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Diagnosis and Management of Acute Kidney Injury Epidemiology Of Disclosures Diagnosis and Management Consultant for Baxter of Acute Kidney Injury Patent on 0.5% citrate anticoagulant solution for CRRT Ashita Tolwani, M.D., M.S. Professor of Medicine University of Alabama at Birmingham 2017 AKI Outline Epidemiology Definition Epidemiology of AKI Pathophysiology and differential diagnosis Overview of prevention and management 1 Acute Kidney Injury: Why Do We Care? AKI is common (KDIGO definition) 21% of all hospital admissions >50% of ICU patients AKI is associated with increased risk of CKD, ESKD, CV disease, and death Worldwide, 2,000,000 Dialysis‐requiring AKI ICU patients have the worst outcomes 11% of ICU patients with AKI require dialysis and 10‐30% survivpeople will die this year ors remain dialysis dependent at time of hospital discharge of AKI! AKI can be preventable, treatable, and reversible Healthcare workers are not well informed about AKI and its consequences Mehta RL et al. Lancet 2015 Pannu et al. CJASN 2013 Cerda, et al. CJASN 2015 2 Definition More than 30 different definitions exist with a variety of quoted incidence rates, risk factors, and morbidity and mortality rates A staging system is needed to stratify patients so that both accurate identification and prognostication are possible Definition of AKI www.ADQI.net Using RIFLE, Patients with AKI Mortality Risk in Hospitalized Patients Have Poorer Outcomes Analysis of 71,000 pts/13 studies to validate RIFLE Criteria Mild AKI have poor outcomes > 0.3 > 0.5 > 1.0 > 2.0 ↑SCr mg/dL Source: Ricci Z. Kidney Int. 73: 538-546, 2008 Chertow et al, JASN 16: 3365-3370, 2005 3 AKIN Criteria (Rifle V2.0) KDIGO AKI Guidelines: Definition of AKI Increased SCr x1.5 UO < .5ml/kg/h OR > 0.3 mg/dL R (I) x 6 hr High Sensitivity Increased SCr x2 UO < .5ml/kg/h I (II) x 12 hr Increase SCr x3 UO < .3ml/kg/h or SCr 4mg/dl x 24 hr or High F (III) (Acute rise of 0.5 mg/dl) Anuria x 12 hrs Specificity RRT Started Modifications proposed by AKIN Criterion must be Amsterdam, 2005 reached within 48hr KDOQI Commentary AJKD 2013 Problems with Serum Creatinine Serum Creatinine and GFR in AKI Creatinine is influenced by age, muscle mass, gender, and Muscle mass ethnicity Nutrition Infection Creatinine does not reflect the presence or absence of structural injury and thus provides no guidance on AKI etiology or the Protein metabolism likelihood of response to various targeted therapies Edema The rise is serum creatinine is delayed by 2‐3 days after the injury has occurred Serum creatinine Volume of Fluid therapy may dilute serum creatinine and therefore delay distribution diagnosis Inter‐laboratory variation in measuring creatinine, and bilirubin Renal excretion and other compounds interfere with the colorimetric modified Drugs Nonlinear Jaffe assay hence affect serum creatinine levels Tubular excretion Filtration (GFR) Star RA, Kidney Int, 1998 4 Relationship Between GFR and Creatinine Conceptual Model for AKI 120 80 GFR (mL/min) 40 Increased Kidney 0 Normal Damage GFR Death risk failure 6 Serum 4 Creatinine (mg/dL) 2 Ideal Creatinine 0 0 7 14 21 28 Biomarker Days Gill, N. et al. Chest 2005;128:2847-2863 What Can an Ideal AKI Biomarker Teach Us? Potential Biomarkers for AKI Proximal Tubule Injury •Urine IL-18 •Urine KIM-1 •Urine L-FABP Distal Tubule . Predict and diagnose AKI early (before increase in serum •Urine Cystatin C •Urine NGAL •α1-microglobulin •Urine π-GST creatinine) •β2-microglobulin •Urine α-GST . Identify the primary location of injury (proximal tubule, distal •Urine Netrin-1 •Urine NAG tubule, interstitium) Glomerular Injury • Urine albumin excretion . Pinpoint the type (pre‐renal, AKI, CKD), duration and severity Glomerular Filtration • Serum Creatinine of kidney injury • Blood urine Nitrogen • Serum Cystatin C . Identify the etiology of AKI (ischemic, septic, toxic, • Plasma NGAL combination) Loop of Henle Injury •Uromodulin . Predict clinical outcomes (dialysis, death, length of stay) . Monitor response to intervention and treatment Other Mechanisms / Sites of Injury not specific to the Adapted from Koyner . Expedite the drug development process (safety) Nephron and Parikh‐ Brenner and •Hepcidin – Iron trafficking Rector’s The Kidney •TIMP-2/ IGFBP7 – G1 cell cycle arrest Courtesy of J. Koyner Prasad Devarajan: Biomarkers in Acute Kidney Injury :Search for a Serum Creatinine Surrogate 5 Biomarkers after AKI Early Detection New Paradigm for the Spectrum of AKI Idealized SCr Kim‐1 STRUCTURAL IL‐18 NO AKI (subclinical) AKI Creat (‐) Creat (‐) Biomarker (‐) Biomarker (+) NGAL FUNCTIONAL AKI INTRINSIC AKI (structural & functional) L‐FABP Creat (+) Creat (+) Biomarker (‐) Biomarker (+) Urinary Biomarkers Associated with Tubular Damage Classification of