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In 2010, researchers identified two variants of the APOL1 gene that create a three-to-five-times greater risk of kidney failure in people of African descent (Genovese et al., 2010). Sixteen years later, most patients who carry these variants are unaware. Neither do many of the clinicians treating them. African Americans represent 13% of the U.S. population but account for 32% of patients on dialysis (Kidney Health Initiative, 2024). About half carry at least one APOL1 variant. Thirteen percent carry two of the variants, placing them in the high-risk category (Nadkarni et al., 2018). These patients often present with proteinuria, rapid eGFR decline, and kidney failure at a mean age of 45, arriving at dialysis nine to twelve years earlier than their non-APOL1 counterparts (Freedman et al., 2021). Many patients are asymptomatic until the damage is advanced.

That gap between discovery and awareness is the reason I co-founded the APOL1 Action Alliance with Sharron Rouse, herself a kidney disease, dialysis, and transplant survivor. As a long-term transplant recipient living with multiple chronic conditions, I know both sides of this issue. AAA is the first nonprofit dedicated exclusively to APOL1-mediated kidney disease, bringing together genetic education, testing access, patient advocacy, and connection to precision medicine therapies now in clinical development. Our Know Your Risk campaign is taking APOL1 education into barbershops, churches, HBCUs, and nursing chapters across the Washington, D.C. region. APOL1 genetic testing is available through several clinical and laboratory partners, and in some instances may be provided at no cost.

On June 27, 2026, AAA will hold its inaugural APOL1 Empowerment Summit at the College Park Marriott in Hyattsville, Maryland, from 11:00 a.m. to 3:00 p.m. ET, with a hybrid option for virtual attendees. Register at apol1alliance.org/events. Admission is free. Your patients need you to know about APOL1. Some of them are sitting in your waiting room right now.
 

References

Freedman, B. I., Moxey-Mims, M. M., Alexander, A. A., Astor, B. C., Birdwell, K. A., Bowden, D. W., Bowen, G., Bromberg, J., Colhoun, H. M., Divers, J., Fornoni, A., Fried, L. F., Garg, A. X., Genovese, G., Groopman, E. E., Iyengar, S. K., Kaplan, B., Kao, W. H. L., Kimmel, P. L., … Sedor, J. R. (2021). APOL1 long-term kidney transplantation outcomes network (APOLLO): Design and rationale. Journal of the American Society of Nephrology, 32(2), 299–312. https://doi.org/10.1681/ASN.2020091282

Genovese, G., Friedman, D. J., Ross, M. D., Lecordier, L., Uzureau, P., Freedman, B. I., Bowden, D. W., Langefeld, C. D., Oleksyk, T. K., Uscinski Knob, A. L., Bernhardy, A. J., Hicks, P. J., Nelson, G. W., Vanhollebeke, B., Winkler, C. A., Kopp, J. B., Pays, E., & Pollak, M. R. (2010). Association of trypanolytic ApoL1 variants with kidney disease in African Americans. Science, 329(5993), 841–845. https://doi.org/10.1126/science.1193032

Kidney Health Initiative. (2024). Roadmap for advancing awareness, genetic testing, and clinical studies of APOL1 kidney disease. American Society of Nephrology. https://khi.asn.org

Nadkarni, G. N., Gignoux, C. R., Engel, S. M., Adeyemo, A. A., & Parsa, A. (2018). Association of APOL1 risk variants with kidney disease in a population of African ancestry. The New England Journal of Medicine, 378(18), 1690–1698. https://doi.org/10.1056/NEJMoa1710425

APOL1 Genetic Testing Resources

• Arkana Laboratories. (n.d.). APOL1 genetic testing program. https://www.arkanalabs.com
• Atrium Health Wake Forest Baptist. (n.d.). APOL1 genotyping services. Wake Forest University School of Medicine.
• Labcorp. (n.d.). APOL1 genotyping test. https://www.labcorp.com
• Mayo Clinic Laboratories. (n.d.). APOL1 genotyping, varies. https://www.mayocliniclabs.com

The post The Gene You Have Never Heard Of Is Driving Kidney Failure in Black Communities appeared first on Multiple Chronic Conditions.

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As discussed in the podcast, the implications of TeleNCC extend beyond operational guidance. They speak directly to improving patient outcomes and reducing disparities in access to specialized care. Facilities that adopt these standards can strengthen clinical decision-making, enhance patient safety, and create more consistent care pathways for complex neurologic emergencies. Dr. Yakoby underscores that this work is not only about technology, but about ensuring that every patient, regardless of location, benefits from evidence-based, expert neurocritical care.

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By Rosa Hart, BSN, RN, SCRN, FLAA

When a stroke occurs, the brain enters a period of rapid, dramatic change. In the acute phase, the immediate priority is saving as much brain tissue as possible, because every minute without blood flow costs nearly 1.9 million neurons. This is why the 2026 AHA/ASA Acute Ischemic Stroke Guidelines place such strong emphasis on speed; from mobile stroke units arriving at the scene faster, to expanded eligibility for clot-busting medications and mechanical thrombectomy reaching patients who previously had no options. Once the brain is stabilized and reperfusion is achieved, a natural window of heightened neurological responsiveness opens. The surviving tissue around the injury site becomes especially receptive to rehabilitation, making the early weeks and months after stroke the most intensive period for motor, cognitive, and swallowing recovery. This is the time when the brain is, in many ways, primed and ready to rewire.

What happens after that window is where the story gets more complicated, and where too many patients are told, incorrectly, that they will have reached a plateau. Chronic stroke recovery, defined as recovery beginning roughly six months or more after the event, does slow down; the brain is no longer in that same state of heightened plasticity. But slower is not the same as stopped. The 2026 guidelines now formally recognize technologies that directly address this reality. Brain-computer interfaces (BCI) paired with functional electrical stimulation have demonstrated lasting motor improvements even in chronic stroke survivors, by decoding the brain’s own movement intentions and using them to trigger real physical response, essentially rebuilding the conversation between the brain and the body. Vagal nerve stimulation paired with rehabilitation has shown a threefold improvement in upper extremity function compared to rehabilitation alone; and for patients living with dysphagia long after their stroke, pharyngeal electrical stimulation, now carrying a Class 2a guideline recommendation, offers a pathway to restoring swallowing function that was previously considered out of reach.

The throughline in all of this is neuroplasticity, the brain’s remarkable, lifelong capacity to reorganize itself. Neuroplasticity does not have an expiration date; it has conditions. It requires the right stimulation, the right intensity, and the right consistency over time. What the 2026 guidelines signal is that science is catching up to what many stroke survivors and their families have seen, that recovery is not a destination you arrive at and then leave behind. It is an ongoing process, and the tools available to support it are more powerful than ever. Whether a patient is three days out from their stroke or three years out, the message from the evidence is the same; the brain does not give up, and neither should we.

Rosa Hart is a stroke certified registered nurse with the American Association of Neuroscience Nurses

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