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Approach to Acute Kidney Injury Anna Jin, M.D. LBVA/UCI 7/21/2014

Approach to Acute Kidney Injury Anna Jin, M.D. LBVA/UCI 7/21/2014. Learning Objectives. Definitions and classification of AKI Epidemiology and clinical outcome Diagnosis and etiology Approach and management of AKI Risk factors and preventive strategies. Definition of AKI.

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Approach to Acute Kidney Injury Anna Jin, M.D. LBVA/UCI 7/21/2014

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  1. Approach to Acute Kidney InjuryAnna Jin, M.D.LBVA/UCI7/21/2014

  2. Learning Objectives • Definitions and classification of AKI • Epidemiology and clinical outcome • Diagnosis and etiology • Approach and management of AKI • Risk factors and preventive strategies

  3. Definition of AKI • a sudden, sustained, and usually reversible decrease in the glomerular filtration rate (GFR) occurring over a period of hours to days. > 30 definitions used in published studies

  4. KDIGO Definition of AKI ( 2012 ) Defined by any of the following: • Increase in SCr by ≥0.3 mg/dL within 48 hours • Increase in Scr by ≥1.5 times baseline, which is known or presumed to have occurred within the prior seven days • Urine volume <0.5 mL/kg/h for six hours

  5. KDIGO Classification of AKI ( 2012 ) KDIGO Clinical Practice Guideline for AKI. Kidney Int 2012

  6. Definitions of Terminology • Azotemia - the accumulation of nitrogenous wastes (high BUN) • Uremia – clinical manifestation (symptomatic renal failure) • Oliguria – UOP < 400-500 mL/24 hours • Anuria – UOP < 100 mL/24 hours

  7. Epidemiology • ≈ 5-10% in hospitalized pts • ≈ 70% in critically ill pts • 5-6% ICU pts require RRT • Once AKI occurred, the treatment is supportive, at an annual cost $10 billion in the US.

  8. Incidence of Non-Dialysis AKI Kidney Int 2007

  9. Incidence of Dialysis-Requiring AKI Kidney Int 2007

  10. In-Hospital Mortality Rate 1992-2001 • 33% - AKI requiring dialysis • 27.5% - AKI not requiring dialysis • 4.6% - no AKI JASN 17:1135-1142, 2006

  11. AKI and MortalityBrigham and Womens, 9210 adults Multivariable Odds Ratio for Death Chertow et al, JASN 16:3365-70; 2005

  12. Increase in Serum Creatinine from Baseline Chertow GM et al. J Am Soc Nephrol 2005;16:3365

  13. 90 Day Mortality Rate in 2001 • 44.8% - AKI requiring dialysis • 40.3% - AKI not requiring dialysis • 12.1% - no AKI JASN 17:1135-1142, 2006

  14. N=634 Lai CF et al. Crit Care 2012

  15. Acute kidney injury increases risk of ESRD among elderly N= 233.803 Ishani A et al. J Am Soc Nephrol 2009

  16. Hou SH, Bushinsky DA, Wish JB. Am J Med 1983; 74: 243-8. Nash K, Hafeez A, Hou S. Am J Kidney Dis. 2002; 39: 930-6. Kaufman J, Dhakal M, Patel B, Et al. Am J Kidney Dis 1991; 17: 191-8.

  17. Etiology of AKI ATN is the cause in more than 90%. Sepsis is the leading cause of ATN

  18. To function properly kidneys require: • Normal renal blood flow • Prerenal d/t renal hypoperfusion • Functioning glomeruli and tubules • Renal (Intrinsic) • Clear urinary outflow tract for drainage and elimination of formed urine • Post renal obstruction

  19. Prerenal AKI Intrinsic AKI Postrenal AKI Acute Tubular Necrosis Acute Interstitial Nephritis Acute GN Acute Vascular Syndromes Intratubular Obstruction Classification of the Etiologies of AKI Acute Renal Injury

  20. Prerenal AKI • Intravascular volume depletion: -bleeding, GI loss, Renal loss, Skin loss (burn), Third space loss, poor oral intake (NPO, AMS, anorexia) • Decreased effective circulating volume: -congestive heart failure, cirrhosis, nephrotic syndrome, sepsis • Decreased flow through renal artery: -RAS or occlusion (compartment syndrome), hepatorenal syndrome, hypercalcemia -pharmacologic impairment (RAAS blocker, NSAIDs, CNI)

