CJASN
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Published ahead of print on May 10, 2006
Clin J Am Soc Nephrol 1: 869-873, 2006
© 2006 American Society of Nephrology
doi: 10.2215/CJN.00450206
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
CJN.00450206v1
1/4/869    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Liu, K. D.
Right arrow Articles by Chertow, G. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Liu, K. D.
Right arrow Articles by Chertow, G. M.

Special Features

Evolving Practices in Critical Care and Potential Implications for Management of Acute Kidney Injury

Kathleen D. Liu*, Michael A. Matthay{dagger}, and Glenn M. Chertow*,{ddagger}

* Division of Nephrology, Department of Medicine; {dagger} Departments of Medicine and Anesthesiology and Cardiovascular Research Institute; and {ddagger} Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, California

Address correspondence to: Dr. Glenn M. Chertow, University of California San Francisco, Department of Medicine Research, UCSF Laurel Heights, Suite 430, 3333 California Street, San Francisco, CA 94118-1211. Phone: 415-476-2173; Fax: 415-476-1700; chertowg{at}medicine.ucsf.edu


   Introduction
Top
 Introduction
Acute Respiratory Distress...
 Early Goal-Directed Therapy,...
 Corticosteroids, AKI, and...
 Future Directions
 Conclusion
 References
 
Acute kidney injury (AKI) is a common complication in hospitalized patients, with an incidence of 3 to 10% (1–4). In-hospital mortality rates that are associated with AKI remain high, in the range of 30 to 70% (5–8), despite significant improvements in dialytic technology as well as important advances in critical care, which have resulted in improved survival for other critical illnesses, including acute lung injury and sepsis (9). These improvements include continuous renal replacement therapies, which allow for continuous removal of solutes and fluid and may be tolerated better from a hemodynamic standpoint, and biocompatible dialysis membranes, which are associated with reduced complement and granulocyte activation.

In general, indications for dialysis in the acute care setting have been extrapolated from those that are applied in chronic kidney disease, including volume overload that is refractory to diuretic therapy; electrolyte abnormalities (in particular hyperkalemia); uremic complications (pericarditis or pleuritis); severe acidosis (pH < 7.20); and selected toxic ingestions, such as methanol, ethylene glycol, and other water-soluble agents (10,11). However, the evidence base supporting specific dialysis practices in the acute care setting is limited. For example, several studies that were completed in the 1960s and 1970s compared "early" and "late" initiation of dialysis, using blood urea nitrogen (BUN) to define early and late (Table 1). These studies primarily were cohort studies that used historical controls, not randomized, clinical trials. The results of these investigations, along with extrapolation from the ESRD population, promoted recent practice patterns. Currently, many nephrologists often delay dialysis in the acute care setting until the patient has an impending complication of AKI, such as hyperkalemia leading to cardiac arrhythmias, acidosis resulting in hypotension, or oliguria leading to volume overload or hypoxemia, or until the BUN exceeds 100 mg/dl (18). Given differences in protein catabolism, diet, comorbid conditions, and severity of illness, it may be inappropriate to extrapolate any BUN or creatinine cutoff for dialysis initiation in the chronic setting to patients with AKI.


View this table:
[in this window]
[in a new window]

  		Table 1. Timing of initiation of dialysis and its association with mortality

 
Practice patterns regarding decisions to initiate dialysis in the acute care setting have not been well described and have not been subjected to randomized trials. Further investigation is needed to describe and provide evidence for these clinical practices. However, nephrologists and intensivists should recognize that recent evidence-based changes in the practice of critical care medicine have significant effects on the parameters that trigger the decision to initiate dialysis. For example, aggressive volume resuscitation for sepsis will exacerbate volume overload in an oliguric patient; as a result that patient may require dialysis earlier in the course of AKI to avoid complications of volume overload, including hypoxemia. In this article, we review recent changes in critical care practice and the potential effects of these practices on metabolic factors that may influence dialysis practice. In so doing, we emphasize the need for randomized clinical trials to examine the optimal timing of dialysis after AKI.


