Dr. Osama El-Shahat Consultant Nephrologist Head of Nephrology department New Mansoura General Hospital (International ) (Egypt)

Objectives Treatment  Non- dialytic support  Dialytic support Diagnosis  Incidence  Mortality  Biomarkers Definatinon ARF AKI

1802: Ischuria Renalis (William Heberden) 1909: Acute Bright’s Disease (William Osler) W.W.I: War Nephritis W.W.II: Acute Kidney Insufficiency (Bywaters & Beall) 1951: Acute Renal Failure (Homer W. Smith) 2006 : Acute Kidney Injury (AKI Network)

 By AKI we actually mean “loss of small solute clearance” (urea/creatinine increase in blood)  This implies loss of GFR  So…clinically we actually mean “acute decrease in GFR” What do we mean by AKI?

Lameire N, Van BW, Vanholder R. Nat Clin Pract Nephrol 2006; 2: 364–377. Can we do staging for AKI?

AKIN Classification

What is the advantages of RIFLE Criteria?  Applying the RIFLE criteria revealed new insights.  Firstly, the RIFLE classification is feasible and fairly straightforward.  Secondly, the patients categorized as RIFLE-F had a far higher mortality than RIFLE-I and -R patients. Max Bell et al; Nephrol Dial Transplant :354 –360

Number of ARF Hospitalizations: 1979 to 2002 Rates per 1,000 persons Source: National Center for Health Statistics, National Hospital Discharge Survey

Kidney International advance online publication, 1 May 2013 Mortality in AKI

Causes of AKI Pre renal Intrinsic renal Post renal Decrease in effective blood volume. Arterial occlusion Or stenosis. Homodynamic Form. Vascular Vasculitis. Malignant hypertension Acute Glomerulo nephritis Acute Interstitial nephritis Acute Tubular necrosis Ischemic.Nephrotoxic. Obstruction Of Collecting System Or Extra renal drainage Exogenous Antibiotic Radio contrast cisplatin Endogenous Intra tubular pigment Intra tubular protein. Intra tubular crystal.

CAUSES OF AKI Post-OP, sepsis, shock,multi-organ failure 70% Obstructive uropathy 15% Glomerulonephritis 5% Nephrotoxic agents 10% reduced blood flow ischemia acute tubular necrosis

Timing nephrology consultation (Mehta, Am J Med 2002) In-hospital mortalityEarly consultDelayed P 40%67%<0,001 Early nephrologist involvement in patients with AKI may reduce the risk of a further decrease in kidney function. Am J Kidney Dis. 2011;57(2):

Kidney International (2013) 83, 901–908 Early Referral

Biomarkers are foot prints of actual organ damage  Creatinine Not A Biomarker  The creatinine level is influenced by multiple non-renal factors, such as age, gender, muscle mass, muscle metabolism, diet, medications, and hydration status  In AKI, the serum creatinine level can take several hours or days to reach a new steady state and thus does not reflect the actual decrease in GFR in the acute setting  Because of renal reserve, the serum creatinine level may not rise until more than half of the kidney function has been lost

Creatinine is late, or is it too late?

New urinary biomarkers for the early detection of acute kidney disease Han, Bonventre,Current Opin Crit Care 2004, 10:476–482 Neutrophil gelatinase associated lipocalin

Early detection of AKI by Cystatin C Definition of AF Area under the ROC Day - 2Day - 1Day 0 ≥ 50 % increase ≥ 100 % increase ≥ 200 % increase Changes in cystatin C were able to detect the onset of AKI one to two days earlier than comparable changes in serum creatinine 1.RIFLE- R ( ≥ 50 % increase ): 1.5 ± 0.6 days earlier 2.RIFLE- I ( ≥ 100 % increase): 1.2 ± 0.9 days earlier 3.RIFLE- F ( ≥ 200 % increase): 1.0 ± 0.6 days earlier Herget-Rosenthal et al, Kidney Int 2004, 66:

Indications of Renal Biopsy 1 Urine No cast FENa<1% Muddy brown cast FENa>1% Red cell cast White cell cast eosinophil Pre-renal ATNGlomerular Interstitial Biopsy 2. Unknown cause 3. Prolonged ATN

Loop diuretics in AKI Diuretics, particularly high doses of loop diuretics, are frequently administered to patients with acute renal failure. This is done in part in an attempt to convert oliguric to nonoliguric acute renal failure. However, a retrospective observational report found that the use of diuretics in this setting may increase the risk of death and no recovery of renal function B : We recommend not using diuretics to prevent AKI. ( 1B ) C : We suggest not using diuretics to treat AKI, except in the management of volume overload. ( 2C )

There is insufficient evidence that the low-dose dopamine improves survival or obviates the need for dialysis in persons with acute renal failure. The routine use of low-dose dopamine should be discouraged until a prospective, randomized, placebo-controlled trial establishes its safety and efficacy. Is the administration of dopamine associated with adverse or favorable outcomes in acute renal failure? Auriculin Anaritide Acute Renal Failure Study Group. Low Dose Dopamine in AKI : We recommend not using low-dose dopamine to prevent or treat AKI. (1A)

IV Fluids in AKI B 3.1.1: In the absence of hemorrhagic shock, we suggest using isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume in patients at risk for AKI or with AKI. (2B)

Contrast Induced AKI i.vvolumeexpansion 1A : We recommend i.v. volume expansion with either isotonic sodium chloride or sodium bicarbonate solutions, rather than no i.v. volume expansion, in patients at increased risk for CI-AKI. ( 1A ) not using prophylactic intermittent hemodialysis IHD hemofiltrationHF 2C : We suggest not using prophylactic intermittent hemodialysis (IHD) or hemofiltration (HF) for contrast-media removal in patients at increased risk for CI-AKI. ( 2C ) oralNACtogetherwithi.visotoniccrystalloids 2D : We suggest using oral NAC, together with i.v. isotonic crystalloids, in patients at increased risk of CI-AKI. ( 2D ) iso-osmolar low-osmolar 1B : We recommend using either iso-osmolar or low-osmolar iodinated contrast media, rather than high-osmolar iodinated contrast media in patients at increased risk of CI-AKI. ( 1B )

Bicarbonate or Saline Among the large randomized trials there was no evidence of benefit for hydration with sodium bicarbonate compared with sodium chloride for the prevention of CI-AKI. Contrast Induced AKI

Stage-based management General Principles Risk Stage 1 (Risk) Risk for more severe AKI Monitor (prevent progression) Injury Stage 2 (Injury) Risk of AKI-related mortality/morbidity high Conservative therapy) Failure Stage 3 (Failure) Highest risk of death Consider RRT Avoid subclavian catheters if possible Discontinue all nephrotoxic agents when possible Consider invasive diagnostic workup Consider Renal Replacement Therapy 12 3 Non-invasive diagnostic workup Ensure volume status and perfusion pressure Check for changes in drug dosing AKI Stage Consider functional hemodynamic monitoring Monitoring Serum creatinine and urine output Consider ICU admission Avoid hyperglycemia Consider alternatives to radiocontrast procedures Risk Injury Failure High Risk

Conclusions Early detection and treatment of AKI may improve outcomes. Even a minor acute reduction in kidney function has an adverse prognosis. Hunting AKI in ICU….use a RIFLE. Early referral will improve outcome