ReviewNephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association2017
Therapeutics for APOL1 nephropathies: putting out the fire in the podocyte.
Review in Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Genome-wide association studies suggest that APOL1-environment interactions more likely trigger kidney disease in African Americans with nondiabetic nephropathy than strong APOL1-second gene interactions.Kidney international · 2018Pooled it
- Article
- Age and the Diurnal Oscillatory Features of the Human Chronobiome.medRxiv : the preprint server for health sciences · 2026Article
- Association of atherogenic index of plasma with cardiovascular disease mortality in patients with type 2 diabetes mellitus and diabetic kidney disease: a cross-sectional study.BMC cardiovascular disorders · 2025Article
- Clinical implications of apolipoprotein L1 testing in patients with focal segmental glomerulosclerosis: a review of diagnostic and prognostic implications.Annals of medicine and surgery (2012) · 2025Review
- Mechanistic Insights Into Redox Damage of the Podocyte in Hypertension.Hypertension (Dallas, Tex. : 1979) · 2025Review
- Black Patients Equally Benefit From Renal Genetics Evaluation but Substantial Barriers in Access Exist.Kidney international reports · 2023Article
- Article
- APOL1 Risk Variants Associated with Serum Albumin in a Population-Based Cohort Study.American journal of nephrology · 2022Article
- Article
- Kidney disease and APOL1.Human molecular genetics · 2021Review
- A focus on the association of Apol1 with kidney disease in children.Pediatric nephrology (Berlin, Germany) · 2021Review
- A bidirectional Mendelian randomization study supports causal effects of kidney function on blood pressure.Kidney international · 2020Article
- Apolipoprotein L1-Specific Antibodies Detect Endogenous APOL1 inside the Endoplasmic Reticulum and on the Plasma Membrane of Podocytes.Journal of the American Society of Nephrology : JASN · 2020Article
- Racial disparities in end-stage renal disease in a high-risk population: the Southern Community Cohort Study.BMC nephrology · 2019Article
- Apolipoprotein L1, Cardiovascular Disease and Hypertension: More Questions than Answers.Cardiology clinics · 2019Review
- Discovery of endoplasmic reticulum calcium stabilizers to rescue ER-stressed podocytes in nephrotic syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Antisense oligonucleotide treatment ameliorates IFN-γ-induced proteinuria in APOL1-transgenic mice.JCI insight · 2019Article
- Recruitment of APOL1 kidney disease risk variants to lipid droplets attenuates cell toxicity.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Worldwide Frequencies of APOL1 Renal Risk Variants.The New England journal of medicine · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 5 institutions in 1 country.
Funding
Abstract
APOL1 nephropathies comprise a range of clinical and pathologic syndromes, which can be summarized as focal segmental glomerulosclerosis, in various guises, and arterionephrosclerosis, otherwise known as hypertensive kidney diseases. Current therapies for these conditions may achieve therapeutic targets, reduction in proteinuria and control of blood pressure, respectively, but often fail to halt the progressive decline in kidney function. It appears that current therapies fail to address certain underlying critical pathologic processes that are driven, particularly in podocytes and microvascular cells, by the APOL1 renal risk genetic variants. Mechanisms hypothesized to be responsible for APOL1 variant-associated cell injury can be summarized in five domains: increased APOL1 gene expression, activation of inflammasomes, activation of protein kinase R, electrolyte flux across plasma or intracellular membranes, and altered endolysosomal trafficking associated with endoplasmic reticulum stress. We briefly review the available evidence for these five mechanisms and suggest possible novel therapeutic approaches.
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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.