Long-term safety of living kidney donors aged 60 and older.

In Japan, kidney transplantation procedures are usually dependent upon live donors. As the recipient ages have been increasing, so has there been a corollary increase in the age of the live donors. Despite this being controversial, the use of older donors is becoming increasingly common. The purpose of our study was to evaluate the long-term safety of accepting older living kidney donors and graft survival rates. We retrospectively analyzed long-term donor outcomes for consecutive patients at our institution between January 1990 and December 2011. Older live kidney donors were defined as ≥ 60 years and younger live kidney donors were defined as <60 years old. Thirty-three were ≥ 60 years and 55 donors were <60 years. The mean follow-up term was 7 years and 4 months. Predonation, older donors had a lower estimated glomerular filtration rate (eGFR) level (77.1 ± 9.5 mL/min/1.73 m(2)) than younger donors (85.8 ± 14.6 mL/min/1.73 m(2); P < .01). More older donors had a history of hypertension (42.4% vs 9.1%; P < .01). In both groups, eGFR levels decreased about 40% immediately after nephrectomy. Residual renal function though was stable on long-term follow-up. The incidence of de novo hypertension and proteinuria after nephrectomy was not different between the 2 groups. In older donors, there were no perioperative complications that required extended hospital stays. Graft survival over a period of 10 years was similar in both groups. In our study, donor age had no influence on the deterioration of renal function after nephrectomy. Regardless of age, careful evaluation and follow-up are important for the donor's long-term safety after donation.

Charcoal hemoperfusion in the treatment of phenytoin overdose.

In the case of phenytoin, a drug that is generally highly protein bound, there is a lack of consensus on the use of charcoal hemoperfusion in cases of overdose. We performed charcoal hemoperfusion on a phenytoin-overdosed patient to assess the effectiveness of this treatment. The plasma concentrations of total and free phenytoin fell rapidly, from 40.0 microg/mL and 3.6 microg/mL to 16.2 microg/mL and 1.5 microg/mL, respectively, after 3 hours of hemoperfusion. The total phenytoin elimination half-life was 3.9 hours. The fraction of protein-bound phenytoin was constant (90.8% +/- 0.5%) before, during, and after the procedure. The relations between the in vitro protein binding and adsorption of phenytoin to activated charcoal were also examined. Interestingly, bound phenytoin was found to dissociate from plasma proteins in the presence of activated charcoal and subsequently became adsorbed to the activated charcoal. Considering that phenytoin is bound to albumin with a large number of binding sites (n = 6) and a small binding constant (K = 6 x 10(3/)mol/L), the extent of adsorption to activated charcoal may depend on the magnitude of the binding constant of the drug to plasma proteins. The current results suggest that charcoal hemoperfusion is effective for the removal of drugs that bind to plasma proteins with a low binding constant.

HTLV-I seroprevalence in patients with malignancy.

Since many malignancies often occur in patients with smoldering type adult T-cell leukemia (ATL) (5 of 18 cases in this report), the relationship between HTLV-I (human T-cell leukemia virus type I) infection, which is closely associated with ATL, with other malignancies in an HTLV-I endemic area was examined. Among the 394 patients with malignancies and who had not had blood cell transfusions, 61 (15.5%) tested positive for HTLV-I antibody. The prevalence was significantly higher in males older than age 40 years and females of all ages compared to age- and sex-matched healthy individuals. The overall seroprevalence (26.1%) in 291 patients with malignancies and who had had blood cell transfusions was higher than that of those who had not had blood transfusions. There was no significant correlation between the site of malignancy and antibody prevalence. These results suggest the possibility that development of malignancy may contribute to expression of latent HTLV-I infection and that HTLV-I infection may contribute to the risk of other malignancies.