Resistance to Erythropoiesis-Stimulating Agents Is Associated with Arterial Microcalcification in Early Hemodialysis Patients

Abstract

The aim of this study was to evaluate the relationship between arterial microcalcification (AMiC) and erythropoiesis-stimulating agents (ESA) hyporesponsiveness in hemodialysis patients. The presence of AMiC was confirmed by pathologic examination of von Kossa-stained arterial specimens acquired during vascular access surgery. We assessed the ESA hyporesponsiveness index (EHRI), defined as the weekly ESA dose per kilogram body weight divided by the hemoglobin level. AMiC was detected in 33 (40.2%) of 82 patients. Patients with diabetes had a higher incidence of AMiC than patients without diabetes. The serum levels of albumin and cholesterol were higher in patients without AMiC than in patients with AMiC. The serum levels of intact parathyroid hormone were lower in patients with AMiC than in patients without AMiC. The serum levels of phosphate and calcium-phosphorus product did not differ between the two groups. The mean EHRI value was higher in patients with AMiC than in patients without AMiC. In multivariate analyses, ESA hyporesponsiveness and diabetes showed a significant association with AMiC. In conclusion, ESA hyporesponsiveness may be a clinical relevant parameters related to AMiC in hemodialysis patients.

Vascular calcification and cardiac function according to residual renal function in patients on hemodialysis with urination

“…Therefore, retained β2-microglobulin seems to further contribute to the vascular calcification process in the uremic milieu. In addition, oxidative stress and inflammation are also considered to play a key role [ 5 ]. Interestingly, Won et al showed that ESA resistance was associated with vascular calcification, which could be explained based on oxidative stress and inflammation [ 5 ].…”

“…In addition, oxidative stress and inflammation are also considered to play a key role [ 5 ]. Interestingly, Won et al showed that ESA resistance was associated with vascular calcification, which could be explained based on oxidative stress and inflammation [ 5 ]. Meanwhile, Stompor et al described that higher residual renal function in dialysis patients was responsible for better clearance of proinflammatory cytokines [ 39 ].…”

“…Vascular calcification is a common pathologic finding among patients with ESRD that has a variety of forms, including the deposition of calcium in the intimal and/or medial vessel layer [ 3 , 4 ]. Previous studies suggested that this change in vessels might be induced by multiple factors such as using calcium-based phosphate binder, calcium-phosphorous products, oxidative stress, inflammation, and erythropoietin stimulating agent (ESA) resistance [ 5 , 6 ]. Eventually, vascular calcification greatly contributes to the exceedingly high cardiovascular disease mortality in this population [ 7 ].…”

Use of the esa resistance index to guide dosing for anaemia management

“…There is a paucity of published anaemia management studies that incorporated various RI measures, and most focused specifically on the ERI RI. The RI was utilized to explore such relationships as the effect of high‐flux dialysis (Schneider et al 2012), dialysate purity (Molina et al 2007), pentoxifylline (Johnson et al 2014), arterial microcalcification (Won et al 2014), cardiovascular events (Chung et al 2012), left ventricular function (Chung et al 2012), choice of medication (ERI vs DRI) (Portolés et al 2008), route (subcutaneous or intravenous) (Bommer et al 2008) or frequency of administration (Molina et al 2008) on ESA dosing and resistance. The weakness of a few reports, which included patients on DRI, was that they mathematically converted its dosing to that for ERI using a fixed 1:200 ratio (Bommer et al 2008; Portolés et al 2008; Johnson et al 2014; Won et al 2014).…”