Acute Kidney Injury IM Resident Lecture. Yongen Chang, MD, PhD Nephrology July 2018
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1 Acute Kidney Injury IM Resident Lecture Yongen Chang, MD, PhD Nephrology July 2018
2 Objectives Epidemiology Definition and Staging Etiology and Diagnostic Approach Specific syndromes of AKI Treatment Biomarkers
3 Epidemiology Global incidence is estimated 22% among hospitalized patients (Meta-analysis, >3.5 million patients). 57.3% ICU patients experience AKI in first week of ICU admission (Cross-sectional study of 97 ICU from 33 countries).
4 AKI and CKD AKI associated with: - 9 fold higher risk of CKD - 3 fold higher risk of ESRD Hsu RK, Hsu CY, Semin Nephrol 2016
5 Definition and Staging R=Risk, I=Injury, F=Failure, L=Loss, E=End Stage
6 Key Points UOP decrease often proceeds increase in SCr Early intervention prevents severe AKI and resultant CKD
7 Etiology Pre-renal: hemodynamic Intrinsic renal: parenchymal Post-renal: obstructive
8 Etiology: Pre-renal A physiologic response to renal hypoperfusion without tubular injury. A functional change in GFR due to intravascular volume depletion. Volume depletion Redistribution Capillary leak Congestion heart failure Hepatorenal Syndrome
9 NSAIDS ACEI/ARB Volume depletion Redistribution Capillary leak CHF HRS
10 Cardiorenal Syndrome Treatment is to treat the underlying cause.
11 Hepatorenal Syndrome (HRS)
12 Hepatorenal Syndrome (HRS) Type 1 HRS: Creatinine doubling to 2.5 or above in < 2 weeks 90 day survival rate <10% Type 2 HRS: Gradual onset Median survival is 6 months
13 HRS Criteria Diagnosis of Exclusion Urine Na typically <10 Portal HTN physiology Precipitating factors Paolo Angeli et al, Journal of Hepatology 2015
14 HRS Treatment Goal is to raise MAP by 10mmHg Vasopressors Midodrine: mg TID Octreotide 50mcg/hr IV or mcg SQ TID Albumin: 1g/kg/day at least 2 days Terlipressin: vasopressin analogue (not available in US) Combination Therapy: Terlipressin (1-2mg q4-6hr IV) +/- albumin Midodrine, octreotide and albumin
15 HRS Treatment Transjugular intrahepatic portosystemic shunt (TIPS) Liver Transplant Renal replacement therapy (RRT) as bridge to liver transplant
16 Etiology Pre-renal: hemodynamic Intrinsic renal: parenchymal Post-renal: obstructive
17 Post-renal: obstructive Pre-renal: hemodynamic Consider obstruction in every patient with ARF Urine volume variable. Sites of obstruction leading to ARF: Bladder neck obstruction Bilateral ureters
18 Diagnostic Approach Renal US +/- PVR bladder scan Bladder catheterization Non-contrast CT Renal scan IV pyelogram
19 Renal Scan Ureteropelvic Junction obstruction
20 IV Pyelogram
21 Treatment Depends on the level of obstruction Ureteral stenting +/- stone retrieval Nephrostomy tube placement Foley catheter placement Treat BPH Reconstructive surgery Timely relief of obstruction is key
22 Etiology Pre-renal: hemodynamic Intrinsic renal: parenchymal Post-renal: obstructive
23 Intrinsic Renal Disease
24 Tubular Ischemic ATN: Hemodynamic changes Septic ATN Agents with direct tubular toxicity Crystal Osmotic Heme Pigment Induced ATN Contrast induced nephropathy
25 Direct tubular Toxicity Antibiotics Chemotherapy agents Iodine contrast (NOT gadolinium) Heavy metal Organic solvants
26 Crystals Uric acid (Tumor lysis syndrome) Oxalate (ethylene glycol) Methotrexate Acyclovir Sulfonamides Indinavir Phospho Soda (bowel prep) Ca oxalate Uric Acid
27 Indinavir
28 Sucrose (IVIG) Mannitol Iodine contrast Dextran Hydroxyethyl starch Osmotic Agents
29 Heme Pigment Induced ATN Rhabdomyolysis Intravascular hemolysis Light chains Mechanism: Vasoconstriction precipitation/obstruction toxicity of breakdown products Concomitant volume depletion Rx: correct underlying cause, volume expansion
30 Contrast-induced nephropathy
31 Contrast-induced nephropathy Mehran R, J Am Coll Cardiol 2004
32 Atheroembolic Disease
33 AIN Triad of fever, rash, eosinophilia Drugs: PCN, cephalosporins, vancomycin PPI NSAIDS Allopurinol T cell modulators Onset is days after exposure Usually resolves after withdrawal of medication Role of glucocorticoids
34 CASES
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