   Acute Respiratory Distress Syndrome, AKI, and Acidosis
Top
 Introduction
 Acute Respiratory Distress...
Early Goal-Directed Therapy,...
 Corticosteroids, AKI, and...
 Future Directions
 Conclusion
 References
 
Acute respiratory distress syndrome (ARDS) historically has been associated with a mortality rate of 40 to 50%. The ARDS Network demonstrated that a lung-protective, low tidal volume ventilation strategy markedly improves survival (19). In the ARDS Network trial, 861 patients who had acute lung injury and were mechanically ventilated were randomly assigned to either conventional tidal volumes of 12 ml/kg or to low tidal volumes of 6 ml/kg of predicted body weight. There was an 8.8% absolute reduction in death (31.0 versus 39.8%; P = 0.007) before discharge home or breathing without assistance with the low tidal volume ventilation strategy. A subsequent ARDS Network trial compared higher and lower levels of positive end-expiratory pressure (PEEP) (20) and found a further reduction in mortality (26%) in patients who were ventilated with the low tidal volume strategy. Therefore, the current standard of care for patients with acute lung injury is to use tidal volumes in the range of 4 to 6 ml/kg ideal body weight with a plateau pressure <30 cm H2O, maintaining acceptable oxygenation by modulating PEEP and fraction of inspired oxygen (21). However, the low volume ventilatory strategy can lead to acidemia, resulting from respiratory acidosis, a strategy that is known as permissive hypercapnia (22). In the original ARDS Network trial, 57 (14%) of 423 patients who were ventilated with low tidal volumes had a serum pH <7.30 on day 1 of the trial, compared with 22 (6%) of 386 patients in the high tidal volume therapy arm of the trial despite no difference in the incidence of AKI in the two groups. In the face of respiratory acidosis, the functioning kidney generates bicarbonate to maintain pH balance. However, the renal capacity to compensate for respiratory acidosis is limited after AKI. Indeed, the mild metabolic acidosis that often accompanies early AKI will compound the respiratory acidosis of permissive hypoventilation. Without correction of the metabolic acidosis, hyperkalemia, hypotension, and other complications may ensue. Intravenous sodium bicarbonate may transiently correct the metabolic acidosis but may have adverse effects, including hypoxemia from volume overload as well as intracellular acidosis (23). Therefore, in the face of kidney injury, dialysis may be required for control of acidemia.

It is interesting that recent animal and human studies have suggested that low tidal volume ventilation may be renoprotective. In several animal models, injurious ventilatory strategies have been shown to result in AKI (24–26). In the ARDS Network trial (19), patients who were ventilated with the low tidal volume strategy were slightly less likely to develop AKI (number of "renal failure–free days" 20 ± 11 versus 18 ± 11 in control subjects; P = 0.005). Although low tidal volume may protect against AKI (a finding that will require confirmation), it is important to recognize that patients who develop AKI in the setting of acute lung injury may require dialysis earlier when low tidal volume ventilation is applied, to prevent the complications of a mixed metabolic and respiratory acidosis.


   Early Goal-Directed Therapy, AKI, and Volume Overload
Top
 Introduction
 Acute Respiratory Distress...
 Early Goal-Directed Therapy,...
Corticosteroids, AKI, and...
 Future Directions
 Conclusion
 References
 
Approximately 750,000 patients in the United States develop severe sepsis each year (27). Severe sepsis is associated with a mortality rate of approximately 30% (27). It has been recognized that patients with the sepsis syndrome may benefit from early goal-directed therapy, that is, early and aggressive volume resuscitation and vasopressor management (28). Indeed, the 2004 Surviving Sepsis Campaign guidelines (from organizations e.g., the American College of Chest Physicians, the American Thoracic Society, the European Society of Intensive Care Medicine, and the Society for Critical Care Medicine) recommend resuscitation of patients on the basis of the protocol described by Rivers et al. (29). In this protocol, tissue oxygen delivery is optimized in patients with early severe sepsis using a stepwise approach of goal-directed volume resuscitation (using a central venous catheter to guide management), followed by the use of vasopressors, transfusion, and inotropic agents to achieve and maintain a central venous oxygen saturation of >70%.

