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20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
20 Saxena   Acute Renal Failure
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20 Saxena Acute Renal Failure

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  • Panel B shows reduced perfusion pressure within the autoregulatory range. Normal glomerular capillary pressure is maintained by afferent vasodilatation and efferent vasoconstriction.
  • Panel C shows reduced perfusion pressure with a nonsteroidal antiinflammatory drug (NSAID). Loss of vasodilatory prostaglandins increases afferent resistance; this causes the glomerular capillary pressure to drop below normal values and the GFR to decrease.
  • Panel D shows reduced perfusion pressure with an angiotensin-converting–enzyme inhibitor (ACEI) or an angiotensin-receptor blocker (ARB). Loss of angiotensin II action reduces efferent resistance; this causes the glomerular capillary pressure to drop below normal values and the GFR to decrease.
  • This slide depicts the inverse relationship between P Cr and GFR (measured by inulin clearance) in a large number of subjects with varying degrees of renal function. The hyperbolic relationship between P Cr and GFR complicates the use of absolute increments in P Cr (e.g., > 0.5 or 1.0 mg/dl) as yardsticks for defining acute renal failure.
  • Relationship between GFR and serum creatinine in ARF One of the things to bear in mind when we are talking about acute renal failure is that our marker for acute renal failure is generally the serum creatinine concentration, but this is a relatively poor marker of renal function. Certainly, there are issues related to the correlation between creatinine and level of GFR related to protein mass so that a creatinine of 1 does not represent the same level of GFR in a cachectic 70-year-old as in a highly muscular 25-year-old, but in addition the change in serum creatinine that occurs lags behind the change in GFR that is seen with acute renal failure. Here you see the abrupt drop in GFR in a patient with acute renal failure, but the serum creatinine lags behind so that it may not start going up for 24 or 36 hours after the acute insult and certainly when we see a patient with aggressively rising serum creatinine, that does not mean that the renal function is continuing to deteriorate. The GFR may be close to 0 and be maintained at that level close to 0 during that period of time. The creatinine has not come back into a steady state at this new very low GFR.
  • ARF is indeed a very powerful independent predictor of a poor outcome. This is particularly seen in vascular cardiac literature where ARF independently increases mortality rate. One example of this was published about ten years ago looking at cardiac surgery patients who were absolutely matched in terms of all their illness severity and comorbidities. For those patients who required dialysis from their acute renal failure it was a 63% mortality rate compared to those patients that went on their merry way without acute renal failure with 4.3% mortality. So again, this is a huge, huge issue.
  • Dilatation of the collecting system is detectable by ultrasonography within 24 hrs of urinary outflow obstruction. Thus, it is possible (but very unusual) that patients evaluated within only a couple hours of the onset of obstruction may still have normal renal ultrasounds
  • Transcript

    • 1. Acute Renal failure (Acute Kidney Injury) Anil K. Saxena, MD; FRCP (Dublin) Renal Physician, Nephrology Division, Al- Rahba Hospital - Johns Hopkins Medicine, Abu Dhabi, UAE Renal autoregulation, Definitions, Pathogenesis, Diagnosis & General Principles of Management
    • 2. To function properly kidneys require: <ul><li>Normal renal blood flow </li></ul><ul><li>Functioning glomeruli and tubules </li></ul><ul><li>Clear urinary outflow tract </li></ul><ul><ul><li>for drainage and elimination of formed urine from the body. </li></ul></ul>
    • 3. RENAL BLOOD FLOW “ Effective Circulating Volume” Normal RBF/RPF Intrarenal Autoregulation GFR, FF Renal Perfusion Pressure Cardiac out put Mean Arterial Pressure
    • 4. Renal Autoregulation <ul><li>Autoregulation is the maintenance of a near normal intrarenal hemodynamic environment (RBF, RPF, FF and GFR) despite large changes in the systemic blood pressure </li></ul>
    • 5. Renal autoregulation <ul><li>RBF - blood perfusing the kidneys each minute (1200 ml/min) </li></ul><ul><li>Renal Plasma Flow (RPF) - plasma flowing to kidneys each minute (670 ml/min or 55-60% of RBF) </li></ul><ul><li>GFR - amount of plasma filtered each minute by the glomeruli . (Normal GFR -125 ml /min for men and 100 ml/min for women) </li></ul><ul><li>Filtration Fraction (FF) - the ratio of GFR to RPF (Normal - .18 - .22) </li></ul>
