1. Acute Kidney Injury Also known as Acute Renal Failure

2. What is it? Abrupt decrease in renal function Occurring over hours to days Results in retention of nitrogenous waste Elevated BUN/Creatinine Current Criteria: – Increase in serum creatinine of 0.5mg/dl – 25% increase in serum creatinine – 25% decrease in GFR

3. Epidemiology Varies 1-2% of hospital admissions 2-5% during hospitalization Up to 20% of ICU patients Slightly more women than men 140 million+ patients per year in western countries

4. Three Main Etiology Categories Prerenal – Fall in Glomerular Perfusion Decreased extracellular fluid – Hemorrhage, burn, vomiting, diuretics Decreased circulating volume – Heart failure, cirrhosis, sepsis Intrinsic Renal – Wait for it… Post-renal – Obstruction Prostatic enlargement, abdominal/pelvic tumor

5. Intrinsic Renal Etiologies Acute Tubular Necrosis-most common – Ischemia Untreated Pre-renal azotemia – Sepsis – Nephrotoxins Exogenous: – Antibiotics, CONTRAST, chemo, ACEi Endogenous: – Proteins-myeloma – Pigments: hemoglobin, myoglobin – Tumor Lysis Syndrome – Crystals-oxalate or uric acid

6. Intrinsic Renal Etiologies Acute Interstitial Nephritis – Antibiotics, NSAIDs Vasculitis – Wegeners, microscopic polyarteritis – Cryoglobulinemia Glomerulonephritis – Post-infectious, Goodpasture Syndrome Urinary Tract Infection/Pyelonephritis Atheroemboli-esp after procedures like heart catheterization

7. Symptoms Often, if already hospitalized, labs come first – Elevated BUN/Creatinine, oliguria “Uremic” Symptoms – Fatigue, loss of appetite – Weakness – Nausea/vomiting – Metallic taste in mouth – Itching – Confusion – Fluid retention and Hypertension

8. Physical Exam Often, nothing notable Signs of fluid retention “Uremic” Signs – Pericardial friction rub – Asterixis – Mental status changes (without other cause) Oliguria/Anuria Can see tachypnea due to acidosis Livedo reticularis-atheroemboli

9. Laboratory Studies This is how you make the diagnosis Elevated BUN and serum Creatinine Other possible serum abnormalities – Hyperkalemia – Low Bicarbonate

10. Laboratory Studies (cont.) Urinalysis is IMPORTANT-can help with etiology – Finely granular casts/hyaline casts-Prerenal – Dirty Brown coarse, granular casts-ATN – Tubular epithelial cells-ATN – Protein, blood – RBC casts-Glomerulonephritis – WBC casts-pyelonephritis Without bacteria? Think AIN – Oxalate or Uric Acid crystals

11. Work up History And Physical/Review Hospital stay – This can often be most helpful to determine cause Then determine which of the 3 categories it is: – Urinalysis with sediment – Urine osmolality – BUN/Creatinine Ratio – Fractional Excretion of Sodium (FENa) Fractional Excretion of Urea (FEurea) – Renal Ultrasound-if doesn’t look like prerenal or intrinsic cause

12. How the Lab work can help: Lab workPrerenal AzotemiaAcute Tubular Necrosis Urine Sodium<20>40 Urine Osmolality>500<450 FENa<1%>1% BUN/Creatinine Ratio>20:1<20:1

13. Other Causes of Elevated BUN GI bleed Catabolic State High Protein Diet Systemic Steroid Use

14. Management Best to PREVENT it if possible. Mostly Symptomatic and dependent on cause Prerenal? Improve circulating volume – IV fluids, stop diuretics, treat sepsis, CHF, or liver disease Avoid Nephrotoxins – Metformin, diuretics, ACEi, further contrast studies Treat Complications

15. Complications Hyperkalemia – Check the ECG->measure of the sum of the effects of Hyperkalemia, Hypocalcemia, acidosis. Fluid Overload – Strict I&Os judicious loop diuretic use Uremia Acidosis Calcium/Phosphate Imbalance

16. Emergent Dialysis for: A: acidosis refractory to medical therapy E: electrolyte abnormalities – namely hyperkalemia I: intoxications-e.g Lithium, Ethylene Glycol O: Overload (fluid) U: Uremia-severely symptomatic or BUN<80

17. Prevention Avoid Nephrotoxins – Especially in elderly, volume depletion, or CKD Hydration before and after radiocontrast studies. Allopurinol before treating large tumors to prevent tumor lysis syndrome.

18. Prophylaxis Strategies for Contrast Induced Nephropathy JAMA. 2006;295:2765-2779. Review article. No RCT to address all possibilities. Hydration: Do it. Unless there is contraindication. – Normal Saline vs. Bicarbonate Why bicarbonate? Alkalinization of urine to prevent tubular damage. Studies show slight improvement or at least no worse outcome with bicarbonate (compared to normal saline), so that is the current recommendation. 3mL/kg (D5 + 150mEq bicarbonate) x 1 hr pre-procedure then 1mL/kg of same fluid x 6 hr post-procedure. This is difficult to get done here. – N-acetylcysteine: currently recommended 1200mg BID x2 doses before procedure then 1200mg BID x2 doses post- procedure.

19. Important Notes Most people who develop AKI while hospitalized will not die of renal disease. Many/Most will recover enough renal function to not require dialysis after discharge. – This is true for those with normal renal function prior to this incident, not necessarily for those with underlying CKD. Most common cause of mortality is INFECTION- keep HD lines and other wounds clean to avoid iatrogenic cause of the infection.

20. References: Sabatine, M. Nephrology section of Pocket Medicine. Shaver, M.J. and S.V. Shah Acute Renal Failure. ACP Medicine 2005. Pannu, N. et. al Prophylaxis Strategies for Contrast Induced Nephropathy JAMA. 2006;295:2765-2779