Table 2 Potential pitfalls of AKI diagnosis based on creatinine and urine criteria
From: Acute kidney injury 2016: diagnosis and diagnostic workup
Clinical scenario | Consequence |
|---|---|
Administration of drugs which interfere with tubular secretion of creatinine (i.e. cimetidine, trimethoprim) | Misdiagnosis of AKI (rise in serum creatinine without change in renal function) |
Reduced production of creatinine (i.e. muscle wasting, liver disease, sepsis) | Delayed or missed diagnosis of AKI |
Ingestion of substances which lead to increased generation of creatinine independent of renal function (i.e. creatin, cooked meat) | Misdiagnosis of AKI |
Obesity | Overdiagnosis of AKI if using actual weight when applying urine output criteria |
Conditions associated with physiologically increased GFR (i.e. pregnancy) | Delayed diagnosis of AKI |
Interference with analytical measurement of creatinine (i.e. 5-fluorocytosine, cefoxitin, bilirubin) | Misdiagnosis and delayed diagnosis of AKI (depending on the substance) |
Fluid resuscitation and overload | Delayed diagnosis of AKI (dilution of serum creatinine concentration) |
Progressive CKD with gradual rise in serum creatinine | Misdiagnosis of AKI |
Extrinsic creatinine administration as a buffer in medications (i.e. in dexamethasone, azasetron) | Pseudo-AKI |
Oliguria due to acute temporary release of ADH (i.e. post-operatively, nausea, pain) enhanced by maximal sodium reabsorption in the setting of volume/salt depletion | Misdiagnosis of AKI |