These strategies frequently result in the administration of several liters of crystalloid, usually 0.9% saline or other isotonic solutions, with the goal of maintaining a central venous pressure of 8 to 12 mmHg and sustaining organ perfusion (28). Indeed, the use of a central venous catheter per protocol to maintain central venous pressure resulted in a significant increase in crystalloid administration during the first 6 h of the protocol. Whereas volume expansion may abrogate prerenal azotemia, the effects of the Rivers et al. protocol on other causes of AKI and its complications remain untested. The recently completed Acute Respiratory Distress Syndrome Network Fluid and Catheter Treatment Trial (FACTT) study may shed important light on the effects of targeted volume resuscitation. However, when there is concomitant AKI, the capacity of the kidneys to maintain salt and water balance, as well as acid-base homeostasis, is reduced. In particular, in the setting of oliguria, patients with AKI may become rapidly volume overloaded. Moreover, the expansion of body water by crystalloid administration may mask the severity of AKI by increasing the total body water space, thereby diluting creatinine and other markers of kidney function (30).

In the setting of volume overload, diuretic agents can be used to augment urine output, although several observational studies and a large randomized trial (31–33) have indicated no benefit and even potential harm associated with the use of high-dose furosemide and other diuretic agents in the intensive care unit (ICU). Even in the setting of diuretic-responsive AKI, there is a diminished capacity to induce a large net negative fluid balance (which usually is required, given obligate fluid requirements in the form of antibiotics, vasopressor agents, and parenteral or enteral nutrition) and may be limited further by hemodynamic effects (e.g., venodilation) and metabolic complications, including hypokalemia and hyponatremia (34). In the setting of acute lung injury, volume overload may be poorly tolerated because an increase in extravascular lung water and pleural effusions may impair oxygenation and ventilation further. Therefore, in the setting of oliguric AKI, aggressive fluid resuscitation may necessitate earlier initiation of dialytic support for control of volume status and to remove extravascular fluid.

In addition, depending on the choice of intravenous fluids administered, the patient may develop a hyperchloremic metabolic acidosis, exacerbating the acidemia described in the previous section. Hyperchloremic metabolic acidosis is more likely to occur when 0.9% saline is used. In the Rivers study (28), patients in the early goal-directed therapy arm received an average of 4.9 L of fluid during the first 6 h of their hospital course. The effects of crystalloid administration on acid-base balance have not been studied carefully in the critically ill. In the Saline versus Albumin Fluid Evaluation (SAFE) trial, patients received relatively little crystalloid by post-Rivers standards (1565 ± 1526 ml during the first 24 h) and equal amounts of nonstudy fluids, rendering evaluation of the intervention on acid-base balance difficult (35). Furthermore, the SAFE study, along with recent meta-analyses, demonstrated that there is no benefit to colloid administration in the critically ill, compared with crystalloid administration. This also may result in increased crystalloid administration to critically ill patients, which, in the presence of kidney injury and depending on the choice of intravenous fluid, may worsen acidosis. In a randomized clinical trial from the surgical literature, Scheingraber et al. (36) randomly assigned 24 women who were undergoing gynecologic surgery to receive 0.9% saline or Ringer’s lactate solution. These patients received an average of 5 L of crystalloid during the first 2 h of surgery, approximately the same volume of fluid that patients in the Rivers study received during the first 6 h of resuscitation. Women who received 0.9% saline had a reduction in pH from 7.41 to 7.28, with no associated change in Paco2 but with an increase in serum chloride from 104 to 115 mmol/L. Therefore, rapid infusion of chloride-containing solutions may have significant effects on pH, in particular in the setting of other therapeutic interventions such as permissive hypercapnia (Figure 1).


Figure 1
View larger version (21K):
[in this window]
[in a new window]
[as a PowerPoint slide]
  		Figure 1. Potential indications for dialysis in the intensive care unit. On the right, evidence-based strategies to reduce mortality in the critical care setting are described. The effects of these strategies on indications for dialysis are indicated by arrows.

