## Why "Acute hemorrhage into cysts and recurrent cyst infections requiring antibiotics with good cyst penetration" is right The bilateral massively enlarged kidneys in ADPKD (marked **A**) are characterized by innumerable cysts throughout the cortex and medulla that can undergo hemorrhage, infection, and calcification. Cyst infections are a well-recognized complication and are notoriously difficult to treat because antibiotics must penetrate the cyst fluid; fluoroquinolones and trimethoprim-sulfamethoxazole are preferred over aminoglycosides. Acute hemorrhage into cysts is also a common cause of acute flank pain in ADPKD patients. Harrison 21e Ch 309 emphasizes these complications as key clinical manifestations of the massively enlarged kidneys in ADPKD. ## Why each distractor is wrong - **Isolated proteinuria without hematuria or hypertension**: ADPKD patients typically present with hematuria (micro or gross) and hypertension as early manifestations due to RAAS activation from cyst-compressed nephrons. Isolated proteinuria without these features is not characteristic of ADPKD. - **Rapid progression to ESRD within 2 years despite optimal management**: While ADPKD does progress to ESRD, the natural history is much slower—typically by the 5th–6th decade in PKD1 disease. Two years is far too rapid and does not reflect the typical disease course. - **Unilateral kidney involvement with normal contralateral kidney function**: ADPKD is by definition bilateral; the hallmark feature is bilateral massively enlarged kidneys with innumerable cysts in both organs. Unilateral involvement would suggest a different diagnosis (e.g., unilateral renal cystic disease or sporadic cystic kidney disease). **High-Yield:** Bilateral massively enlarged kidneys in ADPKD are prone to hemorrhage and infection; cyst infections require antibiotics with good cyst penetration (fluoroquinolones > aminoglycosides). [cite: Harrison 21e Ch 309]
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