作者:Shilpa Sharma, Sushrut S. Waikar 来源:AJKD 日期:2013-02-26
Phosphate Balance in Continuous Venovenous Hemofiltration
Continuous renal replacement therapy (CRRT) was introduced to enable dialytic treatment of hemodynamically unstable patients for whom intermittent hemodialysis could be difficult to administer.1 CRRT has potentially harmful unintended effects, including excessive removal of amino acids, trace elements, and electrolytes such as phosphate.2 Phosphate is the most abundant intracellular anion and is essential for multiple biological functions. Because hypophosphatemia is a complication reported in >10% of patients undergoing CRRT,3, 4, 5 we investigated phosphate balance during continuous venovenous hemofiltration (
CVVH), hypothesizing that CRRT leads to a negative phosphate balance despite protocol-driven phosphate repletion strategies and normalization of serum phosphate levels.
We studied 35 patients with acute kidney injury who underwent CVVH by using a partial effluent collection device that diverted ∼1% of the total effluent volume to a collection bag. CVVH was performed using biocompatible polyethersulfone membranes, bicarbonate or citrate (phosphate-free) replacement solution delivered prefilter at rates of 1,600-4,000 mL/h, and blood flow rates of 200-250 mL/min. We calculated phosphate balance by subtracting urinary and CVVH losses from dietary (enteral or parenteral) intake. Baseline characteristics are described in Tables 1 and S1. We found a significant correlation between total effluent volume and net phosphate removal (Fig 1; r = 0.86; P < 0.001). The lowest recorded serum phosphate concentration during the study was 2 mg/dL (median, 2.6 [range, 2-8.6] mg/dL). According to reference laboratory values (2.5-4.3 mg/dL), 34.2% of patients had overt hypophosphatemia. All patients were in negative phosphate balance during CVVH despite protocol-driven phosphate repletion strategies (Table S2 and Fig S1). Our estimates of negative phosphate balance are slight underestimates because we did not collect stool, which may contain ∼500 mg/d of phosphate.6 Using univariate regression analyses, the predictors of natural log–transformed net phosphate balance were age (β coefficient, −0.02; P = 0.05), medical versus surgical intensive care unit (β = −0.60; P = 0.02), pre-CVVH serum phosphate level (β = 0.19; P = 0.004), effluent volume (β = 0.0047 [per 1 L]; P < 0.001), and days of CVVH (β = 0.26; P < 0.001). We found no association between phosphate balance and in-hospital mortality (P = 0.1; OR, 2.26; 95% CI, 0.76-6.70). Of the 15 patients for whom balance studies were performed for at least 3 days, 87% required intravenous phosphate repletion even though they were hyperphosphatemic at CVVH initiation. Negative phosphate balance was highest at CVVH initiation, reflecting phosphate excess. Although daily phosphate balance became less negative over time as steady state was achieved and nutrition was introduced, it remained persistently negative even after a week of CVVH (Table S3). In the 6 patients who had serial CVVH effluent collections for 7 consecutive days, cumulative net phosphate balance ranged between −6.1 and −13.7 (median, −8.9) g. We found a persistent net negative phosphate balance even on day 7 of treatment with CVVH (range, −449 to −1,259 mg). Our calculations of negative phosphate balance are underestimates because we did not measure phosphate losses in gastrointestinal secretions or surgical drains due to concerns over feasibility.
http://www.ajkd.org/article/S0272-6386(13)00031-0/fulltext