    • 6. Renal autoregulation <ul><li>F =  P </li></ul><ul><li>R </li></ul>F = Flow  P = Pressure Changes R = Resistance RBF = Renal blood flow R aff = Afferent arteriolar resistance RAP = Renal arterial pressure R eff = E fferent arteriolar resistance RAP RBF R aff + R eff ~
    • 7. Renal blood flow (RBF) <ul><li>Major sites of renal vascular resistance -Glomerular afferent (R aff ) and efferent (R eff ) arterioles </li></ul><ul><li>Changes in R aff and R eff affect RBF. </li></ul>
    • 8. Intrarenal autoregulation <ul><li>Vasoconstrictors </li></ul><ul><ul><li>Renin </li></ul></ul><ul><ul><li>Angiotensin II </li></ul></ul><ul><ul><li>Endothelin </li></ul></ul><ul><ul><li>ADH </li></ul></ul><ul><li>Vasodilators </li></ul><ul><ul><li>PGs </li></ul></ul><ul><ul><li>Kinins </li></ul></ul><ul><ul><li>NO </li></ul></ul><ul><ul><li>ANP </li></ul></ul>RBF GFR Figure : RBF / GFR is maintained by a balance between vasodilators and vasoconstrictors of Afferent and Efferent arterioles
    • 9. Intrarenal Mechanisms for Autoregulation Figure - shows normal conditions normal renal perfusion pressure and a normal GFR. RBF R eff / R aff ratio =N N Engl J Med 357;8 August 23, 2007 Afferent Arteriole P GC GFR. Glomerulus Efferent Arteriole Tubule
    • 10. Intrarenal Mechanisms for Autoregulation under decreased Perfusion Pressure RBF Afferent Arteriole P GC GFR . Efferent Arteriole PGE Ang II Figure: shows reduced perfusion pressure within the autoregulatory range. Normal glomerular capillary pressure is maintained by afferent vasodilatation and efferent vasoconstriction. MAP R eff / R aff ratio = N Engl J Med 357;8 August 23, 2007
    • 11. R eff / R aff ratio Figure: Loss of vasodilatory PGs increases afferent resistance causing drop in the glomerular capillary pressure below normal values and the fall in GFR RBF P GC GFR. Ang II Afferent Arteriole Efferent Arteriole PGE NSAID Θ Reduced perfusion pressure with a NSAID. N Engl J Med 357;8 August 23, 2007
    • 12. Reduced perfusion pressure with an ACEI or ARB. P GC GFR. Ang II Afferent Arteriole Efferent Arteriole PGE ACEI /ARB Θ Figure: Loss of angiotensin II action reduces efferent resistance; this causes the glomerular capillary pressure to drop below normal values and the GFR to decrease. R eff / R aff ratio RBF N Engl J Med 357;8 August 23, 2007
    • 13. Renal autoregulation failure <ul><li>Renal autoregulation breaks down as MAP falls below 80 mm Hg, </li></ul><ul><li>Further adjustments in intra-renal hemodynamics are unable to maintain RBF and GFR </li></ul><ul><li>Hallmark of ARF </li></ul><ul><li>After age 30, RBF/ GFR decreases progressively with age; at 80 years it is nearly half of that at 20 years </li></ul>
    • 14. Renal autoregulation failure <ul><li>Failure to decrease arteriolar resistance </li></ul><ul><li>Structural changes in renal arterioles and small arteries </li></ul><ul><ul><li>Old age, Atherosclerosis </li></ul></ul><ul><ul><li>Chronic HTN, Malignant or accelerated HTN </li></ul></ul><ul><ul><li>CKD </li></ul></ul><ul><li>Reduction in vasodilatory prostaglandins </li></ul><ul><ul><li>NSAIDs </li></ul></ul><ul><ul><li>Cyclooxygenase-2 inhibitors </li></ul></ul>N Engl J Med 357;8 August 23, 2007
    • 15. Renal autoregulation failure <ul><li>Afferent glomerular arteriolar vasoconstriction </li></ul><ul><ul><li>Sepsis </li></ul></ul><ul><ul><li>Hypercalcemia </li></ul></ul><ul><ul><li>Hepatorenal syndrome </li></ul></ul><ul><ul><li>Cyclosporine or tacrolimus </li></ul></ul><ul><ul><li>Radiocontrast agents </li></ul></ul><ul><li>Failure to increase efferent arteriolar resistance </li></ul><ul><ul><li>ACEI </li></ul></ul><ul><ul><li>Angiotensin-receptor blockers </li></ul></ul><ul><li>Renal - artery stenosis </li></ul>N Engl J Med 357;8 August 23, 2007
    • 16. ARF - definition <ul><li>An abrupt fall in GFR over a period of minutes to days with rapid & sustained rise in nitrogenous waste products in blood. </li></ul><ul><li>(Rate of production of metabolic waste exceeds the rate of renal excretion) </li></ul>
    • 17. Definitions … <ul><li>Well over 30 definitions used in published studies (Ranging from subtle increases in S. Cr. levels – requirement of dialysis) </li></ul><ul><li>Multiple aetiologies </li></ul><ul><li>Different outcomes </li></ul><ul><li>Classification according to severity and outcome - elusive </li></ul>
    • 18.  
