Acute Renal Failure

1. Acute Renal Failure

2. Definition and Classification Epidemiology Pathophysiology and Etiology Prerenal ARF Intrinisic ARF Postrenal ARF Pharmacologic Management of ARF RRT in ARF

3. Definition

5. MDRD eGFR= 186 x Screat� �?�54 X Age ��?��� X 1.21 [if black] X o.74 [if female] Undersetimates GFR in healthy people (when GFR >60 ml/min) Cockcroft-Gault formula (140-Age) X Mass (In KG) X [o.85 if female]/72 X Serum Creat The non-steady-state conditions that prevail in ARF preclude estimation of GFR using standard formulae derived from patients with chronic kidney disease.

7. Shortcomings The assignement of corresponding changes in serum creat and changes in urine output to the same strata is not based on evidence. The criteria that results in the least favorable rifle strata to be used. The patient would progress from "risk" on day one to "injury" on day two and "failure" on day three, even though the actual GFR has been <10 mL/min over the entire period. It is impossible to calculate the change in serum creatinine in patients who present with ARF but without a baseline measurement of the serum creat. The authors of the RIFLE criteria suggest back-calculating an estimated baseline creat using the four-variable MDRD equation, assuming a baseline GFR of 75 mL/min per 1.73 m2 .

8. Diagnostic criteria Abrupt (within 48 hours) absolute increase in the serum creatinine concentration of = 0.3 mg/dL (26.4 micromol/L) from baseline. Or a percentage increase in the serum creatinine concentration of = 50 percent. Or oliguria of less than 0.5 mL/kg per hour for more than six hours.

10. 3 categories based on the pathophysiology3 categories based on the pathophysiology

11. Epidemiology of ARF

12. The observed incidence, etiology, and outcomes of ARF are highly dependent upon the populations studied and the definition of ARF employed. The absence of centralized registries to track the incidence and outcomes of patients with ARF has hindered our understanding of its epidemiology.

13. Nature Clinical Practice Nephrology (2006) 2,364-377 The changing epidemiology of acute renal failure

15. Exceeds community acquired ARF by 5-10 times 35000 in79 to 650000 in2002, 13% /yearExceeds community acquired ARF by 5-10 times 35000 in79 to 650000 in2002, 13% /year

16. 5-20% of critically ill people suffer from ARF5-20% of critically ill people suffer from ARF

18. Key Points The absolute incidence of acute renal failure (ARF) has increased in the past two decades, while the mortality rate has remained relatively static The lack of a standard definition of ARF complicates the process of identifying the factors that underlie changes in epidemiology of this condition. Despite the use of different definitions in different studies, various factors that have contributed to altered epidemiology of ARF in the past few decades have been identified These factors include geographical site of disease onset (developed vs developing countries; community vs hospital vs intensive care unit), patient age, infections (HIV, malaria, leptospirosis and hantavirus), concomitant illnesses (cardiopulmonary failure, hematooncological disease), and interventions (hematopoietic progenitor cell and solid organ transplantation)

19. Prerenal Acute Renal Failure

20. GFR is reduced as a result of hemodynamic disturbances that decrease glomerular perfusion. The defining feature of prerenal ARF is the absence of cellular injury and the normalization of renal function with reversal of the altered hemodynamic factors.

22. Of Prerenal ARF Pathophsiology

25. Factors that alter intrarenal hemodynamics, either by increasing afferent arteriolar constriction or by causing efferent arteriolar vasodilatation, may also play a significant role in the development of prerenal azotemia by decreasing glomerular capillary pressure. Factors that alter intrarenal hemodynamics, either by increasing afferent arteriolar constriction or by causing efferent arteriolar vasodilatation, may also play a significant role in the development of prerenal azotemia by decreasing glomerular capillary pressure.