 

   Corticosteroids, AKI, and Azotemia
Top
 Introduction
 Acute Respiratory Distress...
 Early Goal-Directed Therapy,...
 Corticosteroids, AKI, and...
Future Directions
 Conclusion
 References
 
Recent studies suggest that relative adrenal insufficiency may be underrecognized in critically ill patients. The diagnosis (and therefore the incidence) of relative adrenal insufficiency remain controversial, but it has been estimated that 10 to 30% of critically ill patients have relative adrenal insufficiency (37,38). Annane et al. (39) reported in a randomized clinical trial that low-dose hydrocortisone (50 mg, four times per day) and fludrocortisone (50 µg, once a day) for 7 d enhanced survival with no increase in complications among ICU patients with septic shock; a large multicenter clinical trial is ongoing. Meta-analyses of recent studies also have suggested that low-dose corticosteroids may have survival benefit (40,41). Although the survival benefit of steroids remains an area of clinical debate, these studies have led to wider recognition of relative adrenal insufficiency and treatment of more critically ill patients with low-dose corticosteroids.

It is well established that steroids contribute to the hypercatabolism of critically ill patients. Slotman et al. (42) reported a significant increase in BUN over the entire first 7 d in critically ill patients who had sepsis and were treated with methylprednisolone for a 24-h period, when compared with patients who were treated with placebo (26 versus 11%; P < 0.01). There was no associated increase in serum creatinine, suggesting that the increase in BUN primarily was the result of increased protein catabolism and not AKI. Therefore, patients who are treated with steroids and who have AKI are likely to experience an abrupt increase in nitrogenous waste products, which may result in uremic complications and also diminish the ability to provide nutritional support. Hypercatabolism will be exacerbated further by acidosis, as a result of the effects on acidosis on the ubiquitin-proteasome pathway (43). Finally, the mineralocorticoid effects of methylprednisolone, prednisone, or fludrocortisone will promote fluid retention and volume overload by increasing sodium reabsorption in the distal tubule. Therefore, patients who are treated with glucocorticoids may require earlier dialytic intervention primarily for azotemia but also for volume overload (Figure 1).


   Future Directions
Top
 Introduction
 Acute Respiratory Distress...
 Early Goal-Directed Therapy,...
 Corticosteroids, AKI, and...
 Future Directions
Conclusion
 References
 
Randomized trials that focus on several aspects of the dialysis prescription, including the preferred modality of dialysis in the critically ill and the optimal method of nutrition support for AKI, should be designed and carried out. The optimal dose of dialysis is the focus of the ongoing Acute Renal Failure Trial Network study (44), a multicenter, randomized trial to compare intensive versus conventional dialysis dose for treatment of severe AKI.

Recent changes in clinical practice in the ICU highlight the need for clinical trials to determine the optimal timing of the initiation of dialysis after AKI. Earlier provision of dialysis may be associated with increased risks (11); these include an increased risk for infection from an indwelling dialysis catheter, hypotension associated with therapy, and leukocyte activation from contact with dialysis membranes, although some of these factors may be attenuated by the use of biocompatible membranes and extended treatment duration, either in the form of slow low efficiency dialysis or continuous renal replacement therapy. Moreover, earlier provision of dialysis might result in procedures’ being performed on patients who otherwise eventually would have recovered kidney function. The effects of dialysis on recovery of kidney function are unclear. Animal studies have suggested that autoregulation of blood flow is impaired after ischemic injury; whether this applies to human disease is unclear but cannot be excluded by current data. Although continuous or hybrid dialysis modalities have not been shown definitively to enhance survival or recovery of kidney function after AKI, these modalities tend to be associated with less intradialytic hypotension than intermittent hemodialysis. However, continuous and hybrid therapies are relatively new methods of renal replacement, and the full spectrum of their effects has not been characterized fully.

Ultimately, whether the hypothetical risks are outweighed by potential benefits of earlier dialysis initiation will require a rigorously conducted randomized clinical trial. Early intervention will require careful consideration of patients’ inclusion criteria; for example, patients might be enrolled after experiencing a 200% increase in serum creatinine (the "injury" criteria of the new Acute Dialysis Quality Initiative RIFLE criteria for acute renal failure) and randomly assigned to start dialysis when prespecified levels of BUN are attained. Biomarkers that better predict the course of AKI would be helpful to incorporate into clinical trial design, although reliable, valid biomarkers may not be available for several years or more. Pilot studies will be needed to test feasibility and acceptance by nephrologists and non-nephrologists alike.


