are needed to better understand the diversity among Hispanic subgroups in the United States and to delineate the clinical implications of these baseline findings.
The causes of racial and ethnic inequities among individuals with CKD are speculated to be of diverse origins, including patient (e.g., biologic, socioeconomic, environmental), provider (e.g., bias, communication), and healthcare system-related (e.g., access to services) factors (22–23). Reasons for these reported disparities in Hispanics have been infrequently examined. Some have argued that differences in sociodemographic and recognized clinical factors account for much of observed disparities in health outcomes (27). Others have contended that intrinsic biologic and genetic predispositions toward CKD and its complications along with differential responses to treatment may contribute substantially to these disparities for Hispanics (7). Moreover, few studies incorporated detailed data on socioeconomic status, health insurance and access to care (3, 8). Of those that did, the observed disparities in regard to higher rates of ESRD among Hispanics appear to be only partially explained by these factors (7). By virtue of its prospective longitudinal design and detailed collection of patient level data, the H-CRIC and CRIC studies are poised to identify additional genetic, biologic, and sociocultural factors that contribute to racial/ethnic differences in CKD-related outcomes.
As in other observational analyses, inferences regarding causality are limited by residual bias and confounding. However, methodologic strategies have been adopted to minimize these concerns (17–18). Another potential limitation pertains to the generalizability of findings from the CRIC and H-CRIC participants. As previously described (17–18), the CRIC cohort oversampled certain subgroups (i.e., African Americans) and recruited participants from select geographic sites, and therefore is not a population-based sample like the NHANES CKD cohort. Similarly, a large majority of Hispanic participants in CRIC/H-CRIC were comprised of Mexican Americans (69%) and recruited from the Chicago metropolitan area (85%). While many characteristics of our Hispanic cohort, including country of origin, education, income, and primary language are similar to representative samples such as those in NHANES (21, 41–42), it is important to recognize that our Hispanic cohort does not include robust representation from all Hispanic subgroups and geographic regions of the U.S.; therefore, findings reported here may not fully generalize to all U.S. Hispanics with CKD. Lastly, although a recent study has indicated that the CKD-EPI equation for eGFR is relatively accurate among Hispanics (43), this equation has not been validated in large diverse samples of Hispanics. Hence, eGFR findings reported here across racial/ethnic groups may be subject to bias.
In conclusion, Hispanics with CKD in CRIC/H-CRIC Studies are disproportionately burdened with lower socioeconomic status, more frequent diabetes mellitus, worse blood pressure control, lower receipt of ACE inhibitor/ARB medications, and more severe CKD with disproportionate associated metabolic complications than their non-Hispanic White and Black counterparts. The consequences of these observed differences across racial and ethnic groups are less clear. Although multiple studies have found an increased burden of adverse sociodemographic characteristics, clinical risk factors, and ESRD among Hispanics compared with Whites (2–4, 6–10, 29), a decreased risk of cardiovascular events and death among Hispanics with CKD and ESRD has been observed (7, 24–27), which is consistent with a phenomenon observed elsewhere called the ‘Hispanic Paradox’ (44). Therefore, longitudinal analyses are critically needed to fully examine the impact of these baseline health disparities as potential mediators of racial/ethnic variation in CKD-related clinical outcomes. Improving our understanding of the causes and consequences of health disparities in Hispanics with CKD has the potential to allow us to more effectively identify and address barriers to health care and improve outcomes for this population (22–23).
We thank the CRIC participants for their time and commitment to the study.
A portion of the results presented in this paper were presented in abstract and poster form at the National Kidney Foundation Annual Meeting in Orlando, FL., on April 13–17, 2010.
