Background: Matrix metalloproteinase-10 (MMP-10) levels increase progressively starting from early diabetic kidney disease (DKD) stages. Vitamin D-3 (vitD(3)) deficit is associated with a higher risk of diabetic microangiopathy. Reduced MMP-10 expression has been observed after exposure to vitD(3). Aim: to assess how vitD(3) status is related to MMP-10 levels in patients with Type 2 diabetes (T2D). Methods: 256 patients with T2D were included in this cross-sectional study. Demographic, clinical and serum MMP-10 and 25-hydroxyvitamin D-3 (25(OH)D-3) levels were collected from each patient. The association between MMP-10 and (25(OH)D-3) levels was assessed using a correlation analysis and fitting a multivariate linear regression model. Results: Serum MMP-10 levels were inversely correlated with circulating 25(OH)D-3 (rho = -0.25; p < 0.001). In the subgroup analysis this correlation was significant in patients with DKD (rho = -0.28; p = 0.001) and in subjects with vitD(3) deficit (rho = -0.24; p = 0.005). In the regression model adjusted for kidney function, body adiposity, smoking and vitD supplementation MMP-10 levels were 68.7 pg/mL lower in patients with 25(OH)D-3 > 20 ng/mL, with respect to <= 20 ng/mL (p = 0.006). Conclusions: vitD(3) repletion status is an independent predictor of MMP-10 levels in T2D patients. Perhaps, high 25(OH)D-3 values should be targeted in these patients in order to prevent vascular complications.

Matrix metalloproteinases have been implicated in diabetic microvascular complications. However, little is known about the pathophysiological links between MMP-10 and the renin-angiotensin system (RAS) in diabetic kidney disease (DKD). We tested the hypothesis that MMP-10 may be up-regulated in early stage DKD, and could be down-regulated by angiotensin II receptor blockade (telmisartan). Serum MMP-10 and TIMP-1 levels were measured in 268 type 2 diabetic subjects and 111 controls. Furthermore, histological and molecular analyses were performed to evaluate the renal expression of Mmp10 and Timp1 in a murine model of early type 2 DKD (db/db) after telmisartan treatment. MMP-10 (473¿±¿274¿pg/ml vs. 332¿±¿151; p¿=¿0.02) and TIMP-1 (573¿±¿296¿ng/ml vs. 375¿±¿317; p¿<¿0.001) levels were significantly increased in diabetic patients as compared to controls. An early increase in MMP-10 and TIMP-1 was observed and a further progressive elevation was found as DKD progressed to end-stage renal disease. Diabetic mice had 4-fold greater glomerular Mmp10 expression and significant albuminuria compared to wild-type, which was prevented by telmisartan. MMP-10 and TIMP-1 are increased from the early stages of type 2 diabetes. Prevention of MMP-10 upregulation observed in diabetic mice could be another protective mechanism of RAS blockade in DKD.

To investigate whether arterial spin labeling (ASL) MRI could detect renal hemodynamic impairment in diabetes mellitus (DM) along different stages of chronic kidney disease (CKD).

The Kidney Transplant Program started at the Clinica Universidad de Navarra (Pamplona, Spain) in September of 1969. The 1000th kidney transplant was performed in September 2015. Data from kidney transplants have been included in the Collaborative Transplant Study since 1983.

The results of kidney transplantation have improved significantly in the last decade with patient and graft survival rates that range from 92% to 95%. Our observations suggest great improvement of early results of renal transplantation in recent years, including complex cases. In this 3-year period we had a patient survival rate of 98% and a graft survival rate of 96% of cases. Further dedicated prospective studies that aim to evaluate or to propose possible recipient-related predictors for kidney transplantation outcomes in different

Our aim was to study the potential effect of PTX on anaemia in haemodialysis patients. Patients and method: Retrospective observational case-control study on 18 patients (treated with PTX) and 18 controls (without PTX matched by age and sex) on HD (Clínica Universidad de Navarra). Four patients received PTX due to vascular disease and 14 due to refractory anaemia (which was defined as haemoglobin [Hb] <11g/dl in the last three months despite high doses of ESA and transferrin saturation of >20%). Hb, MIRCERA® dose and C-reactive protein were recorded before starting PTX treatment (baseline), at 3 months and at the end of the study. Results: In patients who received PTX, there was an increase in Hb (P<.001) over three months and a decrease in the ESA dose at the end of the study (P=.002). The baseline differences in Hb between groups (lowest of all cases) (P<.001) and ESA dose (highest of all cases) (P=.006), disappeared at 3 months. At the end of the study, 11/18 (61.1%) of patients treated with PTX had adequate Hb levels and received doses of ESA comparable with those of the controls. Conclusions: In HD patients, PTX in doses of 800mg/day improves Hb significantly and in the short term (3 months) in HD patients (around 61% response) and allows the required ESA dose to be reduced in the medium-long term. This effect is sustained over time and treatment is tolerated well.