    • 19.  
    • 20.  
    • 21. Clinical markers of ARF <ul><li>Reduced GFR </li></ul><ul><li>Raised S.Creatinine </li></ul>
    • 22. Relationship between GFR and serum creatinine in ARF Serum Creatinine (mg/dl) GFR (ml/min per 1.73m 2 ) 1.0 0 2.0 3.0 4.0 5.0 6.0 7.0 8.0 9.0 40 60 80 100 120 140 160 180 20 0
    • 23. Relationship between GFR and serum creatinine in ARF <ul><li>S.Cr. poor marker of renal function. </li></ul><ul><li>Poor correlation between S.Cr. and level of GFR related to muscle mass. </li></ul><ul><li>S.Cr. of 1.0 does not represent the same level of GFR in a cachectic 70-year-old as in a highly muscular 25-year-old. </li></ul>
    • 24. <ul><li>Figure: The abrupt drop in GFR but the S.Cr. does not start going up for 24 or 36 hours after the acute insult . </li></ul>40 80 0 GFR (mL/min) 0 7 14 21 28 4 Days 2 0 6 Serum Creatinine (mg/dL)
    • 25. Acute Kidney Injury Network (AKIN- 2005) Continuum of the renal injury STAGE I RISK (R) STAGE II INJURY (I) STAGE V ESRD (E) STAGE III FAILURE (F) STAGE IV LOSS (L) Severity Outcome
    • 26. – RIFLE criteria/staging system
    • 27. D/D of Azotemia <ul><li>Acute rise in S. Creatinine </li></ul><ul><li>Medications that block tubular creatinine secretion </li></ul><ul><ul><li>Trimethoprim </li></ul></ul><ul><ul><li>Cimetidine </li></ul></ul><ul><li>Substances that interfere with creatinine assay </li></ul><ul><ul><li>Cefoxitin </li></ul></ul><ul><ul><li>Flucytosine </li></ul></ul>
    • 28. D/D of Azotemia <ul><li>Acute elevation of BUN </li></ul><ul><ul><li>Protein loading </li></ul></ul><ul><ul><li>Catabolic state - severe sepsis </li></ul></ul><ul><ul><li>GI bleeding </li></ul></ul><ul><ul><li>Corticosteroid therapy </li></ul></ul><ul><ul><li>Antibiotics -Tetracycline </li></ul></ul>
    • 29. Definitions…. <ul><ul><li>Azotemia - silent </li></ul></ul><ul><ul><li>Uremia - symptomatic </li></ul></ul><ul><ul><li>Oliguria - < 400 mL/24 h </li></ul></ul><ul><ul><li>Anuria - < 100 mL/24 h </li></ul></ul><ul><ul><li>Nonoliguric ARF - > 400 ml / 24 h </li></ul></ul>
    • 30. D/D of Azotemia <ul><li>Acute rise in S. Creatinine </li></ul><ul><li>Medications that block tubular creatinine secretion </li></ul><ul><ul><li>Trimethoprim </li></ul></ul><ul><ul><li>Cimetidine </li></ul></ul><ul><li>Substances that interfere with creatinine assay </li></ul><ul><ul><li>Cefoxitin </li></ul></ul><ul><ul><li>Flucytosine </li></ul></ul>
    • 31. D/D of Azotemia <ul><li>Acute elevation of BUN </li></ul><ul><ul><li>Protein loading </li></ul></ul><ul><ul><li>Catabolic state - severe sepsis </li></ul></ul><ul><ul><li>GI bleeding </li></ul></ul><ul><ul><li>Corticosteroid therapy </li></ul></ul><ul><ul><li>Antibiotics -Tetracycline </li></ul></ul>
    • 32. ARF: Life threatening consequences <ul><li>Volume overload </li></ul><ul><li>Hyperkalaemia </li></ul><ul><li>Uremia: </li></ul><ul><ul><li>Pericarditis </li></ul></ul><ul><ul><li>Encephalopathy </li></ul></ul><ul><ul><li>Platelet dysfunction </li></ul></ul><ul><li>Metabolic acidosis </li></ul>
    • 33. Epidemiology <ul><li>INCIDENCE </li></ul><ul><li>1-5% of all patients </li></ul><ul><li>7-23 % in the ICU </li></ul><ul><li>Crit Care Med 16 (11): 1106-1109, 1998 </li></ul>
    • 34. ARF- Community vs. Hospital Acquired Obialo, C. I. et al. Arch Intern Med 2000;160:1309-1313.