the Etiologies of AKI AKI Pathophysiology and Differential Diagnosis of AKI Prerenal Intrinsic Post-renal AKI AKI AKI Acute Acute Acute Acute Intratubular Tubular Interstitial Vascular GN Obstruction Necrosis Nephritis Syndromes 6 Non ‐ICU ICU Evaluation of Cause of AKI Form of AKI BUN:Cr UNa (mEq/L) FENa Urine Sediment Prerenal >20:1 <10 < 1% Normal, hyaline casts Post‐renal >20:1 >20 variable Normal or RBC’s Intrinsic ATN <10:1 >20 > 2% Muddy brown casts; tubular epithelial cells, granular casts AIN <20:1 >20 >1% WBC’s WBC casts, RBC’s, eosinophils AGN variable <20 <1% Dysmorphic RBC’s, RBC casts Vascular variable >20 variable Normal or RBC’s Fractional Excretion of Na+ (FENa) Fractional Excretion of Urea (FEurea) (Urine Na x Serum Cr) X 100 < 1% = pre‐renal (Serum Na x Urine Cr) > 2% = ATN (Urine UN x Serum Cr) X 100 < 35% = Pre‐renal (Serum UN x Urine Cr) > 50% = ATN Normal renal function <1% Most accurate with oliguric AKI . Better than FENa in patients on diuretics Caveat: . Rationale: Urea reabsorbed in proximal tubule + inner . < 1% without volume depletion medulla, not affected by loop and thiazide diuretics . Contrast nephropathy . Acute GN . Rhabdomyolysis . Possibly > 2% with prerenal state: . Diuretics, severe CKD Steiner AJM 1984:77:699-702 7 Pre-renal AKI – Decreased Renal Blood Flow Pre-renal Urine Sediment Cause Examples Volume depletion Renal losses; GI fluid losses; hemorrhage; burns Decreased cardiac output Heart failure; massive pulmonary embolus; acute coronary syndrome Systemic vasodilation Sepsis; cirrhosis; anaphylaxis; anesthesia Intrarenal vasoconstriction Drugs (NSAIDs, COX‐2 inhibitors, amphotericin B, calcineurin inhibitors, contrast agents); hypercalcemia; hepatorenal syndrome Efferent arteriolar vasodilation Renin inhibitors; ACE inhibitors; ARBs Hyaline Casts A prolonged pre‐renal state can lead to ATN Pathogenesis of Pre-renal AKI Impaired Autoregulation Can Lead to “Normotensive AKI” Congestive Heart Failure Liver Volume Failure Depletion Sepsis + Renal Angiotensin II Vasoconstriction - + Nitric oxide Adrenergic nerves - + Prostaglandins Vasopressin Decreased GFR Abuelo JG. N Engl J Med 2007;357:797-805 8 Intrarenal Mechanisms for Autoregulation of the GFR Pre-renal Azotemia: Medications Angiotensin‐converting enzyme inhibitors Nonsteroidal anti‐inflammatory drugs NSAIDS ACEI/ARB Abuelo JG. N Engl J Med2007;357:797-805. Systemic Effects of Increased Abdominal Abdominal Compartment Syndrome Pressure Intra‐abdominal hypertension: Cardiac GI Intra‐abdominal pressure ≥12 mm Hg; or venous return splanchnic perfusion Abdominal perfusion pressure <60 mm Hg cardiac output CNS CVP, PCWP & SVR intracranial pressure, Abdominal compartment syndrome Pulmonary perfusion pressure Intra‐abdominal pressure ≥20 mm Hg; and intrathoracic & Renal One or more new organ failures airway pressures renal perfusion PaO2 GFR PaCO2 urinary output 9 Clinical Settings for ACS Abdominal Compartment Syndrome Diagnosis Trauma patients following massive volume Measurement of intra‐abdominal pressure resuscitation Clamp drainage tube of Foley catheter Massive ascites Instill 25 mL sterile water into the bladder via the aspiration port Measure pressure using a manometer or transducer attached to Post liver transplant the aspiration port. Mechanical limitations to the abdominal wall The manometer or transducer should be zeroed at the level of the mid‐axillary line at the iliac crest Tight surgical closure Burn injuries Treatment Bowel obstruction Abdominal decompression Pancreatitis Intrinsic Renal Disease Treatment of Pre-renal AKI Glomerulonephritis Interstitial • Postinfectious GN nephritis Correction of volume depletion • Endocarditis‐associated GN • Systemic vasculitis •drugs Discontinuation/dose adjustment of medications • Membranoproliferative GN –penicillins • NSAIDs Rapidly progressive GN –sulphonamides • IgA nepropathy –rifampin RAAS blockers –NSAID's CNIs –phenytoin Evaluation for causes of “effective” volume depletion –allopurinol Heart failure •infections Small blood vessels •systemic disease Cirrhosis • Malignant hypertension –SLE Nephrotic syndrome • HUS/TTP –sarcoid Sepsis • (Pre)Eclampsia –sjogrens • DIC •malignancy Treat hypercalcemia • Scleroderma •idiopathic Recognize and treat abdominal compartment syndrome • Vasculitis • Cholesterol emboli Acute tubular necrosis 10 Pathogenesis of Ischemic AKI Acute Tubular Necrosis Ischemia Causes Ischemic: causes of prolonged prerenal AKI Innate Acute Tubular Drug‐induced: aminoglycosides; vancomycin; polymyxins; lithium; Microvascular Injury Immunity Injury amphotericin B; pentamidine; cisplatin; foscarnet; tenofovir; Vasoconstriction DAMPS Apoptosis cidofovir; carboplatin; ifosfamide; zoledronate; contrast agents; Leukocyte Adhesion Immune Cells
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