Modeled Daily Ingested, Absorbed and Bound Phosphorus: New Measures of Mineral Balance in Hemodialysis Patients.

BACKGROUND: Control of predialysis serum phosphorus in hemodialysis patients is challenging. We explored the utility of a novel kinetic phosphorus modeling program. METHODS: As part of a quality assurance program, urea kinetic modeling results were combined with those from phosphorus kinetic modeling to compute modeled daily ingested phosphorus (DIP) and components making up this metric, including absorbed, bound, and nonabsorbed, nonbound phosphorus. RESULTS: In 182 hemodialysis patients, DIP averaged 1,089 ± 348 mg/day in men and 934 ± 292 in women (p < 0.002) and correlated substantially with body weight. DIP/kg bodyweight (12.8 ± 3.40 mg/kg) was not significantly different between the sexes. Prescribed equivalent binder dose (EBD) was 4.98 ± 3.61 and 4.53 ± 3.02 g/day in men and women, respectively (p NS). Protein catabolic rate (PCR) was significantly higher in men (64.4 ± 18) g/day vs. women (48.2 ± 15.6, p < 0.001), and the DIP/PCR ratio was 17.4 ± 4.81 in men vs. 20.1 ± 5.76 in women (p < 0.001). Presence of residual kidney function was associated with a lower prescribed EBD dose (4.08 ± 2.62 vs. 5.38 ± 3.81 g/day, p < 0.01). Self-reported poor binder compliance was associated with higher DIP or DIP/kg as well as higher prescribed EBD. In anuric patients, DIP/kg was increased in patients consuming diets with high phosphate additive content and those reporting poor compliance with the prescribed dose of phosphate binders. CONCLUSIONS: The combination of urea kinetic and phosphorus modeling can be used to estimate measures related to phosphorus intake. High DIP/PCR or DIP/kg body weight values in anuric patients suggest consumption of a diet high in phosphorus additives or noncompliance with the prescribed amount of phosphorus binders.

Ferric gluconate reduces epoetin requirements in hemodialysis patients with elevated ferritin.

The Dialysis Patients Response to IV Iron with Elevated Ferritin (DRIVE) study demonstrated the efficacy of intravenous ferric gluconate to improve hemoglobin levels in anemic hemodialysis patients who were receiving adequate epoetin doses and who had ferritin levels between 500 and 1200 ng/ml and transferrin saturation (TSAT) < or = 25%. The DRIVE-II study reported here was a 6-wk observational extension designed to investigate how ferric gluconate impacted epoetin dosage after DRIVE. During DRIVE-II, treating nephrologists and anemia managers adjusted doses of epoetin and intravenous iron as clinically indicated. By the end of observation, patients in the ferric gluconate group required significantly less epoetin than their DRIVE dose (mean change of -7527 +/- 18,021 IU/wk, P = 0.003), whereas the epoetin dose essentially did not change for patients in the control group (mean change of 649 +/- 19,987 IU/wk, P = 0.809). Mean hemoglobin, TSAT, and serum ferritin levels remained higher in the ferric gluconate group than in the control group (P = 0.062, P < 0.001, and P = 0.014, respectively). Over the entire 12-wk study period (DRIVE plus DRIVE-II), the control group experienced significantly more serious adverse events than the ferric gluconate group (incidence rate ratio = 1.73, P = 0.041). In conclusion, ferric gluconate maintains hemoglobin and allows lower epoetin doses in anemic hemodialysis patients with low TSAT and ferritin levels up to 1200 ng/ml.

Efficacy of tissue plasminogen activator for thrombolysis in central venous dialysis catheters.

BACKGROUND: Low blood flow is a frequent complication of central-vein (CV) dialysis catheters. Since thrombotic occlusion accounts for many cases of reduced blood flow, it is common practice to administer empiric thrombolytic therapy in an attempt to restore catheter patency and improve function. METHODS: We prepared tissue plasminogen activator (tPA) from 50 mg lyophilized powder, which was diluted (1 mg/mL) in sterile water for injection. A volume of 1 mL was frozen in 3 cc polystyrene syringes at -20 degrees C and thawed at room temperature when needed. tPA was then administered into the arterial and venous ports of the central venous catheter in a volume equal to the manufacturer's stated luminal volume and was allowed to dwell for 30 minutes. RESULTS: tPA was administered 62 times in 25 patients with 30 catheters (11 Tesio, 17 PermCath, 2 Shiley) for treatment of low blood flow (pump speed < 250 mL/min). Complete restoration of patency was achieved in 23 episodes (mean blood flow pre-tPA 130 mL/min; post-tPA 320 mL/min); partial restoration of patency was achieved in 20 episodes (mean blood flow pre-tPA 69 mL/min; post-tPA 233 mL/min). tPA was just as likely to be effective in patients with complete catheter occlusion (i.e., no blood flow) as it was when some initial blood flow was present. Nineteen episodes failed to respond to tPA. These episodes occurred in 13 catheters, 12 of which ultimately underwent radiologic evaluation; an extraluminal cause for low blood flow was found in all 12 catheters (6 malpositioned, 6 fibrin sheaths). CONCLUSIONS: tPA at a dose of 1 mg/mL is effective for restoring patency in CV dialysis catheters. Failure to respond to tPA strongly suggests an extraluminal cause of catheter malfunction.

Caring for the renal failure patient: optimizing iron therapy.

The effectiveness of anemia management in patients with end stage renal disease (ESRD) has increased over the past 4 years. However, approximately 26% of treated patients still do not meet the minimum hemoglobin (Hgb) value of 11 g/dl that is recommended by the K/DOQI Clinical Practice Guidelines (National Kidney Foundation [NKF], 2001). One of the main obstacles to good patient outcome may be iron deficiency, which is common in both the predialysis and dialysis period. Since iron is needed for Hgb synthesis, iron depletion exacerbated anemia and reduces the response to recombinant erythropoietin (rEPO) therapy. Health care providers can significantly improve patient outcome by addressing iron deficiency more rigorously. A good starting point is the establishment of an iron deficiency management protocol that includes early evaluation of iron status and aggressive iron therapy. Iron therapy, in turn, can be optimized by administering safe and effective iron supplements and by implementing maintenance iron regimens to prevent the recurrence of iron deficiency. By making these simple improvements to their treatment approach, clinicians can enhance the effectiveness of anemia management in patients with ESRD.