   Conclusion
Top
 Introduction
 Acute Respiratory Distress...
 Early Goal-Directed Therapy,...
 Corticosteroids, AKI, and...
 Future Directions
 Conclusion
References
 
Randomized clinical trials are urgently needed with the goal of reducing the exceptionally high mortality rates that are associated with AKI. While awaiting the results of randomized clinical trials, nephrologists and other intensivists should recognize that changes in evidenced-based ICU practice may necessitate earlier initiation of dialysis in selected circumstances, particularly among patients who are treated with low tidal volume ventilation, early goal-directed therapy for sepsis, and corticosteroids for adrenal insufficiency.


   Footnotes
 
Published online ahead of print. Publication date available at www.cjasn.org.


   References
Top
 Introduction
 Acute Respiratory Distress...
 Early Goal-Directed Therapy,...
 Corticosteroids, AKI, and...
 Future Directions
 Conclusion
 References
 

  1. Brivet FG, Kleinknecht DJ, Loirat P, Landais PJ; for the French Study Group on Acute Renal Failure: Acute renal failure in intensive care units: Causes, outcome and prognostic factors of hospital mortality—A prospective, multicenter study. Crit Care Med 24: 192–198, 1996[CrossRef][Medline]
  2. Liano F, Pascual J: Outcomes in acute renal failure. Semin Nephrol 18: 541–550, 1998[Medline]
  3. Nolan C, Anderson R: Hospital-acquired acute renal failure. J Am Soc Nephrol 9: 710–718, 1998[Medline]
  4. Pruchnicki MC, Dasta JF: Acute renal failure in hospitalized patients: Part I. Ann Pharmacother 36: 1261–1267, 2002[Abstract]
  5. Metnitz P, Krenn C, Steltzer H, Lang T, Ploder J, Lez K, Le Gall, J-R, Druml W: Effect of acute renal failure requiring renal replacement therapy on outcome in critically ill patients. Crit Care Med 30: 2051–2058, 2002[CrossRef][Medline]
  6. Mehta R, Pascual M, Soroko S, Savage B, Himmelfarb J, Ikizler T, Paganini E, Chertow G: Spectrum of acute renal failure in the intensive care unit: The PICARD experience. Kidney Int 66: 1613–1621, 2004[CrossRef][Medline]
  7. Ympa YP, Sakr Y, Reinhart K, Vincent JL: Has mortality from acute renal failure decreased? A systematic review of the literature. Am J Med 118: 827–832, 2005[CrossRef][Medline]
  8. Uchino S, Kellum JA, Bellomo R, Doig GS, Morimatsu H, Morgera S, Schetz M, Tan I, Bouman C, Macedo E, Gibney N, Tolwani A, Ronco C: Acute renal failure in critically ill patients: A multinational, multicenter study. JAMA 294: 813–818, 2005[Abstract/Free Full Text]
  9. Lameire N, Van Biesen W, Vanholder R: Acute renal failure. Lancet 365: 417–430, 2005[Medline]
  10. Dollins M, Kraus M, Molitoris B: Intensive care nephrology. In: The Kidney, 7th Ed., edited by Brenner BM, Philadelphia, W.B. Saunders, 2003, pp 2697–2732
  11. Palevsky PM, Baldwin I, Davenport A, Goldstein S, Paganini E: Renal replacement therapy and the kidney: Minimizing the impact of renal replacement therapy on recovery of acute renal failure. Curr Opin Crit Care 11: 548–554, 2005[CrossRef][Medline]
  12. Parsons F, Hobson S, Blagg C, McCracken B: Optimum time for dialysis in acute reversible renal failure. Lancet 277: 124–129, 1961
  13. Fischer R, Griffin W, Clark D: Early dialysis in the treatment of acute renal failure. Surg Gynecol Obstet 123: 1019–1023, 1966[Medline]
  14. Kleinknecht D, Jungers P, Chanard J, Barbanel C, Ganeval D: Uremic and non-uremic complications in acute renal failure: Evaluation of early and frequent dialysis on prognosis. Kiney Int 1: 190–196, 1972
