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. 2025 Dec 9;29:100429. doi: 10.1016/j.metop.2025.100429

Fig. 1.

Fig. 1

Geller syndrome pathophysiology. In normal gestation, progesterone acts as an antagonist of the mineralocorticoid receptor (MR). Contrary, in Geller syndrome, a gain-of-function mutation in the NR3C2 gene, specifically a serine-to-leucine substitution at position 810 (S810L), alters the receptor's ligand specificity, allowing progesterone to hyper-activate the MR. This leads to kaliuresis, hypokalemia, and arterial hypertension. Created with Biorender.com.