27. Diagnosis of Prerenal ARF Hx P/E Urine sediment (usually normal, without cellular elements or abnormal casts, unless chronic kidney disease is present) UNa< 15 meq/L (>20 in ATN) U/Pcreat> 20 (<15 in ATN) FeNa <1% (>1% in ATN) UNa/K <1/4 BUN/creat >20

28. BUN/CREAT of >20 is typical, BUT is not specific to prerenal ARF and may also be seen: Obstructive uropathy Gastrointestinal bleeding Other states associated with increased urea production.

29. FE Urea Patients on diuretics Prerenal azotemia due to vomiting on NG suctioning. FE Na may be low is sepsis, RCN, myoglobinuria, nonoliguric ATN, acute GN, urinary tract obstruction and renal allograft rejection

30.   Significance of the fractional excretion of urea in thedifferential diagnosis of acute renal failure  102 patients were divided into three groups: Prerenal azotemia (N 50) Prerenal azotemia treated with diuretics (N 27) ATN (N 25) Kidney International, Vol. 62 (2002), pp. 2223�2229

31. FENa was low only in the patients with untreated plain prerenal azotemia while it was high in both the prerenal with diuretics and the ATN groups. FEUN was essentially identical in the two pre-renal groups (27.9 2.4% vs. 24.5 2.3%), and very different from the FEUN found in ATN (58.6 3.6%, P < 0.0001). 92% of the patients with prerenal azotemia had FENa <1%. 48% of those patients with prerenal and diuretic therapy had FENa <1% 89% of patients with prerenal azotemia and on diuretics had a FEUN< 35%.

32. FE UREA Low FE urea <=35% is a more sensitive and specific index than FE Na in differentiating between ARF due to prerenal azotemia and that due to ATN, especially if diuretics have been administered.

33. ARF Associated with ACE Inhibitors and Angiotensin Receptor Blockers

35. Acute renal failure can develop acutely, when ACEI or ARB therapy is initiated, or in patients receiving chronic therapy, especially in patients with underlying CHF The mean increase in serum creatinine in patients with CKD treated with ACEI or ARB is, however, less than 30% The mean increase in serum creatinine in patients with CKD treated with ACEI or ARB is, however, less than 30%

36. Predisposing factors: Advanced cardiac failure with low mean arterial pressure Volume depletion due to diuretic therapy The presence of renal vascular disease The concomitant use agents with vasoconstrictor effects (NSAIDs, cyclooxygenase-2 inhibitors, cyclosporine, and tacrolimus) CKD: The risk of ARF is higher in patients with chronic kidney disease of any cause than in patients with normal renal function

37. Serum creatinine and electrolyte concentrations should be measured before and 1 wk after initiating or changing the dose of therapy An increase in serum creatinine of >0.5 mg/dl if the initial serum creatinine is <2.0 mg/dl, or a rise of >1.0 mg/dl if the baseline serum creatinine is >2.0 mg/dl, has been suggested as a threshold for discontinuation of therapy

38. The development of ARF should prompt an evaluation for cardiac failure, hypotension, volume depletion, use of a concomitant vasoconstrictive agent, or renovascular disease. There is no need to discontinue ACEI or ARB therapy in response to smaller increments in serum creatinine. Once reversible factors, such as volume depletion, have been treated and renal function has returned to baseline, therapy with ACEI or ARB can be cautiously reinstituted. There is no need to discontinue ACEI or ARB therapy in response to smaller increments in serum creatinine. Once reversible factors, such as volume depletion, have been treated and renal function has returned to baseline, therapy with ACEI or ARB can be cautiously reinstituted.

39. Acute Renal Failure Associated with NSAIDS

40. Nonsteroidal anti-inflammatory drugs (NSAID) agents inhibit the synthesis of vasodilatory prostaglandins in the kidney.

42. Risk factors: Severe CHF Advanced liver disease Severe atherosclerotic vascular disease CKD

43. Elderly patients are at increased risk due to the increased prevalence of cardiac dysfunction, occult renal vascular disease, and subclinical chronic kidney disease.

