Acute kidney injury (AKI) frequently occurs in the setting of critical illness and its management poses a challenge for the intensivist. Optimal management of volume status is critical in the setting of AKI in the ICU patient. The use of urine sodium, the fractional excretion of sodium (FeNa), and the fractional excretion of urea (FeUrea) are common clinical tools used to help guide fluid management especially further volume expansion but should be used in the context of the patient’s overall clinical scenario as they are not completely sensitive or specific for the finding of volume depletion and can be misleading. In the case of oliguric or anuric AKI, diuretics are often utilized to increase the urine output although current evidence suggests that they are best reserved for the treatment of volume overload and hyperkalemia in patients who are likely to respond to them. Management of volume overload in ICU patients with AKI is especially important as volume overload has several negative effects on organ function and overall morbidity and mortality. 1. Introduction Acute kidney injury (AKI) is a frequent complication in critically ill patients in the intensive care unit (ICU) with an incidence ranging from 17.5% to 78% [1–5]. Management of volume status in critically ill patients with AKI is difficult as it is often accompanied by oliguria or anuria as well as total body fluid overload and tissue edema. AKI increases the risk of mortality and often occurs in the setting of sepsis or other forms of shock [6]. While the early goal-directed therapy study showed the benefit of adequate volume repletion in critically ill patients with septic shock [7], there are detrimental effects associated with salt and water overload which can result from resuscitation with crystalloids or colloids. These include worsening of lung function and difficulty of wound healing [8, 9]. In this paper we will focus on the role of intravenous fluids (IVFs) and diuretics for the management of volume status in critically ill patients with AKI. We will also discuss the differences between oliguric and nonoliguric renal failure and the effects on outcomes of “converting” patients from oliguric to nonoliguric renal failure. 2. Epidemiology and Mortality of AKI in the ICU The Acute Dialysis Quality Initiative (ADQI) published the Risk, Injury, Failure, Loss, End-Stage Kidney Disease (RIFLE) definitions for AKI in 2004 [10], developing a consensus definition of AKI that could be used in studies rather than the 30 plus definitions that had been used in previous studies. This was revised
References
[1]
L. Englberger, R. M. Suri, Z. Li et al., “Clinical accuracy of RIFLE and Acute Kidney Injury Network (AKIN) criteria for acute kidney injury in patients undergoing cardiac surgery,” Critical Care, vol. 15, no. 1, article R16, 2011.
[2]
A. Q. Lam and B. D. Humphreys, “Onco-nephrology: AKI in the cancer patient,” Clinical Journal of the American Society of Nephrology, vol. 7, no. 10, pp. 1692–1700, 2012.
[3]
C. Y. Lin, Y. C. Chen, F. C. Tsai et al., “RIFLE classification is predictive of short-term prognosis in critically ill patients with acute renal failure supported by extracorporeal membrane oxygenation,” Nephrology Dialysis Transplantation, vol. 21, no. 10, pp. 2867–2873, 2006.
[4]
S. G. Coca, P. Bauling, T. Schifftner, C. S. Howard, I. Teitelbaum, and C. R. Parikh, “Contribution of acute kidney injury toward morbidity and mortality in burns: a contemporary analysis,” American Journal of Kidney Diseases, vol. 49, no. 4, pp. 517–523, 2007.
[5]
H. R. Samimagham, S. Kheirkhah, A. Haghighi, and Z. Najmi, “Acute kidney injury in intensive care unit: incidence, risk factors and mortality rate,” Saudi Journal of Kidney Diseases and Transplantation, vol. 22, no. 3, pp. 464–470, 2011.
[6]
S. M. Bagshaw, C. George, and R. Bellomo, “A comparison of the RIFLE and AKIN criteria for acute kidney injury in critically ill patients,” Nephrology Dialysis Transplantation, vol. 23, no. 5, pp. 1569–1574, 2008.
[7]
E. Rivers, B. Nguyen, S. Havstad et al., “Early goal-directed therapy in the treatment of severe sepsis and septic shock,” The New England Journal of Medicine, vol. 345, no. 19, pp. 1368–1377, 2001.
[8]
R. W. Schrier, “Fluid administration in critically I11 patients with acute kidney injury,” Clinical Journal of the American Society of Nephrology, vol. 5, no. 4, pp. 733–739, 2010.
