ArticleJCI insight2022
Cell stress response impairs de novo NAD+ biosynthesis in the kidney.
Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- States of quinolinic acid excess in urine: A systematic review of human studies.Frontiers in nutrition · 2022Pooled it
- Association of dietary niacin intake with cardiovascular-kidney-metabolic syndrome risk and mortality.American journal of preventive cardiology · 2026Article
- Effects of NAD⁺ repletion with Nicotinamide riboside on obesity-induced chronic kidney disease and renal cell lipotoxicity.Scientific reports · 2026Article
- Protection against cisplatin-induced acute kidney injury by hellgrammite extract: insights from comprehensive metabolomics.Frontiers in pharmacology · 2026Article
- NAD + in fatty liver disease: mechanistic insights and associated targets.Cell biology and toxicology · 2025Review
- Cockayne syndrome mice reflect human kidney disease and are defective in de novo NAD biosynthesis.Cell death and differentiation · 2025Article
- NADNature biomedical engineering · 2025Article
- Pediatric acute kidney injury is associated with impairment in nicotinamide adenine dinucleotide (NAD+) metabolism.Pediatric nephrology (Berlin, Germany) · 2025Observational
- NADTrends in molecular medicine · 2025Review
- Multiomics analysis unveils an inosine-sensitive DNA damage response in neurogenic bladder after spinal cord injury.JCI insight · 2025Article
- What do we know about micronutrients in critically ill patients? A narrative review.JPEN. Journal of parenteral and enteral nutrition · 2025Review
- A metagenome-wide study of the gut virome in chronic kidney disease.Theranostics · 2025Article
- Derangement in Nicotinamide Adenine Dinucleotide Metabolism is Observed During Acute Kidney Injury Among Male Agricultural Workers at Risk for Mesoamerican Nephropathy.Kidney international reports · 2024Article
- Tubular insulin-induced gene 1 deficiency promotes NADEMBO molecular medicine · 2024Article
- The Role of Mitochondrial Sirtuins (SIRT3, SIRT4 and SIRT5) in Renal Cell Metabolism: Implication for Kidney Diseases.International journal of molecular sciences · 2024Review
- Exposome and Metabolome Analysis of Sugarcane Workers Reveals Predictors of Kidney Injury.Kidney international reports · 2024Article
- Effects of Physical Cues on Stem Cell-Derived Extracellular Vesicles toward Neuropathy Applications.Biomedicines · 2024Review
- U-shaped association between dietary niacin intake and chronic kidney disease among US elderly: a nationwide cross-sectional study.Frontiers in endocrinology · 2024Article
- Unraveling the nexus of NAD+ metabolism and diabetic kidney disease: insights from murine models and human data.Frontiers in endocrinology · 2024Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 8 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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. We also provide evidence that the endoplasmic reticulum (ER) stress response may impair de novo NAD+ biosynthesis by repressing QPRT transcription. In conclusion, NAD+ biosynthesis impairment is an early event in AKI embedded with the ER stress response, and persistent reduction of QPRT expression is associated with AKI to CKD progression. This finding may lead to identification of noninvasive metabolic biomarkers of kidney injury with prognostic and therapeutic implications.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.