Present quantitative analysis clearly provided the first evidence that arterial calcification of lower limbs' arteries was closely associated with the prevalence and severity of PAD in HD patients. Furthermore, arterial calcification of below-knee arteries and micro-inflammation represented as CRP were the independent associating factors for low TBI, which was the independent associating factor for PAD and CLI in HD patients.

This pilot study suggested that LC delayed progression of CAC in patients on HD compared with CC.

Atherosclerotic complications have a significant effect on mortality in patients undergoing hemodialysis (HD) therapy. However, anti-atherosclerotic and cardioprotective effects of on-line hemodiafiltration (HDF) remain to be elucidated. We prospectively compared the anti-atherosclerotic and cardioprotective effects in two randomly divided groups, i.e. on-line HDF group (n = 13) and conventional HD group (n = 9) for 1 year. Surrogate markers were brachial-ankle pulse wave velocity (baPWV), intima-media thickness (IMT) of carotid artery as an atherosclerosis marker, and cardiac functional surrogate markers included left ventricular mass index (LVMI), ejection fraction (EF), and LV diastolic capacity represented as E/A and deceleration time (DT). LVMI in on-line HDF patients showed significant regression after 1 year of treatment (131.9 Ϯ 25.8 to 116.5 Ϯ 24.7 g/m ). Levels of baPWV in HD patients showed a significant increase (11.4%) from basal levels, while on-line HDF groups showed no significant increase. Furthermore, HD patients showed significant worsening of LV diastolic capacity (E/A: from 0.87 Ϯ 0.12 to 0.79 Ϯ 0.08, P = 0.03), while it was not shown in on-line HDF patients. Ejection fraction and IMT did not show any significant change in both groups. Serum albumin, C-reactive protein, b2 microglobulin, blood pressure, and anti-hypertensive drug use did not change in both groups. On-line HDF showed a significant improvement in LVMI and prevented a significant worsening of baPWV or LV diastolic capacity compared with patients on conventional HD therapy.

AKI is more common among hospitalized patients and patients with AKI are more severely ill in winter.

Acute kidney injury (AKI) is a major clinical problem that still has no established treatment. We investigated the efficacy of cultured human peripheral blood mononuclear cells (PBMNCs) for AKI. Ischemia/reperfusion injury (IRI) was used to induce AKI in male nonobese diabetic (NOD/severe combined immunodeficiency) mice aged 7 to 8 wk. PBMNCs were isolated from healthy volunteers and were subjected to quality and quantity controlled (QQc) culture for 7 d in medium containing stem cell factor, thrombopoietin, Flt-3 ligand, vascular endothelial growth factor, and interleukin 6. IRI-induced mice were divided into 3 groups and administered (1) 1 × 106 PBMNCs after QQc culture (QQc PBMNCs group), (2) 1 × 106 PBMNCs without QQc culture (non-QQc PBMNCs group), or (3) vehicle without PBMNCs (IRI control group). PBMNCs were injected via the tail vein 24 h after induction of IRI, followed by assessment of renal function, histological changes, and homing of injected cells. Blood urea nitrogen and serum creatinine (Cr) 72 h after induction of IRI in the QQc PBMNCs group dramatically improved compared with those in the IRI control and the non-QQc PBMNCs groups, accompanied by the improvement of tubular damages. Interstitial fibrosis 14 d after induction of IRI was also significantly improved in the QQc PBMNCs group compared with the other groups. The renoprotective effect noted in the QQc PBMNCs group was accompanied by reduction of peritubular capillary loss. The change of PBMNCs’ population (increase of CD34+ cells, CD133+ cells, and CD206+ cells) and increased endothelial progenitor cell colony-forming potential by QQc culture might be one of the beneficial mechanisms for restoring AKI. In conclusion, an injection of human QQc PBMNCs 24 h after induction of IRI dramatically improved AKI in mice.