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Risk Factors for Acute Kidney Injury in Congenital Heart Defects Ronald G. Grifka, MD Chief, Cardiology Division Helen DeVos Children’s Hospital Professor of Pediatrics MSU College of Human Medicine Risk Factors for Acute Kidney Injury in Congenital Heart Defects The Elephant… Risk Factors for Acute Kidney Injury in Congenital Heart Defects The Elephant… Risk Factors for Acute Kidney Injury in Congenital Heart Defects What I Will Not Discuss • • • • Hypertension FeNa GFR Calculations Lupus Risk Factors for Acute Kidney Injury in Congenital Heart Defects Cardiac Hemodynamics • Normal cardiac index = 3.5 L/min/m2 • Cardiac index = cardiac output/BSA • For a newborn: 3.2 kg, 0.22 m2 • Cardiac output = 770 ml/min • If HR = 140/min • Each heart beat = 5.5 ml • RBF = 20% of the CO - RBF = 1.1 ml/heart beat Risk Factors for Acute Kidney Injury in Congenital Heart Defects Cardiac Hemodynamics • Low cardiac output state: CI = 2.0 L/min/m2 • For a newborn: 3.2 kg, 0.22 m2 • Cardiac output = 440 ml/min • If HR = 170/min • Each heart beat = 2.6 ml • RBF = 20% of the CO • RBF = 0.52 ml/heart beat Risk Factors for Acute Kidney Injury in Congenital Heart Defects Types of Heart Failure • Acute vs. Chronic • New post-op, Myocarditis vs. Dilated CM, DMD, old post-op • Right ventricle vs. Left ventricle • TOF, Pulm HTN vs. Anomalous left cor art from PA, DCM • High output vs. Low output • Anemia, Hyperthyroid vs. DCM, Myocarditis • Congenital vs. Acquired • Mitochondrial disorder, DMD vs. Kawasaki disease, Myocarditis Risk Factors for Acute Kidney Injury in Congenital Heart Defects 5 Physiologies of Congenital Heart Defects • Left to right shunts • VSD, PDA, AV Canal, ASD • Right to left shunts • TOF, Pulmonary atresia • Transposition physiology • Obstructive / Regurgitant defects • AS, PS, CoA, “HLHS”, MS, MR, AI • Cardiomyopathy • Dilated, Hypertrophic, Restrictive Risk Factors for Acute Kidney Injury in Congenital Heart Defects Physiology #1 Left to Right Shunt • VSD, AV Canal, PDA, ASD, Ao-PA Window, Truncus arteriosus, Single V without PS • Results in pulmonary overcirculation • *RARELY causes heart failure (”CHF”), renal failure • Tx: Diuretics, ACE inhibitor, ± digoxin • *Neonates - Truncus Arteriosus, Premie (PDA) - Intestinal steal NEC, Renal failure Risk Factors for Acute Kidney Injury in Congenital Heart Defects Physiology #2 Right to Left Shunt • Tetralogy of Fallot, Pulmonary atresia, Single ventricle with PS • Does not cause pulmonary overcirculation! • Does not cause heart failure (”CHF”) • Does cause: Cyanosis, Polycythemia, Bleeding • Partial exchange transfusion if Hct > 62-65% Risk Factors for Acute Kidney Injury in Congenital Heart Defects Physiology #3 Transposition Physiology • Blue blood to the body, red blood to the lungs • Not compatible with life as we know it! • Profoundly cyanotic, hypoxic, acidotic, hypotensive • Can cause multi-system organ damage if not treated immediately • Immediate treatment: • PDA (PGE1 infusion) • ASD (Balloon atrial septostomy) Risk Factors for Acute Kidney Injury in Congenital Heart Defects Physiology #4 Obstructive/Regurgitant Defects • Aortic stenosis/regurge, Pulmonary stenosis, Coarctation of the aorta, “HLHS”, Mitral stenosis or regurge • CAN cause heart failure! • CAN cause inadequate perfusion to: • Coronaries (infarction) • Intestines (NEC) • Kidneys (ARF) Risk Factors for Acute