Another interesting Nephsap teaching point by a question was an under recognized cause of acquired apparent mineralcoritcoid access.
Liver cirrhotic patients with elevated bilirubins and sickle cell crisis patients who have elevated bilirubins have this happen to them. When total bilirubin levels are very high, it is hypothesized that worsening cholestasis led to greater bile acid inhibition of 11B - HSDH type II in the distal nephron and this allows for K wasting via cortisol mediation and HTN as well.
Case reports have been reported in liver cirrhosis and sickle cell crisis patients?
Wonder if we see this or its noticed in Post BMT - VOD syndrome?
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