Kidney Week

Abstract: PUB242

A Case of Hyponatremia Due to Unilateral Renal Hypoperfusion from a Type B Aortic Dissection

Session Information

• Publication Only

Category: Fluid, Electrolytes, and Acid-Base Disorders

• 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Authors

• Lin, Andrew A., University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, United States

Andrew A. Lin, PhD

• Al Haddad, Nadia, Penn Medicine, Philadelphia, Pennsylvania, United States

Nadia Al Haddad, MD

• Tillquist, Kristen N., Penn Medicine, Philadelphia, Pennsylvania, United States

Kristen N. Tillquist, DO

• Cohen, Jordana B., University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, United States

Jordana B. Cohen, MD, MS, FASN

• Reisinger, Nathaniel, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, United States

Nathaniel Reisinger, MD, FASN

Introduction

Hypoosmolar hyponatremia in euvolemic patients has a broad differential diagnosis and significant potential morbidity. Much of the underlying pathophysiology in hypoosmolar, euvolemic hyponatremia stems from ADH secretion, whether from ectopic overproduction or the body attempting to regulate perceived osmolar and volume status. Here, we present a case of severe symptomatic hyponatremia due to unilateral renal hypoperfusion.

Case Description

A 64-year-old male with a past medical history of hypertension and type A aortic dissection presented with a new type B aortic dissection. Blood pressure was elevated to the 170s/90s and was quickly controlled with carvedilol, hydralazine, and clonidine. On admission, the patient’s sodium was 137. Late on hospital day 2, the patient became confused and unable to follow commands. The sodium was now 120 with urine sodium 30, urine osmolality 786, and serum osmolality 259. On physical exam, he was euvolemic with a blood pressure of 121/89. Jugular venous distention, pulmonary rales, and edema were absent. Repeat urine sodium was 10 and urine osmolality was 521. The patient received multiple 3% hypertonic saline boluses which stabilized his sodium at 128 on day 4. Review of the patient’s imaging demonstrated the right renal artery arising from the false lumen of his dissection with decreased contrast uptake, versus the left renal artery which arose from the true aortic lumen. We hypothesized that the patient’s hyponatremia was due to unilateral renal hypoperfusion causing increased renin secretion by the right kidney, leading to stimulation of sodium resorption by angiotensin II, and ultimately increased ADH secretion leading to hyponatremia. The patient was placed on fluid restriction and his sodium stabilized at 133; he was discharged with instructions for close nephrology follow-up.

Discussion

While renal hypoperfusion such as in unilateral renal artery stenosis can cause hyponatremia, this is usually accompanied by hypertension (hyponatremic hypertensive syndrome). Here, the patient’s euvolemia and initial urine studies suggested SIADH until revisiting his abdominal imaging. A high degree of clinical suspicion is thus required for alternative anatomic causes of hyponatremia and ADH secretion in response to perceived hypovolemia.