Initial experience of a nephrologist-operated vascular access center.

A nephrology practice in Alabama did not feel in control of vascular access management. Scheduling delays, as well as variable techniques and outcomes, leading to high morbidity and mortality, caused frustration with the existing care system for vascular access. Our objective was to develop an integrative system of vascular access care, involving nephrologists along with the other caregivers, and to demonstrate an improvement in outcomes. Nephrology Vascular Labs (NVL), a recent RMS-Lifeline acquisition, opened a vascular access center (VAC) as an extension of the nephrology practice. Both pre-ESRD and ESRD patients are evaluated and treated in the VAC. Treatment is rendered in a timely fashion, to the benefit of the patients. Nephrologists serve as the interventionists. More than 90% of vascular access problems detected at dialysis are treated at the VAC. More than 2000 procedures have been performed over 2 years. Procedures carried out include thrombolysis with angioplasty, fluoroscopy alone or with angioplasty, placement of cuffed and noncuffed catheters, removal of cuffed catheters, and minor surgeries. Success rates have been high. Minor and major complications have been relatively low. Referrals to both surgeons and radiologists are shown to emphasize the role of the VAC as part of an integrative system of vascular access care. Results of a patient satisfaction survey were excellent. The VAC has fulfilled the vision of creating a seamless integration of care for vascular access. Hospitalization rate has been reduced and it is suspected that the global cost of access care is markedly lower than prior to the VAC. Multiple nephrologists can rotate as the VAC's interventionist and jointly obtain good outcomes and have little variability among them. Several reasons for using a nephrologists as the interventionist are discussed.

Losartan, an angiotensin II type 1 receptor antagonist, lowers hematocrit in posttransplant erythrocytosis.

The mechanism by which angiotensin-converting enzyme inhibitors reduce red cell mass in renal transplant recipients with erythrocytosis is unclear. To examine the role of angiotensin II in this disorder, losartan (a competitive antagonist of the angiotensin II type 1 [AT1] receptor) was administered to 23 patients with erythrocytosis. Fourteen patients took 25 mg/d for 8 wk; nine others were treated with 50 mg/d for 8 wk. Hematocrit decreased from 0.527 +/- 0.027 to 0.487 +/- 0.045 after 8 wk (P < 0.01)--by at least 0.04 in 19 patients. Decrement in hematocrit in the initial 8 wk of therapy was significantly greater in patients administered 50 mg/d than in patients on 25 mg/d. Twelve of 14 patients initially treated with 25 mg/d showed a small change in hematocrit; the dose was increased to 50 mg/d for 8 more wk. Hematocrit decreased from 0.528 +/- 0.030 before losartan treatment to 0.483 +/- 0.055 after 16 wk (P < 0.01). After therapy, serum erythropoietin significantly decreased in eight patients with elevated baseline levels, but not in 15 patients with normal baseline levels; however, hematocrit significantly decreased in both groups. Losartan was withdrawn in 16 patients; hematocrit increased from 0.440 +/- 0.057 to 0.495 +/- 0.049 after 8.9 +/- 7.5 wk (P < 0.001), without change in serum erythropoietin. Thus, specific blockade of AT1 receptors inhibited erythropoiesis, suggesting a pathogenic role for angiotensin II in posttransplant erythrocytosis.