Kidney disease, leading to kidney failure, afflicts disproportionately more black people than white people. Thus, there is a huge burden of kidney health care costs among black people all over the world.
For instance, in the US, although the black population is only 13% to 14% of the total, black people account for one third of the patients with end-stage kidney disease requiring dialysis or transplantation.
Hypertension, diabetes and HIV, which also cause kidney failure, tend to cause more severe kidney damage and rapid deterioration in black people than in white people.
For many decades, researchers wondered why these differences exist. It was only in the last decade and a half that reasons began to emerge. Research found that black people have a genetic variation which emerged to protect the body from a parasitic disease called trypanosomiasis, or sleeping sickness. This disease was common in the west African region. The gene prompts the immune system to produce a protein that dissolves the membrane of the parasite, destroying it.
Over time, the parasite developed resistance to the gene variant’s effects. Then new variants emerged to restore immunity against the new forms of the parasite. But this came with a drawback: individuals who have the new gene variants (called APOL1 G1 and G2) also have an increased risk of developing kidney disease.
Over the last two decades there has been growing evidence that these variants cause kidney damage in African Americans, even if they don’t have diabetes.
However, until recently this link between the gene and kidney disease had not been confirmed or fully described among people on the African continent—where the genetic variant first evolved.
This was the aim of a study that began over a decade ago in Africa, called Human Heredity and Health in Africa (H3Africa), by the Kidney Disease Research Network.
As part of this effort, our recently published study found that having APOL1 G1 or G2 significantly increased the risk of having kidney disease compared to those who do not have the gene variants.
This finding might lead to improvements in screening for risk of kidney disease, reveal more about how kidney disease affects west Africans in particular, and result in treatment opportunities.
The current prevalence of kidney disease is 13.7% in Nigeria and 28% among Ghanaians.
Our research
The Kidney Disease Research Network assembled researchers in Nigeria, Ghana, South Africa, Ethiopia and Kenya. Among the aims of the research were to study and describe 8,000 cases and controls, and conduct genetic studies associated with kidney diseases. Over 40 researchers collaborated on the project, including nephrologists, geneticists, genetic statisticians and laboratory scientists.
The study enrolled 8,355 participants in Ghana and Nigeria, including 4,712 with kidney disease of varying severity and 2,777 without kidney disease. Extensive and sophisticated genetic studies were done on the materials obtained from the participants with their consent.
The gene variants that could cause kidney disease are called APOL1 G1 or G2. The variant that does not cause kidney disease is called G0. Individual people can have different combinations of these three variants.
We found that the APOL1 genes are more common among west African populations, including Nigerians and Ghanians, than among populations from other regions of Africa.
In our study, 43% (3,592) participants had just one of the variants, while 29.7% (2,481) participants had double variants of APOL1. Participants with double G1 or G2 variants were more likely to have chronic kidney disease than those with one of those variants. And participants with one variant were more likely to have chronic kidney disease than those who had none.
Our study thus confirmed what was found in people of African descent in the US: the genetic origin underpinning the excess risk of developing kidney disease among black Africans, wherever they live.
What our findings mean
The study established, for the first time, the association of APOL1 with chronic kidney disease in sub-Saharan Africa.
This opens up opportunities:
- improving the survival of kidney transplant patients by screening donors who may have the high-risk variants
- targeted treatment of those with high-risk variants.
A new drug, Inaxaplin, which inhibits APOL1 function, reduces proteinuria, the hallmark of kidney disease. This opens the possibility of treating patients with APOL1 mediated chronic disease with medications. Studies are continuing in this area.
This article is republished from The Conversation under a Creative Commons license. Read the original article.
Citation:
West Africans have a high risk of kidney disease. New study confirms genetic cause (2025, February 12)
retrieved 12 February 2025
from https://medicalxpress.com/news/2025-02-west-africans-high-kidney-disease.html
This document is subject to copyright. Apart from any fair dealing for the purpose of private study or research, no
part may be reproduced without the written permission. The content is provided for information purposes only.
