Prevalence of ICD-9-CM codes for chronic kidney disease in individuals with cardiovascular disease risk factors.

BACKGROUND: Chronic kidney disease (CKD) is a risk factor for cardiovascular disease (CVD). METHODS: We determined the prevalence of diagnosed CKD in 87,128 members older than 40 years of age without CVD who were enrolled in a regional medical care plan with at least 1 claim for medical care. RESULTS: The prevalence of diagnosed CKD was 4%, and 8%, 6%, 5% and 10% in patients with diabetes, hypertension, hyperlipidemia and all 3 risk factors, respectively. In multivariate analysis, the odd ratios for CKD were 1.8 (95% confidence interval [95% CI], 1.7-2.0) for older age, 2.5 (95% CI, 2.3-2.8) for diabetes, 2.2 (95% CI, 2.2-2.4) for hypertension, 1.5 (95% CI, 1.4-1.7) for hyperlipidemia and 4.4 (95% CI, 2.8, 5.1) for all 3 risk factors. CONCLUSION: Prevalence of diagnosed CKD among patients with CVD risk factors is low but increases with age and number of risk factors, suggesting inadequate awareness of CKD. This may have implications for control of CVD risk factors in patients with CKD.

Managing erythropoietin hyporesponsiveness.

The anemia of chronic kidney disease is associated with cardiovascular disease, decreased quality of life, and mortality. The introduction of recombinant human erythropoietin (rHuEPO) has transformed the management of this condition. However, a significant proportion of patients fail to respond to even high doses of rHuEPO. Several factors have been implicated in the hyporesponsiveness to rHuEPO. Iron deficiency, whether absolute or functional, is considered the most important, and maintenance of adequate iron stores reduces rHuEPO requirements among patients on hemodialysis. However, traditional indices of iron that are currently utilized may not reflect iron stores accurately, and there is also increasing concern regarding the potential long-term toxicity of parenteral iron therapy. Infection and inflammation also influence the response to rHuEPO, both by disruption of iron metabolism and by eliciting the release of cytokines that inhibit erythropoiesis. Oxidative stress may contribute to rHuEPO hyporesponsiveness directly by promoting lipid peroxidation in cell membranes, leading to increased erythrocyte fragility and reduced life span and also through its strong association with inflammation. Severe hyperparathyroidism can lead to a reduced number of erythroid progenitor cells. Inadequate dialysis dose, aluminum overload, nutritional factors such as deficiencies of carnitine, vitamin B12, folic acid, and vitamin C can also reduce the efficacy of rHuEPO therapy. Hyporesponsiveness to rHuEPO presents a challenge to both diagnosis and management in an era where optimizing response to rHuEPO is critical both in limiting the burgeoning costs of anemia management and improving clinical outcomes in the dialysis population.