On January 15th, our amazing PGY2 Simi Sharma presented a case of a middle-aged man with alcoholic cirrhosis presented with decreased urine output, worsening leg swelling, and shortness of breath for one day. His labs revealed acute renal failure with a Cr of 5.8, up from a baseline of 1.2 only weeks before. Urinalysis did not show pyuria and only had 4 RBCs after Foley catheter placement, 11-20 granular casts were noted.
For this patient, getting urine electrolytes (Urine Cr, sodium, +/- urea) can be a valuable next step in finding the etiology of his acute renal failure. However, FENa calculations tend to be overused to determine the cause of AKI in hospitalized patients.
In order to use FENa (fractional excretion of sodium) to determine the cause of AKI, your patient should be oliguric without underlying CKD and NOT be on diuretics.
If your patient is not oliguric, FENa is not reliable to differentiate between prerenal AKI and ATN. In adults, oliguria is defined as a urine output of <0.5mL/kg/h or <300mL of urine per 24 hours.
If your patient has CKD, their sodium excretion may be enhanced or impaired to an unpredictable degree. Therefore, FENa may not be accurate.
If your patient is on diuretics, their sodium excretion will be increased regardless of the etiology of their kidney injury. FEUrea is a better way to distinguish between prerenal AKI and ATN in these patients. However, urine sodium should still be measured as an indication of hydration (if the urine sodium is low despite diuretics, they are likely very volume down).
The FENa should only be used to differentiate between prerenal AKI and ATN. It cannot exclude other causes of intrinsic kidney disease (glomerulonephritides etc) or postrenal kidney disease. Many causes of intrinsic AKI may have a FENa that looks prerenal.
Hepatorenal syndrome is acute renal failure without other etiology in a patient with advanced cirrhosis and portal hypertension. It is essentially a diagnosis of exclusion. Their urinalysis should be bland, they should not be in shock or have an infection such as SBP, and they should not be on nephrotoxic drugs. Prerenal AKI should be excluded by volume expansion via albumin infusion 1g/kg body weight per day. If Cr rises despite this and other etiologies are excluded, HRS can be diagnosed.
HRS is classified in two different types. Type 1 HRS is rapidly progressive and defined by at least a twofold increase in serum Cr to a level of >2.5 during a period of less than 2 weeks. Type 2 HRS is any lesser degree of renal impairment.
Treatment of HRS type 1 includes ICU admission, octreotide infusion, and vasopressor support (usually norepinephrine in type 1 HRS) with continued albumin infusion of 25-50g/d until octreotide and pressors are discontinued. Treatment is continued for a total of 2 weeks. If there is some, but not total improvement in renal function, treatment duration may be extended, but if no improvement is noted, treatment is likely futile and prognosis is very poor. Hemodialysis can sometimes be used as a bridge to liver transplant or when there is a possibility of improvement in liver function, and therefore renal function, such as in potentially reversible causes of renal failure like Tylenol overdose.
However, if there is no possibility of listing a patient for liver transplant, HRS type 1 carries an 84% mortality at 6 months. For all patients with HRS type 1, palliative care and end of life discussions should be strongly considered.