Kidney disease, leading to kidney failure, afflicts disproportionately more black people than white people. Thus, there is a huge burden of kidney health care costs among black people all over the world. For instance, in the US, although the black population is only 13% to 14% of the total, black people account for one third of the patients with end-stage kidney disease requiring dialysis or transplantation. Hypertension, diabetes and HIV, which also cause kidney failure, tend to cause more severe kidney damage and rapid deterioration in black people than in white people. For many decades, researchers wondered why these differences exist. It was only in the last decade and a half that reasons began to emerge. Research found that black people have a genetic variation which emerged to protect the body from a parasitic disease called trypanosomiasis, or sleeping sickness. This disease was common in the west African region. The gene prompts the immune system to produce a protein that dissolves the membrane of the parasite, destroying it. Over time, the parasite developed resistance to the gene variant’s effects. Then new variants emerged to restore immunity against the new forms of the parasite. But this came with a drawback: individuals who have the new gene variants (called APOL1 G1 and G2) also have an increased risk of developing kidney disease. Over the last two decades there has been growing evidence that these variants cause kidney damage in African Americans, even if they don’t have diabetes. However, until recently this link between the gene and kidney disease had not been confirmed or fully described among people on the African continent—where the genetic variant first evolved. This was the aim of a study that began over a decade ago in Africa, called Human Heredity and Health in Africa (H3Africa), by the Kidney Disease Research Network. As part of this effort, our recently published study found that having APOL1 G1 or G2 significantly increased the risk of having kidney disease compared to those who do not have the gene variants. This finding might lead to improvements in screening for risk of kidney disease, reveal more about how kidney disease affects west Africans in particular, and result in treatment opportunities. The current prevalence of kidney disease is 13.7% in Nigeria and 28% among Ghanaians. The Kidney Disease Research Network assembled researchers in Nigeria, Ghana, South Africa, Ethiopia and Kenya. Among the aims of the research were to study and describe 8,000 cases and controls, and conduct genetic studies associated with kidney diseases. Over 40 researchers collaborated on the project, including nephrologists, geneticists, genetic statisticians and laboratory scientists. The study enrolled 8,355 participants in Ghana and Nigeria, including 4,712 with kidney disease of varying severity and 2,777 without kidney disease. Extensive and sophisticated genetic studies were done on the materials obtained from the participants with their consent. The gene variants that could cause kidney disease are called APOL1 G1 or G2. The variant that does not cause kidney disease is called G0. Individual people can have different combinations of these three variants. We found that the APOL1 genes are more common among west African populations, including Nigerians and Ghanians, than among populations from other regions of Africa. In our study, 43% (3,592) participants had just one of the variants, while 29.7% (2,481) participants had double variants of APOL1. Participants with double G1 or G2 variants were more likely to have chronic kidney disease than those with one of those variants. And participants with one variant were more likely to have chronic kidney disease than those who had none. Our study thus confirmed what was found in people of African descent in the US: the genetic origin underpinning the excess risk of developing kidney disease among black Africans, wherever they live. The study established, for the first time, the association of APOL1 with chronic kidney disease in sub-Saharan Africa. This opens up opportunities: A new drug, Inaxaplin, which inhibits APOL1 function, reduces proteinuria, the hallmark of kidney disease. This opens the possibility of treating patients with APOL1 mediated chronic disease with medications. Studies are continuing in this area. This article is republished from The Conversation under a Creative Commons license. Read the original article. Citation: This document is subject to copyright. Apart from any fair dealing for the purpose of private study or research, no
Our research
What our findings mean
West Africans have a high risk of kidney disease. New study confirms genetic cause (2025, February 12)
retrieved 12 February 2025
from https://medicalxpress.com/news/2025-02-west-africans-high-kidney-disease.html
part may be reproduced without the written permission. The content is provided for information purposes only.