Kidney Injury in Congenital Heart Defects Physiology #5 Cardiomyopathy • Dilated, Hypertrophic, Restrictive • CAN cause heart failure! • LHF: Inadequate organ perfusion, Pulm edema, SOB, Activity • RHF: 1° or 2°, Hepato-splenomegally, systemic edema • DCM: Diuresis, ACE inhibitor, Inotrope, ± Anti-arrhythmic • HCM: NO: diuresis or inotrope (unless end stage) YES: beta blocker, ± Anti-arrhythmic, AICD • End stage Tx: LVAD (DCM), Heart transplant Risk Factors for Acute Kidney Injury in Congenital Heart Defects Cardiac Related Renal Injury • Acute insult • Chronic insult • An acute insult to a chronic condition Risk Factors for Acute Kidney Injury in Congenital Heart Defects Cardiac Related Renal Injury - Acute Insult • Myocarditis • Acute bacterial endocarditis • CHD with acute decompensation (URI) • Aortic stenosis, CoA, DCM • Catheterization / IV Contrast • Open heart surgery / CPB • Heart transplant • Rejection, meds, infection • Trauma (hemorrhage, etc) Risk Factors for Acute Kidney Injury in Congenital Heart Defects Cardiac Related Renal Injury - Chronic Insult • (Systemic) Ventricular failure • • • • CHD, DCM natural history Post-op failure Myocarditis Transplant: Coronary vasculopathy, rejection, meds, infection • Cyanosis • Repetitive embolic events • Arrhythmia, thrombotic substrate Risk Factors for Acute Kidney Injury in Congenital Heart Defects Peri-Operative Renal Insults • • • • • • • • Nephrotoxic antibiotics Furosemide, mannitol Diuresis, but IVF not replaced Epi, Norepi, high dose Dopamine Renal vasoconstriction Anesthetic agents Hypotension Low cardiac output, low blood pressure Sepsis Pre-existing renal disease (cyanosis, Hct, low cardiac output) Cardiopulmonary bypass Risk Factors for Acute Kidney Injury in Congenital Heart Defects Cardiopulmonary Bypass - Positives • • • • Allows surgery in a bloodless field Arrests the heart, decreases MVO2 Perfuses other organs during surgery Can adjust the blood flow, add medications Risk Factors for Acute Kidney Injury in Congenital Heart Defects Risk Factors for Acute Kidney Injury in Congenital Heart Defects Cardiopulmonary Bypass – Negatives • • • • • • • Fragments RBC’s Activates platelets Alters clotting factors Liberates vasoactive compounds Hypothermic insult (18-25° C) Metabolic acidosis Perfuses organs during surgery with NON-PULSATILE flow • P/O transfusions Risk Factors for Acute Kidney Injury in Congenital Heart Defects Peri-Operative Treatment • Phenoxybenzamine pre-op • Increase renal blood flow • Dopamine, fenoldapam, neseritide • Intra-op, Post-op diuretics • ± IVF replacement: colloid vs. crystalloid • Increase BP • But pressors SVR, HR , ? CO • Peritoneal dialysis BenephitTM Infusion System (FlowMedica, Inc., Fremont, CA) FDA (510K) Cleared January 2004 Intrarenal infusion -Dopamine, Fenoldopam -Nesiritide (BNP) Risk Factors for Acute Kidney Injury in Congenital Heart Defects Cyanotic Heart Disease • • • • • • • Enlargement of the glomerular capillary tuft Mesangial hypercellularity Accumulation of eosinophilic material Capillary basement membrane thickening IgM deposits in the mesangium Fibrin in the glomerular capillary walls Clinically – GN: hematuria, proteinuria, HTN Risk Factors for Acute Kidney Injury in Congenital Heart Defects Infective Endocarditis • Kidneys normal to slightly enlarged • Glomerular immune complex deposition - C3, IgG. Occasionally IgM, IgA • Treat SBE, renal function improves • Advanced SBE disease • Microabcesses • Embolization, infarction • May not recover renal function Risk Factors for Acute Kidney Injury in Congenital Heart Defects Contrast Induced Nephropathy • Well described entity in adults • Adults have more pre-existing renal disease, HTN • Rare in children following cardiac cath • New contrast much safer • IVF from anesthesiologist and catheter flushes • Contrast given over several hour cath procedure - Up to 12 ml/kg over 7 hr procedure • Much IV fluids, foley The Evolution of Contrast Media Molecular Structure I CH3CONH COO–Na+/Meg+ I I R Era 1950s R I I R R 1980s I R I II R R I R COO–Na+/Meg+ I 1980s I R II I R R R I Ionic monomer Diatrizoate Iothalamate Comment High Osmolality, 5 – 8 blood Nonionic monomer Iopamidol Iohexol Ioversol Low Osmolality, 2 – 3 blood, improved hydrophilicity Ionic dimer Ioxaglate Low Osmolality, ~2 blood Nonionic dimer Iodixanol (Iotrolan) Iso-osmolality Osmolality = blood R I I Examples 1990s Osmolality (mOsm/kg H2O) Osmolalities of Contrast Media * 320 mg I/mL † 350 mg I/mL ‡ 370 mg I/mL 2500 ‡ + 2000 1500 1000 500 * † * ‡ ‡ † † † * 0 Iodixanol is a nonionic dimer, formulated with balanced levels of Ca2+ and Na+, that is isosmolar with plasma at all iodine concentrations Reduced nephron mass vulnerable to injury Associated factors: diabetes, poor renal perfusion, others Contrast enters renal vasculature Endothelium-independent transient vasodilation (minutes) Adenosine release from macula densa (tubulo-glomerular feedback) Prostaglandin dysregulation Endothelin release Decreased Nitric Oxide Synthesis/Release Sustained intrarenal vasoconstriction (hours) Prolonged contrast transit time in kidneys Increased contrast exposure to renal tubular cells Contrast direct cellular injury and death Medullary hypoxia Ischemic injury and death Catalytic iron-driven oxidative Stress, inflammation, other organ injury processes McCullough PA, JACC 2008 Acute Kidney Injury 73 y/o with multiple myeloma, Cr 2.3 mg/dl, CrCl=23 ml/min, Cr rise 0.3 mg/dl Nephrol Dial Transplant (2004) 19: 1654–1655 One-Year Kaplan-Meier Survival Curves Stratified by CrCl Levels after Primary Angioplasty in CADILLAC 100 CrCl >60 CrCl 50-60 Survival (%) 90 CrCl 40-50 CrCl 30-40 80 70 CrCl 20-30 60 CrCl <20 50 P<.0001 (all groups) 40 0 50 100 150 200 250 300 350 400 450 500 Time (days) Sadeghi HM et al. Circulation. 2003;108:2769– 2775. Calculate eGFR or CrCl Assess contrast-induced AKI risk eGFR <30 ml/min eGFR 30-59 mL/min Start/continue statin Discontinue NSAIDs, other nephrotoxic drugs, metformin Start/continue statin Discontinue NSAIDs, other nephrotoxic drugs, metformin • Hospital admission • Other strategies as for eGFR 30-59 ml • Nephrology consultation* • Consider hemofiltration pre- and post-procedure • IV isotonic (NaCl/NaHCO3) •1.0-1.5 ml/kg/min 3-12 hrs pre and 6-24 post •Ensure urine flow rate > 150 ml/hr Discontinue metformin Good clinical practice • Iso-osmolar contrast •DM, ACS, other added risks • Low osmolar contrast •No other added risks occurs and dialysis is required N-Acetylcysteine •< 30 cc diagnostic •<100 cc diagnostic+intervention • Consider adjunctive *Plans should be made in case AKI † Potentially beneficial agents: • Limit contrast volume Serum Cr before discharge or 24–72 hr Expectant Care eGFR ≥60 ml/min medications† •Antioxidants •N-acetylcycteine 1200 mg po bid preand post-procedure or •Ascorbic acid 3 g po