acute kidney injury also known as acute renal failure

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• Livedo reticularis-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

How the Lab work can help:Lab work Prerenal Azotemia Acute Tubular

NecrosisUrine Sodium <20 >40

Urine Osmolality >500 <450

FENa <1% >1%

BUN/Creatinine Ratio >20:1 <20:1

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