Pilot study to assess increased dialysis efficiency in patients with limited blood flow rates due to vascular access problems.

In the last few years, the number of hemodialysis patients with inadequate blood flow (Qb) rates has increased due to vascular access problems. To avoid a clinical status of underdialysis, these patients need long-lasting dialysis sessions. However, other factors aimed to optimize the dialysis dose have to be considered. High-efficiency convective therapies, such as online hemodiafiltration (HDF), are claimed to be superior to high-flux hemodialysis (HF-HD) in improving the dialysis efficacy, but treatment efficacy is strongly related to blood flow rate and infusion volumes. Online mid-dilution (HDF-MD) with the Nephros OL-pure MD190 represents a new HDF concept to increase the removal of middle molecules. In a cross-over clinical trial, 8 patients, with Qb eff <300 mL/min, received either online HDF-MD or HF-HD; Qd was 700 mL/min, the time duration was 240 min, and the filtration volume in HDF-MD was 112+/-7 mL/min. No differences were found for Kt/V, urea, and creatinine clearances. Clearance of both small phosphate (P) large beta(2)-microglobulin (beta(2)m), and leptin (L) solutes was significantly greater for MD (P 217+/-32, beta(2)m 85.5+/-10, L 42.6+/-18 mL/min) than for HF-HD (P 178+/-32, beta(2)m 71.9+/-13, L 32.1+/-12 mL/min). The results of this study indicate that HDF remains the best means of providing increased removal of large-molecular weight solutes even in patients with vascular access problems.

Metabolic effects of a corticosteroid-free immunosuppressive regimen in recipients of pancreatic transplant.

BACKGROUND: A corticosteroid (CS)-free immunosuppressive regimen may be considered less diabetogenic than treatments including CSs principally after pancreas transplantation. METHODS: To test whether a CS-free immunosuppressive treatment is metabolically superior to a regimen including CSs, we prospectively studied 19 CS-free simultaneous pancreas and kidney (SPK) transplant recipients (body mass index=22+/-1 kg/m2; cyclosporine dose=400+/-19 mg/kg/day; azathioprine dose=77+/-8 mg/day; basal plasma C-peptide=1.3+/-0.12 ng/mL) and 12 matched CS-treated SPK transplant recipients (prednisone dose=9+/-1 mg/day; basal C-peptide=2.2+/-0.2 ng/mL) by means of the 6,6-2H(2)-glucose infusion and the euglycemic insulin clamp (1 mU/kg/min, insulin infusion rate). In addition, six renal transplant recipients receiving a CS-free regimen were also studied as a control group. RESULTS: In the postabsorptive state, CS-treated SPK transplant recipients demonstrated comparable plasma glucose levels but higher plasma insulin levels than CS-free SPK transplant recipients. Plasma triglyceride levels were significantly higher in CS-treated SPK patients than in CS-free SPK patients (1.16+/-0.16 mg/dL vs. 0.88+/-0.08; P<0.05). High-density lipoprotein and apoprotein A(1) levels were similar in both groups. No difference was observed in pyruvate, lactate, beta-OH-butyrate, and basal endogenous glucose production in all three groups of patients studied. During euglycemic hyperinsulinemia, the inhibition of endogenous glucose production and the stimulation of tissue glucose disposal were not statistically different among the three groups. CONCLUSIONS: SPK recipients receiving chronic low-dose CS maintenance therapy do not present a lower glucose disposal than CS-free recipients. Nonetheless, this is obtained at the expense of a higher endogenous insulin secretion, which can cause an alteration of the triglyceride profile.

BK polyomavirus interstitial nephritis in a renal transplant patient with no previous acute rejection episodes.

A renal transplant patient treated with tacrolimus and mycophenolate-mofetil (MMF) developed progressive graft function deterioration 10 months after transplantation. Biopsy of the graft showed severe, focally accentuated interstitial inflammation with focal tubulitis and tubular necrosis, and medium-severe interstitial fibrosis with focal tubular atrophy. Glomerular and vascular structures were preserved. On careful examination, in some sections, tubular epithelial cells showed a definite increase with deformation of the nuclear shape, chromatin irregularities with peripheral dislocation and inclusion bodies. These cytopathic changes suggested polyoma virus infection ("decoy cells"). Subsequent screening of the urinary sediment confirmed the presence of many "decoy cells". Immunohistochemical analysis of the biopsy showed many tubular cells were strongly positive for the SV 40 antigen, specific for BK polyoma virus. A diagnosis of interstitial nephritis due to BK polyoma virus was made, though the coexistence of cellular rejection could not be excluded. At variance with previous reports, our patient had not had repeated episodes of rejection before biopsy or heavy immunosuppressive treatment, such as ALG, OKT3, after transplantation. This case shows that even in the absence of vigorous anti-rejection therapy an immunosuppressive regimen based on tacrolimus and MMF may involve the risk of BK polyoma virus- associated interstitial nephritis.