Biologics Appear Renal-Safe in Psoriasis, IL-17 Agents Show Kidney Promise

Kidney disease is one of the quieter threats shadowing people with moderate to severe psoriasis, and the biologic drugs that reshaped their treatment long carried an open question of whether they eased that threat or deepened it. A review published in Frontiers in Immunology weighed that concern and reported that biologic agents, taken as a class, did not worsen renal function in most treated patients and that interleukin (IL)-17 inhibitors may even help stabilize it.¹

Systemic Inflammation Links Skin Disease and Kidney Risk

Psoriasis has increasingly been recognized as a systemic disorder rather than a skin-limited condition, with the term "psoriatic nephropathy" introduced in 2005 to describe its renal spectrum. A meta-analysis of more than 700,000 patients found pooled HRs of 1.65 for chronic kidney disease (CKD) and 1.37 for end-stage renal disease, with risk rising alongside disease severity. In a cohort of 219 patients, 17.35% carried a moderate CKD risk, 5.02% a high risk, and 3.66% a very high risk, while microalbuminuria tracked with disease duration, severity, and psoriatic arthritis. A separate cross-sectional analysis identified CKD in 12.5% of 104 patients, concentrated among those with severe, long-standing disease.

The mechanistic rationale rested on a shared inflammatory axis. Foundational immunology work established that IL-23 drives IL-17-producing T cells to mount a self-amplifying inflammatory response in the skin, the same signaling that modern psoriasis biologics disrupt, and that this systemic inflammation was associated with comorbidities including CKD.² That overlap offered a plausible basis for how agents designed to quiet cutaneous disease could also ease inflammatory pressure on the kidney.

Biologic Classes Held Renal Function Steady

The review synthesized clinical and experimental evidence across tumor necrosis factor (TNF)-α, IL-17, and IL-12/23 inhibitors.¹ A retrospective study of 601 patients with severe psoriasis treated continuously for at least 2 years found no significant change in estimated glomerular filtration rate (eGFR) or CKD stage, regardless of biologic class; only 2.2% experienced CKD progression, and every patient receiving an anti-IL-17 agent maintained a stable CKD stage.

An observational analysis of 6294 adults initiating methotrexate or a biologic reported comparable renal safety between the 2, with CKD affecting roughly 1.5% over 5 years and an adjusted HR near unity (1.03). Among 211 patients with ankylosing spondylitis receiving anti-TNF therapy, a small eGFR decline lost clinical relevance after adjustment for confounders.

IL-17 Inhibitors Pointed Toward Renal Benefit

Beyond stability, some evidence pointed toward improvement. In patients with moderate to severe plaque psoriasis, serum creatinine fell significantly after 1 year of biologic therapy, with the degree of renal improvement tracking psoriasis remission. Case reports described patients with erythrodermic psoriasis or immunoglobulin A nephropathy and end-stage disease on hemodialysis who cleared skin lesions with secukinumab without renal deterioration and, in some cases, with modest renal recovery.

Comorbidities Shaped Renal Outcomes More Than Therapy

Across studies, patient characteristics rather than biologic exposure drove renal trajectories. Diabetes emerged as an independent risk factor for renal deterioration during treatment, alongside older age, baseline renal impairment, and dyslipidemia. A CKD cohort underscored the stakes, with each 1 mL/min/1.73 m² drop in eGFR associated with a 2.2% increase in acute kidney injury risk and an 8% increase in bleeding risk.

The authors framed the results as "a dual opportunity: effective disease control and potential renal protection," while cautioning that the mechanisms of renal benefit remained incompletely understood.

Case Reports and Small Series Temper the Conclusions

The evidence base carried notable limits. Much of it derived from case reports and small series that can flag safety signals but cannot establish causality or incidence, and longitudinal renal data in biologic-treated patients remained sparse. As a narrative review, the article synthesized heterogeneous study designs rather than pooling standardized outcomes, and its authors called for prospective, randomized trials and registries combining dermatology and nephrology data to clarify whether specific agents offer superior renal protection and whether existing kidney damage can be reversed.

For now, the authors recommended baseline and periodic renal monitoring, individualized risk assessment, and multidisciplinary care for patients with psoriasis and kidney concerns.

References

1. Tang Z, Wu J, Dong M, Li C, Wang R. Navigating renal safety in the biologic treatment of psoriasis: from immunologic mechanisms to clinical practice. Front Immunol. 2026;17:1787836. doi:10.3389/fimmu.2026.1787836
2. Hawkes JE, Yan BY, Chan TC, Krueger JG. Discovery of the IL-23/IL-17 signaling pathway and the treatment of psoriasis. J Immunol. 2018;201(6):1605-1613. doi:10.4049/jimmunol.1800013