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Kidney Week

Abstract: PO0114

Brain Got Spongy at Angry Kidneys

Session Information

Category: Trainee Case Report

  • 102 AKI: Clinical, Outcomes, and Trials


  • Madera Sanchez, Ubaldo R., Hospital Universitario Ramon Ruiz Arnau, Bayamon, United States
  • Rodriguez Cintron, Christian, Doctors Center Carolina, Carolina, Puerto Rico, United States

Brain edema is a rare complication of acute kidney injury in patients who have not received renal replacement therapy. Immunologic and pro-inflammatory cascades mediate brain edema that is not dependent on the uremia, and instead, it is due to crosstalk between the kidneys and brain in the so-called reno-cerebral reflex. We are presenting an 88-year-old female with a history of hypertension and hypothyroidism with acute colitis that developed acute kidney injury and cerebral edema. We want to raise awareness of the need for early diagnosis and treatment to prevent severe clinical outcomes.

Case Description

88-year-old woman with a past medical history of hypertension, hypothyroidism came to the ER complaining of green-colored non-bloody diarrhea with associated epigastric pain for 2 days. Examination remarkable for left lower quadrant tenderness, tachycardia, alerted, awake, oriented to person only, cooperative and following commands. Labs were remarkable for leukocytosis with neutrophilia, fecal leukocyte positive, and metabolic alkalosis. Abdominal CT showed acute colitis localized to descending colon and sigmoid. The patient was admitted with acute colitis. On day 2 of admission creatinine went up to 2.35 from 1.07. On urine, sediment was evident with renal tubular epithelial cells and oxalate crystal. Renal sonogram with no renal abnormality. On day 3 the creatinine continued increasing doubled to 4.4. The patient's mental status started declining, and metabolic acidosis was present. Renal replacement therapy was advised, but the patient’s family member refused it and signed off DNR. The creatinine keeps trending up to 9.37. Brain CT without contrast was done and showed diffuse cerebral edema with no acute hemorrhage or ischemic changes. On day 11, the patient passed away.


The brain edema seen in this patient was a byproduct of oxidative stress, activation of the immunologic pathway, and activation of the Reno-cerebral reflex occurring in acute kidney injury that is entirely independent of the mechanism seen in uremia. Not every functional or structural brain alteration in acute kidney injury is caused by uremic encephalopathy. Many pathways are activated in acute kidney injury that contributes to the effects of the kidneys in distant organs being the brain one of them. This case will serve to raise awareness to study the crosstalk between organs to prevent complications and improve outcomes.