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  • 1.  Rapid loss of renal function leading to abnormal water, electrolyte and solute balance. Occurs over a period of hours to days. Usually associated with oliguria. Some patients develop non oliguric ARF eg. After radiocontrast media. It can be reversed with treatment of the cause. Acute-on top of chronic renal failure may occur. 2
  • 2. RIFLE classification of acute kidney injury Grade GFR criteria UO criteria SCr × 1.5 UO < 0.5 mL/kg/hour Risk × 6 hours SCr × 2 UO < 0.5 mL/kg/hour Injury × 12 hours SCr × 3 or SCr > 350 UO < 0.3 mL/kg/hour Failure mol/L with an acute rise × 24 hours > 40 mol/L Persistent AKI > 4 weeks Loss Persistent renal failure > ESKD 3 monthsAKI, acute kidney injury; ESKD, end-stage kidney disease, GFR,glomerular filtration rate; SCr, serum creatinine; UO, urine output. 3
  • 3. Acute Renal FailurePre-renal Intrinsic renal Post-renal causes causes causesGlomerular Tubular Interstitial Vasculardisease injury nephritis disease Ischaemic Toxic 4
  • 4. Causes of Acute Renal FailurePrerenal (Reduced renal perfusion)1) Volume depletion:  Renal loss – diuretics, osmotic diuresis (DKA). Addisonian crisis.  Extrarenal loss – vomiting, diarrhea, skin losses (burns, excessive sweating).  Hemorrhage.  Pancreatitis.2) Hypotension (regardless of cause):3) Cardiovascular:  Congestive heart failure, reduced myocardial function, arrhythmias.  Severe valvular heart disease. 5
  • 5. 4) Hemodynamic (intense intrarenal vasoconstriction):  Radiographic contrast.  Prostaglandin inhibition (NSAIDs).  Cyclosporine and tacrolimus.  ACE inhibitors.  Amphotericin.  Hypercalcemia.5) Hepatorenal syndrome (bland urinary sediment, oliguria, low urine sodium, not reversed with volume repletion, reversible with successful liver transplant). 6
  • 6. Intrinsic or intrarenal1) Vascular:  Renal infarction, renal artery stenosis, renal vein thrombosis.  Malignant hypertension, scleroderma renal crisis, atheroemboli.2) Tubular:  Ischemic-prolonged prerenal state, sepsis syndrome, systemic hypotension.  Nephrotoxic-aminoglycosides, methotrexate, cisplatin, myoglobin (rhabdomyolysis), hemoglobin (intravascular hemolysis). 7
  • 7. 3) Glomerular:  Acute glomerulonephritis.  Good pasture syndrome.  Vasculitis (Wegener’s granulomatosis, polyarteritis).  Thrombotic microangiopathy (hemolytic uremic syndrome, TTP).4) Interstitium:  Medications–penicillins, cephalosporins, ciprofloxacin, NSAIDs, phenytoin.  Tumor infiltration (lymphoma, leukemia).  Sarcoidosis, sjogren syndrome. 8
  • 8. Postrenal (obstruction) Prostate hypertrophy, neurogenic bladder Intraureteral obstruction-crystals stones, clots, tumor. Extraureteral obstruction-tumor (cervical, prostate), retroperitoneal fibrosis. Ureteric ligation during pelvic surgery. 9
  • 9. * Pre-renal failure : - There is hypotension with signs of poor preripheral perfusion. - Postural hypotension. - Signs of hypovolemia. - Manifestations of the cause. - Metabolic acidosis and ↑ K may be present.* Established renal ARF : - Oliguria (urine volume < 400ml/d) or anuria (< 100ml/d). - Disturbances of water, electrolyte and acid base balance (↑ K, ↓ pH, Dilutional ↓ Na). - Uremic features include anorexia, nausea, vomiting, hiccough, acidotic breathing …. 10
  • 10. * Post-renal (ARF) : - Loin pain (which may be constant or intermittent) - Complete anuria with bilateral obstruction or complete obstruction of single kidney. - Infection may → fever, septicaemia. - Bladder outflow obstruction → Hesitancy, weak urine stream, terminal drippling, re-tension with overflow may occur - Screening of urinary tract by sonar is essential. 11
  • 11. Probable Causes of Acute Renal Failure Based on the Findings of The HistoryHistory Probable causes of acute renal failureReview of systemsPulmonary system Sinus, upper respiratory or pulmonary Pulmonary-renal syndrome or vasculitis symptomsCardiac system Symptoms of heart failure Decreased renal perfusion Intravenous drug abuse, prosthetic Endocarditis valve or valvular diseaseGastrointestinal System Diarrhea, vomiting or poor intake. Hypovolemia Colicky abdominal pain radiating from Urolithiasis flank to groinGenitourinary System Symptoms of benign prostatic Obstruction hypertrophy. Bone pain in the elderly Multiple myeloma or prostate cancer Trauma or prolonged immobolization Rhabdomyolysis (pigment nepbropathy)12
