Urinary Sodium Is a Potent Correlate of Proteinuria: Lessons from the Chronic Renal Insufficiency Cohort StudyWeir M.R.a · Townsend R.R.b · Fink J.C.a · Teal V.b · Sozio S.M.c · Anderson C.A.c · Appel L.J.c · Turban S.c · Chen J.d · He J.d · Litbarg N.e · Ojo A.f · Rahman M.g · Rosen L.b · Steigerwalt S.h · Strauss L.g · Joffe M.M.b · on behalf of the CRIC study Investigators
aUniversity of Maryland School of Medicine, Baltimore, Md., bUniversity of Pennsylvania, Philadelphia, Pa., cJohns Hopkins Medical Institutions, Baltimore, Md., dTulane University School of Medicine, New Orleans, La., eUniversity of Illinois School of Medicine, Chicago, Ill., fUniversity of Michigan School of Medicine, Ann Arbor, Mich., gCase Western Reserve School of Medicine, Cleveland, Ohio, and hSt. Claire Specialty Center, Lakewood, Wash., USA Am J Nephrol 2012;36:397–404 (DOI:10.1159/000342966)
Background: While higher blood pressure is known to increase proteinuria, whether increased dietary sodium as estimated from 24-hour urinary excretion correlates with increased proteinuria in patients with chronic kidney disease (CKD) is not well studied. Methods: We measured 24-hour urinary sodium, potassium and protein excretion in 3,680 participants in the Chronic Renal Insufficiency Cohort study, to determine the relationship between urinary sodium and potassium and urinary protein excretion in patients with CKD. We stratified our data based on the presence or absence of diabetes given the absence of any data on this relationship and evidence that diabetics had greater urinary protein excretion at nearly every level of urinary sodium excretion. Multiple linear regressions were used with a stepwise inclusion of covariates such as systolic blood pressure, demographics, hemoglobin A1c and type of antihypertensive medications to evaluate the relationship between urinary electrolyte excretion and proteinuria. Results: Our data demonstrated that urinary sodium (+1 SD above the mean), as a univariate variable, explained 12% of the variation in proteinuria (β = 0.29, p < 0.0001), with rising urinary sodium excretion associated with increasing proteinuria. The significance of that relationship was only partially attenuated with adjustment for demographic and clinical factors and the addition of 24-hour urinary potassium to the model (β = 0.13, R2 = 0.35, p < 0.0001). Conclusions: An understanding of the relationship between these clinical factors and dietary sodium may allow a more tailored approach for dietary salt restriction in patients with CKD.
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