hydrocholorothiazide is DOC for Nephrogenic Diabetes insipidus because it paradoxically causes an increase in BP by increasing sodium absorption and thus water absorption, Pathoma explains this nicely.

Desmopressin is incorrect because upon fasting (fluid restriction) ADH is increased meaning ADH is being released Centrally but is not working in the kidneys at the V2 receptors of the epithelial renal cells at Collecting duct.

On that note, Amiloride is used for Lithium induced nephrogenic DI.

according to uptodate thiazides cause a mild hypovolemic state thus your PCT will see more Na and H2O --> by principle that the PCT always reabsorbs 60% of what it sees, it will reabsorb more water and Na.

Patient has nephrogenic Diabetes Insipidus. One of the treatments is Hydrochlorthiazide.

Just to add thought process. Pt has excessive thirst, and urinating frequently but his Serum osmolality is increased...which means he has to omuch solute in his blood and his ADH is not working.

ADH not working can be due to Central DI or Nephrogenic DI. Central DI is when pt has lack of ADH but in this vignette they say the ADH is increased --> must be nephrogenic.

I don't think you need to know that HCTZ paradoxically works for nephrogenic. I think you can save time and just memorize FA's tx choices for Nephrogenic DI - HCTZ, amiloride, and indomethacin. You could argue it's good to know mechanisms, but I think knowing the drug names and their MOA, you'd be able to figure it out if they went for a 4th order reasoning (there's already enough thinking to do in this question)