APOL1 G1 — kidney disease risk variant
One copy of the APOL1 G1 risk allele detected.
You have one copy of the APOL1 G1 kidney risk version. On its own, one copy doesn't meaningfully raise your risk.
One copy alone does not meaningfully elevate kidney disease risk. The clinical effect emerges with two risk alleles (G1/G1, G1/G2, or G2/G2).
One copy on its own doesn't meaningfully raise your kidney disease risk. The clinical effect only really shows up when you carry two risk copies in any combination (G1/G1, G1/G2, or G2/G2).
What this means
APOL1 evolved to protect against trypanosome parasites (sleeping sickness). The G1 and G2 variants are protective against trypanosomes but, when inherited in pairs, substantially increase risk of several forms of kidney disease. The effect is "recessive": one copy is fine, two copies (G1/G1, G1/G2, or G2/G2) raises risk by several-fold. APOL1 testing is increasingly part of pre-kidney-transplant evaluation.
APOL1 is a gene that evolved to fight off the trypanosome parasite that causes sleeping sickness, which is why the G1 and G2 versions are common in people with recent sub-Saharan African ancestry. The trade-off is that having two risk copies — any combination of G1 and G2 — raises the risk of several kidney diseases several-fold. One copy is essentially fine; two copies is what matters. APOL1 testing is becoming a routine part of kidney transplant evaluation. Most people with two copies still don't develop kidney disease, but the risk shift is large enough that blood pressure and diabetes control matter even more than usual.
Caveats
- Effect is recessive — single-allele carriers have little additional risk.
- The effect is large *relative* to baseline but most carriers never develop kidney disease.
- Blood pressure and diabetes control remain the dominant modifiable factors.
Populations
- Found almost exclusively in people of recent sub-Saharan African ancestry