  15. Conger J: A controlled evaluation of prophylactic dialysis in post-traumatic acute renal failure. J Trauma 15: 1056–1063, 1975[Medline]
  16. Gettings L, Reynolds H, Scalea T: Outcome in post-traumatic acute renal failure when continuous renal replacement therapy is applied early vs late. Intensive Care Med 25: 805–813, 1999[CrossRef][Medline]
  17. Bouman CS, Oudemans-Van Straaten HM, Tijssen JG, Zandstra DF, Kesecioglu J: Effects of early high-volume continuous venovenous hemofiltration on survival and recovery of renal function in intensive care patients with acute renal failure: A prospective, randomized trial. Crit Care Med 30: 2205–2211, 2002[CrossRef][Medline]
  18. Mehta RL: Indications for dialysis in the ICU: Renal replacement versus renal support. Blood Purif 19: 227–232, 2001[CrossRef][Medline]
  19. The Acute Respiratory Distress Syndrome Network: Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 342: 1301–1308, 2000[Abstract/Free Full Text]
  20. Brower R, Lanken P, MacIntyre N, Matthay M, Morris A, Ancukiewicz M, Schoenfeld D, Thompson B; for the National Heart, Lung and Blood Institute Clinical Trials Network: Higher versus lower positive end-expiratory pressures in patients with the acute respiratory distress syndrome. N Engl J Med 351: 327–336, 2004[Abstract/Free Full Text]
  21. Brower R, Ware L, Berthiaume Y, Matthay M: Treatment of ARDS. Chest 120: 1347–1367, 2001[CrossRef][Medline]
  22. Schmidt G, Hall J, Wood L: Ventilatory failure. In: Textbook of Respiratory Medicine, edited by Murray JB, Nadel J, Philadelphia, W.B. Saunders, 2000, pp 2443–2470
  23. Graf H, Leach W, Arieff A: Evidence for a detrimental effect of bicarbonate therapy in hypoxic lactic acidosis. Science 227: 754–756, 1985[Abstract/Free Full Text]
  24. Choi WI, Quinn DA, Park KM, Moufarrej RK, Jafari B, Syrkina O, Bonventre JV, Hales CA: Systemic microvascular leak in an in vivo rat model of ventilator-induced lung injury. Am J Respir Crit Care Med 167: 1627–1632, 2003[Abstract/Free Full Text]
  25. Chien CC, King LS, Rabb H: Mechanisms underlying combined acute renal failure and acute lung injury in the intensive care unit. In: Sepsis, Kidney and Multiple Organ Dysfunction, edited by Ronco C, Bellomo R, Brendolan A, Basel, Karger, 2004, pp 53–62
  26. Kuiper JW, Groeneveld AB, Slutsky AS, Plotz FB: Mechanical ventilation and acute renal failure. Crit Care Med 33: 1408–1415, 2005[CrossRef][Medline]
  27. Angus D, Linde-Zwirble W, Lidicker J, Clermont G, Carcillo J, Pinsky M: Epidemiology of severe sepsis in the United States: Analysis of incidence, outcome and associated costs of care. Crit Care Med 28: 1303–1310, 2001
  28. Rivers E, Nguyen B, Havstad S, Ressler J, Muzzin A, Knoblich B, Petersen E, Tomlanovich M; for the Early Goal-Directed Therapy Collaborative Group: Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med 345: 1368–1377, 2001[Abstract/Free Full Text]
  29. Dellinger R, Carlet J, Masur H, Gerlach H, Calandra T, Cohen J, Gea-Banacloche J, Keh D, Marshall J, Parker M, Ramsay G, Zimmerman J, Vincent J, Levy M; for the Surviving Sepsis Campaign Management: Surviving Sepsis Campaign guidelines for management of severe sepsis and septic shock. Crit Care Med 32: 858–873, 2004[CrossRef][Medline]
  30. Moran S, Myers B: Pathophysiology of protracted acute renal failure in man. J Clin Invest 76: 1440–1448, 1985[Medline]
  31. Mehta R, McDonald B, Gabbai F, Pahl M, Farkas A, Pascual M, Zhuang S, Kaplan R, Chertow G: Nephrology consultation in acute renal failure: Does timing matter? Am J Med 113: 456–461, 2002[CrossRef][Medline]
