Glomerular disease, manifesting as steroid resistant nephrotic syndrome and/or persistent haematuria or albuminuria, is the second most common cause of chronic kidney disease in children and adults in Singapore and worldwide. To date, there are about 500 genes known to cause monogenic kidney diseases, of which 100 are known to cause glomerular diseases. About 20-30 percent of children with steroid-resistant nephrotic syndrome (SRNS) and 10 percent of adults with focal segmental glomerulosclerosis have genetic causes; this number rises to 60-90 percent if there are predisposing risk factors like positive family history, extrarenal manifestations and/or glomerular basement membrane changes. Among these, Alport syndrome genes (COL4A3, COL4A4, COL4A5) are the most common genetic causes. Genetic testing in glomerular diseases has numerous clinical impacts on the patient, such as directing immunosuppressive strategies, negate the need for kidney biopsy, kidney donor selection and cascade testing. Early introduction of renin-angiotensin-aldosterone system (RAAS) blockade can delay CKD progression especially in male patients with X-linked Alport Syndrome. Early initiation of RAAS blockade in these patients at the microalbuminuria stage or even prior to the onset of any urinary anomalies can delay kidney failure by >15 years. Such impactful treatment is possible only if there is early diagnosis based on genetic testing. Furthermore, Coenzyme Q10 (CoQ10) deficiency can also cause genetic glomerulopathy, and treatment with coenzyme Q10 supplements can decrease proteinuria and delay CKD progression.