pre2 g po bid post-procedure Ascorbic acid Aminophylline Prostaglandin E1 None approved for this indication AKI=acute kidney injury Cr = creatinine CrCl=creatinine clearance; eGFR=estimated glomerular filtration rate NSAIDs= nonsteroidal anti-inflammatory drug IV Hydration and Urine Output Change in Cr from Baseline (mg/dL) r = -0.36, F = 5.73, P = 0.005 Urine Flow Rate (mL/hr), beta = -0.36, t = -3.33, P = 0.001 Baseline CrCI (mL/min), beta = 0.10, t = 0.93, P = 0.36 4.5 3.5 2.5 1.5 0.5 -0.5 -1.5 0 60 120 180 240 Urine Flow Rate (mL/h) Stevens MA et al. J Am Coll Cardiol. 1999. 300 Regression 95% CI Treitl M, et al, Nephrol Dial Transplant (2008) Hemofiltration Hemofiltration works to ensure – Adequate intravascular volume – Reduce uremic toxins which may worsen AKI – Provides stability to the high risk patient after the procedure reducing the risks of oliguria, volume overload, and electrolyte imbalance that are associated with short-term mortality. Double lumen catheter is placed in a jugular or femoral vein for blood withdrawal and reinfusion and connected to an extracorporeal circuit. 6 hours before contrast: Peristaltic pump (e.g. Prisma hemofiltration pump) at 100 mL/min. Isotonic replacement fluid (post-dilution hemofiltration) 1000 mL/h, matched with the rate of ultrafiltrate production so no net fluid loss occurs. 5000 IU heparin bolus before initiation followed by a continuous heparin infusion of 500 to 1000 IU/h through the inflow side of the catheter. At the time of the cardiac procedure, the hemofiltration treatment should be stopped, the circuit temporarily filled with a saline solution and short-circuited to exclude the patient without interruption of the flow. Immediately after the cath, hemofiltration should be restarted for 12-18 hours. AKI (Cr >0.5 mg/dL [> 44.2µmol/L]) Dialysis 9 (30%) 3 (10%) 0 (0%) P=0.002 3 (10%) 0 (0%) P=0.03 Death 6 (20%) NS 50 47 42 40 P<0.001 30 % 20 10 3 0 Control Posthemofiltration group Pre/posthemofiltration group Marenzi G et al. Am J Med. 2006 Feb;119(2):155-62. Anatomical Basis: The Coronary Sinus MCV 69 y.o. with CRI, SCr. 2.9, CTO, 240cc dye Sensor (Optical Reflectance) • Delivery fiber shines visible light into blood monochromatic, • Interactions between light and blood cells results into back-scattering of photons, which are captured by detection fiber • Amount of scattered light is proportional to optical density of blood (i.e. number of blood cells per volume). • Signal drop registered when contrast bolus passes by tip of sensor system [1] Signal represents contrast presence in coronary sinus Delivery Detection Contrast Detection Signal [1] In-Vivo Contrast Removal • Successful device deployment in CS • Arterial injection of contrast • Appropriate size & seal at CS level • Contrast recovery: 70%* Source: CAN-12 CD1_IMG008 * Contrast recovery established by UV Spectrometry Risk Factors for Acute Kidney Injury in Congenital Heart Defects This is not the end. Nor is it the beginning of the end. But perhaps, this is the end of the beginning. Risk Factors for Acute Kidney Injury in Congenital Heart Defects Thank you, and looking toward the future in Grand Rapids…. Risk Factors for Acute Kidney Injury in Congenital Heart Defects Risk Factors for Acute Kidney Injury in Congenital Heart Defects Ronald G. Grifka, MD Chief, Cardiology Division Helen DeVos Children’s Hospital Professor of Pediatrics MSU College of Human Medicine