  • 12. (Cont.)History Probable causes of acute renal failureSkin Rash Allergic interstitial nephritis, vasculitis, systemic lupus erythematosus, atheroemboli or thrombotic thrombocytopenic purpura.Constitutional symptoms Fever, weight loss, fatigue or anorexia Malignancy or vasculitisPast medical historyMultiple sclerosis, diabetes mellitus Neurogenic bladderor strokePast surgical historyRecent surgery or procedure Ischemia, atheroemboli, endocarditis or exposure to contrast agentMedication historyAngiotensin-converting enzyme Decreased renal perfusion, acuteinhobitors, nonsteroidal anti- tubular necrosis or allergic interstitialinflammatory drugs, antibiotics or nephritisacyclovir (Zovirax) 13
  • 13. Probable Causes of Acute Renal Failure Based on the Physical FindingsPhysical Probable causes of acute renal failureExaminationVital signs Temperature Possible infection. Blood Hypertension: G.N or malignant hypertension. pressure Hypotension: volume depletion or sepsis.Weight loss or Hypovolemia or hypervolemia.gainMouth DehydrationJugular veins Hypovolemia or hypervolemiaand axillae(perspiration)Pulmonary Signs of pneumonia, cavitations, pleurisy.systemHeart New murmur of endocarditis or signs of congestive heart failure 14
  • 14. (Cont.)Physical Probable causes of acute renal failureExaminationAbdomen Bladder distention suggesting uretheral obstructionPelvis Pelvic massRectum Prostate enlargementSkin Rash of interstitial nephritis, purpura of microvascular disease, livedo reticularis suggestive of atheroembolic disease, or splinter hemorrhages or Osler’s nodes of endocarditis. 15
  • 15. * Blood urea nitrogen and serum creatinine are elevated.* ABG, electrolytes, CBC, and serology.* U/S kidneys (The size of the kidneys is usually normal.* Serology: ANA, ANCA, Anti DNA, HBV, HCV, Anti GBM. Cryoglobulin, CK, urinary myoglobin. 16
  • 16. * Urine analysis : - Unremarkable in pre and post renal causes. - Differentiates ATN vs. AIN. vs. AGN  Granular casts in ATN.  WBC casts in AIN.  RBC casts in AGN. - Urine electrolytes (Na) and osmolality.* Hansel stain for Eosinophiluria. 17
  • 17. LAB Findings of Specific Types of Acute Renal Failure Findings on blood tests Diagnosis to considerVery high uric acid level Suggestive of malignancy or tumor lysis syndrome leading to uric acid crystals; also seen in prerenal acute renal failure.Elevated creatinine kinase or Rhabdomyolysis.myoglobin levelsElevated prostate-specific antigen Prostate cancer.Abnormal serum protein Multiple myeloma.electrophoresisLow complement levels Systemic lupus erythematosus, postinfectious glomerulophritis, subacute bacterial endocarditisPositive antineurtrophic Small-vessel vasculitis (Wegener’scytoplasmic antibody (ANCA) granulomatosis or polyartheritis nodosa) 18
  • 18. LAB Findings of Specific Types of Acute Renal Failure (Cont.) Findings on blood tests Diagnosis to considerPositive antinuclear antibody to Systemic lupus erythematosusdouble-stranded DNAPositive antibody to glomerular Goodpasture’s syndromebasement membranePositive antibodies to streptolysin Poststreptocaccal glomerulonephritis.O, streptokinase or hyaluronidaseSchistocytes on peripheral smear, Hemolytic uremic syndrome ordecreased hepatoglobin level, thrombotic thrombocytopenic purpuraelevated lactate dehydrogenaselevel or elevated serum bilirubinlevelLow albumin levels Liver disease or nephrotic syndrome 19
  • 19. Laboratory Findings in Acute Renal Failure To Differentiate Pre-Renal from Renal Failure Index Prerenal Azotemia Oliguric Acute Renal Failure (ATN) BUN/PCR Ratio > 20 : 1 10-15 : 1Urine sodium (UNa) < 20 > 40 meg/L Urine osmolality, > 500 < 350 mosmol/L H2OFractional excretion <1% >2% of sodium Response to Improvement No improvement volume Urinary Sediment Bland ATN: muddy brown granular casts, cellular debris, tubular epithelial cells 20
  • 20.  ARF is common in the ICU. ARF is an independent factor for prognosis in the ICU. The incidence of ARF in the ICU 40-60% compared to 1-3% in the ward. ARF still has a mortality of 50% since it occurs in very sick patients with multiorgan failure. 21
  • 21.  Predisposing factors to ARF include old age sepsis pre existing renal disease heart disease and chronic liver disease. Mechanical ventilation has an adverse effect on renal blood flow and GFR and subsequent renal function. 22
