ReviewAmerican journal of physiology. Renal physiology2019
APOL1 polymorphisms and kidney disease: loss-of-function or gain-of-function?
Review in American journal of physiology. Renal physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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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.
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Who cites it
27 citing papers in PubMed, 34 citations in OpenAlex.
- APOL1 kidney disease: a critical narrative review of molecular mechanisms, clinical heterogeneity, and the emerging therapeutic landscape.International urology and nephrology · 2026Review
- Erythroid Atypical Chemokine Receptor 1 Deficiency Aggravates Immune-Mediated Kidney Disease.Journal of the American Society of Nephrology : JASN · 2026Article
- Molecular Mechanisms of APOL1-Associated Kidney Disease.International journal of molecular sciences · 2026Review
- A novelRenal failure · 2025Article
- Article
- Review
- Carrying APOL1 G1 allele is associated with cardiovascular complications during COVID-19 in an admixed population.Human genomics · 2025Article
- Multiethnic prevalence of theClinical kidney journal · 2025Article
- IFI16 Is Indispensable for Promoting HIF-1α-Mediated APOL1 Expression in Human Podocytes under Hypoxic Conditions.International journal of molecular sciences · 2024Article
- Novel Therapies inKidney international reports · 2023Review
- The Roles of Fatty Acids and Apolipoproteins in the Kidneys.Metabolites · 2022Review
- The evolving story of apolipoprotein L1 nephropathy: the end of the beginning.Nature reviews. Nephrology · 2022Review
- APOL1 Risk Variants, Acute Kidney Injury, and Death in Participants With African Ancestry Hospitalized With COVID-19 From the Million Veteran Program.JAMA internal medicine · 2022Article
- Cholesterol Metabolism in Chronic Kidney Disease: Physiology, Pathologic Mechanisms, and Treatment.Advances in experimental medicine and biology · 2022Article
- Article
- Emerging Insights Into Chronic Renal Disease Pathogenesis in Hypertension From Human and Animal Genomic Studies.Hypertension (Dallas, Tex. : 1979) · 2021Review
- The First Thousand Days: Kidney Health and Beyond.Healthcare (Basel, Switzerland) · 2021Review
- The glomerular filtration barrier: a structural target for novel kidney therapies.Nature reviews. Drug discovery · 2021Review
- APOL1 risk variants and the development of HIV-associated nephropathy.The FEBS journal · 2021Review
- APOL1 genotype-associated morphologic changes among patients with focal segmental glomerulosclerosis.Pediatric nephrology (Berlin, Germany) · 2021Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The mechanism that explains the association of APOL1 variants with nondiabetic kidney diseases in African Americans remains unclear. Kidney disease risk is inherited as a recessive trait, and many studies investigating the intracellular function of APOL1 have indicated the APOL1 variants G1 and G2 are associated with cytotoxicity. Whether cytotoxicity results from the absence of a protective effect conferred by the G0 allele or is induced by a deleterious effect of variant allele expression has not be conclusively established. A central issue hampering basic biology studies is the lack of model systems that authentically replicate APOL1 expression patterns. APOL1 is present in humans and a few other primates and appears to have important functions in the kidney, as the kidney is the primary target for disease associated with the genetic variance. There have been no studies to date assessing the function of untagged APOL1 protein under native expression in human or primate kidney cells, and no studies have examined the heterozygous state, a disease-free condition in humans. A second major issue is the chronic kidney disease (CKD)-associated APOL1 variants are conditional mutations, where the disease-inducing function is only evident under the appropriate environmental stimulus. In addition, it is possible there may be more than one mechanism of pathogenesis that is dependent on the nature of the stressor or other genetic variabilities. Studies addressing the function of APOL1 and how the CKD-associated APOL1 variants cause kidney disease are challenging and remain to be fully investigated under conditions that faithfully model known human genetics and physiology.
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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.