    • 35. Epidemiology <ul><li>MORTALITY </li></ul><ul><li>20-70% Overall </li></ul><ul><li>79% for patients requiring RRT (ICU) </li></ul><ul><li>Nephrol Dial Transplant. 1994:9 S179-S182 </li></ul>
    • 36. Epidemiology <ul><li>MORTALITY </li></ul><ul><li>ARF Outcome ~ Severity of Underlying Disease </li></ul><ul><li>Significant Mortality difference - </li></ul><ul><li>Ischemic -30% vs. Nephrotoxic- 10% </li></ul>
    • 37. MORTALITY <ul><li>ARF is an independent predictor of a poor renal outcome </li></ul><ul><li>Vascular/ cardiac surgery – ARF increases mortality </li></ul><ul><li>Cardiac surgery patients </li></ul><ul><li>Matched illness severity / comorbidities </li></ul><ul><ul><ul><li>63% mortality dialysis </li></ul></ul></ul><ul><ul><ul><li>4.3 % mortality intact renal function </li></ul></ul></ul>Am J Med 1998; 104 (4) 343-348
    • 38. Predictors of mortality <ul><ul><li>Multisystem failure </li></ul></ul><ul><ul><li>Mechanical ventilation </li></ul></ul><ul><ul><li>Hypoalbuminemia </li></ul></ul><ul><ul><li>Hyperbilirubinemia </li></ul></ul><ul><ul><li>Severe Lactic acidosis </li></ul></ul><ul><li>Dialysis requirement </li></ul>
    • 39. Spectrum of AKI <ul><li>Prerenal : renal hypoperfusion </li></ul><ul><li>Renal (Intrinsic) : </li></ul><ul><ul><li>Glomerular </li></ul></ul><ul><ul><li>Tubular </li></ul></ul><ul><ul><li>Vascular </li></ul></ul><ul><ul><li>Interstitial </li></ul></ul><ul><li>Post renal: obstruction </li></ul>injury
    • 40. Spectrum …. <ul><li>Hemodynamic AKI (≈30%) </li></ul><ul><li>Parenchymal AKI (65%) </li></ul><ul><ul><li>Acute tubular necrosis (55%) </li></ul></ul><ul><ul><li>Acute glomerulonephritis (≈5%) </li></ul></ul><ul><ul><li>Vasculopathy (3%) </li></ul></ul><ul><ul><li>Acute interstitial nephritis (≈2%) </li></ul></ul><ul><li>Obstruction (≈5%) </li></ul>
    • 41. PRE-RENAL ( Hemodynamic ) AKI PRERENAL AKI Generalized or localized reduction in RBF <ul><li>Hypovolaemia </li></ul><ul><li>Haemorrhage </li></ul><ul><li>Volume depletion </li></ul><ul><li>( vomiting, </li></ul><ul><li>diarrhoea, </li></ul><ul><li>inappropriate diuresis, burns) </li></ul>Hypotension Cardiogenicshock Distributive shock (sepsis, anaphylaxis) Oedema states Cardiac failure Hepatic cirrhosis Nephrotic syndrome Renal Hypoperfusion NSAIDs ACEI / ARBs AAA RAS /occlusion Hepatorenal syndrome Reduced GFR
