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Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
Acute kidney injury and urine output in ICU
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Acute kidney injury and urine output in ICU

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  • 1. Acute kidney Injury in ICU Gagan Kumar MD Fellow Pulmonary & Critical Care
  • 2. Why should we be concerned? • Increased risk of death • Marker of severity
  • 3. Outcomes in AKI • BEST study* (Beginning and Ending Supportive Therapy for the Kidney) – The prevalence of AKI requiring renal replacement therapy (RRT) ~ 4% – 28 days in-hospital mortality in patients with AKI was ~ 60% • RIFLE criteria – In-hospital mortality with AKI is in the range of • • • • 5 to 10% with no renal dysfunction 9 to 27% in patients classified as at risk 11 to 30% with injury 26 to 40% with failure *Clin J Am Soc Nephrol. 2007 May;2(3):431-9. Septic acute kidney injury in critically ill patients: clinical characteristics and outcomes.
  • 4. Definitions – RIFLE criteria
  • 5. AKIN criteria 1. Increase the sensitivity of the RIFLE criteria by recommending that a smaller change in serum creatinine (≥26.2 µmol/L) be used as a threshold to define the presence of AKI and identify patients with Stage 1 AKI (analogous to RIFLE-Risk) 2. A time constraint of 48 h for the diagnosis of AKI was proposed. 3. Any patients receiving renal replacement therapy (RRT) were to now be classified as Stage 3 AKI (RIFLEFailure) Bagshaw SM, George C, Bellomo R; ANZICS Database Management Committe. A comparison of the RIFLE and AKIN criteria for acute kidney injury in critically ill patients. Nephrol Dial Transplant. 2008 May;23(5):1569-74. Epub 2008 Feb 15.
  • 6. Is ↓UO= renal failure? • Does ↓UO = ↓GFR? • May be physiological to preserve body volume or electrolyte homeostasis. • Severe tubular dysfunction can lead to increased urine output despite low GFR. • Bottom line: urine output alone is less severe marker if used alone.
  • 7. Normal GFR GFR = Kf[(PGC-PBS) –(ΠGC-ΠPB)] Kf = filtration coefficient ΠPB = zero, since no protein A higher renal plasma flow will induce a reduction in filtration fraction (i.e., ratio of ultrafiltration to renal plasma flow) with a lesser increase of capillary plasma protein concentration along the glomerular capillaries. When the renal plasma flow is reduced, the glomerular filtration rate decreases but with an increase in the filtration fraction
  • 8. What if renal blood flow increases?
  • 9. What if renal perfusion pressure increases? • the ultrafiltrate will be mainly generated on the first portion of the afferent side of the capillary network and to cease when hydraulic and oncotic pressures become equal along the glomerular capillary network • Therefore the oncotic pressure becomes the limiting factor of glomerular filtration
  • 10. Clinical implication • When you resuscitate patient with crystalloids  you are diluting the serum proteins thereby decreasing the plasma oncotic pressure. • Hence the urine response you may be seeing is simply due to decreased oncotic pressure !!!
  • 11. What if renal perfusion pressure decreases?
  • 12. What happens in chronic kidney disease? • Decreased glomerular surface area • Glomerular hydraulic pressure becomes major determinant of GFR.
  • 13. Relation between renal blood flow and GFR • the renal blood flow is autoregulated, which means that it remains unchanged when arterial blood pressure varies • Mediated by – Myogenic mechanism: FAST – Tubuloglomerular feedback: SLOW
  • 14. How long can kidneys suffer low perfusion? • Interruption of blood flow x >30min followed by reperfusion  tubular and microvascular damage • But this scenario is not what we encounter. • This is seen in supra renal aortic surgery where aorta has to be clamped for some time!
