Abstract: TH-PO0093
More than Just Cysts: Obstructive Uropathy Masquerading as Progression in ADPKD
Session Information
- AKI: Pathogenesis and Disease Mechanisms
November 06, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Tully, Hannah, Wright State University Boonshoft School of Medicine, Dayton, Ohio, United States
- Barnes, Eric W., Wright State University Boonshoft School of Medicine, Dayton, Ohio, United States
Introduction
Autosomal Dominant Polycystic Kidney Disease (ADPKD) is a common inherited disorder characterized by progressive cystic and kidney enlargement as well as indolent decline in estimated glomerular filtration rate (eGFR) over decades. However, sudden or rapid worsening in kidney function warrants prompt evaluation for superimposed pathology, such as cyst hemorrhage, infection, or obstruction. Though uncommon, extrinsic ureteral obstruction from expanding cysts may be an underrecognized and reversible contributor to renal injury in ADPKD.
Case Description
A 73-year-old male with history of chronic kidney disease stage 3bA2 due to known ADPKD, hypertension, and type 2 diabetes mellitus was referred to nephrology clinic for worsening renal function from a baseline serum creatinine (SCr) from 1.1-1.3 to 2.0 mg/dL. Urinalysis showed no hematuria and minimal proteinuria. A vasculitis panel and SPEP were negative. A renal ultrasound showed multiple bilateral renal cysts with advanced parenchymal atrophy on the right. A follow up MRI abdomen was obtained which demonstrated numerous bilateral cysts with severe right-sided hydronephrosis. The patient was referred to urology and underwent a retrograde pyelogram with ureteral stent placement at the right ureteropelvic junction (UPJ), resulting in improved SCr and reduced hydronephrosis. Despite this, eGFR increased only modestly. A Lasix renogram showed severely reduced right renal function (11%) compared to the left (88%). To avoid chronic stenting, he underwent right ureteroscopy and robotic-assisted cyst decortication. Postoperatively, renal function remained stable without further intervention.
Discussion
This case illustrates a rare but treatable cause of renal decline in ADPKD—extrinsic ureteral compression by renal cysts. While ADPKD progression is usually intrinsic, secondary obstruction should be considered with asymmetrical findings or rapid functional decline. Renal imaging and functional studies were crucial in differentiating chronic parenchymal loss from a reversible obstructive process. Surgical cyst decortication alleviated obstruction and preserved function, emphasizing the role of timely urologic intervention and multidisciplinary care in complex ADPKD presentations.