[9]
B. Brandstrup, H. T？nnesen, R. Beier-Holgersen et al., “Effects of intravenous fluid restriction on postoperative complications: comparison of two perioperative fluid regimens—a randomized assessor-blinded multicenter trial,” Annals of Surgery, vol. 238, no. 5, pp. 641–648, 2003.
[10]
R. Bellomo, C. Ronco, J. A. Kellum, R. L. Mehta, and P. Palevsky, “Acute renal failure—definition, outcome measures, animal models, fluid therapy and information technology needs: the second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group,” Critical Care, vol. 8, no. 4, pp. R204–R212, 2004.
[11]
R. L. Mehta, J. A. Kellum, S. V. Shah et al., “Acute kidney injury network: report of an initiative to improve outcomes in acute kidney injury,” Critical Care, vol. 11, no. 2, article R31, 2007.
[12]
E. Macedo, R. Malhotra, J. Bouchard, S. K. Wynn, and R. L. Mehta, “Oliguria is an early predictor of higher mortality in critically ill patients,” Kidney International, vol. 80, no. 7, pp. 760–767, 2011.
[13]
J. Gotfried, J. Wiesen, R. Raina, and J. V. Nally Jr., “Finding the cause of acute kidney injury: which index of fractional excretion is better?” Cleveland Clinic Journal of Medicine, vol. 79, no. 2, pp. 121–126, 2012.
[14]
S. M. Bagshaw, M. Bennett, P. Devarajan, and R. Bellomo, “Urine biochemistry in septic and non-septic acute kidney injury: a prospective observational study,” Journal of Critical Care. In press.
[15]
A. J. Vaz, “Low fractional excretion of urine sodium in acute renal failure due to sepsis,” Archives of Internal Medicine, vol. 143, no. 4, pp. 738–739, 1983.
[16]
H. L. Corwin, M. J. Schreiber, and L. S. T. Fang, “Low fractional excretion of sodium. Occurrence with hemoglobinuric- and myoglobinuric-induced acute renal failure,” Archives of Internal Medicine, vol. 144, no. 5, pp. 981–982, 1984.
[17]
L. S. T. Fang, R. A. Sirota, T. H. Ebert, and N. S. Lichtenstein, “Low fractional excretion of sodium with contrast media-induced acute renal failure,” Archives of Internal Medicine, vol. 140, no. 4, pp. 531–533, 1980.
[18]
S. Zarich, L. S. T. Fang, and J. R. Diamond, “Fractional excretion of sodium. Exceptions of it diagnostic value,” Archives of Internal Medicine, vol. 145, no. 1, pp. 108–112, 1985.
[19]
K. Lopau, D. Kleinert, J. Erler, L. Schramm, E. Heidbreder, and C. Wanner, “Tacrolimus in acute renal failure: does L-arginine-infusion prevent changes in renal hemodynamics?” Transplant International, vol. 13, no. 6, pp. 436–442, 2000.
[20]
M. N. Pépin, J. Bouchard, L. Legault, and J. éthier, “Diagnostic performance of fractional excretion of Urea and fractional excretion of sodium in the evaluations of patients with acute kidney injury with or without diuretic treatment,” American Journal of Kidney Diseases, vol. 50, no. 4, pp. 566–573, 2007.
[21]
M. Darmon, F. Vincent, J. Dellamonica et al., “Diagnostic performance of fractional excretion of Urea in the evaluation of critically ill patients with acute kidney injury: a multicenter cohort Study,” Critical Care, vol. 15, article R178, 2011.
[22]
A. P. Wheeler, G. R. Bernard, B. T. Thompson et al., “Pulmonary-artery versus central venous catheter to guide treatment of acute lung injury,” The New England Journal of Medicine, vol. 354, no. 21, pp. 2213–2224, 2006.
[23]
M. E. Grams, M. M. Estrella, J. Coresh, R. G. Brower, and K. D. Liu, “Fluid balance, diuretic use, and mortality in acute kidney injury,” Clinical Journal of the American Society of Nephrology, vol. 6, no. 5, pp. 966–973, 2011.
[24]
H. P. Wiedemann, A. P. Wheeler, G. R. Bernard et al., “Comparison of two fluid-management strategies in acute lung injury,” The New England Journal of Medicine, vol. 354, no. 24, pp. 2564–2575, 2006.