44. Abdominal Compartment Syndrome

45. Unusual cause of decreased renal perfusion associated with increased intra-abdominal pressure Trauma patients who require massive volume resuscitation Mechanical limitations of the abdominal wall (tight surgical closures or scarring after burn injuries) Medical etiologies that are characterized by intraabdominal inflammation with fluid sequestration, such as bowel obstruction, pancreatitis, and peritonitis.

46. Clinical manifestations Respiratory compromise Decreased cardiac output Intestinal ischemia Hepatic dysfunction Oliguric renal failure

47. The renal insufficiency results from decreased renal perfusion and correlates with the severity of the increased intraabdominal pressure. Oliguria develops when the intraabdominal pressure exceeds 15 mmHg, with anuria developing at pressures >30 mmHg. It was initially thought that the renal dysfunction resulted from increased renal parenchymal pressure; however, data now suggest that decreased perfusion associated with increased renal venous pressure is the primary mechanism of renal dysfunctionIt was initially thought that the renal dysfunction resulted from increased renal parenchymal pressure; however, data now suggest that decreased perfusion associated with increased renal venous pressure is the primary mechanism of renal dysfunction

48. Diagnosis The diagnosis should be suspected in patients with a tensely distended abdomen and progressive oliguria. Measurement of intraabdominal bladder pressure. Abdominal compartment syndrome can be excluded when the bladder pressure is <10 mmHg and is virtually always present if the pressure is >25 mmHg.

49. Treatment Abdominal decompression: Paracentesis if massive ascites. Surgical decompression is required in the majority of patients. Renal failure usually recovers promptly after relief of the increased intraabdominal pressure

50. Postrenal Acute Renal Failure

51. Postrenal acute renal failure is caused by the anatomic obstruction to the flow of urine. When urinary tract obstruction is unilateral and the contralateral kidney is normal, the plasma creatinine concentration is usually normal or only minimally elevated and clinical ARF does not develop. Renal failure becomes manifest when the obstruction is bilateral (or below the level of the bladder) or is unilateral with dysfunction or absence of the contralateral kidney. Postrenal acute renal failure is caused by the anatomic obstruction to the flow of urine. When urinary tract obstruction is unilateral and the contralateral kidney is normal, the plasma creatinine concentration is usually normal or only minimally elevated and clinical ARF does not develop. Renal failure becomes manifest when the obstruction is bilateral (or below the level of the bladder) or is unilateral with dysfunction or absence of the contralateral kidney.

53. Urine output? The obstruction: Complete Anuria

54. Pathophysiology After the acute onset of obstruction, GFR declines progressively, but it does not fall to zero. Factors that maintain GFR include continued salt and water reabsorption along the nephron, dilatation of the collecting system, and alterations in renal hemodynamics. Intratubular pressure rises acutely, but it begins to decline within the first 4 to 8 h, returning to nearly normal by 24 h.

56. Complete obstruction Recovery after relief of obstruction depends on: Severity Duration Less than 1 wk duration, recovery complete. Little or no recovery after 12 wk.

57. Partial obstruction The course after relief of partial obstruction is less predictable Depends on Severity Duration Presence of infection or preexisting renal disease.

58. Relief of obstruction may be accompanied by a post-obstructive diuresis; Excretion of salt and water retained during the obstruction. Persistent salt-wasting and impaired urinary concentrating ability .

59. Diagnosis Elderly male patients Measurement of a post-voiding residual bladder volume, either by an bedside ultrasound bladder scan or by placement of an indwelling bladder catheter.

60. Diagnosis Ultrasonography Sensitivity and specificity are high Non diagnostic Early in the course of postrenal ARF. Severe volume depletion. Obstruction is due to retroperitoneal disease (e.g., retroperitoneal fibrosis, tumors, adenopathy) encasing the ureter and preventing dilatation

61. Diagnosis Computed tomography Non-contrasted CT scanning may be particularly useful for the identification of obstructing kidney stones

62. Intrinsic ARF

63. Etiology of Intrinsic ARF

64. Intrinsic processes that result in ARF are categorized according to the primary site of anatomic injury Intrinsic processes that result in ARF are categorized according to the primary site of anatomic injury

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68. Acute tubular necrosis is the most common form of intrinsic ARF (85 %) Tubular injury Nephrotoxic (35%) Ischemic (50%) Multifactorial. Profound ischemic injury may result in bilateral cortical necrosis.

