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Acute Kidney Injury. Also known as Acute Renal Failure. 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
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Acute Kidney Injury Also known as Acute Renal Failure
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
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
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
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
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
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
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 • Livedoreticularis-atheroemboli
Laboratory Studies • This is how you make the diagnosis • Elevated BUN and serum Creatinine • Other possible serum abnormalities • Hyperkalemia • Low Bicarbonate
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
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
Other Causes of Elevated BUN • GI bleed • Catabolic State • High Protein Diet • Systemic Steroid Use
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
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
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
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.
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.
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.
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