Diabetes is associated with renal calcium and magnesium wasting, but the molecular mechanisms of these defects are unknown. We measured renal calcium and magnesium handling and investigated the effects of diabetes on calcium and magnesium transporters in the thick ascending limb and distal convoluted tubule in streptozotocin (STZ)-induced diabetic rats. Rats were killed 2 weeks after inducing diabetes, gene expression of calcium and magnesium transporters in the kidney was determined by real-time polymerase chain reaction, and the abundance of protein was assessed by immunoblotting. Our results showed that diabetic rats had significant increase in the fractional excretion for calcium and magnesium (both P < 0.01), but not for sodium. Reverse transcriptase-polymerase chain reaction revealed significant increases in messenger RNA abundance of transient potential receptor (TRP) V5 (223 +/- 10%), TRPV6 (177 +/- 9%), calbindin-D28k (231 +/- 8%), and TRPM6 (165 +/- 8%) in diabetic rats. Sodium chloride cotransporter was also increased (207 +/- 10%). No change was found in paracellin-1 (cortex: 108 +/- 8%; medulla: 110 +/- 10%). Immunofluorescent studies of renal sections showed significant increase in calbindin-D28k (238 +/- 10%) and TRPV5 (211 +/- 10%), but no changes in paracellin-1 in Western blotting (cortex: 110 +/- 7%; medulla: 99 +/- 7%). Insulin administration completely corrected the hyperglycemia-associated hypercalciuria and hypermagnesiuria, and reversed the increase of calcium and magnesium transporter abundance. In conclusion, our results demonstrated increased renal calcium and magnesium transporter abundance in STZ-induced diabetic rats, which may represent a compensatory adaptation for the increased load of calcium and magnesium to the distal tubule.

Vascular access thrombosis (VAT) is an important cause of morbidity for chronic haemodialysis (HD) patients. Some risk factors for VAT have been well-defined for chronic HD patients from western countries. However, only a few such factors have been confirmed for Taiwanese patients. This study attempted to determine the association between hyperhomocysteinaemia and the incidence of VAT for chronic HD patients in Taiwan. We retrospectively enrolled a total of 196 patients into this study during 2003. The patients were separated into VAT (n = 142) and control (n = 54) group. The participants of the VAT group were identified as those having one or more VAT, and the participants of the control group were those with no VAT in the past. The mean follow-up period was 48 months. The mean serum homocysteine levels were 29.5 +/- 9.6 and 29.1 +/- 9.5 micromol/l for the VAT (n = 142) and the control (n = 54) group, respectively. There was no significant difference in the level of homocysteine between the VAT and the control group (p = 0.70). Female chronic HD patients had significantly greater mean total homocysteine levels than male (30.89 micromol/l, 95% CI 28.84-32.94 vs. 28.06 micromol/l, 95% CI 26.32-29.82, respectively, p = 0.038). That synthetic graft was a significant risk factor for VAT was determined using multivariate logistic regression analysis. There was no association between serum total homocysteine levels and the incidence of VAT in chronic HD patients in Taiwan.