69. 2 ends of the spectrum of renal reponse to hypoperfusion2 ends of the spectrum of renal reponse to hypoperfusion

72. The initiation phase refers to that period during which patients are subject to factors known to cause ATN�e.g., hypotension, ischemia, sepsis, and nephrotoxins�but have not yet developed overt parenchymal injury. It is during this period that ARF is potentially preventable. With the development of overt tubular injury, there is an abrupt fall in GFR and the clinical syndrome of ATN becomes manifest. During the maintenance phase, which typically lasts 1 to 2 wk but is highly variable and may be as short as a few days or as long as 4 to 6 wk, GFR remains markedly depressed. Urine volume during this phase is variable�although many patients are oliguric, patients may be non-oliguric with urine volumes greater than 400 to 500 ml/d. During the recovery phase, cellular regeneration and repair restore tubular integrity and GFR increases to normal or near normal values.The initiation phase refers to that period during which patients are subject to factors known to cause ATN�e.g., hypotension, ischemia, sepsis, and nephrotoxins�but have not yet developed overt parenchymal injury. It is during this period that ARF is potentially preventable. With the development of overt tubular injury, there is an abrupt fall in GFR and the clinical syndrome of ATN becomes manifest. During the maintenance phase, which typically lasts 1 to 2 wk but is highly variable and may be as short as a few days or as long as 4 to 6 wk, GFR remains markedly depressed. Urine volume during this phase is variable�although many patients are oliguric, patients may be non-oliguric with urine volumes greater than 400 to 500 ml/d. During the recovery phase, cellular regeneration and repair restore tubular integrity and GFR increases to normal or near normal values.

73. Pathogenesis of ATN

76.  Recovery from Ischemic Injury In contrast to the heart and brain, where ischemic injury results in permanent cell loss, the kidney is able to completely restore its structure and function after acute ischemic or toxic injury. The recovery from tubular necrosis involves the dedifferentiation and proliferation of remaining viable tubular epithelial cells followed by reestablishment of cellular polarity, normal histologic appearance, and physiologic function.

77. Under normal circumstances, renal tubular cells in vivo are quiescent and do not divide in response to growth factors. After ischemic or toxic injury, alterations in gene expression are observed that are similar to those induced in vitro by growth factors. Multiple growth factors, including (IGF-1), (EGF), and (HGF), and their receptors are upregulated during the regenerative process after renal injury Administration of exogenous IGF-1, EGF, or HGF to experimental animals after ischemic or toxic renal injury accelerates renal regeneration. Concern has been raised, that growth factors may also have a deleterious effect, augmenting tubulointerstitial injury and fibrosis.

78. Short-term Outcomes The outcome of ATN is highly dependent on the severity of comorbid conditions. Uncomplicated ATN is associated with mortality rates of 7 to 23% Mortality of ATN in postoperative or critically ill patients with multisystem organ failure is high as 50 to 80%. Mortality rates increases with the number of failed organ systems

79. Long-term Outcomes Long term outcomes in ARF in patients treated with continuous RRT. Am J Kidney Dis, 2002 Long-term outcomes of patients who survive are good. Of a population of 979 critically ill patients with ARF who required RRT (predominately patients with ATN), in-hospital mortality was 69%. Patients who survived to hospital discharge, 6-mo survival was 77%, 1-yr survival was 69%, and 5-yr survival was 50% 59% of surviving patients had no residual renal insufficiency, and only 10% required chronic dialysis therapy.

