Contrast-induced acute kidney injury following iodine opacification other than by intravascular injection
A 57-year-old woman having two stomies due to a long history of intestinal resections was admitted to the intensive care unit (ICU) because of an acute rise in serum creatinine level (from 67 to 134 µmol/L in 24 h) with oliguria and drowsiness. Three days before, she developed fever with C-reactive protein elevation attributed to a digestive bacterial translocation and was treated by Imipenem 500 mg t.i.d without any other change in her current medication. On the same day, looking for a peritoneal fistula, a trans-jejunostomy enteroclysis was performed with 300 mL of Iopamiro 300 (low-osmolar CM; 90 g iodine load), which showed no intestinal leak. Since ICU admission, the patient remained haemodynamically stable and after rehydration a normal diuresis resumed. To note, the urine sediment was normal, in particular without leukocyturia nor eosinophiluria, while the urinary βNAG and lysozyme were markedly increased. Thereafter, the serum creatinine level continued to increase rapidly up to 481 µmol/L on Day 6 after enteroclysis and then slowly returned to baseline within a month ().\nIn the attempt to find the reason for this acute renal failure, it turned out that the radiologist had noticed the presence of CM in the urinary tracts already during the enteroclysis. For this reason, he had performed a native abdominal computed tomography (CT)-scan 1 h later, which confirmed the unexpected presence of CM in both renal pelvis and ureters, without evidence for any peritoneal resorption of CM (). Therefore, although no intravascular-iodinated CM had been administered to this patient, we considered the diagnosis of CI-AKI on the basis of the presence of CM in both urinary tracts associated with a typical clinical evolution. As no leak of CM into the peritoneal space was detected on the CT-scan, we assumed that the rapid absorption of CM occurred through the intestinal mucosa, the permeability of which was apparently increased by the local inflammatory state. Moreover, in our patient, the transmucosal resorption of CM could have been sustained, as suggested by the persistence of CM in the caecum on a native CT-scan made 7 days after the enteroclysis.