Inpatient / Nephrology

Acute Kidney Injury (AKI)

If You Remember Nothing Else

The vast majority of AKI seen inpatient are due to prerenal etiology or ATN and thus most AKIs are fixed with fluids (hypotension), Lasix (CHF), or a foley (retention). You can usually start with a small bolus challenge unless the patient has obvious overload or may be difficult to get fluid out of (ESRD, CHF, cirrhosis). In general, unless profound, you can wait 48 hours to see if the AKI resolves on its own with fluids or diuresis. If it's ATN, the only therapy is patience.

In general, urine studies are difficult to interpret if you've received fluids or diuretics. However, urinalysis is great for picking up many (but not all) of the don’t miss diagnoses of AKI (glomerulonephritis, vasculitis, rhabdo, AIN, obstruction 2/2 cancer). Acute renal failure will rarely require dialysis, but if it does, remember the indications (AEIOU) - Acidosis pH <7 w/ bicarb, Electrolytes refractory hyperK, Intoxication with ethylene glycol or methanol, Overload with anuria, Uremia causing encephalopathy or clinically significant pericarditis.
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Clinical Pearls

• AKI is defined by a rise in serum Cr >0.3 over 48 hours or >1.5x baseline over 1 week OR UOP <0.5cc/kg/hr over 6 hours
• GFR is not used to measure the extent of an AKI - it is validated for tracking CKD
• Because of the non-linear relationship (see image here) between creatinine/cystatin C and GFR, relatively small initial increases in these markers represent significant decreases in GFR; as such, the difference in GFR change when going from a creatinine of 0.5 to 1.0 is much more significant than a change from 3.5 to 4.0
• Creatinine is a product of muscle breakdown - its levels change based on a patient's diet and muscle mass; Cystatin C can thus be a more accurate measure of GFR in patients who have a good deal of muscle mass or muscle breakdown
• The majority of inpatient AKI is from prerenal or ATN - in general, okay to trial fluids, and if AKI resolves within 48 hours, it was likely prerenal and you don’t have to go digging
• Most AKIs are fixed with a fluid (hypotension), Lasix (CHF), or a foley (retention)
• In general, it’s usually easier to get fluids in than to get them out. Yet, 1L of LR is almost always okay, and if the AKI resolves within 48 hours you’re done. UNLESS ESRD, ADHF or cardiogenic shock, cirrhosis/ascites, RV failure (PE, pHTN)
• If it’s ATN, the only therapy is patience
• Prerenal AKI is caused by decreased renal perfusion and thus decreased GFR whereas intrinsic AKI is due to direct damage to the kidneys - prolonged prerenal injury leads to intrinsic injury via ischemia and tubular necrosis
• Why do we consider the BUN/Cr ratio, FeNa, and UOsm? Classically >20 is prerenal and <20 is intrarenal. The usual ratio of BUN/Cr is 5-20 to 1. In healthy kidneys, BUN is absorbed more than creatinine  - if the intrinsic ability of the kidney to reabsorb is lost due to damage, the BUN in the blood will be lower and you will thus see a lower BUN/Cr ratio (<15-20)Moreover, when prerenal AKI, the kidney activates RAAS which leads to absorption of more Na, H20, AND BUN, leading to a higher BUN/Cr ratio.This is also why FENa is low (<1%), FeUrea is low (<35%) and UOsm is high (>500) in pre-renal - more Na and H2O are reabsorbed due to RAAS activation in the kidney that is able to re-absorb and concentrate urine.
• However, urine studies are often useless; patient needs to be off diuretics and ideally not received fluids; however, if Urine Osm >500, less likely ATN since damaged kidneys are not able to concentrate
• Urinalysis is great for the don’t miss diagnoses (glomerulonephrtiis, vasculitis, rhabdo, AIN, obstruction 2/2 cancer) - look for blood and RBCs (nephritis, myoglobin in rhabdo), protein (nephritis, SLE), WBCs (AIN)
• Why do ACE/ARBs cause pre-renal AKI? They decrease the effective circulating volume (RAAS is decreased and thus less Na and H20 absorbed) and can lead to lower BP than the body has become accustomed to seeing - together GFR and perfusion can decrease
• NSAIDs cause prerenal due to afferent arteriole constriction decreasing GFR
• Crystalline nephropathy is caused by acyclovir, tumor lysis, ethylene glycol 
• TTP/HUS/MAHA can cause small vessel occlusion leading to intrinsic AKI 
• Hypercalcemia causes diuresis which can lead to pre-renal physiology and AKI
• What’s the deal with ATN diuresis/polyuria? ATN polyuria is due to the inability of the tubules to reabsorb after the insult - filtering via glomeruli recovers faster than the tubular system which re-absorbs - GFR returns, but can’t reabsorb water from the filtrate - usually happens days after the insult and can last 1-3 weeks
• Venous injections of contrast likely does not cause true AKI and should not be cited as the reason to not get an otherwise needed scan - it may lead to transiently elevated creatinine, but its very unlikely this represents a clinically meaningful injury to the kidney; that being said, only contrast from the 1950's likely was nephrotoxic

Trials and Literature

• AKIKI Trial- ICU patients with AKI do not have better mortality if RRT is started early (within 6 hours) vs when patients met certain lab or clinical criteria (NEJM, 2016)
• Review on How to Use... serum creatinine, cystatin C, and GFR (BMJ, 2017)
• Controversies in Contrast-Material Induced Acute Kidney Injury (Radiology, 2015)

Other Resources

• Clinical Problem Solvers - AKI Schema, Intrinsic AKI Schema, Post-Renal AKI Schema
• EMCrit Project - Contrast Nephropathy, Myth Thereof
• IBCC Podcast on Contrast Nephropathy

Video