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Nephrology · IgA Nephropathy

Current Standard of Care and Treatment Options

At a Glance

IgA nephropathy treatment uses layered kidney protection: a low-sodium diet and blood pressure control with an ACE inhibitor or ARB form the foundation, while SGLT2 inhibitors, sparsentan, or targeted-release budesonide may be added when risk remains high.

Treating IgA Nephropathy (IgAN) has evolved significantly in recent years. The current standard of care follows a “layered” approach, starting with a strong foundation of supportive care and adding disease-specific therapies if the risk of kidney decline remains high [1][2].

The primary goal of all these treatments is to protect your kidney function by reducing the amount of protein leaking into your urine (proteinuria). Current guidelines aim for a proteinuria level below 0.5 g/day, though reaching levels below 0.3 g/day may offer even greater long-term protection [3][1].

Layer 1: The Foundation (Supportive Care)

Before starting newer drugs, every patient should have “optimized” supportive care. This foundation alone can significantly slow the progression of the disease for many people.

  • RAAS Blockade: This is the use of ACE inhibitors (like lisinopril) or ARBs (like losartan). These drugs do more than just lower blood pressure; they reduce the pressure inside the kidney’s filters, which helps stop protein from leaking out [4][2]. Doctors aim for the “maximally tolerated dose” to get the most benefit. Monitoring of blood potassium and creatinine is required. ACE inhibitors and ARBs are generally avoided during pregnancy.
  • Blood Pressure Control: Guidelines suggest aiming for a properly standardized clinic systolic blood pressure below 120 mm Hg when tolerated to protect the kidneys from further strain [1].
  • Dietary Sodium Restriction: Limiting salt to less than 2 grams of sodium per day (about one teaspoon of salt) is essential, as salt can interfere with the effectiveness of your blood pressure medications [1].

Layer 2: Kidney Protection (SGLT2 Inhibitors)

If your risk remains high despite the foundation, your doctor may add an SGLT2 inhibitor (such as dapagliflozin or empagliflozin). Originally used for diabetes, these drugs have been shown to provide significant “kidney-protective” benefits for people with IgAN, even if they do not have diabetes [5][6].

  • What to expect: When you first start an SGLT2 inhibitor, it is normal to see a small, temporary dip in your kidney function numbers (eGFR). This is usually a sign the drug is working to reduce pressure in the kidney [7], but a large or persistent fall should be evaluated.
  • Side effects: Common risks include an increased chance of genital yeast infections, volume depletion, and more rarely, a serious condition called ketoacidosis. These medications are often temporarily stopped during periods of severe illness or surgery (“sick day rules”) [8][9].

Layer 3: Disease-Specific Therapies

For patients who still have high levels of protein in their urine (typically >0.5 g/day or >1 g/day) despite Layer 1 and 2, newer targeted therapies may be considered [1].

Sparsentan (Filspari)

Sparsentan is a newer type of medication called a Dual Endothelin-Angiotensin Receptor Antagonist (DEARA). Unlike other drugs that are added to your ACE inhibitor or ARB, Sparsentan is usually used instead of them [10]. It must not be co-administered with an ACE inhibitor or ARB.

  • How it works: It blocks two different pathways that cause kidney stress and scarring. In clinical trials, it reduced proteinuria by approximately 40% to 50% more than standard ARB treatment alone [11][10].
  • Monitoring: Because it can affect fluid levels and liver function, patients require regular blood tests and monitoring for low blood pressure, hyperkalemia, or swelling (edema) [11]. It carries serious warnings for embryo-fetal toxicity, requiring strict pregnancy prevention and contraception.

Targeted-Release Budesonide (Tarpeyo/Nefecon)

This is a specialized steroid designed to release its medicine in a specific part of the gut (the ileum) to target mucosal immunity [12].

  • How it works: By targeting the gut, it seeks to modulate the immune activity that causes IgAN. It is typically taken for a 9-month course [12].
  • Side effects: While it is designed to be more “targeted” than traditional steroids, it remains a corticosteroid, meaning patients must be monitored for adrenal suppression, increased infection risk, mood or metabolic effects, swelling (edema), high blood pressure, and acne [12][13].

Finding Your Path

These therapies are not “one-size-fits-all.” Eligibility depends on your specific eGFR levels, your biopsy results (MEST-C score), and how your body responds to the foundational treatments [1][2]. Your care team will use these tools to select the options that are right for your risk profile. Additionally, systemic glucocorticoids (like prednisone) may be considered in carefully selected high-risk patients, while rapidly progressive disease may require urgent specialist treatment with glucocorticoids plus cyclophosphamide.

Common questions in this guide

What is the usual starting treatment for IgA nephropathy?
Treatment usually begins with optimized supportive care. This may include an ACE inhibitor or ARB at the highest dose you can safely tolerate, careful blood pressure control, and limiting sodium to reduce protein leakage and protect kidney function.
What protein level in urine is the treatment target?
Current guidance generally aims to reduce protein in the urine below 0.5 grams per day. A level below 0.3 grams per day may provide even more long-term kidney protection, but your target should be individualized with your healthcare team.
Can an SGLT2 inhibitor help if I do not have diabetes?
Yes. Dapagliflozin and empagliflozin may protect kidney function in some people with IgA nephropathy even without diabetes, especially when risk remains high after supportive care. A small temporary decline in the kidney filtration estimate can occur when treatment starts, but a large or lasting decline needs prompt review.
Can I take sparsentan with an ACE inhibitor or ARB?
No. Sparsentan is generally used instead of an ACE inhibitor or ARB and must not be taken with either one. Your clinician should supervise the switch and monitor blood pressure, potassium, fluid retention, and liver function.
How long is targeted-release budesonide used for IgA nephropathy?
The usual course is nine months. Although the medicine is designed to release in the gut, it is still a corticosteroid, so monitoring may include adrenal effects, infections, blood pressure, swelling, mood, and metabolic changes.
What lifestyle and monitoring steps are part of IgA nephropathy care?
Limiting sodium to less than 2 grams per day, tracking home blood pressure, and attending regular laboratory checks are important parts of care. A standardized clinic systolic blood pressure below 120 mm Hg may be targeted when tolerated, but your clinician should set the goal for you.

