People with IgA nephropathy gradually lose kidney function over decades. Therapies could slow it, not stop it. On July 7, 2026, the FDA approved the first medicine to intervene in the immunological origin of the disease: Trutakna (atacicept) from Vera Therapeutics blocks the two cytokines that trigger pathological antibody production, destroying kidneys.
What IgA nephropathy is and who it affects
IgA nephropathy (IgAN) is the world's most common primary glomerulonephritis, an inflammation of the kidney corpuscles. According to a long-term analysis of 1,012 patients published in PLOS ONE, the kidney function survival rate after 30 years is only 50.3 percent. About 10 percent of all dialysis patients worldwide have IgAN as their underlying disease.
The mechanism is immunological: B cells produce galactose-deficient immunoglobulin A1 (Gd-IgA1). The immune system forms autoantibodies against this faulty protein, which together with the Gd-IgA1 form immune complexes. These deposit in the glomeruli and trigger chronic inflammation and scarring. Elevated levels of two cytokines from the tumor necrosis factor family drive this process: B-cell activating factor (BAFF) and A proliferation-inducing ligand (APRIL). Studies in Frontiers in Nephrology and Kidney International show their levels correlate with disease severity.
Why all previous therapies miss the root
Until 2026, there were three FDA-approved therapies for IgAN. None interrupted the BAFF/APRIL-driven B-cell cascade that produces pathological Gd-IgA1:
- Tarpeyo (budesonide, approval 2021, full approval 2023): Delayed-release corticosteroid that preferentially releases in the distal small intestine, where some of the pathological IgA originates. Acts anti-inflammatory locally, does not affect BAFF and APRIL.
- Sparsentan (Filspari, 2023): Dual receptor blocker for endothelin-1 and angiotensin II that lowers filtration pressure in the glomeruli and thus reduces proteinuria. No immunological intervention.
- Iptacopan (Fabhalta, 2024): Inhibits complement factor B in the inflammation cascade. One level deeper than BAFF/APRIL but still downstream of B-cell activation.
Atacicept is a TACI-Fc fusion protein that binds and neutralizes both BAFF and APRIL. It intervenes at the point from which all downstream processes depend. It is the first substance to interrupt the autoimmune cascade in IgAN at its source. The injection of 150 milligrams occurs once weekly subcutaneously, administered by the patient via an autoinjector.
What the ORIGIN-3 study data show
The FDA approval is based on a pre-specified interim analysis of the ongoing Phase 3 trial ORIGIN 3. According to Vera Therapeutics, patients in the Trutakna group achieved a 46 percent reduction in proteinuria from their baseline after 36 weeks and a statistically highly significant 42 percent reduction compared to placebo (p less than 0.0001). Eighty-one percent of treated patients showed hematuria remission, the disappearance of blood in urine, which is a sign of active glomerulitis in IgAN. Surprisingly, severe adverse events occurred in 0.5 percent of the atacicept group versus 5 percent in the placebo group.
The approval is an accelerated approval (Accelerated Approval) based on the surrogate endpoint of proteinuria reduction, not on the clinically decisive endpoint of kidney function retention over time. The FDA can revoke an Accelerated Approval if confirmation data do not show clinical benefit. The process gives patients faster access while the confirmation study is ongoing.
Trutakna compared to other IgAN therapies
The IgAN therapy field has evolved from a niche to the most active development area in nephrology between 2021 and 2026. What all three previous therapies have in common: they intervene in downstream processes. Trutakna is the first substance to directly interrupt BAFF/APRIL-mediated B-cell activation, preventing all downstream complexes of Gd-IgA1 and autoantibodies from forming in the first place.
In earlier Phase 2b atacicept studies published in Kidney International, significant reductions of Gd-IgA1 itself of up to 60 percent compared to placebo at the 75 mg dose demonstrated the mechanistic promise of the substance. The American patient network NephroCure called the approval, per its press release of July 7, 2026, a "turning point for patients who previously only had the choice between slowing and dialysis." One caveat remains: Trutakna is classified as a specialty biologic, which typically means high list prices in the US. Vera Therapeutics has not yet announced an official price.
What Q3 2026 decides about full approval
Vera Therapeutics announced it will publish primary endpoint data on kidney function retention from the confirmation portion of ORIGIN 3 in the third quarter of 2026. These data measure whether atacicept slows or stops the decline in glomerular filtration rate (eGFR), the only endpoint that clinically determines whether patients live longer without dialysis. If the data come out positive, the FDA will convert the accelerated approval to a regular approval. If negative, withdrawal threatens.
For the IgAN field, positive confirmation would be a signal beyond Trutakna: it would be the first direct evidence that an upstream intervention in the B-cell cascade translates into measurable kidney function retention. This would establish the BAFF/APRIL axis as a validated therapeutic target for an entire family of new drugs.