Members of the CRIC Study Group are as follows; an asterisk denotes an Ancillary Investigator. University of Pennsylvania Scientific & Data Coordinating Center: Harold I. Feldman, MD, MSCE (PI); J. Richard Landis, PhD; Dina H. Appleby, MS; Shawn Ballard, MS; Denise Cifelli, MS; Robert M. Curley, MS; Jennifer Dickson; Marie Durborow; Stephen Durborow; Melanie Glenn, MPH; Asaf Hanish, MPH; Christopher Helker, MSPH; Elizabeth S. Helker, RN; Amanda Hyre Anderson, PhD, MPH; Marshall Joffe, MD, PhD, MPH; Scott Kasner, MD, MSCE, FAHA; Stephen E. Kimmel, MD, MSCE; Shiriki Kumanyika, PhD, MPH; Lisa Nessel, MSS, MLSP; Emile R. Mohler, III, MD; Steven R.Messe, MD; Nancy Robinson, PhD; Leigh Rosen, MUEP; J. Sanford Schwartz, MD; Sandra Smith; Joan Stahl, MS; Kelvin Tao, PhD, MS; Valerie L. Teal, MS; Xin Wang, MS; Dawei Xie, PhD; Peter Yang, PhD; Xiaoming Zhang, MS. University of Pennsylvania Medical Center: Raymond R. Townsend, MD (PI); Manjunath Balaram; *Thomas P. Cappola, MD, ScM; Debbie Cohen, MD; Magdalena Cuevas; Mark J. Duckworth; *Daniel L. Dries, MD; ; Virginia Ford, MSN, CRNP; Colin M. Gorman; *Juan Grunwald, MD; Holly M. Hannah; Peter A. Kanetsky, PhD, MPH; Krishna Kellem; Lucy Kibe, MS; *Mary B. Leonard, MD, MSCE; *Maureen Maguire, PhD; Stephanie McDowell; John Murphy, MD; *Muredach Reilly, MB; *Sylvia E. Rosas, MD; Wanda M. Seamon; Angie Sheridan, MPH; Karen Teff, MD. The Johns Hopkins University: Lawrence J. Appel, MD, MPH (PI); Cheryl Anderson, PhD, MPH; Jeanne Charleston, RN; Nyya Etheredge; Bernard Jaar, MD, MPH; Kelly Mantegna; Carla Martin; Edgar “Pete” Miller, MD; Patience Ngoh; Julia Scialla, MD; Steve Sozio, MD, MHS; Sharon Turban, MD, MHS; Hemalatha Venkatesh. University of Maryland: Jeffrey Fink, MD, MS (Co-PI); Wanda Fink, RN, BSN; Afshin Parsa, MD, MPH; Beth Scism; Stephen Seliger, MD, MS; Matthew Weir, MD. University Hospitals of Cleveland Case Medical Center: Mahboob Rahman, MD (PI); Valori Corrigan RN ; Renee Dancie, CMA; Genya Kisin MA; Radhika Kanthety; Louise Strauss, RN; Jackson T. Wright, Jr., MD, PhD. MetroHealth Medical Center: Jeffrey Schelling, MD (Co-PI); Patricia Kao, MD (Co-PI); Ed Horowitz, MD (Co-PI); Jacqui Bjaloncik; Theresa Fallon; John R. Sedor, MD; Mary Ann Shella, RN,BSN; Jacqueline Theurer; J. Daryl Thornton, MD, MPH. Cleveland Clinical Foundation: Martin J. Schreiber, MD (Co-PI); Martha Coleman, RN; Richard Fatica, MD; Sandra Halliburton, PhD; Carol Horner, BSN, RN; Teresa Markle, BS; Mohammed A. Rafey, MD, MS; Annette Russo; Stephanie Slattery, RN; Rita Spirko, RN, MSN; Kay Stelmach, RN; Velma Stephens, LPN; Lara Danziger-Isakov MD MPH. University of Michigan at Ann Arbor: Akinlolu Ojo, MD, PhD (PI); Baskaran Sundaram, MD; Jeff Briesmiester; Denise Cornish-Zirker, BSN; Crystal Gadegbeku, MD; Nancy Hill; Kenneth Jamerson, MD; *Matthias Kretzler, MD; Bruce Robinson, MD; Rajiv Saran, MD; Bonnie Welliver, BSN, CNN; Jillian Wilson; Eric Young, MD, MS. St. John’s Health System: Susan P. Steigerwalt, MD (Co-PI); Keith Bellovich, DO; Jennifer DeLuca; Sherry Gasko, BSRN; Gail Makos, RN, MSN; Chantal Parmelee; Shahan Smith; Kathleen Walls. Wayne State University: John M. Flack, MD, MPH (Co-PI); James Sondheimer, MD; Mary Maysura; Stephen Migdal, MD; M. Jena Mohanty, MD; Yanni Zhuang, BSN. University of Illinois at Chicago: James P. Lash, MD (PI); Jose Arruda, MD; Carolyn Brecklin, MD; Eunice Carmona, BA; Janet Cohan, MSN; Michael