As part of our free webinar series, we conducted a webinar in December 2020 clarifying the diagnostic criteria for acute kidney injury (AKI), acute tubular necrosis (ATN), and acute on chronic kidney disease (CKD). We present the highlights below, including case studies and coding tips.

Over the past twenty years there have been several attempts to come up with diagnostic standards for AKI/renal failure, most notably in JAMA (2003), at the 2004 RIFLE conference, and in the Acute Kidney Injury Network (AKIN) report (2007). Finally, in 2012 the Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Guidelines combined the best of these previous efforts, providing an authoritative diagnostic standard for AKI that is now accepted world-wide.

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Acute Kidney Injury (AKI)

Seemingly small changes in creatinine reflect a significant loss of renal function: a creatinine increase of 1.5 times the baseline level corresponds to a 25% loss of renal function, and an increase to twice the baseline level corresponds to a 50% loss of renal function. Identifying and treating acute kidney injury as early as possible is therefore crucial.

KDIGO specifies three different criteria for AKI, any one of which is sufficient for diagnosis:

1. Increase in creatinine to ≥ 1.5 times baseline (within a 7-day period), or
2. Increase in creatinine of ≥ 0.3 mg/dL within 48 hours, or
3. Urine output < 0.5 ml/kg/hr for 6 hours

Criterion 1 can be applied either retrospectively orprospectively. The latter is more common, since the baseline creatinine is usually not known upon admission, and the creatinine falls after administration of IV fluids; in such cases, if the creatinine measured at admission is 1.5 times greater than a subsequent measurement within 7 days, this is sufficient for diagnosis. The calculation is simple: divide the highest creatinine level by the lowest.

Clinical case A. A patient is admitted with a creatinine of 2.2 and unknown baseline. Over the next three days, their creatinine falls to 1.3, which is now assumed to be the baseline. To calculate the degree of change, the admission creatinine of 2.2 is divided by the baseline of 1.3, yielding 1.7. Since 1.7 is more than 1.5, the diagnosis of AKI present on admission is confirmed.

Criterion 2 requires no baseline creatinine level and is applied prospectively, as it requires two measurements no more than 48 hours apart to show an increase from the first measurement by at least 0.3 mg/dL. If the second creatinine level is lower than the first, this diagnostic criterion cannot be applied—a point sometimes misunderstood by providers and documentation specialists alike.

Clinical case B. An initial creatinine of 1.3 increases to 1.7 in 36 hours. This 0.4 mg/dL increase from the initial level confirms a diagnosis of AKI. 

Clinical case A, revisited. The patient's creatinine fell from 2.2 to 1.8 within 48 hours. This patient did not meet Criterion 2, because the creatinine fell; at 48 hours the patient did not meet Criterion 1, either, because 2.2 divided by 1.8 is less than the required 1.5. In another 24 hours, however, as the creatinine fell further to 1.3, the patient met Criterion 1 for AKI.

Criterion 3 for urinary output is straightforward but less commonly encountered.  The urine output calculation is quantity of urine in ml divided by patient's weight in kg divided by 6 hours. 

Clinical case C.  A 150-pound (68 kg) septic patient has urine output of only 180 ml over 6 hours.  180 ml / 68 kg / 6 hour = 0.44 ml/kg/hour. This meets Criterion 3 for AKI. 

Acute Tubular Necrosis (ATN)

ATN is defined as AKI due to impairment of renal tubule function. It is a clinical diagnosis based on the persistence of AKI with creatinine levels above baseline for at least 72 hours. ATN is most commonly caused by IV contrast, prolonged hypotension or shock, medications, chemicals, toxins, prolonged pre-renal AKI, rhabdomyolysis with myoglobinuria, or tumor necrosis syndrome. AKI due to contrast or myoglobinuria is always caused by ATN.

In the majority of cases, there is no actual necrosis, which is a sign of very severe injury. "Acute tubular injury" would therefore be a more accurate term for this condition overall, but this new terminology has not been officially accepted.

Coding tip: It is important to distinguish AKI from ATN, since the code for AKI is a CC while ATN is an MCC. 

Urinalysis. Urine chemistries may be used to confirm ATN in questionable cases or rule out other diagnoses. Urinary sodium concentration > 40 meq/L and fractional excretion of sodium (FENa) > 2% help confirm the ATN diagnosis but are not required. If the problem is, instead, pre-renal AKI (e.g., dehydration), the urinary sodium concentration is expected to be < 20 meq/L and FENa < 1%. Note that since the vast majority of cases of ATN are functional (without necrosis), the urine sediment will be unremarkable. (“Muddy brown casts” and renal tubular cells appear in the urine only with severe ATN that has led to necrosis)

Clinical case D.  A 58-year-old is admitted with pulmonary embolism, confirmed by CT angiography. Creatinine levels measured over six days were as follows: 0.5, 1.0, 1.4, 1.6, 1.2, 0.8. In this case, the baseline creatinine was 0.5 and increased to 1.0 in one day, which meets the AKI criterion of creatinine increase  > 0.3 within 48 hours. Creatinine remained above baseline for 4 days (> 72 hours) and at discharge, meeting the criterion for ATN. (This was an easy one: AKI due to IV contrast is always ATN.)

Acute on Chronic Kidney Disease (CKD)

Acute on chronic kidney disease is simply the occurrence of AKI in the setting of pre-existing CKD, which makes patients extremely vulnerable to any physiological stress. Separate codes are assigned for AKI and CKD by stage, as ICD-10 has no combination code for this situation. AKI criteria for CKD patients are precisely the same as for non-CKD patients (see first section above).

For CKD to be diagnosed, either of the following criteria must be present for > 3 months:

1. GFR < 60, or
2. Clinical markers of kidney injury (i.e., structural or functional abnormalities).

The CKD stage is determined by the stable GFR. The GFR may fluctuate during the inpatient stay, so the "stable GFR" will be the GFR at or near the time of discharge.

Note that, because the GFR in Stages 1 and 2 is > 60, thereby failing to meet the first criterion, a diagnosis of CKD in those cases will require the finding of at least one clinical marker of kidney injury.  Stages 3-5 CKD often have clinical markers of kidney injury, but these are not required because the GFR in these cases is, by definition, < 60.

Coding tip: Correct documentation of CKD stage is important, since stages 4 and 5 are CCs, while stages 1-3 are non-CCs. If the stage is not documented, providers should be queried for patients with a stable GFR < 60.

Clinical case E. A 60-year-old male with CKD-4 was admitted for COVID-19 and pneumonia with a creatinine level of 4.4 and GFR of 14.  His creatinine level fell to 2.5 and GFR improved to 27 by the time of discharge.  The creatinine at admission (4.4) is 1.8 times the lowest creatinine level (2.5), which meets the AKI criteria of > 1.5 times or more from baseline. The discharge GFR of 27 confirms stage 4 CKD.

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