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Abstract: PO1107

A Salty Goodbye to Diuretic Resistance: Hypertonic Saline

Session Information

Category: Fluid, Electrolyte, and Acid-Base Disorders

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

Author

  • Barnett, Sean, Brooke Army Medical Center, Fort Sam Houston, Texas, United States
Introduction

Understanding the complex interplay of Cardiorenal physiology and pathophysiology in diuretic resistance requires a deep understanding of RAAS, ADH, and virtually all segments of the nephron. To treat, requires not only understanding but also the ability to investigate and differentiate. However, a treatment that can inhibit RAAS (directly and indirectly), stimulate Cardiac Output, improve GFR, and increase natriuesis could be the universal answer. 3% Saline has the ability to improve Cardiac Output and decrease SVR, increase GFR, increase natriuresis, inhibit RAAS and ADH (directly and indirectly), and stimulate ANP. Therefore, the answer to Diuretic Resistance is 3% Saline.

Case Description

A 55 y.o. AAF presented to the hospital for severe edema and shortness of breath. PMHx of HFpEF, DM, HTN, CKDg3a3 (non-nephrotic). She presented with AKI III, severe hyponatremia, and anasarca. Echo revealed EF 40%, biatrial enlargement, RV overload and reduced RV function. She was initially treated with high dose furosemide but did not improve. She was given Metolazone which caused worsening hyponatremia which was treated with 100mL of 3% Saline. This caused an immediate increase in urine output and sodium. She was then changed to a bumex drip and high dose spironolactone (200mg) with some improvement (via objective urine electrolyte assessment) she was still inadequately diuresed. She was then treated with 3% + Loop pulse dosing and sustained a robust diuresis of >3L of urine and maintained urinary sodium >50.

Discussion

The potential causes of diuretic resistance arise from the RAAS system and the individual nephron segments. The RAAS system however is the most universal target (when inhibited). While DCT, ASDN, CD and CCT. are involved, regardless of which segment is primary, targetting the RAAS system would likely have significant benefits in all diuretic resistance. 3% Saline works as a potent IVF to improve Cardiac Output, decrease SVR, improve renal blood flow, inhibit RAAS, inhibit ADH, and stimulate ANP. Using 100mL of 3% saline to augment diuresis (or alone) causes improvement in virtually all Cardiorenal parameters. The NaCl load directly inhibiting RAAS through distal NaCl delivery (salt load also increases salt wasting), this causes decreased afferent arteriolar constriction and thus further improving GFR. It also stimulates ANP in the RA to inhibit RAAS and ADH indirectly.