    • 42. Prerenal AKI <ul><li>Renal hypoperfusion </li></ul><ul><ul><li>Decreased RBF and GFR </li></ul></ul><ul><ul><li>Increased Na and H 2 O reabsorption </li></ul></ul><ul><ul><li>Oliguria </li></ul></ul><ul><ul><li>High U osm (>500) , low U Na ( FeNa >1%) </li></ul></ul><ul><ul><li>Elevated BUN / S.Cr. Ratio </li></ul></ul><ul><ul><li>Bland urinary sediments </li></ul></ul>
    • 43. Renal / Intrinsic AKI Tubular Glomerular Vascular Interstitial ATN Ischemia (50%) Toxins (30%) Ac. Interstitial nephritis Drug induced - NSAIDs, antibiotics Infiltrative - lymphoma Granulomatous- sarcoidosis, tuberculosis Infection related - post-infective, pyelonephritis Vascular occlusions - Renal artery occlusion - Renal vein thrombosis - Cholesterol emboli <ul><li>Ac.GN </li></ul><ul><ul><li>post-infectious, </li></ul></ul><ul><ul><li>SLE, </li></ul></ul><ul><ul><li>ANCA associated, </li></ul></ul><ul><ul><li>anti-GBM disease </li></ul></ul><ul><ul><li>Henoch-Schönlein purpura </li></ul></ul><ul><ul><li>Cryoglobulinaemia, </li></ul></ul><ul><ul><li>Thrombotic microangiopathy </li></ul></ul><ul><ul><ul><li>TTP </li></ul></ul></ul><ul><ul><ul><li>HUS </li></ul></ul></ul>5% 85% 8 -12% < 2% N Engl J Med 1996;334 (22):1448-60
    • 44. ATN <ul><li>Sepsis - 48% </li></ul><ul><li>Hemodynamic (excluding sepsis) - 32% </li></ul><ul><li>Toxic – 20% </li></ul><ul><ul><li>NSAIDS </li></ul></ul><ul><ul><li>Radiocontrast media </li></ul></ul><ul><ul><li>ACEI </li></ul></ul><ul><ul><li>Antibiotics (Gentamicin, Amphotericin) </li></ul></ul><ul><ul><li>Crit care Med 1996; 24(2) 192-198 </li></ul></ul>
    • 45. <ul><li>PaO2 </li></ul><ul><li>50 mm of Hg </li></ul><ul><li>PaO2 </li></ul><ul><li>20 mm of Hg </li></ul>10 mm of Hg PaO2
    • 46. ATN <ul><li>Medullary blood flow constitutes about 10% to 15% of total RBF </li></ul><ul><li>Relative hypoxia in the outer medulla predisposes to ischemic injury in </li></ul><ul><ul><li>S3 segment of the proximal tubule </li></ul></ul><ul><ul><li>Thick ascending limb (more glycolytic machinery for ATP synthesis) </li></ul></ul>
    • 47.  
    • 48. Pathophysiology of ATN: Tubular Epithelial Cell Injury and Repair Loss of polarity Normal Epithelium Migration , Dedifferentiation of Viable Cells Differentiation & Reestablishment of polarity Sloughing of viable and dead cells with luminal obstruction Ischemia/ Reperfusion Apoptosis Necrosis Cell death Adhesion molecules Na + /K + -ATPase Proliferation
    • 49.  
