Too bad to be true: pseudo-AKI due to traumatic bladder rupture


Acute Kidney Injury (AKI) is described as a rapid decline in Glomerular Filtration Rate (GFR), reflected by an increase in serum creatinine (SCr) and/or contraction of diuresis. The traditional paradigm considers pre-renal, renal and post-renal causes of AKI. However, there are some settings in which an elevated SCr does not reflect a real decline in GFR. Here we describe the case of a pseudo-AKI, consequence of a massive intraperitoneal urinary leakage due to a traumatic bladder rupture. Besides the pathophysiological considerations, we want to raise awareness about this condition, especially in relation to patients presenting with oliguria, hematuria, apparent AKI, abdominal pain and ascites, particularly after trauma; we do this not only to prevent late diagnosis complications, but also to avoid costly and risky overtreatment.

Keywords: pseudo-AKI, creatinine, urinary ascites, bladder rupture, trauma

Case report

A young adult, whose medical history includes favism, tabagism, alcohol drinking, drug addiction and no reports of kidney disease, was transported by helicopter to the emergency department after a road accident.

His arterial pressure was 190/80 mmHg, heart rate 103 beats per minute, peripheral oxygen saturation 100% with oxygen therapy, Glasgow Coma Scale 14/15.

Suspecting a seat belt trauma, a Focus Assessment with Sonography for Trauma (FAST) evidenced abdominal effusion, no display of the bladder and no signs of pneumothorax. Urine output was scarce and hematuric. 

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