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Questions to Ask Your Doctor

Curated prompts to bring to your next appointment.

  1. 1.What is my current proteinuria level, and what is the specific target number we are aiming for with my treatment?
  2. 2.Am I on the 'maximally tolerated' dose of my ACE inhibitor or ARB, and if not, can we safely increase it?
  3. 3.Given my latest eGFR and protein levels, am I a candidate for adding an SGLT2 inhibitor to my regimen?
  4. 4.If we consider Sparsentan, how will we transition from my current ACE inhibitor or ARB, and how often will my blood pressure and potassium be checked?
  5. 5.For Targeted-release Budesonide, what side effects (like swelling or acne) should I watch for, and how long would the course of treatment last?

References

References (13)
  1. 1

    IgA Nephropathy in Adults: A Review.

    Stoneman S, Teh JW, O'Shaughnessy MM

    JAMA 2026; (335(9)):799-813 doi:10.1001/jama.2025.25020.

    PMID: 41587026
  2. 2

    IgA Nephropathy: Mechanisms, Risk Stratification, and Precision Therapy.

    Alobaidi S

    Diagnostics (Basel, Switzerland) 2026; (16(9)) doi:10.3390/diagnostics16091259.

    PMID: 42121963
  3. 3

    The Association of Proteinuria Target Achievement Timing and Stability with Adverse Kidney Outcomes among Patients with IgA Nephropathy: A Cohort Study.

    Li R, Hui M, Chen P, et al.

    American journal of nephrology 2026; (57(4)):409-425 doi:10.1159/000547868.

    PMID: 40769132
  4. 4

    Successful targeting of the alternative complement cascade with iptacopan for the treatment of IgA nephropathy: a case report.

    Ingold L, Dickenmann M, Menter T, et al.

    Swiss medical weekly 2025; (155()):4435 doi:10.57187/s.4435.

    PMID: 40811131
  5. 5

    Seven suggestions for successful SGLT2i use in glomerular disease - a standalone CKD therapy?

    McQuarrie EP, Gillis KA, Mark PB

    Current opinion in nephrology and hypertension 2022; (31(3)):272-277 doi:10.1097/MNH.0000000000000786.

    PMID: 35220316
  6. 6

    SGLT2 Inhibitors in Glomerulonephritis: Beyond Nephroprotection?

    Del Vecchio L, Peiti S, Pucci Bella G, Locatelli F

    Journal of clinical medicine 2025; (14(10)) doi:10.3390/jcm14103533.

    PMID: 40429528
  7. 7

    Prescribing SGLT2 Inhibitors in Patients With CKD: Expanding Indications and Practical Considerations.

    Yau K, Dharia A, Alrowiyti I, Cherney DZI

    Kidney international reports 2022; (7(7)):1463-1476 doi:10.1016/j.ekir.2022.04.094.

    PMID: 35812300
  8. 8

    SGLT2 Inhibition for CKD and Cardiovascular Disease in Type 2 Diabetes: Report of a Scientific Workshop Sponsored by the National Kidney Foundation.

    Tuttle KR, Brosius FC, Cavender MA, et al.

    Diabetes 2021; (70(1)):1-16 doi:10.2337/dbi20-0040.

    PMID: 33106255
  9. 9

    Cardiovascular and renal efficacy and safety of sodium-glucose cotransporter-2 inhibitors in patients without diabetes: a systematic review and meta-analysis of randomised placebo-controlled trials.

    Tsai WC, Hsu SP, Chiu YL, et al.

    BMJ open 2022; (12(10)):e060655 doi:10.1136/bmjopen-2021-060655.

    PMID: 36241355
  10. 10

    Sparsentan in patients with IgA nephropathy: a prespecified interim analysis from a randomised, double-blind, active-controlled clinical trial.

    Heerspink HJL, Radhakrishnan J, Alpers CE, et al.

    Lancet (London, England) 2023; (401(10388)):1584-1594 doi:10.1016/S0140-6736(23)00569-X.

    PMID: 37015244
  11. 11

    Efficacy and safety of sparsentan versus irbesartan in patients with IgA nephropathy (PROTECT): 2-year results from a randomised, active-controlled, phase 3 trial.

    Rovin BH, Barratt J, Heerspink HJL, et al.

    Lancet (London, England) 2023; (402(10417)):2077-2090 doi:10.1016/S0140-6736(23)02302-4.

    PMID: 37931634
  12. 12

    Efficacy and safety of a targeted-release formulation of budesonide in patients with primary IgA nephropathy (NefIgArd): 2-year results from a randomised phase 3 trial.

    Lafayette R, Kristensen J, Stone A, et al.

    Lancet (London, England) 2023; (402(10405)):859-870 doi:10.1016/S0140-6736(23)01554-4.

    PMID: 37591292
  13. 13

    Efficacy and safety of budesonide for the treatment of IgA nephropathy: a systematic review and meta-analysis.

    Nabi R, Ansab M, Hussain A, et al.

    International urology and nephrology 2026; (58(9)):3795-3811 doi:10.1007/s11255-026-05043-1.

    PMID: 41649715

This page is for informational purposes only and does not constitute medical advice. Your nephrologist or other healthcare professional should help you choose and monitor treatment for your specific IgA nephropathy risk and health needs.