  21. Prerenal Azotemia Tx • In early stages can be rapidly corrected by aggressive normalization of effective arterial volume. • Correction of volume deficits • Optimization of cardiac function • Discontinuation of antagonizing medications • NSAIDs/COX-2 inhibitors • Diuretics • RAAS blockers

  22. Renal / Intrinsic AKI • Tubule: ATN (sepsis, ischemic, toxins) • Interstitium:AIN (Drug, infection, neoplasm) • Glomerulus:AGN (primary, post-infectious, rheumatologic, vasculitis, HUS/TTP) • Vasculature: • Atheroembolic dz, renal artery thromboembolism, renal artery dissection, renal vein thrombosis • Intratubular Obstruction • myoglobin, hemoglobin, myeloma light chains, uric acid, tumor lysis, drugs (bactrim, indinavir, acyclovir, foscarnet, oxalate in ethylene glycol toxicity)

  23. Sepsis (48%) Ischemia (32%) prolonged prerenal azotemia Hypotension hypovolemic shock cardiopulmonary arrest cardiopulmonary bypass Direct toxic Injury (20%) Exogenous Radiocontrast Aminoglycosides Vancomycin Amphotericin B Cisplatin Acyclovir Calcineurin inhibitors HIV meds (tenofovir) Endogenous (pigment nephropathy) Rhabdomyolysis Hemolysis Acute Tubular Necrosis (ATN)

  24. Laboratory Findings in Acute Kidney Injury

  25. Pitfalls: Fractional Excretion of Na • Pre-existing CKD: FeNa 2-3 even without tubular injury • Poor sensitivity with diuretics use • Picture might be muddied by fluid therapy • Etiologies of FeNa < 1% • hepatorenal syndrome • contrast nephropathy • rhabdomyolysis • acute glomerulonephritis • early obstructive uropathy

  26. Postrenal AKI: Classification • Level of obstruction • Upper tract (ureters) • Lower tract (bladder outlet or urethra) • Degree of obstruction • Partial vs. Complete • Type • Anatomic lesion (unilateral vs. bilateral) • Functional • Duration (Acute vs Chronic) • Cause (Congenital vs Acquired)

  27. Etiologies: Upper tract obstruction Extrinsic: Retroperitoneal or pelvic malignancy Endometriosis/Prolapsed uterus Abdominal aortic aneurysm or Iliac artery aneurysm Retroperitoneal fibrosis • Intrinsic: • Nephrolithiasis • Blood clot • Papillary necrosis • Cancer

  28. Etiologies: Lower tract obstruction • BPH or prostate cancer • Bladder cancer • Urethral strictures • Bladder stones • Blood clots • Functional obstruction as a result of neurogenic bladder

  29. Postrenal AKI tx • Prompt recognition and relief of obstruction can prevent the development of permanent structural damage. • Lower tract obstruction (bladder catheter) • Upper tract obstruction • ureteral stents • percutaneous nephrostomies • Monitor for post-obstructive diuresis • Recovery of renal function dependent upon duration of obstruction.

  30. How do we assess a pt with AKI? • Is this acute or chronic renal failure? • Establish baseline Cr and assess Cr trend • History and examination • Small kidneys on ultrasound (except for in -Diabetes, PCKD, Urinary Tract Obstruction) Hilton et al, BMJ 2006;333;786-790

  31. AKI: Focused History • Prenal hx: N/V/D? Oral intake? Diuretics? Hx of heart dz, liver dz, previous renal dz? • Post-renal sxs: hesitancy, frequency, urgency, weak stream, dribbling, feeling of incomplete bladder emptying, flank pain. h/o kidney stones or BPH? Spinal cord injury? Anticholingergic meds? • Any recent illnesses? Fever? Rashes? • Any recent surgery? • Cardiovascular instability? • Toxin exposure: new medications (Abx, NSAIDs)? IV contrast? • Change in urination, any edema/SOB/Wt. gain? • Look for temporal link of exposure or risk factor to elevation of Cr or decline in UOP