  • 22. • Patients with ICU acquired ARF were classified into the following : A) According to the urine output: - Oliguric (urine volume of < 400 ml/day). - Nonoliguric (urine volume of > 400 ml/day). - Anuric (urine volume of < 100 ml/day). B) According to the cause: 1) Prerenal ARF. 2) Ischemic acute Tubular necrosis. 3) Nephrotoxic ARF (ATN or AIN). 4) Sepsis induced ARF. 5) Hepato-renal syndrome. 6) Other causes (e.g. obstructive uropathy, pigment nephropathy, microangiopathies). 23
  • 23. 1) Prerenal ARF was defined as ARF to renal hypoperfusion with recovery after correction of hemodynamic disturbances.2) Ischemic Acute tubular necrosis (IATN) was diagnosed when renal function did not improve after correction of possible prerenal causes, and when hepatorenal syndrome, vascular, interstitial, glomerular and obstructive aetiologies were excluded. 24
  • 24. • Decreased renal perfusion was identified by the following observations :  Any documented decline in blood pressure to less than 90/60 mmHg.  Overt volume contraction on physical examination (postural hypotension, decreased skin turgor, …), and central venous pressure (CVP) less than 5 cm H2O.  Clinically evident congestive heart failure with improvement in renal function following appropriate treatment of heart failure. 25
  • 25. 3) Nephrotoxic ARF (either AIN or ATN)  Nephrotoxic Acute Interstitial Nephritis (AIN): history of drug ingestion, fever, rash, or arthralgias. Urinary increase in WBCs (frequently eosirophiluria), WBC casts RBCs, and proteinuria, with systemic eosinophilia, if histologically demonstrated by renal biopsy or when there was a high grade of clinical suspicion. 26
  • 26.  Nephrotoxic Acute Tubular Necrosis (ATN): was defined as ARF occurring after administration of drugs known to cause ATN (e.g. aminoglycosides, amphotericin, contrast media etc …).Concurrent administration of vancomycin &aminoglycosides to critically ill septicpatients with normal renal function ofbaseline induces mainly slight and transienttoxic tubular effects. 27
  • 27.  Radiographic contrast media, were determined to be the cause of renal insufficiency when the serum creatinine concentration increased – as defined – within 72 hours following a radiologic procedure employing these agents (e.g. intravenous pyelogram – angiography – computed tomography scan). 28
  • 28. 4) Sepsis induced ARF was diagnosed if ARF is associated with at least one of the following three conditions:  Documented bacteremia.  A known focus of infection  Immunosuppression with neutropenia, and at least two additional findings: rigors – unexplained hyperventilation unexplained sudden fall in blood pressure – abrupt rise in temperature to more than 38C not due to transfusion reaction – unexplained leukocytosis of more than 15.000 mm3. 29
  • 29. 5) Hepatorenal syndrome was assigned as the cause of renal failure if the patient had severe liver failure (e.g. ascites – jaundice, hepatic encephalopathy) – and a urine sodium concentration less than 10 mEq/Liter, and the renal function did not respond to a volume expansion. 30
  • 30. 6) Other causes:  Obstruction was determined to be the cause of renal failure if obstruction was present by physical examination (as enlarged bladder) or by radiological evaluation and if improvement in renal function followed relief of obstruction. 31
  • 31.  Pigment induced-ARF, history suggestive of rhabdomyolysis, urine dispstick positive for blood (heme) without microscopic haematuria hyperkalemia, hyperphosphatemia, hypocalcemia, increased creatine kinase-MM fraction and serum uric acid. 32
  • 32.  Atheroembolic ARF: Associated with emboli of fragments ofatherosclerotic plaque from aorta and other largearteries. Diagnose by history, physical findings(evidence of other embolic phenomena, ischemicdigits, “blue toe” syndrome, etc), low serum C3and C4, peripheral eosinophiluria, rarely WBCcasts. Commonly occur after intravasculerprocedures or cannulation (cardiac catheter,CABG). 33
  • 33. Number of patients admitted in different ICUs with acquired ARF in each ICU ICU No. of admitted No. & % of patients patients with ICU acquired ARF in each ICU Medical ICU 1123 402 (35.7 %) Gynecology ICU 431 98 (22.7 %) Surgical ICU 336 53 (15.7 %) Neurology ICU 116 17 (14.6 %) Chest ICU 409 57 (13.9 %)Coronary Care Unit 722 78 (10.1 %)Cardiosurgery ICU 425 43 (10.1 %) Total 3562 748 (21 %) 34
