Kidney Week

Abstract: FR-PO0876

Clamping the Clamp: Conservative and Individualized Management of Profound Hyponatremia in Advanced CKD

Session Information

• Fluid, Electrolyte, and Acid-Base Disorders: Case Reports - 1
  October 23, 2026 | Location: Exhibit Hall A, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Fluid, Electrolytes, and Acid-Base Disorders

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

Authors

• Hashmi, Razi Haider, Baystate Medical Center, Springfield, Massachusetts, United States

Razi Haider Hashmi, MD

• Abdullin, Marat, Baystate Medical Center, Springfield, Massachusetts, United States

Marat Abdullin, MD, PhD

• Landry, Daniel L., Baystate Medical Center, Springfield, Massachusetts, United States

Daniel L. Landry, DO, FASN

• Braden, Gregory Lee, Baystate Medical Center, Springfield, Massachusetts, United States

Gregory Lee Braden, MD

Group or Team Name

• Clampers

Introduction

Hyponatremia (Na <135 mEq/L) is a common electrolyte disorder with multifactorial causes including ADH-mediated free-water retention, medications, low solute intake, and excess fluid intake. Symptoms range from mild to severe neurologic dysfunction. Management depends on severity, chronicity, etiology, and clinical status, with options including hypertonic saline, fluid restriction, DDAVP, and vasopressin antagonists. Approaches vary widely. This case highlights severe hypotonic hyponatremia in advanced CKD due to excess free-water intake, emphasizing that therapy should be individualized and not all cases require a DDAVP clamp.

Case Description

A 31-year-old male with stage 5 CKD (baseline creatinine 10.6 mg/dL) presented with edema and calf pain after consuming ~4 L/day of fluid for 1 week. Serum sodium was 102 mmol/L, serum osmolality 238 mOsm/kg, and creatinine 13 mg/dL. Urine studies showed osmolality 100 mOsm/kg, urine sodium <20 mmol/L, and urine chloride <20 mmol/L. He was alert, oriented, and hemodynamically stable, with 1+ bilateral lower extremity edema and mild pulmonary congestion on chest X-ray. After brief hypertonic saline in the ED, further hypertonic therapy and DDAVP were withheld. ICU management included 1 L/day fluid restriction, close urine output and sodium monitoring, and avoidance of diuretics or renal replacement therapy. Sodium rose gradually ≤6 mEq/L per 24 hours, and the patient maintained residual urine output of 2–3 L/day, allowing transfer to the floor within 24 hours.

Discussion

ICU-based DDAVP clamps are commonly used to prevent overcorrection in severe hyponatremia but may not benefit all patients. In advanced CKD, reduced nephron mass limits medullary gradient generation and ADH responsiveness via downregulation of aquaporin-2 channels, impairing urine concentration. Despite CKD, this patient maintained low urine osmolality, reflecting preserved diluting capacity and excess free-water intake. Residual urine output and limited maximal free-water clearance constrained rapid sodium shifts, lowering overcorrection risk. Absence of neurologic symptoms suggested chronic adaptation, supporting conservative management with fluid restriction and close monitoring. This case highlights that urine indices and underlying renal physiology should guide hyponatremia therapy rather than routine DDAVP clamp protocols.