  • 15. How long can kidneys suffer low perfusion? • Prolonged period of renal hypo-perfusion does not always results in renal histological damage and renal failure. • Reduced renal blood flow by 80% x 2 hrs no kidney damage
  • 16. In five sheep: renal blood flow (RBF) was reduced by 25, 50 and 75%, respectively, by acute vascular occlusion for 30 min at weekly intervals. In another six sheep: RBF was reduced by 80% for 2 h. Release of occlusion induced brief hyperemia before all measured variables returned to normal within 8 h and remained normal for the following 72 h. At autopsy, the kidneys were histopathologically normal
  • 17. • Rats with LPS infusion to reduce blood flow by 50% • Decrease in cortical PO2 from 6852mHg • Rats with mechanical reduction of blood flow to 50%  anuria • No decrease in PO2 seen • Fluid resuscitation in LPS rats with normalized blood flow • No decrease in cortical Po2
  • 18. Conclusions • Severe transient hypoperfusion is able to reduce GFR and urine output but is not sufficient to induce persistent AKI. • Superimposition of renal hypoperfusion episodes in relation to other insults, such as sepsis or ischemia may induce renal failure • It is expected that preventing a decrease of renal blood flow may prevent or limit the occurrence of AKI in ICU patients
  • 19. E. coli induced hyperdynamic sepsis in sheep
  • 20. • Review of all studies in literature do not show a correlation between TRPF and GFR, implying uncoupling between perfusion(TRPF) and function (GFR), such that ‘for a given decrease in decreased perfusion, there is an unpredictable and much greater loss in function’.
  • 21. Possible explanations for uncoupling between RBF and GFR. 1. Raised bowman’s space pressure secondary to tubular obstruction 2. Failure of active reabsorption of ultrafiltrate 3. Back-leak of tubular ultrafiltrate into the interstitium and circulation 4. Tubulo-glomerular feedbackinduced afferent arteriolar vasoconstriction 5. Decreased efferent arteriolar tone
  • 22. Intra renal blood flow distribution • normal kidneys receive ~20% of cardiac output • medulla receives less than 10% of renal blood flow • In contrast to the cortical microcirculation, the medulla microcirculation appears to be poorly autoregulated, i.e., pressure-dependent. – Regulation of diuretics and natriuresis and, therefore, the response of the kidney to the body fluid composition and volume status – in mammalians kidneys, the ability of the medulla circulation to regulate its own blood flow depends largely on the body volume status
  • 23. • With changes in RPP, the only detectable change in intra-renal perfusion occurs in the inner medulla
  • 24. • In contrast, both renal cortical and medulla are well autoregulated in hydropenic rats. • Because the descending vasa recta provide blood flow to the medulla emerge from efferent arterioles of juxtamedullary glomerules, these data suggest that changes in resistance in the postglomerular circulation of juxtamedullary nephrons might be responsible for the lack of autoregulation of medullary blood flow in volume expended animals
  • 25. Pressure induced diuresis • Increase in renal medullary blood flow – decreases the outer-inner medullar osmotic gradient – increases renal interstitial hydrostatic pressure • which both impair the ability to concentrate urine and participate in the natriuresis response to hypertension in well-hydrated mammalians. • In hydropenic animals, this response is blunted preventing further loss of water and sodium
  • 26. Hypothesis for developing AKI in sepsis • Increased vascular response of the renal microcirculation to vasoconstrictors  elicit intense renal vasoconstriction  induces AKI • Endogenous vasoconstrictors, including angiotensin II – decrease GFR due to decrease in renal blood flow – blunt the natriuresis response after the renal perfusion pressure has been restored • Endotoxemia also can increase urine output and water clearance despite decrease in GFR due to tubular aquaporin-2 dysfunction
  • 27. Tubulo-glomerular feedback • Higher [NaCl] in tubular fluids in macula densa  adenosine release  increase of the glomerular afferent arteriole vascular tone  decreases GFR – Operates for few seconds to minutes – It resets in 30-60 min – Prevents rapid loss of water and electrolytes in condition of tubular dysfunction • Na+ absorption network has the major renal oxygen consumption. • So decrease in GFR  lesser amount of Na reaching distal tubules  decreased oxygen consumption.
