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      The influence of hypophosphatemia on outcomes of low- and high-intensity continuous renal replacement therapy in critically ill patients with acute kidney injury

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          Abstract

          Background

          The purpose of this study was to assess the role of hypophosphatemia in major clinical outcomes of patients treated with low- or high-intensity continuous renal replacement therapy (CRRT).

          Methods

          We performed a retrospective analysis of data collected from 492 patients. We divided patients into two CRRT groups based on treatment intensity (greater than or equal to or less than 40 mL/kg/hour of effluent generation) and measured serum phosphate level daily during CRRT.

          Results

          We obtained a total of 1,440 phosphate measurements on days 0, 1, and 2 and identified 39 patients (7.9%), 74 patients (15.0%), and 114 patients (23.1%) with hypophosphatemia on each of these respective days. In patients treated with low-intensity CRRT, there were 23 episodes of hypophosphatemia/1,000 patient days, compared with 83 episodes/1,000 patient days in patients who received high-intensity CRRT ( P < 0.01). Multiple Cox proportional hazards analysis showed that Acute Physiology and Chronic Health Evaluation (APACHE) III score, utilization of vasoactive drugs, and arterial pH on the second day of CRRT were significant predictors of mortality, while serum phosphate level was not a significant contributor to mortality.

          Conclusion

          APACHE score, use of vasoactive drugs, and arterial pH on the second CRRT day were identified as significant predictors of mortality. Hypophosphatemia might not be a major risk factor of increased mortality in patients treated with CRRT.

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          Most cited references22

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          Hypophosphatemia: an update on its etiology and treatment.

          Phosphate plays a key role in several biological processes. In recent years, new insights have been obtained into the regulation of the phosphate metabolism, including a growing amount of evidence suggesting that factors other than parathyroid hormone (PTH) and vitamin D are involved in maintaining the phosphate balance. A new class of phosphate-regulating factors, the so-called "phosphatonins," have been shown to be important in phosphate-wasting diseases. However, the role of the phosphatonins in the normal human homeostasis remains to be established. The incidence of hypophosphatemia in selected patient series can be more than 20%, with clinical sequelae ranging from mild to life threatening. Only when combined with phosphate depletion does hypophosphatemia become clinically significant. The factors that are involved in the phosphate homeostasis, the pathophysiology, the relevance in patient care, the clinical manifestations, and an appropriate management of phosphate depletion are discussed in this review.
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            Recovery of renal function and survival after continuous renal replacement therapy during extracorporeal membrane oxygenation.

            To assess the outcome of pediatric patients supported by concomitant extracorporeal membrane oxygenation (ECMO) and continuous renal replacement therapy (CRRT). Acute kidney injury is associated with mortality in ECMO patients. CRRT in patients on ECMO provides an efficient and potentially beneficial method of acute kidney injury management. Concern that concomitant CRRT use increases the risk of developing anuria and chronic renal failure limits its use in some centers. We hypothesized that development of chronic renal failure is rare with concurrent ECMO and CRRT. We evaluated the outcomes of 154 ECMO/CRRT patients cared for over 10 yrs at a referral pediatric medical center. None. Among 68 (44%) ECMO/CRRT survivors, 45 were assigned a pediatric risk, injury, failure, loss and end-stage (referred to as "pRIFLE") score at CRRT initiation. Seventeen (38%) patients met the criteria for Risk, 15 (33%) for Injury, and 10 (22%) for Failure. Two Failure patients later met End stage criteria. Of all survivors, 18 (26%) required ongoing renal replacement therapy (15 required continuous veno-venous hemofiltration, two required peritoneal dialysis, and one patient required intermittent hemodialysis) post ECMO discontinuation. Renal recovery occurred in 65 (96%) of 68 patients before discharge. One neonatal patient had sepsis-induced renal injury on transfer, but had normal creatinine 1 month later. Two pediatric patients with vasculitis and primary renal disease at presentation (both meeting Failure criteria) developed end-stage renal disease. One received peritoneal dialysis and subsequent renal transplant. The other has diminished function without need for renal replacement therapy. In the absence of primary renal disease, chronic renal failure did not occur after concurrent use of CRRT with ECMO. Concern for precipitating chronic renal failure by using CRRT during ECMO is not substantiated by this large single-center experience. Consistent with previous reports, mortality is higher in patients receiving concomitant CRRT and ECMO compared with those receiving ECMO alone. Mortality is similar to patients requiring CRRT who are not on ECMO. Additional studies are warranted to determine the optimal role of CRRT use in ECMO patients.
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              Hypophosphatemia in critically ill patients.

              The aim of this study was to assess the association of phosphate concentration with key clinical outcomes in a heterogeneous cohort of critically ill patients. This was a retrospective observational study at a general intensive care unit (ICU) of an Australian university teaching hospital enrolling 2730 adult critically ill patients. We studied 10504 phosphate measurements with a mean value of 1.17 mmol/L (measurements every 28.8 hours on average). Hyperphosphatemia (inorganic phosphate [iP] concentration > 1.4 mmol/L) occurred in 45% and hypophosphatemia (iP ≤ 0.6 mmol/L) in 20%. Among patients without any episodes of hyperphosphatemia, patients with at least 1 episode of hypophosphatemia had a higher ICU mortality than those without hypophosphatemia (P = .004). In addition, ICU nonsurvivors had lower minimum phosphate concentrations than did survivors (P = .009). Similar results were seen for hospital mortality. However, on multivariable logistic regression analysis, hypophosphatemia was not independently associated with ICU mortality (adjusted odds ratio, 0.86 [95% confidence interval, 0.66-1.10]; P = .24) and hospital mortality (odds ratio, 0.89 [0.73-1.07]; P = .21). Even when different cutoff points were used for hypophosphatemia (iP ≤ 0.5, 0.4, 0.3, or 0.2 mmol/L), hypophosphatemia was not an independent risk factor for ICU and hospital morality. In addition, timing of onset and duration of hypophosphatemia were not independent risk factor for ICU and hospital mortality. Hypophosphatemia behaves like a general marker of illness severity and not as an independent predictor of ICU or in-hospital mortality in critically ill patients. Copyright © 2013 Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                Kidney Res Clin Pract
                Kidney Res Clin Pract
                Kidney Research and Clinical Practice
                Korean Society of Nephrology
                2211-9132
                2211-9140
                September 2017
                30 September 2017
                : 36
                : 3
                : 240-249
                Affiliations
                Department of Internal Medicine, Kosin University College of Medicine, Busan, Korea
                Author notes
                Correspondence: Ho Sik Shin, Department of Internal Medicine, Kosin University College of Medicine, 262 Gamcheon-ro, Seo-gu, Busan 49267, Korea. E-mail: 67920@ 123456naver.com
                Article
                krcp-36-240
                10.23876/j.krcp.2017.36.3.240
                5592891
                28904875
                97b8467a-b578-4608-9206-db0ee5243542
                Copyright © 2017 by The Korean Society of Nephrology

                This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 31 January 2017
                : 19 April 2017
                : 20 April 2017
                Categories
                Original Article

                acute kidney injury,continuous renal replacement therapy,hypophosphatemia,intensity,mortality

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