  • 34. Causes of ICU acquired-ARF in 748 patients Causes No. & % of patients iATN 283 (37.8 %) Prerenal 198 (26.5 %) Toxic ARF 80 (10.6 %) Sepsis induced ARF 89 (11.9 %) HRS 73 (9.8 %) Others 25 (3.4 %)iATN = ischemic acute tubuler necrosis. Toxic ARF = toxic acute renalfailure. HRS – hepatorenal syndrome. 35
  • 35. Number & Percentage of patient mortality in each ICU ICU No. of patients Mortality No. & % with ICU acquired in each ICU ARF Medical ICU 402 261 (64.9 %)Coronary Care Unit 78 20 (25.6 %) Chest ICU 57 28 (49.1 %) Neurology ICU 17 9 (52.9 %) Surgical ICU 53 10 (18.8 %)Cardiosurgery ICU 43 19 (44.1 %)Gyne & obst. ICU 98 42 (42.8 %) Total 748 389 36
  • 36. * The initiation of RRT in patients with AKI prevents uremia and immediate death from the adverse complications of renal failure.* It is possible that variations in the timing of initiation, modalities, and/or dosing may affect clinical outcomes.* Multiple modalities of RRT are currently available. These include intermittent hemodialysis (IHD), continuous renal replacement therapies (CRRTs), and hybrid therapies, such as sustained low- efficiency dialysis (SLED). Despite these varied techniques mortality in patients with ARF remains high greater than 50% in severely ill patients. 37
  • 37. 1. Indications for dialysis.2. Timing of initiation of dialysis.3. Optimal modality.4. Optimal Dosing.5. Discontinuation of therapy. 38
  • 38. 1) Refractory fluid overload. 2) Hyperkalemia (plasma potassium concentration > 6.5 meq/L) or rapidly rising potassium levels. 3) Metabolic acidosis (pH less than 7.1). 4) Signs of uremia e.g. pericarditis and decline in mental state. 5) Certain alcohol and drug intoxications.* The likelihood of requiring RRT is increased in patients with underlying CKD (Acute on top of chronic). 39
  • 39.  Studies published during the 1960s and 1970s suggested that improved outcomes were associated with the initiation of hemodialysis when BUN reached exceeded 150 to 200 mg/dL. 40
  • 40.  More recent studies have evaluated the relationship between the timing of RRT initiation and clinical outcomes. Several non-randomized studies have reported that improved outcomes, including survival, are associated with early versus late initiation of RRT. It has been suggested that initiation of RRT dialysis prior to the development of overt symptoms and signs of renal failure due to AKI improves the outcome. 41
  • 41. Can dialysis delay recovery of renal function ? There is at least theoretical concern that dialysis might have detrimental effects on renal function. Three factors may be important in this regard: 1) A reduction in urine output; Both removal of excess volume and of urea contribute to a reduction in or even cessation of the urine output. The fall in urine output should not delay the regeneration of tubules. 2) Induction of hypotension; Autoregulation is impaired in ATN, because vascular endothelial injury reduces the release of vasodilating substances so recurrent ischemic tubular injury is more likely to occur, thereby delaying the restoration of function. 42
  • 42. 3) Complement activation resulting from a blood- dialysis membrane interaction, can lead to neutrophilic infiltration into the kidney (and other tissues) and prolonged acute kidney injury.4) High flux membranes can enhance removal of putative toxins and improve outcome, but may also allow the back transport (from dialysate to blood). 43
  • 43. 1) Intermittent hemodialysis (IHD).2) Continuous renal replacement therapy (CRRT).3) Peritoneal dialysis. 44
  • 44. Principles of dialysis Dialysis = diffusion = passive movement of solutes across a semi- permeable membrane down concentration gradient. * Good for small molecules. (Ultra) filtration = convection = solute + fluid removal across semi permeable membrane down a pressure gradient (solvent drag). * Better for removal of fluid Figure (1): Principles of dialysis and medium-size molecules. (top panel) and filtration (lower panel). 45
