Kidney Week

Abstract: SA-PO0103

Subarachnoid Hemorrhage Reveals Previously Unrecognized ADPKD

Session Information

• ADPKD and Cystic Kidney Disease - 3
  October 24, 2026 | Location: Exhibit Hall A, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Genetic Diseases of the Kidneys

• 1201 Genetic Diseases of the Kidneys: Cystic (Monogenic)

Authors

• Asencio-Torres, Gabriela M., VA Caribbean Healthcare System, San Juan, Puerto Rico

Gabriela M. Asencio-Torres, MD

• Adams Chahin, Juan J., VA Caribbean Healthcare System, San Juan, Puerto Rico

Juan J. Adams Chahin, MD

• Vega-Colon, Jesus Daniel, Universidad de Puerto Rico Escuela de Medicina, San Juan, Puerto Rico

Jesus Daniel Vega-Colon, MD

• Ocasio Melendez, Ileana E., Universidad de Puerto Rico Escuela de Medicina, San Juan, Puerto Rico

Ileana E. Ocasio Melendez, MD, FASN

Introduction

Autosomal dominant polycystic kidney disease (ADPKD) is a genetic disorder characterized by progressive bilateral renal cyst growth with associated extrarenal manifestations and is a major cause of end-stage kidney disease. Intracranial aneurysms and subarachnoid hemorrhage are well-described complications that increase morbidity and mortality. We present a case of previously undiagnosed ADPKD presenting with subarachnoid hemorrhage and severe kidney impairment.

Case Description

A 51-year-old man with untreated hypertension and prior nephrolithiasis sustained a 10-foot fall, resulting in multiple traumatic injuries. Noncontrast head CT demonstrated bilateral sulcal SAH near the vertex. He was markedly hypertensive on presentation. Laboratory studies showed non-anion gap metabolic acidosis, azotemia (creatinine 5.43 mg/dL; BUN 49.6 mg/dL), CK 2,371 U/L, and a urine protein/creatinine ratio of 2,206 mg/g. Abdominal imaging revealed innumerable bilateral renal cysts and multiple hepatic cysts without hydronephrosis, consistent with ADPKD, with a height-adjusted total kidney volume of 891.1 mL/m. Management included oral antihypertensives, alkali therapy, and strict fluid monitoring. His hospital course was complicated by generalized tonic-clonic seizures and a saddle pulmonary embolism with right-heart strain requiring heparin infusion and ICU care. Renal function remained severely impaired but did not necessitate emergent kidney replacement therapy.

Discussion

This case underscores the importance of considering ADPKD as the cause of kidney dysfunction in patients with bilateral renal cysts and hypertension. Early recognition should prompt consideration of intracranial aneurysm screening in patients, at-risk family members, and implementation of risk-reduction strategies to prevent catastrophic outcomes.