A Consultant Nephrologist and Professor of Medicine, Professor Samuel Ajayi, has said the discovery of APOL1 kidney-risk gene variants is transforming the understanding, diagnosis and treatment of chronic kidney disease among people of African ancestry, offering new hope for millions of patients across the continent.

Ajayi disclosed this while delivering a virtual lecture titled “APOL1 and Kidney Disease: A Paradigm Shift in Clinical Research and Management,” organised by the Institute for Advanced Medical Research and Training (IAMRAT) at the University College Hospital (UCH), Ibadan.

He described the discovery as one of the most significant breakthroughs in kidney disease research in recent decades, saying it has helped explain why Africans bear a disproportionate burden of chronic kidney disease.

According to him, chronic kidney disease is a growing global public health challenge, with an estimated 3.2 million people worldwide depending on dialysis or kidney transplantation, while the number requiring renal replacement therapy continues to increase annually.

Ajayi noted that the disease often develops silently and may remain undetected until it reaches an advanced stage.

He said: “Most of the changes leading to kidney disease occur while the kidneys still appear normal. If we can identify those at risk early enough, we can prevent many patients from progressing to kidney failure.”

The nephrologist explained that people of African ancestry are about four times more likely to develop chronic kidney disease than those of European descent. He also cited studies showing that the prevalence of chronic kidney disease in Nigeria is about 17.6 per cent.

While hypertension, diabetes, salt sensitivity, poor access to healthcare and environmental factors have long been linked to kidney disease in Africans, Ajayi said a landmark 2010 study identified APOL1 gene variants as a major factor responsible for the increased risk among people of Sub-Saharan African ancestry.

He explained that the APOL1 gene evolved thousands of years ago to protect Africans against African sleeping sickness, but the same genetic changes can also damage the kidneys.

“The gene developed as a defence mechanism against the parasite that causes sleeping sickness. While it protects against that infection, the same genetic changes can also damage the kidneys,” he said.

Ajayi explained that the APOL1 variants attack specialised kidney cells known as podocytes, causing protein to leak into the urine and gradually leading to chronic kidney disease.

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He, however, stressed that carrying the APOL1 variants does not automatically mean an individual will develop kidney disease, noting that infections such as HIV and COVID-19, as well as inflammation and other environmental factors, may trigger kidney damage in genetically susceptible individuals.

“The genes load the gun, but the environment pulls the trigger,” he added.

Ajayi disclosed that research has shown the high-risk APOL1 variants are common in West Africa, with about 25 per cent of Yoruba people carrying them, compared with about 50 per cent among the Igbo population, making parts of Nigeria among the regions with the highest prevalence worldwide.

He highlighted the contributions of African scientists through the Human Heredity and Health in Africa (H3Africa) Kidney Disease Research Network, a multinational collaboration investigating the role of APOL1 in chronic kidney disease and developing treatments tailored to African populations.

According to him, findings from one of the group’s major studies published in 2025 confirmed a strong association between APOL1 high-risk variants and chronic kidney disease in West Africans, while researchers continue to monitor participants to better understand disease progression and improve early intervention.

Ajayi also announced encouraging progress in the search for targeted treatment.

He said researchers are evaluating inaxaplin, an experimental oral drug designed to block the harmful effects of APOL1, in international clinical trials involving UCH, Ibadan. Early studies, he said, have shown significant reductions in protein leakage among patients with APOL1-related kidney disease.

“If the ongoing studies are successful, this medicine will change the landscape of nephrology because it targets the cause of the disease rather than simply treating its complications,” he said.

Ajayi added that the discovery has important implications for kidney transplantation, noting that doctors are increasingly screening kidney donors for APOL1 high-risk variants because kidneys carrying the variants may have poorer transplant outcomes and a higher risk of graft failure.

While acknowledging ethical and psychological concerns surrounding genetic testing, he expressed optimism that acceptance would increase as effective treatments become widely available.

He said the discovery of APOL1 has reshaped scientific understanding of chronic kidney disease and opened the door to precision medicine, offering hope for earlier diagnosis and more effective treatment for millions of Africans at risk of kidney failure.