Kidney Week

Abstract: TH-PO0763

Sudden Reversal of Anuric AKI After Intubation and Mechanical Ventilation: A pCO2 Effect?

Session Information

• AKI: Critical Care, CKRT, Cardiorenal Syndromes, and Clinical Outcomes
  October 22, 2026 | Location: Exhibit Hall A, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Acute Kidney Injury

• 102 AKI: Clinical, Outcomes, and Trials

Authors

• Onuchic, Laura, Yale University, New Haven, Connecticut, United States

Laura Onuchic, MD

• Barsotti, Gabriel, Yale University, New Haven, Connecticut, United States

Gabriel Barsotti

• Gomez, Daniel, Yale University, New Haven, Connecticut, United States

Daniel Gomez, MD

• Brewster, Ursula C., Yale University, New Haven, Connecticut, United States

Ursula C. Brewster, MD, FASN

Introduction

The effects of mechanical ventilation on hemodynamics are well established. Positive pressure causes reduction in RV preload and LV afterload which can in turn affect cardiac output and lead to changes in GFR. The effect of abrupt changes in blood pH on renal function and urine output, on the other hand, are mostly unknown and literature is scarce.

Case Description

A 79 yo female with history of AS post-TAVR, HFpEF and CKD3 (baseline Cr 1.3 mg/dL) presented with progressive dyspnea consistent with respiratory failure precipitated by RSV infection. 72h later, she developed oligoanuria and Cr increased to 5.0 mg/dL. Norepinephrine was initiated due to hypotension and despite a 200mg lasix challenge, urine output remained minimal (200cc in 3 h). At this time we decided to proceed with mechanical ventilation followed by CRRT. ABG prior to intubation revealed a severe mixed acid-base disturbance: pH 7.12, pCO₂ 86 mmHg, HCO₃^- 24.1 mEq/L. TTE prior to intubation showed EF 61%, flattening of the interventricular septum, RVSP 77mmHg and a non-collapsible IVC with >2.1cm, consistent with volume overload. 1h after intubation patient had spontaneously made 125cc of urine and ABG showed pH 7.31/pCO₂ 50mmHg. Urine output over the next 3h increased to 300cc/h, 400cc/h and 500cc/h and CRRT was not started. Within 6h, Cr decreased to 3.5mg/dL and 48 h after intubation Cr was back to baseline. Repeat TTE showed stable EF, a collapsible IVC with <2.1cm and no septum flattening.

Discussion

The rapidity and completeness of Cr normalization in 48 h argue against tubular injury and favor hemodynamically reversible AKI. Animal data show that severe hypercapnic acidemia decreases both renal blood flow and glomerular filtration rate as a result of vasoconstriction through renal nerve stimulation. Hypercapnia-mediated renal nerve stimulation prevents the decrease in renal afferent arteriolar tone that is expected in response to lowering of renal perfusion pressure. In vivo, these effects can be abolished by renal denervation (Anderson et al, Clnical Science, 1983). In conclusion, the rapidity of correction we observed supports initally a pCO₂-driven correction of hemodynamic AKI which was later followed by a reduction in RV pre-load and improvement in cardiorenal physiology. This case underscores the importance of recognizing hypercapnic acidosis as a driving mechanism of hemodynamic AKI which can be rapidly corrected.