  32. How to assess volume? • History (intake, fluid loss, meds) • Postural blood pressure andpulse • Daily weights • In’s/Out’s, fluid balance/fluid challenge • Signs of volume depletion: -Dry mouth, Increased thirst, Lightheadedness, Muscle cramps, extremities are cool to the touch, palpitations, reduced and dark urine, syncope -PE: Listlessness/AMS/LOC, tachycardic, weak rapid pulse, hypotensive (orthostatic vitals), tachypnic, increased Temp, poor capillary refill, decreased skin turgor, flattened neck veins, little or no urination for several hrs

  33. Further work-up • U/A, Urine protein/Cr, Urine Eosinophilla • FeNa, FeUrea • CPK, uric acid • Urine microscopy: • Muddy brown casts in ATN • WBC casts in AIN • RBC casts in AGN • Post-void residual (>100-150 ml c/w voiding dysfunction) • bladder catheterization • renal ultrasound

  34. Management of AKI: general principle • No therapy to date have shown efficacy in treating AKI. • Identify the etiology and treat the underlying cause • Optimization of hemodynamics to increase renal perfusion • Lack of benefit – low dose dopamine, loop diuretics only if markedly fluid overload • Identify and aggressively treat infection (early removal of foley catheters, and minimize indwelling lines)

  35. Management of AKI: treat complications • Correct fluid imbalances: strict I/O’s, daily wts. determine fluid balance goals daily, fluid selection or diuresis, readjust for UOP recovery, post diuresis or dialysis • Electrolyte imbalances (low K/phos diet, binder) • Metabolic acidosis (Bicarb deficit, mode and rate of replacement) • Nutrition: adjust TPN/protein intake • Medication dosing: adjustment for eGFR to avoid under or over dosing, timing for dialytic therapy, reassess dosing for renal recovery or dialysis modality) • Procedural considerations (prefer non-contrast CT, appropriate to delay contrast exposure, prophylaxis)

  36. Nephrotoxic Drug Exposure • Minimizing nephrotoxin • Avoid Aminoglycosides, Amphotericin, Bactrim, Vancomycin, NSAIDs, IV contrast, Fleet’s enemas • Renal dose medications – especially antibiotics and monitor level • Cautious use (metformin, long acting oral hypoglycemic agents, insulin, gemfibrozil and statins, neurotin, colchicine/allopurinol, morphine/codeine, lmwh)

  37. Ancient Chinese Medical Text • The inferior doctor treats actual illness. • The mediocre doctor attends to impending illness. • The superior doctor prevents illness. 2600 BC - Huang Dee Nai-Chang

  38. Best cure is to prevent! Be aware of pts who are at risk for AKI • Volume depletion or Hypotension • Sepsis • Pre-existing renal, hepatic, or cardiac dz • Diabetes mellitus • Elderly • Exposure to nephrotoxins • Aminoglycosides, amphotericin, immunosuppressive agents, chemo., NSAIDs,, RAAS blockers, intravenous contrast media • Post cardiac or vascular Surgery pts or ICU pts with multiorgan failure

  39. Take Home Messages: AKI • AKI is increasingly common. • It involves high cost of management, carries a high morbidity and mortality risks. • The most common cause of in-hospital AKI is ATN that results from multiple acute insults (sepsis, ischemia, or nephrotoxin). • No drug treatment has been shown to limit the progression of, or speed up recovery from AKI. • Review medications and adjust dose • Recognize risk factors • The Best Treatment is PREVENTION and avoid further renal damage!!!

  40. “Doc, your pt hasn’t peed in 5 hrs....what do you want to do?” • Examine pt: BP? Dry? Septic (vasodilated)? • Flush foley (sediment can obstruct outflow) • Check I/Os (has he been drinking?) • Give IV BOLUS (250-500cc IVF), see if pt pees in next 30-60 min • If he pees, then he was dry • If he doesn’t pee, then he’s either REALLY dry or in renal failure • Check UA, UCx, urine lytes • Consider Renal U/S if reasonable

  41. THANK YOU!

  42. RIFLE Criteria for AKI (2005)

  43. Definition of AKI based on AKIN“Acute Kidney Injury Network” ( 2007 )

  44. RIFLE 2004 AKIN 2007 LIMITATIONS STRENGTHS KDIGO 2012

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