Steroid-resistant nephrotic syndrome (SRNS) has long been a challenge for clinicians due to its poor responsiveness to
immunosuppressants, and rapid progression to
end-stage renal disease. Identifying a monogenic cause for SRNS may
lead to a better
understanding of
podocyte structure and function in the
glomerular filtration barrier. This
review focuses on
genes associated with slit
diaphragm,
actin cytoskeleton,
transcription factors, nucleus,
glomerular basement membrane,
mitochondria, and other
proteins that
affect podocyte biology.