  • 45. Principles of dialysis Hemodialysis = solute passively diffuses down concentration gradient.  Dialysate flows countercurrent to blood flow.  Urea, creatinine, K move from blood to dialysate.  Ca and bicarb move from dialysate to blood. Ultrafiltration = This is the convective flow of water and dissolved solutes down a pressure gradient caused by hydrostatic or osmotic forces. Hemodiafiltration = combination of dialysis and ultrafiltration 46
  • 46. Intermittent hemodialysis (IHD) Oldest and most common technique. Primarily diffusive treatment: blood and dialysate are circulated in countercurrent manner.  Also some fluid removal by ultrafiltration due to pressure driving through circuit. Best for removal of small molecules. Typically performed 4 hours 3x / wk or daily. 47
  • 47. Continuous Renal Replacement Therapy (CRRT) CRRT strategies are particularly useful in haemo- dynamically compromised patients with ARF. They allow slow and gentle removal of solutes and fluid, avoiding major intravascular fluid shifts and minimizing electrolyte disturbances, hypotension and arrhythmias. Inflammatory mediators may also be continuously removed by CRRT, so it may be useful in sepsis syndrome. 48
  • 48. Types of Continuous Renal Replacement Therapies (CRRT)Blood accessContinuous arteriovenous hemofiltration (CAVH).Continuous arteriovenous hemodialysis (CAVHD).Continuous arteriovenous hemodiafiltration (CAVHDF).Continuous venovenous hemofiltration (CVVH).Continuous venovenous hemodialysis (CVVHD).Continuous venovenous hemodiafiltration (CVVHDF).Slow low efficiency dialysis (SLED).Slow continuous ultrafiltration (SCUF).Extended daily dialysis (EDD).Peritoneal accessContinuous equilibrium peritoneal dialysis.Blood acce 49
  • 49. Haemofiltration Provides solute clearance by convection as solutes are dragged down pressure gradient with water. It provides better removal of large MW solutes e.g. B2-microglobulin, improved clearance of low MW uraemic toxins and better cardiovascular stability and Bp control than HD. Inflammatory markers are improved. 50
  • 50. Sustained low-efficiency daily dialysis (SLED): Uses conventional dialysis machines but blood flow of 100-200 ml/M and dialysate flow of only 100 ml/M for 8-24 hr/D. Major advantages: Flexibility of duration and intensity, reduced costs. Excellent tolerability, cardiovascular stability and solute removal. 51
  • 51. Slow continuous ultrafiltration ((SCUF): Used for fluid removal in overloaded CHF patients with refractory edema without severe renal failure. Blood is driven through a highly permeable filter in a venovenous mode to primarily remove water, not solute. The ultrafiltrate produced during membrane transit is not replaced.Haemodiafiltration (HDF): Simultaneous use of HD and UF. It is good with CVS instability. It can remove the inflammatory mediators. 52
  • 52. * Current data suggest that survival and recovery of renal function are similar with both CRRT and IHD.* Advocates for CRRT have claimed that CRRT is associated with the following advantages compared with IHD: 1) Enhanced hemodynamic stability, in hemodynamically unstable patients. 2) Increased net salt and water removal, thereby permitting superior management of volume overload and nutritional requirements. 53
  • 53. 3) Enhanced clearance of inflammatory mediators, which may provide benefit in septic patients, particularly using convective modes of continuous therapy.4) Among patients with acute brain injury or fulminant hepatic failure, continuous therapy may be associated with better preservation of cerebral perfusion. 54
  • 54. Peritoneal dialysis: Least useful form of CRRT in the ICU. Diffusive treatment: Blood in capillaries of peritoneal membrane exposed to dialysate in abdomen. Continuous or intermittent. Inefficient solute/ volume clearance if unstable or poor intestinal blood flow. Can’t use if intra-abdominal pathology – risk of peritonitis. Respiratory burden. 55
  • 55. * Intermittent hemodialysis – Dosing in IHD is based upon the dose delivered per session plus the frequency of sessions.* Improved survival was observed with a higher Kt/V (greater than 1), which was particlarly evident among patients with intermediate levels of illness severity.* Compared with every other day dialysis, daily therapy was associated with a significant reduction in mortality, fewer hypotensive episodes during hemodialysis, and more rapid resolution of acute renal failure. 56