80. Radiocontratst Nephropathy

81. Contrast media induced nephropathy (CMIN) is the third highest cause of hospital-acquired acute renal failure. In nearly half of these patients, CMIN occurred during cardiac diagnostic or interventional procedures such as percutaneous coronary intervention.

84. ARF:increase in serum creat of>50 % above baseline or >1 mg/dl if baseline>2 mg/dl Normal baseline creat negilgible risk Mild to moderate CKD 5-10 % risk Mild to moderate CKD + DM 10- 40 % Advanced renal insufficiency >50 % risk

85. Pathogenesis Haemodynamic alterations and tubuloglomerular feedback The injection of CM induces early, rapid renal vasodilatation followed by prolonged vasoconstriction, with an increase in intrarenal vascular resistances, a reduction of total renal blood flow (RBF) and a decrease in glomerular filtration rate (GFR). Conversely, the effect on the extrarenal vasculature is transient vasoconstriction that precedes a stable decrease in vascular peripheral resistances. The resulting renal ischaemia due to these haemodynamic effects is, in part, responsible for nephropathy

87. Endothelial dysfunction Vasoactive mediators Free radicals and reperfusion damage Haemorheological factors Tubular toxicity and immunological mechanisms

88. Treatment The best treatment of contrast-induced renal failure is prevention. The use, if clinically possible, of ultrasonography, magnetic resonance imaging or CT scanning without radiocontrast agents, particularly in high-risk patients. The use of lower doses of contrast and avoidance of repetitive studies that are closely spaced (within 48 to 72 hours). Avoidance of volume depletion or nonsteroidal antiinflammatory drugs, both of which can increase renal vasoconstriction. The use of low or iso-osmolal nonionic contrast agents.

89. Treatment The administration of Intravenous Saline. Isotonic saline at a rate of 1 mL/kg per hour, begun at least two and preferably 6 to 12 hours prior to the procedure, and continuing for 6 to 12 hours after contrast administration. The administration of the antioxidant Acetylcysteine. Dose of 600 to 1200 mg orally twice daily, administered the day before and the day of the procedure, based upon its potential for benefit and low toxicity and cost.

90. Treatment Routine hemofiltration or hemodialysis for the prevention of contrast nephropathy in patients with stage 3 and 4 CKD is not recommended. More data are needed in stage 5 CKD (Prophylactic use of hemodialysis in patients with stage 5 CKD, can be considered,provided that a functioning access is already available) Extracorporeal blood purification therapies for prevention of radiocontrast-induced nephropathy: a systematic review. Am J Kidney Dis 2006; 48:361. Renal protection for coronary angiography in advanced renal failure patients by prophylactic hemodialysis. A randomized controlled trial. J Am Coll Cardiol 2007; 50:1015.

91. Treatment There is no indication for prophylactic dialysis for the prevention of volume overload in dialysis-dependent patients.

92. Treatment Therapies with Limited Evidence Calcium Channel Blockers Diuretics Atrial Natriuretic Peptide (ANP) Endothelin (ET) Antagonists Prostaglandin E1 ACE Inhibitors

93. The high-osmolal contrast media (osmolality 1500�1800 mOsm/kg) are first generation agents. Low-osmolal contrast media still have an increased osmolality compared with plasma (600�850 mOsm/kg), The newest nonionic radiocontrast agents have a lower osmolality, 290 mOsm/kg, iso-osmolal to plasma

94. In high-risk patient populations (patientswith underlying renal insufficiency and diabetes), both low-osmolar and iso-osmolar contrasts tend to reduce the risk of contrast nephropathy as compared to the high-osmolar compounds.

95. The volume of contrast administered to the patien also appears to correlate with the incidence of nephrotoxicity. In patients who undergo only diagnostic coronary procedures, the volume of dye (approximately 100 mL) is considerably less than in patients who undergo interventional procedures (approximately 250-300 mL).

