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Articles by M. G. Shlipak
Total Records ( 2 ) for M. G. Shlipak
  C. A Peralta , Y Li , C Wassel , S Choudhry , W Palmas , M. F Seldin , N Risch , D Siscovick , D Arnett , B Psaty and M. G. Shlipak
  Background—

Reports show higher prevalence of albuminuria among Hispanics compared with whites. Differences by country of origin or genetic background are unknown.

Methods and Results—

In Multi-Ethnic Study of Atherosclerosis, we studied the associations of both genetic ancestry and country of origin with albumin to creatinine ratio among 1417 Hispanic versus white participants using multivariable linear regression and back transforming beta coefficients into relative difference (%RD, 95% CI). Percentage European, Native American, and African ancestry components for Hispanics were estimated using genetic admixture analysis. The proportions of European, Native American, and African genetic ancestry differed significantly by country of origin (P<0.0001); Mexican/Central Americans had the highest Native American (41±13%), Puerto Ricans had the highest European (61±15%), and Dominicans had the highest African (39±21%) ancestry. Hispanic ethnicity was associated with higher albumin/creatinine ratio compared with whites, but the association varied with the country of origin (adjusted P interaction=0.04). Mexican/Central Americans and Dominicans had higher albumin/creatinine ratio compared with whites after adjustment (RD 19%, 2% to 40% and RD 27%, 1% to 61%), but not Puerto Ricans (RD 8%, –12% to 34%). Higher Native American ancestry was associated with higher albuminuria after age and sex adjustment among all Hispanics (RD 11%, 1% to 21%) but was attenuated after further adjustment. Higher European ancestry was independently associated with lower albumin/creatinine ratio among Puerto Ricans (–21%, –34% to –6%) but not among Mexican/Central Americans and Dominicans.

Conclusions—

Hispanics are a heterogeneous group with varying genetic ancestry. Risks of albuminuria differ across the country of origin groups. These differences may be due, in part, to differences in genetic ancestral components.

  R Deo , N Sotoodehnia , R Katz , M. J Sarnak , L. F Fried , M Chonchol , B Kestenbaum , B. M Psaty , D. S Siscovick and M. G. Shlipak
 

Background— Recent studies have demonstrated an association between moderate kidney dysfunction and sudden cardiac death in people with cardiovascular disease.

Methods and Results— The study was a longitudinal analysis among 4465 participants from the Cardiovascular Health Study without prevalent cardiovascular disease at baseline. Cystatin C and creatinine were measured from baseline sera. Sudden cardiac death (SCD) was defined as a sudden pulseless condition from a cardiac origin in a previously stable individual that occurred out of the hospital or in the emergency room. The association between cystatin C tertiles and SCD was determined with multivariate Cox proportional hazards. A similar analysis compared SCD incidence across creatinine-based estimated glomerular filtration rate (eGFR) tertiles. Over a median follow-up of 11.2 years, 91 adjudicated SCD events occurred. The annual incidence of SCD events increased across cystatin C tertiles: 10 events per 10 000 person years in tertile 1, 25 events per 10 000 person years in tertile 2, and 32 events per 10 000 person-years in the highest cystatin C tertile. These associations persisted after multivariate adjustment: hazards ratio=2.72; 95% confidence interval, 1.44 to 5.16 in tertile 2 and hazards ratio=2.67; 95% confidence interval, 1.33 to 5.35 in tertile 3. After multivariate adjustment, the rate of SCD also increased in a linear distribution across creatinine-based eGFR tertiles: 15 events per 10 000 person-years in tertile 1, 22 events per 10 000 person-years in tertile 2, and 27 events per 10 000 person-years in tertile 3. No significant associations, however, remained between creatinine-based eGFR and SCD after multivariable adjustment.

Conclusions— Impaired kidney function, as measured by cystatin C, has an independent association with SCD risk among elderly persons without clinical cardiovascular disease.

 
 
 
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