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1.  Urinary sodium is a potent correlate of proteinuria: Lessons from the CRIC Study 
American journal of nephrology  2012;36(5):397-404.
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.
We measured 24-hour urine sodium, potassium, and protein excretion in 3,680 participants in the Chronic Renal Insufficiency Cohort (CRIC) 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 (SBP), demographics, hemoglobin A1C, and type of antihypertensive medications to evaluate the relationship between urinary electrolyte excretion and proteinuria.
Our data demonstrated that urinary sodium (+1SD above the mean), as a univariate variable, explained 12% of the variation in proteinuria (β=0.29, p<.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<.0001).
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.
PMCID: PMC4448958  PMID: 23076013
proteinuria; sodium; potassium; blood pressure
2.  The influence of creatinine versus GFR on NSAID prescriptions in CKD 
American journal of nephrology  2012;36(1):19-26.
Non-steroidal anti-inflammatory drugs (NSAIDs), including cyclo-oxygenase-2 (COX-2) inhibitors, are generally contraindicated in chronic kidney disease (CKD). This investigation sought to identify the frequency of NSAID/COX2 prescription and determine the influence of serum Cr versus estimated GFR on this practice pattern.
An established Veterans Health Administration (VHA) CKD safety cohort (n = 70,154) was examined to determine the frequency of NSAID/COX2 in fiscal year 2005 (FY05) for up to 30 days preceding the index hospitalization and as many as 365 days during that year. Binomial regression was used to determine adjusted prevalence ratios for prescription of NSAID/COX2 with respect to continuous eGFR measurement and serum creatinine (Cr) categories. CKD was defined as eGFR < 60 ml/min/1.73m2.
15.4% of subjects had an NSAID/COX2 prescription during the observation period with the proportion prescribed these agents decreasing with declining renal function, but remained significant at any stage of CKD given the renal harm related to these medications. At specific GFR estimates, serum creatinine (Cr) remained a significant predictor of NSAID/COX prescription. At GFR set at 42 ml/min/1.73, the predicted proportion prescribed NSAID/COX2 was 0.29 (95% CI: 0.24,0.36); 0.23 (95% CI: 0.22,0.26); 0.20 (95%: 0.19,0,22); 0.12 (95% CI: 0.10,0.14) for Cr strata of ≤ 1.3 mg/dl, 1.4 – 1.6 mg/dl, 1.7 –2.1 mg/dl, ≥ 2.2 mg/dl, respectively (all p < 0.05).
A significant proportion of individuals with CKD continue to be prescribed NSAID/COX2 and serum Cr remains an influential guide to NSAID/COX2 prescription, even in GFR ranges where these agents are ill-advised.
PMCID: PMC3417055  PMID: 22699456
chronic kidney disease; safety; recognition; NSAIDs

Results 1-2 (2)