96.  Heme pigment-induced acute tubular necrosis Myoglobinuria: rhabdomyolysis. Hemoglobinuria: intravascular hemolysis.

97. Rhabdomyolysis The release of muscle cell contents as the result of traumatic or nontraumatic injury of skeletal muscle Physical findings may consist of Tender, �doughy� muscles Edema weakness Compartmental compression symptoms with signs and symptoms of neurovascular compromise may develop, necessitating the need for emergent fasciotomy.

98. The majority of cases of rhabdomyolysis are nontraumatic Muscle compression from immobilization as in drug induced comaMuscle compression from immobilization as in drug induced coma

99. Hemolysis Transfusion reactions due to ABO incompatible blood are probably the most frequently encountered hemolytic processes that can lead to acute renal failure. Severe acute hemolytic episodes in patients with glucose-6-phosphate dehydrogenase deficiency.

100. Laboratory abnormalities Obstruction with intratubular heme pigment casts. Proximal tubular cell injury mediated by free chelatable iron and by the heme center of myoglobin. Concurrent volume depletion and renal ischemia. With crush injury of muscle, for example, Obstruction with intratubular heme pigment casts. Proximal tubular cell injury mediated by free chelatable iron and by the heme center of myoglobin. Concurrent volume depletion and renal ischemia. With crush injury of muscle, for example,

101. The urine may have a low FENa despite tubular injury. Positive dipstick test for heme pigment without red blood cells on microscopic exam should suggest myoglobinuria. Heme-pigmented granular casts. Plasma is normal color in myoglobinuria and red brown in hemoglobinuria

102. Treatment IVF Isotonic saline at 1 to 2 liters per hour Fluids are titrated to maintain a urine output of 200 to 300 mL/hour Continue until the urine discoloration clears, and plasma creatine kinase decreases to less than 5,000 to 10,000 U/L (or there is cessation of hemolysis), or symptomatic fluid overload develops.

103. Treatment Alkalinization. Mannitol diuresis. urine alkalinization prevents heme-protein precipitation with Tamm-Horsfall protein, and therefore intratubular pigment cast formation. Alkalinization may also minimize the conversion of hemoglobin to the more toxic methemoglobin.urine alkalinization prevents heme-protein precipitation with Tamm-Horsfall protein, and therefore intratubular pigment cast formation. Alkalinization may also minimize the conversion of hemoglobin to the more toxic methemoglobin.

104. Acute Interstitial Nephritis Acute interstitial nephritis (AIN) is a syndrome of ARF associated with an inflammatory infiltrate involving the renal interstitium

105. Drug hypersensitivity Penicillin Cephalosporin Sulfonamide Fluoroquinolone Rifampin NSAIDs Phenytoin Furosemide Thiazide diuretics Allopurinol Alpha interferon Cimetidine Omeprazole

107. Methicillin induced AIN Renal symptoms typically develop 2 to 3 weeks after the initiation of treatment: Hematuria Pyuria with white blood cell casts Proteinuria < 1g/d (can be nephrotic with NSAIDs) Renal failure in 50% of patients Extrarenal manifestations: Fever in 80% Eosinophilia in 80% Rash in 25%

108. Other kinetics Within 2 to 3 days after rechallenge with a drug with previous sensitisation De novo in response to a med previoulsy tolerated medication

109. Renal failure is the most prominent feature Develops within 3 wk of initiation of drug therapy in 80% Hematuria and pyuria each are present in only 50% of patients. Extrarenal manifestations, including fever, maculo-papular rash, arthralgias, and eosinophilia are each present in fewer than 50% All of them together in <5%

110. Eosinophiluria Diagnostic value is poor. Other conditions associated with Eosinophiluria Prostatitis RPGN Bladder Cancer Renal Atheroembolic disease

111. Eosinophiluria PPV for AIN of only 50 %. NPV of 90%? Thus, the presence of eosinophiluria is not strongly predictive of a diagnosis of AIN; however, its absence is useful in excluding the diagnosis.

