Evaluation of Acute Kidney Injury

Along with hyponatremia, acute kidney injury was one of the most common reasons for consultation on my rotation. To diagnose acute kidney injury, you need one out of the following three criteria

• An increase in serum creatinine of ≥0.3 mg/dL (≥26.5 micromol/L) within 48 hours
• An increase in serum creatinine of ≥1.5 times baseline, which is known or presumed to have occurred within the prior seven days; or
• Urine volume <0.5 mL/kg per hour for more than six hours

Before I would go and see the patient, I would look through their chart and ask myself the following questions

• What is the patient's baseline creatinine? (is this acute kidney injury of acute on chronic kidney injury?)
• Has the patient received any IV contrast? 
• Have they been on any antibiotics as an outpatient or inpatient that are nephrotoxic (aminoglycosides, sulfonamides...)
• Has the patient been on any medications that could cause acute kidney injury? (NSAIDS, ACEi, diuretics, chemotherapy agents, antivirals or immunosuppressants)
• Does the patient have anything in their history that would decrease renal blood flow? (diarrhea, vomiting, decreased oral intake, sepsis, hypotensive episodes charted on vitals, third spacing of fluids)
• Any reason to suspect obstruction to urine outflow? (BPH, hx of uterine cancer, nephrostomy tubes or ureter stents)

Once I would gather the history from the chart, I would go see the patient and do a thorough H and P. I would try to assess their volume status by examining the following

• Mucous membranes moist or dry?
• Skin turgor?
• Evidence of poor perfusion? 
• Any evidence of fluid overload on exam? (JVD, ascites or edema)
• I/Os

Gathering the data above would usually give me a give me a high suspicion of the etiology of the patient's renal failure. Acute kidney injury causes can be divided into three categories: Pre-renal, Intrinsic and Post-renal

Pre-Renal Failure-This is the most common cause of acute kidney injury. A decrease in mean arterial blood pressure will cause an increase in sympathetic tone which leads to increase in renin which leads to vasoconstriction of the efferent arterioles causing a decrease in renal perfusion and thus an increase in creatinine. Causes for pre-renal failure include...

• True volume depletion-GI (vomiting, diarrhea, bleeding), Renal losses (diuretics, osmotic agents), loss through skin (sweating and burns) and third space sequestration (crush injury and skeletal fracture)
• Edematous states-Heart failure, cirrhosis and nephrotic syndrome
• Selective renal ischemia-Renal artery stenosis made worse by treatment with ACE inhibitors, Ang II blockers
• Drugs that affect the glomerular hemodynamics-decrease the arteriole dilation (NSAIDs decrease prostaglandins) or that increase efferent constriction (ACEi or Arbs which cause vasoconstriction of the efferent arteriole) 

Intrinsic Renal Failure-Etiology is damage to the renal parenchyma (intrinsic renal injury) and Acute Tubular Necrosis is the most common cause of intrinsic renal failure so I will focus on ATN and the three major causes of ATN.

• Severe renal ischemia-severe hypotension, thombotic event
• Sepsis-again, it is due to decreased perfusion but you also get an increase in cytokines and activation of neutrophils which cause inflammation of the renal tissue
• Nephrotoxic agents administered

Post-Renal Failure-when there is a long term obstruction to urine flow, the urine will back up through the ureters and can cause hydronephrosis. There is a point where the damage to the kidneys is so severe that it is not reversible.

• Obstruction within the urinary system-stones, blood clots
• Obstruction outside the urinary system-Enlarged prostate, strictures, retroperitoneal fibrosis or tumors

So, again the hx and physical will more than likely point you in one of these directions but there are a few lab test and treatment that you can do to help with the etiology. 

• UA-Examine the sediment. Are there any type of casts? Eosinophils present?
• FENA- looks at urine lytes and intact kidney function. <1% is more consistent with prerenal failure and >1% more consistent with intrinsic and post renal failure. 
• Response to fluid repletion-This is the gold standard for the distinction between pre-renal and ATN. With fluid repletion, the return of creatinine to baseline within 24-72 hours is consistent with pre-renal failure. The only exception to this is pre-renal failure secondary to edematous states. These patients are fluid overloaded but need to mobilize the fluid back into the intravascular space.
• Post-void bladder scan and renal US-If a pt has >200 cc of fluid after voiding, they have urinary retention which is more consistent with post-renal failure. A look at the kidneys with an US can tell you if there is any hydronephrosis present which would also point you towards post-renal failure.