  • 28. • In ischemic kidneys: – Diversion of oxygen consumption from Na+ reabsorption to other oxygen-consuming pathways illustrated by an increase of the ratio oxygen consumption/Na Reabsorp +
  • 29. Postcardiac surgery patients with (n = 12) and without (n = 37) acute kidney injury were compared with respect to renal blood flow, glomerular filtration, RVO2, and renal oxygenation. In the acute kidney injury group, GFR (-57%), renal blood flow (-40%), filtration fraction (-26%), and sodium resorption (-59%) were lower, renal vascular resistance (52%) and renal oxygen extraction (68%) were higher, whereas there was no difference in renal oxygen consumption between groups. Renal oxygen consumption for one unit of reabsorbed sodium was 2.4 times higher in acute kidney injury
  • 30. • Oxygen consumption to absorptive work mismatch is not well understood and may result from: – higher production of reactive oxygen species by infiltrative immune cells – high level of NO, which regulates the renal oxygen consumption • This may partially explain why strategies designed to inhibit renal oxygen consumption (e.g., loops diuretics) have failed to improve the prognosis of patients suffering from AKI
  • 31. Distant effects of renal ischemia/reperfusion injury J Am Soc Nephrol 14: 1549–1558, 2003
  • 32. Acute renal failure leads to dysregulation of lung salt and water channels Kidney International, Vol. 63 (2003), pp. 600–606
  • 33. Summary • Decrease urine output can mirror a decrease in creatinine clearance. • Although a decrease in renal blood flow and/or a decrease in renal perfusion pressure is a major determinant of GFR, plasma oncotic pressure appears to be central in the glomerular hydrodynamic forces. • Colloids increase the oncotic pressure and may reduce filtration rate
  • 34. Summary • Fluid administration may be found inappropriate and even harmful in numerous situations due to the inconstant relationship between renal blood flow or renal perfusion pressure and diuresis/natriuresis due to complex neurohormonal control. • systemic inflammation can induce natriuresis and diuresis changes due to functional changes unrelated to hypoperfusion, histological, or tubular damage
  • 35. How to identify early AKI ? • Is creatinine good enough? • Use it with Urine output • What about prediction equations: MDRD or Cockroft & Gault. – In critical care where creatinine is changing rapidly, these formulas cannot be used to predict GFR. – Cannot be used in oliguric/anuric patients. – These are used only for steady states
  • 36. Is FeNa useful? Crit Care Med. 2007 Jun;35(6):1592-8.
  • 37. Is FeNa useful? • Although a low UNa or FeNa (e.g., FeNa <1%) suggest a preserved renal tubular reabsorptive capacity, there is NO evidence for a correlation between urinary biochemical modifications and tissue damage. • Control of urinary Na+ excretion results from a complex neurohumoral regulation and is influenced by • fluid resuscitation • arterial pressure • infusion of diuretics
  • 38. How do I predict renal prognosis? • FeNa and FeUrea are not helpful • Neutrophil Gelatinase associated lipocalin (NGAL)
  • 39. Neutrophil Gelatinase associated lipocalin (NGAL) • Plasma NGAL had an area under the ROC curve of 0.71 (95% confidence interval (CI), 0.55-0.88) for predicting AKI progression and of 0.78 (95% CI, 0.61-0.95) for need for renal replacement therapy • Area under the ROC curve of 0.82 (95% CI, 0.7-0.95) for predicting the use of renal replacement therapy • Urine NGAL remains low in patients admitted in the emergency department with prerenal azotemia versus AKI
  • 40. Cystatin-C • 13 kD endogenous cysteine-proteinase inhibitor that is produced by all cells. • Freely filtered across the glomerulus and, in contrast to creatinine, it is not secreted by renal epithelial cells. • Rises earlier than creatinine in ICU patients with AKI Kidney Int. 2004 Sep;66(3):1115-22.
  • 41. Conclusions • These urinary markers have been poorly studied among critically ill patients. • Recent reviews of experimental and human sepsis have highlighted the paucity of available studies and their design heterogeneity regarding urinary findings in septic AKI • there is no evidence that these urinary biochemical findings can predict the response to hemodynamic optimization in terms of renal injury and renal function
  • 42. How should we assess renal perfusion in ICU patient? • Doppler-based determination of resistive index • Problems – Need data with respect to GFR, Crclearance, FeNa and oxygen consumption – Need baseline data before the insult – Difficult technically and in obese persons
  • 43. Can We Predict Which Patient in the ICU Will Develop AKI ? • There are risk factors but no prediction score. – Age – Sepsis – Cardiac surgery – Infusion of contrast – Diabetes – Rhabdomyolysis – Preexisting renal disease – Hypovolemia and shock
  • 44. How do we protect kidneys? • Improve Renal perfusion 1. Volume status – fluid resuscitation 2. Pressors
  • 45. Fluids • How much? • What type?