112. Renal biopsy Failure to improve after discontinuation of potential offending drug If the potential offending drug is critical for therapy If immunosupressive therapy is considered

113. Supportive Dicontinue offending drug Prednisone 1mg/kg/d for 4 weeks Controversial Rcommended if biopsy proven AIN and who have persistent renal failure 1 week after DC the offending medication ?adjunct cyclophosphamide Treatment

114. Hepatorenal syndrome ARF in HRS results from profound renal vasoconstriction in the setting of histologically normal kidneys. Although many of the features of HRS resemble prerenal azotemia, the defining feature is a lack of improvement in renal function with volume expansion. Recovery of renal function is usually observed after restoration of hepatic function after liver transplantation

115. Picture on pathophysiology of HRSPicture on pathophysiology of HRS

117. Diagnostic criteria Chronic or acute hepatic disease with advanced hepatic failure and portal hypertension A plasma creatinine concentration above 1.5 mg/dL (133 �mol/L) that progresses over days to weeks. The absence of any other apparent cause for the renal disease, including shock, ongoing bacterial infection, current or recent treatment with nephrotoxic drugs, and the absence of ultrasonographic evidence of obstruction or parenchymal renal disease. Urine red cell excretion of less than 50 cells/HPF and protein excretion less than 500 mg/day. Lack of improvement in renal function after volume expansion with intravenous albumin (1 g/kg of body weight per day up to 100 g/day) for at least two days and withdrawal of diuretics. Urine Na<10 As noted above, the rise in plasma creatinine with reductions in glomerular filtration rate may be minimized by the marked reduction in creatinine production. It is particularly important to exclude spontaneous bacterial peritonitis, which is complicated by acute renal failure that may be reversible in 30 to 40 percent of patients. As noted above, the rise in plasma creatinine with reductions in glomerular filtration rate may be minimized by the marked reduction in creatinine production. It is particularly important to exclude spontaneous bacterial peritonitis, which is complicated by acute renal failure that may be reversible in 30 to 40 percent of patients.

118. Treatment Management of underlying cause Stop diuretics Low salt diet and free water restriction if hyponatremia Midodrine + Octreotide + Albumin Terlipressin + Albumin RRT TIPS

119. �The management of patients with acute renal failure or acute kidney injury (AKI) is principally supportive, with renal replacement therapy (RRT) indicated in patients with severe kidney injury.

120. Treatment of ARF

121. Prevention Renal hypoperfusion is a predisposing factor to the development of renal failure. Optimizing vascular hemodynamics to ensure adequate renal perfusion is a fundamental principle in avoiding renal failure. Avoidance or discontinuation of drugs that increase renal vaso-constriction, such as NSAID and selective COX-2 inhibitors. Potentially nephrotoxic medications should be avoided, particularly in high-risk patients, whenever possible. Using alternative imaging techniques such as MRI scanning should be considered in patients at high risk for contrast .

122. Pharmacologic Treatment of Acute Renal Failure Dopamine Loop diuretics ANP Thyroxine IGF-1

123. Indications for RRT Refractory fluid overload Hyperkalemia (plasma potassium concentration >6.5 meq/L) or rapidly rising potassium levels Metabolic acidosis (pH less than 7.1) Signs of uremia, such as pericarditis, neuropathy, or an otherwise unexplained decline in mental status

124. Timing of initiation of RRT It is not possible to specify a specific duration of renal injury or level of azotemia at which RRT should be optimally initiated. It is unproven whether initiation of earlier or prophylactic dialysis offers any clinical or survival benefit.

125. The optimal timing for initiation of RRT in patients with AKI will require an adequately powered prospective randomized trial. Adequate design of such a trial is limited by the current inability to quickly prospectively identify patients with early AKI who will have protracted renal injury and eventually require RRT.

126. Initiation of dialysis prior to the development of symptoms and signs of renal failure due to AKI is recommended.

127. Current data do not support the superiority of either CRRT or IHD.

128. Learning objectives Understanding the limitations of serum creat Formulation of a DDx Understanding of the pathophysiology of ARF Prevention of ARF

129. Thank you