Genetic variants, including apolipoprotein L1 (APOL1), myosin-9 (MYH9), alpha-thalassemia (HBA1/HBA2 deletions), those affecting hemoglobin regulation (e.g., BCL11A), heme degradation (HMOX1) and the renin–angiotensin system genes (e.g., ACE), were identified as key risk factors of albuminuria and/or glomerular filtration in SCD populations. This evidence concerns the gene HBA2 and alpha thalassemia spectrum.