  32. Cantarovich F, Rangoonwala B, Lorenz H, Verho M, Esnault V; for High-Dose Furosemide in Acute Renal Failure Study Group: High-dose furosemide for established ARF: A prospective, randomized, double-blind, placebo-controlled, multicenter trial. Am J Kidney Dis 44: 402–409, 2004[Medline]
  33. Lassnigg A, Schmidlin D, Mouhieddine M, Bachmann L, Druml W, Bauer P, Hiesmayr M: Minimal changes of serum creatinine predict prognosis in patients after cardiothoracic surgery: A prospective cohort study. J Am Soc Nephrol 15: 1597–1605, 2004[Abstract/Free Full Text]
  34. Wilcox C: Diuretics. In: The Kidney, 7th Ed., edited by Brenner BM, Philadelphia, W.B. Saunders, 2003, pp 2345–2380
  35. Finfer S, Bellomo R, Boyce N, French J, Myburgh J, Norton R: A comparison of albumin and saline for fluid resuscitation in the intensive care unit. N Engl J Med 350: 2247–2256, 2004[Abstract/Free Full Text]
  36. Scheingraber S, Rehm M, Sehmisch C, Finsterer U: Rapid saline infusion produces hyperchloremic acidosis in patients undergoing gynecologic surgery. Anesthesiology 90: 1265–1270, 1999[CrossRef][Medline]
  37. Cooper M, Stewart P: Corticosteroid insufficiency in acutely ill patients. N Engl J Med 348: 727–734, 2003[Free Full Text]
  38. Hamrahian A: Adrenal function in critically ill patients. Cleve Clin J Med 72: 427–432, 2005[Abstract/Free Full Text]
  39. Annane D, Sebille V, Charpentier C, Bollaert P-E, Francois B, Korach J-M, Capellier G, Cohen Y, Azoulay E, Troche G, Chaumet-Riffaut P, Bellissant E: Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock. JAMA 288: 862–871, 2002[Abstract/Free Full Text]
  40. Annane D, Bellissant E, Bollaert P, Briefel J, Keh D, Kupfer Y: Corticosteroids for severe sepsis and septic shock: A systematic review and meta-analysis. BMJ 329: 480–488, 2004[Abstract/Free Full Text]
  41. Minneci P, Deans K, Banks S, Eichacker P, Natanson C: Meta-analysis: The effect of steroids on survival and shock during sepsis depends on the dose. Ann Intern Med 141: 47–56, 2004[Abstract/Free Full Text]
  42. Slotman GJ, Fisher CJ Jr, Bone RC, Clemmer TP, Metz CA: Detrimental effects of high-dose methylprednisolone sodium succinate on serum concentrations of hepatic and renal function indicators in severe sepsis and septic shock. The Methylprednisolone Severe Sepsis Study Group. Crit Care Med 21: 191–195, 1993[Medline]
  43. Mitch WE, Medina R, Grieber S, May RC, England BK, Price SR, Bailey JL, Goldberg AL: Metabolic acidosis stimulates muscle protein degradation by activating the adenosine triphosphate-dependent pathway involving ubiquitin and proteasomes. J Clin Invest 93: 2127–2133, 1994[Medline]
  44. Palevsky P, O’Connor T, Zhang J, Star R, Smith M; for the VA/NIH Acute Renal Failure Trials Network: Design of the VA/NIH Acute Renal Failure Trial Network (ATN) study: Intensive versus conventional renal support in acute renal failure. Clin Trials 2: 423–435, 2005[Abstract/Free Full Text]



This article has been cited by other articles:


Home page
 CJASNHome page
K. D. Liu and M. A. Matthay
Advances in Critical Care for the Nephrologist: Acute Lung Injury/ARDS
Clin. J. Am. Soc. Nephrol., March 1, 2008; 3(2): 578 - 586.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
CJN.00450206v1
1/4/869    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Liu, K. D.
Right arrow Articles by Chertow, G. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Liu, K. D.
Right arrow Articles by Chertow, G. M.

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS