Septic Shock, Tubular Necrosis, and Central Diabetes Insipidus: A Challenging Syndrome

The association between septic shock, acute tubular necrosis, and central diabetes insipidus is infrequent: our recent clinical observation invited us to deepen its pathophysiological features.

We reported an unusual case report of a young, healthy man with a septic shock, severe dehydration with a hematocrit of 70.6% caused by gastrointestinal infection and refractory renal failure, and persistent polyuria.

The patient presented severe dehydration, hypovolemic shock with a hematocrit of 70.6%, and acute renal failure. The subsequent laboratory exams demonstrated a gastrointestinal infection of Campylobacter Upsaliensis and Helicobacter pylori. The persistent renal failure and polyuria later 20 days made it mandatory for further investigations. A Magnetic brain Resonance excluded encephalic lesions but demonstrated a posterior pituitary lobe hypointense.

This cascade of pathological events seems originated from a septic shock: the consequent increase in hematocrit and blood viscosity, estimated double the normal, with severe hypotensive shock correlated, decelerated the microcirculatory blood flow, until a proper blood stasis in the venous system. These factors caused hypoxia and possible venous thromboses, electively affecting the pituitary hypothalamic nuclei and their axons in the post-hypophysis and its portal system.