  • 56. * In contrast, the Acute Renal Failure Trial Network (ATN) Study did NOT find a difference in mortality associated with a more intensive dosing strategy for renal replacement therapy.* The Hanover Dialysis Outcome study compared extended duration dialysis, provided for approximately 8 hours per day, to a more intensive regimen where additional 8-hour treatment sessions were provided to maintain the BUN < 42 mg/dL. No difference in survival or recovery of kidney function was observed with more intensive treatment. 57
  • 57. • The Randomized Evaluation of Normal versus Augmented Legal of RRT study and two meta- analyses were performed. All studies found that, compared with standard intensity dialysis, higher intensity dialysis did not result in improved survival or clinical benefits.• It is recommended that IHD be provided 3 times/week with monitoring of the delivered dose of therapy to ensure a minimum delivered Kt/V of 1.2 per treatment. 58
  • 58. RRT is usually continued until the patientmanifests evidence of recovery of kidneyfunction.1. Increase in urine output.2. A progressive decline in serum creatinine concentration after initial attainment of stable values (assessed daily during CRRT or predialysis in patients managed with IHD) despite a constant dose of renal support.3. Measurement of creatinine clearance e.g. on six- hour timed urine collections obtained when the urine output exceeded 30 mL/hour based on an average serum creatinine at the beginning and end of the timed collection. 59
  • 59. A precise level of kidney function needed toallow discontinuation of renal support has notbeen established; however,Creatinine clearance < 12 mL/min → no discontinuation.Creatinine clearance > 20 mL/min → discontinue.Creatinine clearance 12 to 20 mL/min → optional. 60
  • 60. 1) No drugs are currently available to enhance or hasten renal recovery once ARF occurs.2) There is now clear evidence that ARF is associated with excess mortality, irrespective of whether the patient requires renal replacement therapy.3) Hense prevention is the only powerful tool to improve outcome of AKI. 61
  • 61. Identification of patients at high risk to developAKI-Elderly, DM, HT. Sepsis etc .... Non Pharmacological Pharmacological Ensuring adequate  Loop diuretics, hydration (reversing  Mannitol, dehydration,  Dopamine & Maintenance of Fenoldopam. adequate mean  Natriuretic Peptides. arterial pressure, Minimizing exposure to nephrotoxins. 62
  • 62.  NS, albumin, plasma …. CVP = 8-12 cm H2O, MAP > 65 mmHg. Optimal rate of infusion remain unclear and should be individualized. Target MAP ≥ 65 mmHg. Which vasopressors to be used. Role of low dose dopamine.. 63
  • 63.  Noradrenaline is the drug of choice in AKI in sepsis. Norepinephrine has been demonstrated to preserve splanchnic blood flow better than dopamine. Optimise fluid before starting vasopressors. Low dose dopamine should not be used for renal protection in severe sepsis. 64
  • 64. Meta-analysis: Low-Dose Dopamine IncreasesUrine Output but Does Not Prevent RenalDysfunction or DeathLow-dose dopamine offers transientimprovements in renal physiology, but nogood evidence shows that it offersimportant clinical benefits to patients withor at risk for acute renal failure. 65
  • 65.  In animal studies the use of mannitol and loop diuretic minimize the degree of renal injury if given at the time of ischemic injury. Loop diuretics decrease the active Na transport in the thick ascending loop decreasing the energy requirement. 66
  • 66.  Increasing the urine output by loop diuretic make the management easier but does not affect cell injury or the severity of the renal damage. Loop diuretic increase the urine output in the remaining nephrons and therefore huge doses are required that may cause deafness. 67
  • 67.  ANP had been tried in experimental models without any benefit despite their ability to increase renal blood flow and Na excretion. Calcium channel blockers decrease Ca influx to the cells that lead to cell injury. Most human studies were done on established ATN. 68
  • 68.  Uncontrolled studies showed that those patients who respond to diuretics or mannitol may have better outcome but these patients has less severe disease. Controlled studies failed to show any evidence that low dose dopamine have any protection of cell injury in ischemic renal damage. 69
  • 69. 70