Kidney Week

Abstract: SA-OR54

Respiratory Alkalosis Accounts for Nearly Half of Cases of Low Serum Bicarbonate in Patients with Cirrhosis with AKI

Session Information

• Fluid, Electrolyte, and Acid-Base Disorders: Clinical Advances
  October 26, 2024 | Location: Room 4, Convention Center
  Abstract Time: 05:50 PM - 06:00 PM

Category: Fluid, Electrolytes, and Acid-Base Disorders

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

Authors

• Johnson, Kirsten, UQ-Ochsner Clinical School, New Orleans, Louisiana, United States

Kirsten Johnson

• Chalmers, Dustin R., LSU Internal Medicine, Baton Rouge, Louisiana, United States

Dustin R. Chalmers, MD, MS

• Shetty, Sumukh, UQ-Ochsner Clinical School, New Orleans, Louisiana, United States

Sumukh Shetty, MS

• Ellis, Montana D., UQ-Ochsner Clinical School, New Orleans, Louisiana, United States

Montana D. Ellis, MS

• Hashem, Ghaith, UQ-Ochsner Clinical School, New Orleans, Louisiana, United States

Ghaith Hashem

• Varghese, Vipin, University of Michigan Division of Nephrology, Ann Arbor, Michigan, United States

Vipin Varghese, MD

• Velez, Juan Carlos Q., Department of Nephrology, Ochsner Health, New Orleans, Louisiana, United States

Juan Carlos Q. Velez, MD, FASN

Group or Team Name

• Ochsner Group.

Background

Metabolic (Met) acidosis (Acid) is the most common acid-base disorder in the context of acute kidney injury (AKI). As a result, a low serum carbon dioxide (sCO₂) level from a chemistry panel in a patient with AKI is usually presumed to be caused by Met Acid. Respiratory (Resp) alkalosis (Alk) is the most common acid base disorder in cirrhosis. However, whether the predominance of Resp Alk prevails in cirrhosis even during AKI has not been investigated. We hypothesized that Resp Alk is a frequent cause of low sCO₂ in cirrhosis with AKI.

Methods

We prospectively collected data of patients seen in nephrology consultation for AKI who had a urine specimen subjected to microscopic examination of the urinary sediment (uSEDI) as part of the clinical evaluation. Within this cohort, we identified patients with cirrhosis with a low sCO₂ (< 22 mEq/L) in which acid-base status was assessed by either arterial blood gas (ABG) or venous blood gas (VBG) analysis. VBG results were corrected to an ABG equivalent (venous pH + 0.03 = arterial pH; venous pCO₂ – 6 = arterial pCO₂).

Results

Among 801 patients assessed by uSEDI over a 5-year period, 267 (33%) had cirrhosis. A low sCO₂ was recorded in 225/267 (84%). Among those with low sCO2, 109 (48%) had acid-base status assessed (77 ABG, 32 VBG). Mean age was 53 years, 44% women, 74% White, 16% Black, 4% Hispanic. Main causes of cirrhosis were alcoholic (58%) and NASH (20%). Main causes of AKI were ischemic/toxic acute tubular injury (49%) and hepatorenal syndrome (40%). Median serum creatinine at diagnosis was 3.6 mg/dL. The most common single acid-base disorders were Resp Alk in 25 (23%) and Met Acid in 24 (22%). Combined 2 disorders included Resp Alk + Met Acid in 34 (31%) and Met Acid + Resp Acid in 12 (11%) and Resp Alk and Met Alk in 6 (6%). A triple disorder was found in 16 (15%). Altogether, Resp Alk was found in 65 (60%). Furthermore, 27 (42%) of patients with isolated Resp Alk or combined Resp Alk + Met Acid (with pH > 7.35) were treated with oral or intravenous bicarbonate.

Conclusion

In patients with cirrhosis and AKI, sCO2 is often caused by Resp Alk. Default administration of bicarbonate supplementation without assessment of acid-base status should be avoided.