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20 Saxena Acute Renal Failure
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
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3. RENAL BLOOD FLOW “ Effective Circulating Volume” Normal RBF/RPF Intrarenal Autoregulation GFR, FF Renal Perfusion Pressure Cardiac out put Mean Arterial Pressure
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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
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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
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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
34. ARF- Community vs. Hospital Acquired Obialo, C. I. et al. Arch Intern Med 2000;160:1309-1313.
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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
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64. Red blood cell cast Marker of glomerular injury Granular cast
66. May- Grünwald - Giemsa staining Marker of acute interstitial nephritis.
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Hinweis der Redaktion
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
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