Renal injury in cardiorenal syndrome type 1 is mediated by albumin

Yoshio Funahashi1, Mizuko Ikeda1, Rumie Wakasaki1

  • 1Anesthesiology & Perioperative Medicine, Oregon Health & Science University, Portland, Oregon, USA.

Physiological Reports
|February 12, 2022
PubMed

Insights

Cardiorenal syndrome type 1 (CRS-1) causes acute kidney injury (AKI) and albuminuria. Albumin injures kidney tubular cells, worsening AKI, suggesting caution with albumin treatments in CRS-1 patients.

Area of Science:

  • Nephrology
  • Cardiology
  • Physiology

Background:

  • Cardiorenal syndrome type 1 (CRS-1) is a severe complication of acute cardiovascular disease, leading to acute kidney injury (AKI) and albuminuria.
  • Albuminuria is linked to kidney disease progression and tubular injury, but its role in CRS-1 is unclear.

Purpose of the Study:

  • To investigate albumin's role in CRS-1 pathophysiology.
  • To determine if CRS-1 alters renal albumin handling and its impact on AKI.

Main Methods:

  • Utilized in vivo (cardiac arrest/cardiopulmonary resuscitation model) and in vitro (HK2 cells) CRS-1 models.
  • Assessed albuminuria, tubular injury, albumin filtration, and tubular uptake using microscopy and cell-based assays.

Main Results:

  • Cardiac arrest/cardiopulmonary resuscitation induced significant albuminuria and tubular cell death.
  • Exogenous albumin administration exacerbated AKI in CRS-1 models.
  • Albumin uptake by proximal tubules became saturated, and albumin directly injured kidney tubular cells in vitro.

Conclusions:

  • CRS-1 disrupts normal renal albumin handling, increasing tubular albumin exposure and causing injury, thereby worsening AKI.
  • Findings suggest albumin may be detrimental in CRS-1 and warrant careful consideration during resuscitation therapies.

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