Methods for treating hyperaldosteronism with therapeutic renal neuromodulation and associated systems and methods are disclosed herein. One aspect of the present technology, for example, is directed to methods that at least partially inhibit sympathetic neural activity in renal nerves proximate a renal blood vessel of a human patient. One or more measurable physiological parameters corresponding to hyperaldosteronism of the patient can thereby be improved. Moreover, central sympathetic drive in the patient can be reduced in a manner that treats the patient for hyperaldosteronism. Renal sympathetic nerve activity can be modulated along the afferent and/or efferent pathway. The modulation can be achieved, for example, using an intravascularly positioned catheter carrying a neuromodulation assembly, e.g., a neuromodulation assembly configured to use electrically-induced, thermally-induced, and/or chemically-induced approaches to modulate the renal nerve.