[25]
K. Sw？rd, F. Valsson, J. Sellgren, and S. E. Ricksten, “Differential effects of human atrial natriuretic peptide and furosemide on glomerular filtration rate and renal oxygen consumption in humans,” Intensive Care Medicine, vol. 31, no. 1, pp. 79–85, 2005.
[26]
S. M. Bagshaw, A. Delaney, D. Jones, C. Ronco, and R. Bellomo, “Diuretics in the management of acute kidney injury: a multinational survey,” Contributions to Nephrology, vol. 156, pp. 236–249, 2007.
[27]
R. L. Mehta, M. T. Pascual, S. Soroko, and G. M. Chertow, “Diuretics, mortality, and nonrecovery of renal function in acute renal failure,” Journal of the American Medical Association, vol. 288, no. 20, pp. 2547–2553, 2002.
[28]
S. Uchino, G. S. Doig, R. Bellomo et al., “Diuretics and mortality in acute renal failure,” Critical Care Medicine, vol. 32, no. 8, pp. 1669–1677, 2004.
[29]
I. R. Shilliday, K. J. Quinn, and M. E. M. Allison, “Loop diuretics in the management of acute renal failure: a prospective, double-blind, placebo-controlled, randomized study,” Nephrology Dialysis Transplantation, vol. 12, no. 12, pp. 2592–2596, 1997.
[30]
F. Cantarovich, B. Rangoonwala, H. Lorenz, M. Verho, and V. L. M. Esnault, “High-dose furosemide for established ARF: a prospective, randomized, double-blind, placebo-controlled, multicenter trial,” American Journal of Kidney Diseases, vol. 44, no. 3, pp. 402–409, 2004.
[31]
P. H. J. Van Der Voort, E. C. Boerma, M. Koopmans et al., “Furosemide does not improve renal recovery after hemofiltration for acute renal failure in critically ill patients: a double blind randomized controlled trial,” Critical Care Medicine, vol. 37, no. 2, pp. 533–538, 2009.
[32]
V. C. Wu, C. F. Lai, C. C. Shiao, et al., “Effect of diuretic use on 30-day postdialysis mortality in critically ill patients receiving acute dialysis,” PloS One, vol. 7, no. 3, article e30836, 2012.
[33]
J. R. Prowle, J. E. Echeverri, E. V. Ligabo, C. Ronco, and R. Bellomo, “Fluid balance and acute kidney injury,” Nature Reviews Nephrology, vol. 6, no. 2, pp. 107–115, 2010.
[34]
L. Dalfino, L. Tullo, I. Donadio, V. Malcangi, and N. Brienza, “Intra-abdominal hypertension and acute renal failure in critically ill patients,” Intensive Care Medicine, vol. 34, no. 4, pp. 707–713, 2008.
[35]
M. Heung, D. F. Wolfgram, M. Kommareddi, Y. Hu, P. X. Song, and A. O. Ojo, “Fluid overload at initiation of renal replacement therapy is associated with lack of renal recovery in patients with acute kidney injury,” Nephrology Dialysis Transplantation, vol. 27, no. 3, pp. 956–961, 2012.
[36]
K. V. Desai, G. A. Laine, R. H. Stewart et al., “Mechanics of the left ventricular myocardial interstitium: effects of acute and chronic myocardial edema,” American Journal of Physiology, vol. 294, no. 6, pp. H2428–H2434, 2008.
[37]
R. P. Dellinger, M. M. Levy, J. M. Carlet, et al., “Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock,” Critical Care Medicine, vol. 36, no. 1, pp. 296–327, 2008.
[38]
J. L. LeTourneau, J. Pinney, and C. R. Phillips, “Extravascular lung water predicts progression to acute lung injury in patients with increased risk,” Critical Care Medicine, vol. 40, no. 3, pp. 847–854, 2012.
[39]
P. E. Marik, X. Monnet, and J. L. Teboul, “Hemodynamic parameters to guide fluid therapy,” Annals of Intensive Care, vol. 1, no. 1, article 1, 2011.
[40]
P. E. Marik, A. Levitov, A. Young, and L. Andrews, “The use of NICOM (Bioreactance) and Carotid Doppler to determine volume responsiveness and blood flow redistribution following passive leg raising in hemodynamically unstable patients,” Chest. In press.
[41]
S. Uchino, R. Bellomo, H. Morimatsu et al., “Pulmonary artery catheter versus pulse contour analysis: a prospective epidemiological study,” Critical Care, vol. 10, article R174, 2006.