  • 46. FACTT trial • Selected patients with acute lung injury, conservative fluid management may not be detrimental to kidney function. • Fluid balance over 7 days was -136 ml in the conservative group versus +6,992 ml in the liberal fluid strategy group • Not associated with an increase in the frequency of RRT, which occurred in 10% of the conservative-strategy group and 14% of the liberal-strategy group
  • 47. Fluid resuscitation in AKI • Although fluid resuscitation and optimization of renal perfusion pressure are central to the prevention and treatment of AKI, excessive fluid resuscitation may be harmful in some critically ill patients
  • 48. Problems with fluid overload • Aggressive fluid resuscitation  increases renal blood flow  but can be ineffective in restoring renal microvascular oxygenation due to hemodilution with no increase in blood-oxygen carriage capacities. • Positive fluid balance can deteriorate cell oxygenation and prolong mechanical ventilation. • Fluid overload may lead to central venous congestion and decrease of renal perfusion pressure, which will promote the development of AKI in patients with acute heart failure or sepsis
  • 49. Which is better – crystalloids or colloids ?
  • 50. • Hyperosmotic colloids can be associated with development of renal dysfunction Schortgen F et al. Effects of hydroxyethylstarch and gelatin on renal function in severe sepsis: a multicentre randomised study. Lancet 2001;357:911–916.
  • 51. Brunkhorst FM et al. Intensive insulin therapy and pentastarch resuscitation in severe sepsis. N Engl J Med 2008;358:125–139
  • 52. SAFE study • No differences between the groups in – Patients who required RRT (1.3% and 1.2%) – the mean number of days of RRT (0.5 ±2.3 and 0.4 ± 2.0; P =0.41) – number of days of mechanical ventilation (4.5 ± 6.1 and 4.3 ± 5.7; P = 0.74). N Engl J Med. 2004 May 27;350(22):2247-56
  • 53. • Fuid resuscitation with crystalloids or gelatin is associated with a lower incidence of AKI than resuscitation with artificial hyperoncotic colloids • Dextran in 3% of patients and starches in 98% of patients (adjusted odds ratio, 2.48) or • Hyperoncotic albumin (adjusted odds ratio, 5.99) Schortgen F, Girou E, Deye N, Brochard L. The risk associated with hyperoncotic colloids in patients with shock. Intensive Care Med 2008;34:2157–2168.
  • 54. Recommendations* • Consider fluid resuscitation with crystalloids to be as effective and safe as fluid resuscitation with hypooncotic colloids (gelatins and 4% albumin) • Based on current knowledge, hyperoncotic solutions (dextrans, hydroxyethyl starches, or 20–25% albumin) not be used for routine fluid resuscitation because they carry a risk for renal dysfunction. *An Official ATS/ERS/ESICM/SCCM/SRLF Statement:Prevention and Management of Acute Renal Failure in the ICU Patient. Am J Respir Crit Care Med Vol 181. pp 1128– 1155, 2010
  • 55. Role of vasoactive drugs • Titrate to what ? • What pressors should I use? • Don’t the vasopressors cause renal afferents to vasoconstrict and worsen renal blood flow?
  • 56. How much MAP is sufficient ? • Unknown whether the current recommendation to maintain a mean arterial pressure (MAP) at or above 65 mm Hg in patients who are critically ill is adequate for preventing AKI. • It is likely that some patients—especially those with history of hypertension and the elderly—may require higher MAP to maintain adequate renal perfusion.
  • 57. • Twenty-eight patients with a diagnosis of septic shock who required fluid resuscitation and pressor agents • to achieve and maintain a mean arterial pressure of 65 mm Hg. • Then they were randomized in two groups: – In the first group (control group, n 14), mean arterial pressure was maintained at 65 mm Hg – in the second group (n 14), mean arterial pressure was increased to 85 mm Hg by increasing the dose of norepinephrine
  • 58. • Increasing the CI to a supra normal level > 4.5 (cardiac-index group) • Increasing mixed venous oxygen saturation to a normal level (oxygen-saturation group)
  • 59. Conclusions • Higher MAP is associated with increased cardiac output but no difference in urine output or creatinine clearance • Normalization of mixed venous oxygen saturation or by increasing oxygen delivery to supranormal levels does not decrease rate of AKI • Resuscitation should be titrated to end points of oxygen metabolism and organ function.
  • 60. Does type of vasopressor has any role? • You would expect NE to cause afferent vessel vasoconstriction and decrease renal blood flow.
  • 61. Does NE infusion improves renal perfusion?
  • 62. • Twelve post-cardiac surgery patients with NEdependent vasodilatory shock and AKI were studied • 2–6 days after surgery. • NE infusion rate was randomly and sequentially titrated to target MAPs of 60, 75 and 90 mmHg.
