Chronic kidney disease (CKD) isn’t a one-size-fits-all condition. It’s a progressive loss of kidney function that can stem from various causes—diabetes, hypertension, autoimmune disorders, genetic factors, and more. These underlying causes, or subtypes, influence how the disease progresses and how it’s best treated. Tailoring treatment to the subtype is key to managing symptoms, slowing progression, and reducing complications.

Diabetic Kidney Disease (DKD)

For people with diabetes, diabetic kidney disease (DKD) is the most common CKD subtype. Treatment here focuses on tight blood sugar control and renin-angiotensin system (RAS) inhibition. Drugs like ACE inhibitors and ARBs are standard not just for lowering blood pressure, but also for reducing proteinuria and protecting kidney function. 

Recently, SGLT2 inhibitors like dapagliflozin and empagliflozin have become a game-changer. Originally developed for glucose control, these drugs now show strong evidence of slowing CKD progression in diabetic patients—even in those with lower kidney function.

Hypertensive Nephrosclerosis

When CKD is primarily due to high blood pressure, treatment hinges on keeping blood pressure low—often aiming below 130/80 mmHg. Again, ACE inhibitors or ARBs are preferred, particularly for patients with proteinuria. Glycemic control isn’t a factor here, so medication choices focus on cardiovascular risk reduction.

Glomerulonephritis (GN)

Glomerulonephritis (GN) is a group of diseases causing inflammation of the kidney’s filtering units. These subtypes—such as IgA nephropathy, lupus nephritis, or membranous nephropathy—often require immunosuppressive therapy. For example, lupus nephritis treatment typically involves corticosteroids and immunosuppressants like mycophenolate mofetil or cyclophosphamide.

Contrast that with IgA nephropathy, where supportive care with blood pressure meds may be enough in mild cases, and steroids are reserved for high-risk patients. Each GN subtype has its own protocol, making biopsy and subtype identification essential.

Polycystic Kidney Disease (PKD)

Polycystic kidney disease (PKD)—categorized as either autosomal-dominant (ADPKD) or autosomal-recessive (ARPKD)—is a genetic subtype where cysts form and grow over time, enlarging the kidneys and eventually impairing function. The only FDA-approved disease-modifying drug is tolvaptan, which slows cyst growth. 

Tolvaptan doesn’t benefit most other CKD subtypes. Lifestyle changes and blood pressure control are also important, but the genetic basis of PKD shifts the focus toward targeting cyst growth specifically.

Alport Syndrome

Alport syndrome involves genetic mutations in collagen that damage tiny filtering units in the kidneys and can scar your kidney tissue. It leads to progressive kidney failure and sometimes hearing loss. There’s no cure, but early use of ACE inhibitors has been shown to delay ESRD onset. Genetic testing is key to diagnosis, especially in families with a history of kidney disease and hearing issues.

FSGS (Focal Segmental Glomerulosclerosis)

Focal segmental glomerulosclerosis (FSGS) is another rare but aggressive glomerular disease. Some forms are genetic; others are caused by secondary factors like obesity or drug toxicity. Treatment varies—steroids or calcineurin inhibitors are used for primary FSGS, while addressing the underlying cause is critical for secondary forms.

Takeaway

CKD is not one disease, and treatment should reflect that. Whether it’s optimizing glucose control, adjusting immunosuppression, or slowing cyst development, the underlying cause of kidney damage shapes the strategy. Personalizing care to the CKD subtype not only improves outcomes but also helps avoid unnecessary or ineffective treatments. As more subtype-specific therapies emerge, understanding your CKD’s root cause is more important than ever.

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