IgA Nephropathy: Mechanism to Targeted Therapy

Clinical Mastery · Visual teaching summary · October 3, 2026

Andrew Bland, MD, FACP, FAAP

Visual summary

A proteinuria reduction is clinically useful but does not by itself settle long-term kidney benefit or safety. Explain the level of evidence supporting the treatment.

IgA Nephropathy: Mechanism to Targeted Therapy: six-panel learning summary. Full text follows below.
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An immune-complex pathway

Abnormal IgA biology, autoantibodies, immune-complex formation, and glomerular deposition contribute to injury. Downstream inflammation and fibrosis determine kidney consequences.

Recognize the phenotype

Hematuria, proteinuria, hypertension, and declining filtration vary widely. Clinical severity is not captured by the biopsy label alone.

Integrate biopsy and trajectory

Assess pathology, persistent proteinuria, kidney function, blood pressure, and competing causes. Prognostic tools complement rather than replace judgment.

Build supportive care

Optimize appropriate kidney-protective treatment and modifiable risk factors before and alongside disease-specific therapy. Monitor tolerance and response.

Compare targets carefully

APRIL, BAFF, complement, endothelin, and targeted steroid approaches intervene at different points. Confirm trial population, endpoint, approval status, and long-term evidence for each.

Keep surrogate and outcome separate

A proteinuria reduction is clinically useful but does not by itself settle long-term kidney benefit or safety. Explain the level of evidence supporting the treatment.

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