    • 50. ATN <ul><li>Renal Tubular obstruction, Tubular back leak </li></ul><ul><ul><li>Decreased GFR, Oliguria </li></ul></ul><ul><ul><li>Decreased Na reabsorption </li></ul></ul><ul><ul><li>Low U osm (< 350), High U Na (FeNa <1%) </li></ul></ul><ul><ul><li>Elevated BUN / S.Cr. </li></ul></ul><ul><ul><li>Urinary sediments- Muddy pigmented granular casts </li></ul></ul>
    • 51. Principal POST-RENAL causes of AKI <ul><li>Intra-luminal </li></ul><ul><li>Stone, </li></ul><ul><li>Blood clots, </li></ul><ul><li>Papillary necrosis </li></ul><ul><ul><li>Pelvic malignancies </li></ul></ul><ul><ul><li>Prolapsed uterus </li></ul></ul><ul><ul><li>Retroperitoneal fibrosis </li></ul></ul>Intrinsic <ul><li>Intra-mural </li></ul><ul><li>Urethral stricture, </li></ul><ul><li>BPH, </li></ul><ul><li>Carcinoma prostate, </li></ul><ul><li>Bladder tumour, </li></ul><ul><li>Radiation fibrosis </li></ul>Extrinsic Post-renal Urinary outflow tract obstruction
    • 52. How do we assess a patient with AKI? <ul><li>Is this acute or chronic renal failure? </li></ul><ul><ul><li>History and examination </li></ul></ul><ul><ul><li>Previous Serum creatinine measurements </li></ul></ul><ul><ul><li>Small kidneys on ultrasound (except for in - Diabetes, PCKD, Urinary Tract Obstruction ) </li></ul></ul>Hilton et al, BMJ 2006;333;786-790
    • 53. <ul><li>Distinguishing between acute and chronic renal failure is important, as – </li></ul><ul><ul><li>The approach to these patients differs greatly. </li></ul></ul><ul><ul><li>This may, save a great deal of unnecessary investigation. </li></ul></ul>
    • 54. <ul><li>Factors that suggest chronicity include – </li></ul><ul><ul><li>Long duration of symptoms, </li></ul></ul><ul><ul><li>Nocturia, </li></ul></ul><ul><ul><li>Absence of acute illness, anaemia, hyperphosphatemia, and hypocalcaemia, </li></ul></ul>
    • 55. <ul><li>Has obstruction been excluded? </li></ul><ul><ul><li>Complete anuria </li></ul></ul><ul><ul><li>Palpable bladder </li></ul></ul><ul><ul><li>Renal ultrasound </li></ul></ul>Hilton et al, BMJ 2006;333;786-790
    • 56. <ul><li>Careful urological evaluation </li></ul><ul><ul><li>P/H Renal stones, </li></ul></ul><ul><ul><li>H/O Symptoms of bladder outflow obstruction- Prostate enlargement </li></ul></ul><ul><ul><li>Prolapsed uterus </li></ul></ul><ul><ul><li>A palpable bladder. </li></ul></ul><ul><ul><li>Catheterization </li></ul></ul>
    • 57. <ul><li>Complete anuria suggests renal tract obstruction </li></ul><ul><ul><li>X-ray KUB </li></ul></ul><ul><ul><li>Renal ultrasonography – detect dilatation of the renal pelvis and calyces, </li></ul></ul><ul><ul><li>CT Scan </li></ul></ul>
    • 58. <ul><li>Is the patient euvolaemic? </li></ul><ul><ul><li>Pulse, JVP/CVP, postural blood pressure, daily weights, fluid balance </li></ul></ul><ul><ul><li>Disproportional increase in urea /creatinine ratio </li></ul></ul><ul><ul><li>Urinary sodium concentration (unless on diuretics) </li></ul></ul><ul><ul><li>Fluid challenge </li></ul></ul>
    • 59.  
    • 60. <ul><li>Does evidence of renal parenchymal disease exist (other than ATN)? </li></ul><ul><ul><li>History and examination (systemic features) </li></ul></ul><ul><ul><li>Urine dipstick and microscopy (red cells, red cell casts, eosinophils, proteinuria) </li></ul></ul>
    • 61. <ul><li>Has a major vascular occlusion occurred? </li></ul><ul><ul><li>Atherosclerotic vascular disease </li></ul></ul><ul><ul><li>Renal asymmetry </li></ul></ul><ul><ul><li>Loin pain </li></ul></ul><ul><ul><li>Macroscopic haematuria </li></ul></ul><ul><ul><li>Complete anuria </li></ul></ul>
    • 62. What investigations are most useful in ARF? <ul><li>Urinalysis: </li></ul><ul><ul><li>Dipstick for blood, protein, or both - Suggests a renal inflammatory process </li></ul></ul><ul><ul><li>Microscopy for cells, casts, crystals - Red cell casts diagnostic in glomerulonephritis </li></ul></ul>Hilton et al, BMJ 2006;333;786-790
    • 63. RBCs <ul><li>Dysmorphic red blood cells suggest glomerular injury. </li></ul>
    • 64. Red blood cell cast Marker of glomerular injury Granular cast
    • 65. Pigmented granular (“muddy brown”) casts Marker of acute tubular necrosis
    • 66. May- Grünwald - Giemsa staining Marker of acute interstitial nephritis.