  • 63. Vasopressin • Binding to the V2-receptors in the inner medullary collecting ducts activates the UTA1 molecules •  increases the urea permeability of collecting duct •  increase the ability to concentrate urine
  • 64. Vasopressin • Increase of plasma vasopressin concentration (independently of any increase of systemic arterial pressure) also influences the pressure-natriuresis/ diuresis relationship in decreasing the medullary blood flow through receptor V1a Crit Care Med. 2004 Sep;32(9):1891-8.
  • 65. • Vasopressin may reduce the progression to severe AKI only in a prespecified subgroup of patients with less severe septic shock (norepinephrine dose ,15 mg/minute) • No difference was observed in the need for RRT in any subgroup. Holmes CL, Mehta S, Granton JT, Storms MM, et al. Vasopressin versus norepinephrine infusion in patients with septic shock. N Engl JMed2008;358:877–887.
  • 66. What about dopamine? Low dose? 7 sheep 6 h of placebo (saline solution) or drugs (MD-NE at 0.4 micro g/kg/min or LDD at 2 micro g/kg/min), Outcomes: cardiac output (CO), and flow to vital organs, lactate, creatinine, and creatinine clearances Chest. 2004 Jun;125(6):2260-7.Increasing renal blood flow: low-dose dopamine or medium-dose norepinephrine.
  • 67. In patients with or at risk for AKI, low-dose dopamine may increase diuresis on the first day of use but it does not protect against the development of AKI
  • 68. Dobutamine • Not been shown consistently to improve renal blood flow.
  • 69. Fenoldopam • Short-acting dopamine receptor-1 agonist • Fenoldopam did not affect the need for RRT and survival at 21 days. • In secondary analysis, however, fenoldopam reduced the need for RRT and the incidence of death in patients without diabetes and in postoperative patients who have undergone cardiothoracic surgery
  • 70. Anything else? • Angiotensin II • In the absence of angiotensin II, volume expansion with no increase in MAP induces natriuresis, whereas the increase in MAP by angiotensin II infusion did not induce a natriuresis response
  • 71. Summary • Norepinephrine and vasopressin may induce, in septic states, an increase of renal blood flow through a combined – increase of renal perfusion pressure (i.e., prerenal mechanism) and – an increase of renal vascular conductance (i.e., intrarenal mechanism) • Increase of renal blood flow does not necessarily translate into GFR increase • Current clinical data are insufficient to conclude that one vasoactive agent is superior to another in preventing development of AKI
  • 72. Renal support • Introduce early • Traditional thresholds used in stable patients may not be appropriate in ICU patients with AKI – impact of renal failure on other failing organs such as the lungs (ARDS, pulmonary edema) and brain (encephalopathy) should be considered in the timing of RRT – the increased catabolism associated with critical illness and the need to administer adequate nutritional protein will lead to increased urea generation – Often difficult to limit fluid intake in these patients, in part due to the administration of intravenous medications (antibiotics, vasopressors, etc.) – patients who are critically ill may be more sensitive to metabolic derangements, and swings in their acidbase and electrolyte status may be poorly tolerated.
  • 73. Program to Improve Care in Acute Renal Disease (PICARD) study • Timing: early vs. late • Odds ratio for adverse outcome of 1.97 (95% confidence interval *CI+ 1.21– 3.20) was associated with late start of RRT (BUN ,76 mg/dl versus BUN .76 mg/dl) Clin J Am Soc Nephrol 1: 915–919, 2006
  • 74. RRT dose • Acute Renal Failure Trial Network study: no difference between CVVHD(22ml/kg/hr) and IHD (>3.9Kt/Vd/Wk) – OR 0.92 (0.73-1.16) • Randomized Evaluation of Normal versus Augmented Level [RENAL] Replacement Therapy Study: CVVHD @ 25 and 40ml/kg/hr. – OR for mortality 1.00 (0.81-1.23)
  • 75. Recommendations • Timing – In patients who are critically ill with AKF we suggest initiating RRT before the development of extreme metabolic derangements or other life-threatening events. • Intensity – For IHD and SLED, we recommend clearances at least equal to minimum requirements for chronic renal failure (3.6 Kt/Vd/wk) – For CRRT (CVVH or CVVHD), we recommend clearance rates for small solutes of 20 m/kg/h (actual delivered dose). – Higher doses of CRRT cannot be generally recommended and should only be considered by teams that can administer them safely *An Official ATS/ERS/ESICM/SCCM/SRLF Statement:Prevention and Management of Acute Renal Failure in the ICU Patient. Am J Respir Crit Care Med Vol 181. pp 1128–1155, 2010
  • 76. Comments & Questions

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