Documentation and coding of acute renal failure can be problematic, as many different criteria may be used to define the condition. Distinguishing between acute and chronic renal failure in the inpatient setting also may require several days of evaluation. What's more, the clinical terminology applied may not correspond with coding requirements. For example, the time-honored terms “renal insufficiency” and “pre-renal azotemia” are considered non-specific and do not translate for coding purposes as “renal failure.” The word “acute” is essential for correct coding; if omitted the code will default to chronic kidney disease or a clinically insignificant “unspecified” status.
The definition of acute renal failure (or acute kidney injury) is a reduction of renal function, usually within a short period of time. This can be measured by a rising serum creatinine or by diminished urine output. Many criteria exist, but a useful article in the February 12, 2003 Journal of the American Medical Association (2003;289:747-751) offers the following:
- Acute renal failure occurs when the serum creatinine level increases by 0.5 mg/dL or more within 2 weeks or less.
- In cases of chronic kidney disease where the baseline creatinine is greater than 2.5 mg/dL, a 20% increase from baseline is required.
The term “acute kidney injury” (AKI) comes from the proposed RIFLE criteria (Critical Care. 2004;8:R204-R212), and is equivalent to acute renal failure. The earliest phase of AKI is recognized as an increase in creatinine of 1.5 times baseline. It doesn't matter which criteria are used, but you should use and apply one set, and document acute renal failure or AKI whenever the criteria are met.
The most common cause of acute renal failure—and an often-missed documentation opportunity—is dehydration. Severe dehydration frequently causes acute renal failure. Even if the only treatment of acute renal failure is rehydration, the important relationship between acute renal failure and dehydration remains valid.
If the baseline creatinine is unknown, then correction of creatinine upon rehydration establishes a new baseline to be compared with the admission creatinine. A difference of 0.5 mg/dL or more provides clinical proof of the presence of acute renal failure on admission, which should then be documented in the medical record.
Another cause of acute renal failure, acute tubular necrosis (ATN), doesn't occur very often, but when it does the diagnosis is extremely important. The creatinine usually increases several-fold and is preceded by oliguria. Structural damage or necrosis of the renal tubules occurs and is typically ischemic in nature or related to drug toxicity.
The urinalysis will show red blood cells (RBCs), white blood cells (WBCs) and casts. The oliguria and elevation in creatinine will persist for several days to six weeks or more, and may be followed by a diuretic phase. There can be residual renal loss, so baseline creatinine may not return to normal.
The distinction between dehydration and ATN as the cause of acute renal failure should be simple. Unless a urinary infection is also present, WBCs and RBCs on urinalysis would not be expected with dehydration, and there would never be tubular casts in the urine. Oliguria is transient and the creatinine usually returns to baseline promptly with treatment of dehydration.
In summary, keep a close eye on patients' creatinine levels and remember to document the presence of acute renal failure whenever the criteria are met, especially when associated with dehydration. Avoid “non-specific” terminology. Monitor urine output and review the urinalysis for evidence of ATN.