    • 67. Biochemistry <ul><li>Serial blood urea, creatinine, electrolytes, Blood gas analysis, serum bicarbonate – </li></ul><ul><ul><li>Important metabolic consequences of ARF include hyperkalaemia, metabolic acidosis, hypocalcaemia, hyperphosphataemia </li></ul></ul>
    • 68. Biochem…. <ul><li>Creatine kinase, myoglobinuria – </li></ul><ul><ul><li>Markedly elevated CK and myoglobinuria suggests rhabdomyolysis </li></ul></ul><ul><li>Serum immunoglobulins, serum protein electrophoresis, Bence Jones proteinuria – </li></ul><ul><ul><li>Immune paresis, monoclonal band on serum protein electrophoresis, and Bence Jones proteinuria suggest multiple myeloma </li></ul></ul>
    • 69. Haematology <ul><li>Full blood count, blood film: </li></ul><ul><ul><li>Eosinophilia may be present in acute interstitial nephritis, cholesterol embolization, or vasculitis (CSS) </li></ul></ul><ul><ul><li>Thrombocytopenia and red cell fragments suggest thrombotic microangiopathy –TTP, HUS </li></ul></ul>
    • 70. Haem…. <ul><li>Coagulation studies </li></ul><ul><ul><li>Disseminated intravascular coagulation associated with sepsis </li></ul></ul>
    • 71. Immunology <ul><li>Antinuclear antibody (ANA) , Anti-double stranded (ds) antibody - </li></ul><ul><ul><li>ANA positive in SLE and other autoimmune disorders;DNA antibodies anti-ds DNA antibodies more specific for SLE </li></ul></ul><ul><li>C3 & C4 complement concentrations- </li></ul><ul><ul><li>Low in SLE, acute post infectious glomerulonephritis, Cryoglobulinemia </li></ul></ul><ul><li>ASO and anti-DNAse B titres </li></ul><ul><ul><li>High after streptococcal infection </li></ul></ul>Hilton et al, BMJ 2006;333;786-790
    • 72. Immunology <ul><li>ANCA </li></ul><ul><ul><ul><li>p-ANCA - Anti PR3 antibodies </li></ul></ul></ul><ul><ul><ul><li>c-ANCA - Anti MPO antibodies </li></ul></ul></ul><ul><ul><li>Associated with systemic vasculitis - Wegener’s granulomatosis; CSS, Microscopic polyangiitis. </li></ul></ul><ul><li>AntiGBM antibodies </li></ul><ul><ul><li>Present in Goodpasture’s disease </li></ul></ul>
    • 73.  
    • 74. serology <ul><li>Hepatitis B and C, HIV serology– </li></ul><ul><ul><li>Important implications for infection control within dialysis area </li></ul></ul><ul><li>Radiology </li></ul><ul><li>Renal ultrasonography </li></ul><ul><ul><li>For renal size, symmetry, evidence of obstruction </li></ul></ul>
    • 75.  
    • 76.  
    • 77. Management principles in ARF <ul><li>Identify and correct pre-renal and post-renal factors </li></ul><ul><li>Optimise cardiac output and RBF- </li></ul><ul><li>Review drugs: </li></ul><ul><ul><li>Stop ACEI, ARBs, NSAIDs </li></ul></ul><ul><ul><li>Adjust doses / monitor drug concentrations (where appropriate) </li></ul></ul>
    • 78. Avoid <ul><li>Aminoglycosides </li></ul><ul><ul><li>33 % of nephrotoxicity “therapeutic levels” </li></ul></ul><ul><li>Amphotericin </li></ul><ul><ul><li>hydration, </li></ul></ul><ul><ul><li>Liposomal formulation </li></ul></ul><ul><li>Radiocontrast media - </li></ul><ul><ul><li>Hydration </li></ul></ul><ul><ul><li>N-acetyl cysteine </li></ul></ul>
    • 79. Management principles.. <ul><li>Accurately monitor fluid balance and daily body weight </li></ul><ul><li>Identify and treat acute complications </li></ul><ul><ul><li>Hyperkalaemia, </li></ul></ul><ul><ul><li>Acidosis, </li></ul></ul><ul><ul><li>Pulmonary oedema </li></ul></ul>
    • 80. Optimise nutritional support <ul><li>Maintaining calories enhances patient survival </li></ul><ul><li>Maintaining protein intake MAY enhance recovery & outcome </li></ul><ul><li>protein intakes of > 1.2- 1.4 g/kg/ day can dramatically increase urea production WITHOUT evidence of outcome benefit </li></ul>
