Cell stress response impairs de novo NAD+ biosynthesis in the kidney.

The biosynthetic routes leading to de novo nicotinamide adenine dinucleotide (NAD+) production are involved in acute kidney injury (AKI), with a critical role for quinolinate phosphoribosyl transferase (QPRT), a bottleneck enzyme of de novo NAD+ biosynthesis. The molecular mechanisms determining reduced QPRT in AKI, and the role of impaired NAD+ biosynthesis in the progression to chronic kidney disease (CKD), are unknown. We demonstrate that a high urinary quinolinate-to-tryptophan ratio, an indirect indicator of impaired QPRT activity and reduced de novo NAD+ biosynthesis in the kidney, is a clinically applicable early marker of AKI after cardiac surgery and is predictive of progression to CKD in kidney transplant recipients.

Percutaneous cannulation for extracorporeal membrane oxygenation (ECMO): A method for pig experimental models.

Pigs are often used for experimental models of cardiogenic shock, cardiac arrest or acute lung injury with veno-arterial (VA) or veno-venous (VV) extracorporeal membrane oxygenation (ECMO) implementation. Percutaneous (as opposed to surgical) cannulation in experimental models has potential advantages, including, less surgical trauma or stressful stimuli and less bleeding complications when compared to open chest cannulation. However, pig anatomy can also be a challenge because of the deep location and angled anatomy of the femoral artery.

Real-Time and Non-invasive Monitoring of the Activation of the IRE1α-XBP1 Pathway in Individuals with Hemodynamic Impairment.

Many stressors that are encountered upon kidney injury are likely to trigger endoplasmic reticulum (ER) stress, subsequently activating transcriptional, translational and metabolic reprogramming. Monitoring early cellular adaptive responses engaged after hemodynamic impairment yields may represent a clinically relevant approach. However, a non-invasive method for detecting the ER stress response has not been developed.