A new study advances the search for accurate acute kidney injury blood markers

Johns Hopkins Medicine researchers report advances in their hunt for more reliable and easier-to-obtain markers to assist predict, manage, and assess therapy of acute kidney injury (AKI) using cells from kidney biopsies. AKI, which is characterized by severe inflammation, can result in rapid loss of kidney function, and clinicians have long sought markers that alert them to AKI status without the need for invasive kidney biopsies.

The findings of this study, which examined 120,985 nuclei from kidney biopsy samples from 24 people, were published on December 13th in the journal Science Translational Medicine.

According to the National Library of Medicine, acute kidney injury (AKI) affects 15% to 20% of hospitalized patients, putting them at a higher risk of in-hospital death and a progressive form of chronic kidney disease that may eventually require dialysis or transplant. The new study was created to address a shortage of noninvasive assessments of maladaptive proximal tubule (PT) repair. As the body’s immune system responds to AKI, PT is characterized by severe inflammation. This PT maladaptation process provides an opportunity to identify noninvasive markers in blood or urine that can predict AKI and manage treatment more accurately and safely.

“Because AKI patients are critically ill and frequently in the ICU, performing kidney biopsies is not feasible due to safety concerns.” “There is an urgent need to identify tissue signatures in the blood or urine that can tell us how kidneys are healing,” says Chirag Parikh, MD, Ph.D., director of the division of nephrology at Johns Hopkins Medicine and the study’s corresponding author.

The Kidney Precision Medicine Project provided a single-nucleus ribonucleic acid (RNA) sequencing technique that was utilized to characterize 120,985 nuclei from kidney biopsy samples from 17 people with AKI and seven healthy participants. The discovery of PT maladaptation markers necessitated the investigation of plasma proteomes in patients undergoing cardiac surgery as well as marathon runners who may have suffered from exercise-related AKI. Researchers discovered maladaptive PT cells in AKI patients and were able to identify six distinct protein markers. Increased transforming growth factor-2 (TGFB2), collagen type XXIII-1 (COL23A1), and X-linked neuroligin 4 (NLGN4X) and decreased plasminogen (PLG), ectonucleotide pyrophosphatase/phosphodiesterase 6 (ENPP6), and protein C (PROC) were among the protein markers discovered.

According to Parikh, “the newer tools available to interrogate the genetic messages in the kidney biopsy tissue and find the corresponding products (proteins) in the blood enables us to track the condition of the kidney during the course of AKI.”

Parikh notes, “the availability of the panel of such proteins is equivalent of a “liquid biopsy” and could assist with therapeutic development as well as assist clinicians with AKI management when a biopsy is not feasible.” Researchers may have moved one step closer to treating AKI as a result of the findings of this study.

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