Markers of Kidney Tubule Dysfunction and Major Adverse Kidney Events.

Acute kidney injury Biomarker Major adverse kidney events Tubules

Journal

Nephron
ISSN: 2235-3186
Titre abrégé: Nephron
Pays: Switzerland
ID NLM: 0331777

Informations de publication

Date de publication:
2023
Historique:
received: 04 05 2023
accepted: 09 07 2023
pubmed: 1 8 2023
medline: 1 8 2023
entrez: 31 7 2023
Statut: ppublish

Résumé

Serum creatinine and albuminuria are primary markers of glomerular function and injury, respectively. Tubular secretion, acid-base homeostasis, protein reabsorption, among other tubular functions, are largely ignored. This mini-review aimed to discuss how two tubular functions, secretion, and acid-base homeostasis are associated with major adverse kidney events (MAKEs). Proximal tubular secretion is an essential function that allows the elimination of endogenous substances and drugs. Recently discovered endogenous markers in urine and plasma allow a noninvasive way of assessing tubular secretion markers. Several studies have found an association between these markers and a higher risk of chronic kidney disease (CKD) progression and mortality. In a study we recently performed among patients with CKD and at risk of cardiovascular events, lower tubular secretion was associated with an increased risk of acute kidney injury and metabolic acidosis, independent of baseline eGFR and albuminuria. The kidney tubules also play a crucial role in acid-base homeostasis. Although the standard clinical assessment of acidosis consists of measuring serum bicarbonate, urinary ammonium excretion decreases before over metabolic acidosis. Urinary ammonium excretion is associated with CKD progression, a higher risk of kidney failure, and an increased mortality risk, independent of baseline eGFR and albuminuria. Novel biomarkers of kidney tubular health consistently associate with MAKEs, above and beyond baseline eGFR, albuminuria, and other CKD risk factors. Tubular markers may provide new opportunities to improve kidney prognosis, drug dosing, and monitoring for adverse events.

Sections du résumé

BACKGROUND BACKGROUND
Serum creatinine and albuminuria are primary markers of glomerular function and injury, respectively. Tubular secretion, acid-base homeostasis, protein reabsorption, among other tubular functions, are largely ignored. This mini-review aimed to discuss how two tubular functions, secretion, and acid-base homeostasis are associated with major adverse kidney events (MAKEs).
SUMMARY CONCLUSIONS
Proximal tubular secretion is an essential function that allows the elimination of endogenous substances and drugs. Recently discovered endogenous markers in urine and plasma allow a noninvasive way of assessing tubular secretion markers. Several studies have found an association between these markers and a higher risk of chronic kidney disease (CKD) progression and mortality. In a study we recently performed among patients with CKD and at risk of cardiovascular events, lower tubular secretion was associated with an increased risk of acute kidney injury and metabolic acidosis, independent of baseline eGFR and albuminuria. The kidney tubules also play a crucial role in acid-base homeostasis. Although the standard clinical assessment of acidosis consists of measuring serum bicarbonate, urinary ammonium excretion decreases before over metabolic acidosis. Urinary ammonium excretion is associated with CKD progression, a higher risk of kidney failure, and an increased mortality risk, independent of baseline eGFR and albuminuria.
KEY MESSAGES CONCLUSIONS
Novel biomarkers of kidney tubular health consistently associate with MAKEs, above and beyond baseline eGFR, albuminuria, and other CKD risk factors. Tubular markers may provide new opportunities to improve kidney prognosis, drug dosing, and monitoring for adverse events.

Identifiants

pubmed: 37524063
pii: 000531946
doi: 10.1159/000531946
doi:

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

713-716

Informations de copyright

© 2023 S. Karger AG, Basel.

Auteurs

Alexander L Bullen (AL)

Nephrology Section, Veterans Affairs San Diego Healthcare System, La Jolla, California, USA.
Division of Nephrology-Hypertension, Department of Medicine, University of California San Diego, San Diego, California, USA.

Alma Fregoso (A)

School of Medicine, University of California San Diego, San Diego, California, USA.

Simon B Ascher (SB)

Kidney Health Research Collaborative, Department of Medicine, San Francisco Veterans Affairs Health Care System and University of California, San Francisco, California, USA.
Division of Hospital Medicine, University of California Davis, Sacramento, California, USA.

Michael G Shlipak (MG)

Kidney Health Research Collaborative, Department of Medicine, San Francisco Veterans Affairs Health Care System and University of California, San Francisco, California, USA.

Joachim H Ix (JH)

Nephrology Section, Veterans Affairs San Diego Healthcare System, La Jolla, California, USA.
Division of Nephrology-Hypertension, Department of Medicine, University of California San Diego, San Diego, California, USA.

Dena E Rifkin (DE)

Nephrology Section, Veterans Affairs San Diego Healthcare System, La Jolla, California, USA.
Division of Nephrology-Hypertension, Department of Medicine, University of California San Diego, San Diego, California, USA.

Classifications MeSH