    • 81. Management principles… <ul><li>Identify and aggressively treat infection; </li></ul><ul><ul><li>Minimise indwelling lines </li></ul></ul><ul><ul><li>Remove bladder catheter if anuric. </li></ul></ul><ul><li>Identify and treat bleeding tendency: </li></ul><ul><ul><li>Prophylaxis - proton pump inhibitor or H2 antagonist, avoid aspirin </li></ul></ul><ul><ul><li>transfuse if required </li></ul></ul>
    • 82. <ul><li>Initiate dialysis before uraemic complications set in. </li></ul>
    • 83. Radiocontrast induced nephropathy (RCIN) <ul><li>Less than 1% in patients with normal renal function </li></ul><ul><li>Increases significantly with renal insufficiency </li></ul><ul><li>Dialysis - rarely needed </li></ul>
    • 84. Risk Factors Patient Related <ul><ul><li>Elderly </li></ul></ul><ul><ul><li>Dehydration </li></ul></ul><ul><ul><li>Underlying CKD </li></ul></ul><ul><ul><li>Diabetes mellitus </li></ul></ul><ul><ul><li>Urgent procedure </li></ul></ul><ul><ul><li>Multiple myeloma </li></ul></ul><ul><ul><li>CHF ( LVEF < 40%) </li></ul></ul><ul><ul><li>Hypertension </li></ul></ul><ul><ul><li>Low hematocrit </li></ul></ul><ul><ul><li>Intra-aortic balloon pump </li></ul></ul>
    • 85. Contrast properties <ul><ul><li>High osmolar contrast </li></ul></ul><ul><ul><li>Ionic contrast </li></ul></ul><ul><ul><li>High viscosity </li></ul></ul><ul><ul><li>Large volume </li></ul></ul>
    • 86. Clinical Characteristics <ul><li>Onset - 24 to 48 hrs after exposure </li></ul><ul><li>Duration - 5 to 7 days </li></ul><ul><li>Non-oliguric (majority) </li></ul><ul><li>Urinary sediment – May contain the “muddy-brown” pigmented casts and renal tubular cells typical of ATN or may be quite bland. </li></ul><ul><li>Low fractional excretion of Na </li></ul>
    • 87. Mechanism <ul><li>Hemodynamic- reduce RBF </li></ul><ul><li>Direct tubulotoxicity </li></ul><ul><li>Cytokine release </li></ul><ul><li>Osmolar injury </li></ul><ul><li>Tubular obstruction </li></ul>
    • 88. <ul><li>Patients who are administered contrast media through an arterial vessel, are at the risk of developing Atheroembolic (cholesterol) AKI </li></ul>
    • 89. Prophylactic Strategies <ul><li>Use I.V. contrast only when necessary </li></ul><ul><li>Hydration with normal saline (1-1.5 mL/Kg/ h) 6 -12 h before and after the procedure. </li></ul><ul><li>Use Low/ iso osmolar (nonionic) contrast media </li></ul><ul><li>Minimize contrast volume </li></ul><ul><li>N-acetylcysteine - 600-1200 mg BID for two doses before and 2 doses after the procedure </li></ul>
    • 90. Conclusions. <ul><li>ARF is common worldwide </li></ul><ul><li>Occurs in all clinical & community settings </li></ul><ul><li>It carries a high morbidity and mortality risks. </li></ul><ul><li>Involves high cost of management. </li></ul>
    • 91. Conclusions.. <ul><li>The most common cause of in-hospital ARF is ATN that results from multiple acute insults e.g. sepsis, Hypotension, and use of nephrotoxic drugs or Radiocontrast media </li></ul>
    • 92. Conclusions <ul><li>ARF is increasingly common, particularly among hospital inpatients, elderly people, and critically ill patients. </li></ul><ul><li>It carries a high mortality </li></ul>
    • 93. Conclusions.. <ul><li>Patients at risk are - elderly people; patients with diabetes, hypertension, or vascular disease; and those with pre -existing renal impairment </li></ul>
    • 94. Conclusions.. <ul><li>ARF is often preventable. </li></ul><ul><li>Rapid recognition of incipient ARF and early treatment of established ARF may prevent irreversible loss of nephrons. </li></ul>
    • 95. Conclusions.. <ul><li>No drug treatment has been shown to limit the progression of, or speed up recovery from, ARF. </li></ul><ul><li>Advice from a nephrologist should be sought for all cases of ARF. </li></ul>

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