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IgAN for Nephrology Nurses and NPs
IgAN: An Overview and Call to Action for Nephrology Nurses and NPs

Released: April 29, 2025

Expiration: April 28, 2026

Kelly B. Chen
Kelly B. Chen, BSN, MSN, NP
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Key Takeaways
  • Immunoglobulin A nephropathy (IgAN) is an immune-mediated chronic kidney disease (CKD) that can lead to kidney failure.
  • Like CKD attributed to other causes, the basis of IgAN management is supportive care to slow or prevent disease progression.
  • Reducing proteinuria to <1 g/day is a surrogate marker of improved kidney outcome and a reasonable treatment target in IgAN.
  • Nephrology nurses and nurse practitioners should be prepared to use new and emerging medications that target IgAN pathogenic processes to reduce proteinuria and improve outcomes.

In the United States, there are too few nephrologists to readily care for all patients with CKD, acute kidney injury, end-stage renal disease, kidney transplants, and other nephrology-related complications. The clinical impact of this shortage is compounded by the high levels of care often needed by nephrology patients, who on average have 5 comorbid conditions, take 5-15 daily medications, and have follow-up appointments on 30- to 90-day cycles. Consequently, nephrology nurses and nurse practitioners (NPs) have increasingly larger roles caring for patients with CKD, including management of patients with more complicated disease courses. IgAN affects approximately 200,000 people in the United States, making it an uncommon condition in the general population. However, it is one of the most common forms of primary glomerulonephritis and a leading cause of CKD and kidney failure, with an estimated 20% to 50% of patients progressing to end-stage renal disease, so it is important that nephrology nurses and NPs understand its pathophysiology and management. 

What causes IgAN?
IgAN is an immune-mediated disease. The pathogenesis of IgAN is currently thought to involve 4 sequential “hits”:

  1. An increase in serum levels of pathogenic IgA1 antibodies with a galactose-deficient hinge region (Gd-IgA1) that can stick together to form polymers
  2. Production of anti–Gd-IgA1 autoantibodies
  3. Formation of immune complexes of polymeric Gd-IgA1 and anti–Gd-IgA1 antibodies that deposit in the glomerular mesangium
  4. Mesangial cell activation and proliferation, leading to inflammation

Mesangial inflammation affects podocyte structure and function, leads to worsening kidney function, and can even cause kidney failure. IgAN generally manifests with proteinuria as well as hematuria, which are both signs of renal inflammation.

How is IgAN diagnosed?
Biopsy with immunohistologic identification of glomerular IgA deposits is the gold standard for IgAN diagnosis. In addition, histological scoring of mesangial hypercellularity (M), endocapillary hypercellularity (E), segmental glomerulosclerosis (S), tubular atrophy/interstitial fibrosis (T), and crescents (C) should be performed to determine an Oxford Classification of IgAN MEST-C score.  The MEST-C score, with other disease characteristics, should be used to assess prognosis. The International IgAN Prediction Tool is particularly helpful for calculating risk of IgAN progression based on disease characteristics.  

The presence of symptoms, such as high blood pressure, swelling in the legs, and blood in the urine, should lead a healthcare professional (HCP) to refer a patient to a nephrology specialist, where kidney biopsy could be performed if needed. If there are no symptoms, or maybe mild symptoms like microscopic hematuria or slightly elevated blood pressure, the need for nephrology referral would typically be identified as proteinuria or hematuria in a lab test. Ultimately, it is up to the HCP to refer the patient to a nephrology specialist as soon as possible, particularly because biopsy and IgAN diagnosis open the door for access to optimal care, including novel therapies.

What is the general approach to care?
Patients who receive a diagnosis of IgAN start on supportive care approaches typical for CKD, including blood-pressure management, angiotensin-converting enzyme inhibitor (ACEi) or angiotensin receptor blocker (ARB) therapy, lifestyle modification, and cardiovascular risk management. Ideally, all patients with IgAN who have proteinuria > 0.5 g/day should receive an ACEi or ARB for renal protection, regardless of whether they have hypertension, to reduce the risk of CKD progression. If a patient does not tolerate an ACEi or ARB, or cannot take one for other reasons, an alternative agent for renal protection, such as an SGLT2 inhibitor, might be considered. Lifestyle modification includes interventions that are also associated with reducing cardiovascular risk, such as dietary adjustments (eg, sodium restriction, heart-healthy choices), smoking cessation, weight control, and regular physical activity. However, many patients are not well-informed regarding lifestyle management, so their care may start with education on topics such as recognizing which foods are high in sodium.

How do you know if treatment is effective? What is the treatment goal?
According to current IgAN treatment guidelines from Kidney Disease | Improving Global Outcomes (KDIGO), reducing proteinuria to under 1 g/day is a surrogate marker of improved kidney outcome and a reasonable treatment target. In addition, patients with proteinuria >0.75-1.00 g/day despite 90 or more days of optimized supportive care are considered to be at high risk for IgAN progression. The KDIGO guidelines recommend that other approaches, such as enrollment in a clinical trial or a course of glucocorticoid therapy, should be considered and discussed with these patients.  

Regulatory agencies, including the FDA, now recognize proteinuria reduction as a surrogate marker for clinical outcomes in IgAN, which is expected to reduce the length of time and number of patients required for clinical trials.  Proteinuria reduction is also being used as a treatment target and marker of improved kidney outcome. Informing patients about proteinuria as a treatment goal has become a key part of their IgAN education. Although serum creatinine levels have been used to assess disease progression, patients and HCPs need to be aware of the shift to using proteinuria as a key indicator of progression risk.

New therapies and a call to action
Bench research based on the multihit hypothesis of IgAN pathogenesis has led to the development of therapies targeting different pathophysiologic processes, which is exciting for HCPs and patients. Because there is still limited experience with the therapies, questions remain regarding their use in practice. As HCPs wait for guideline recommendations for new therapies, it is crucial that they stay up-to-date with available evidence to inform the “best fit” for patients in what ultimately will be a shared decision. In addition, regular monitoring and communication will be needed so therapy can be adjusted to optimize the balance between outcomes and adverse effects.

Nephrology nurses and NPs are not exempt from this call to action. Because IgAN is a CKD, it is in their scope of practice, and many will encounter patients with this disease. In my practice, I see 1-2 patients with IgAN per month. I educate them about the disease, what it means for their lives, and what they can expect. I address therapies that need to be started right away, explain the importance of their therapies and treatment adherence, coordinate labs, and track supportive care. In addition, nephrology nurses and NPs are on the frontline to help patients get access to novel therapies and enrolled in associated programs, such as Risk Evaluation Mitigation Strategies [REMS] programs and patient assistance programs. In this regard, nephrology nurses and NPs, particularly those who become REMS providers, should be well-positioned to facilitate patient care and prevent treatment delays. Because nephrology nurses and NPs have vital roles in caring for patients with IgAN, it is essential that they have the latest information on IgAN as a disease state and advancements in IgAN management.

Join us on May 3, 2025, for a live satellite symposium to learn more about IgAN and improving patient outcomes.

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