Fischer, MD, MSPH; Anne Frydrych, MS, RD; Amada Lopez; *Claudia Lora, MD; Monica Martinez; Adriana Matos; Alejandro Mercado; Brenda Moreno; Patricia Meslar, MSN; Ana Ricardo, MD, MPH; Thomas Stamos, MD; *Eve Van Cauter, PhD. Tulane University Health Science Center: Jiang He, MD, PhD (PI); Brent Alper, MD; Vecihi Batuman, M.D; Lydia A. Bazzano, MD, PhD; Bernadette Borja; Adriana Burridge, MPH; Jing Chen, MD, MSc; Catherine Cooke; Patrice Delafontaine, MD; Karen B. DeSalvo, MD, MPH, MSc; Vivian A. Fonseca, MD ; Lee Hamm, MD; Michelle R. Hurly, RN, BSN; Julie Legarde; Eva Lustigova, MPH; *Paul Muntner, PhD; Maria Patrocollo-Emerson, MPH; Lindsey Powers; Shea Shelton; Claire Starcke; Paul Whelton, MD, MSc. Kaiser Permanente of Northern California: Alan S. Go, MD (PI); Lynn M. Ackerson, PhD; Pete Dorin, MPA; Daniel Fernandez; Nancy G. Jensvold, MPH; Joan C. Lo, MD; Juan D. Ordonez, MD, MPH; Rachel Perloff; Thida Tan, MPH; Daphne Thompson; Gina M. Valladares; Annette Wiggins, RN; Diana B. Wong, RN, MPH; Jingrong Yang, MA. University of California, San Francisco: Chi-yuan Hsu, MD, MSc (Co-PI); Glenn M. Chertow, MD, MPH ; *Nisha Bansal, MD; *Manju Kurella, MD, MPH; *Michael G. Shlipak, MD, MPH; *Kristine Yaffe, MD. NIDDK: John W. Kusek, PhD; Andrew S. Narva, MD. Scientific Advisory Committee: Kathy Faber-Langendoen, MD; Bryce A. Kiberd, MD; Elisa T. Lee, PhD; Julia Lewis, MD; William McClellan, MD, MPH; Timothy Meyer, MD; David Nathan, MD; John B. Stokes, MD; Herman Taylor, MD; Peter W. Wilson, MD. University of New Mexico: *Vallabh Shah, PhD. George Washington University: *Dominic Raj MD, DM. University of Miami: *Myles Wolf, MD, MMSc. Consultant, Harvard School of Medicine: Paul M. Ridker, MD. Central Lab, University of Pennsylvania: Daniel J. Rader, MD; Anna DiFlorio; Ted Mifflin; Linda Morrell; Megan L. Wolfe. GFR Lab, Cleveland Clinic: Phillip Hall, MD; Henry Rolin; Sue Saunders. EBT Reading Center, UCLA: Mathew Budoff, MD; Chris Dailing. ECG Reading Center, Wake Forest: Elsayed Z. Soliman MD, MSc, MS; Zhu-Ming Zhang, MD. Echo Reading Center, University of Pennsylvania: Martin St. John Sutton, MBBS; Martin G. Keane, MD.
Support: In addition to funding under a cooperative agreement from NIDDK (5U01DK060990 , 5U01DK060984, 5U01DK06102 , 5U01DK061021, 5U01DK061028 , 5U01DK60980, 5U01DK060963, 5U01DK060902) and an R01 DK072231 (H-CRIC), this work was supported in part by the following institutional Clinical Translational Science Awards (CTSA) and other National Institutes of Health (NIH) grants: UL1 RR-025005 (Johns Hopkins University), General Clinical Research Center (GCRC) grant M01 RR-16500 (University of Maryland), UL1 RR-024989 (Case Western Reserve University Clinical and Translational Science Collaborative [University Hospitals of Cleveland, Cleveland Clinic Foundation, and MetroHealth]), GCRC M01 RR-000042 (University of Michigan), CTSA UL1 RR-024986, M01 RR-013987-06 (University of Illinois at Chicago Clinical Research Center), RR-05096 (Tulane/LSU/Charity Hospital General Clinical Research Center), CTSA UL1 RR-024134 (University of Pennsylvania), UL1 RR-024131 (Kaiser NCRR UCSF-CTSI), 5K24DK002651. Additional support provided by the National Center for Minority Health and Health Disparities, NIH, and Department of Veterans Affairs Health Services Research and Development Service (Career Development Award to Dr Fischer).
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