Финеренон замедлил прогрессирование болезни почек при генетической форме FSGS

Finerenone may provide adjunctive renoprotection for patients with genetically mediated focal segmental glomerulosclerosis (FSGS), according to a case report detailing what may be the first reported use of the nonsteroidal mineralocorticoid receptor antagonist in  COQ8B -associated disease published in  Kidney Medicine. In a 35-year-old woman with homozygous  COQ8B -related FSGS, finerenone was associated with a reduction in her urine albumin-to-creatinine ratio (uACR) from 6460 mg/g to 1430 mg/g over 12 months. It also helped slow her annual estimated glomerular filtration rate decline from -9.55 to -6.77 mL/min/1.73 m². The patient initially developed persistent proteinuria after preeclampsia during her first pregnancy in 2017. By January 2022, her uACR was 980 mg/g despite normal kidney function. A clear family history of early kidney failure included 2 siblings who underwent kidney transplantation at ages 34 and 36 years. Biopsy identified FSGS with 40% cortical interstitial fibrosis and tubular atrophy; immunofluorescence was negative, and electron microscopy showed focal podocyte foot process effacement. Corticosteroids for 6 months and tacrolimus through May 2024 failed to control progressive proteinuria. Empagliflozin and renin-angiotensin-aldosterone system blockade also produced limited benefit. Genetic testing subsequently identified the c.532C>T p.(Arg178Trp) missense variant in exon 7 of  COQ8B  in probable homozygosity. A trial of coenzyme Q10 was discontinued because of gastrointestinal intolerance, fatigue, and lethargy. Off-label finerenone was initiated at 10 mg daily in May 2024 and increased to 20 mg daily in November. Baseline creatinine was 1.40 mg/dL, estimated glomerular filtration rate was 50 mL/min/1.73 m², and potassium was 4.8 mmol/L. Albuminuria improved and remained partially stabilized for approximately 1 year.  The patient experienced only 1 episode of mild hyperkalemia, with potassium reaching 5.3 mmol/L, which did not require discontinuation of treatment. Rituximab administered in February 2025 also failed to improve proteinuria or kidney function. Symptomatic hypotension ultimately necessitated finerenone discontinuation in June 2025, and attempts to restart treatment were unsuccessful. Subsequently, creatinine increased from 1.56 mg/dL in June 2025 to 2.22 mg/dL in January 2026, while uACR rose from 1430 to 4860 mg/g. The temporal relationship between finerenone exposure, improvement, and subsequent deterioration after withdrawal supports further investigation but does not establish causality. The proposed rationale for therapeutic finerenone involves mineralocorticoid receptor-mediated oxidative stress, inflammation, and profibrotic signaling, pathways that may compound mitochondrial dysfunction and podocyte injury caused by COQ8B-related coenzyme Q10 deficiency. Because podocytes have high energy requirements and depend heavily on oxidative phosphorylation, impaired coenzyme Q10 biosynthesis can increase reactive oxygen species and promote podocyte loss.  Finerenone is a mineralocorticoid receptor antagonist that has demonstrated antifibrotic and anti-inflammatory effects through the reduction of oxidative stress, specifically in diabetic kidney disease. However, its role in hereditary podocytopathies such as hereditary FSGS has not been fully explored. “[I]n this genetically confirmed case of  COQ8B -associated FSGS, finerenone therapy was associated with attenuation of kidney function decline and partial stabilization of proteinuria,” stated the authors. “This report supports further investigation of mineralocorticoid receptor antagonists and trajectory-based outcome measures in hereditary podocytopathies.” This article originally appeared on Rare Disease Advisor References: Aljishi M, Khogali M, Alhussain T, Alnashmi T.  Finerenone use in coenzyme Q8B-related focal segmental glomerulosclerosis.  Kidney Med. Published online August 13, 2026. doi:10.1016/j.xkme.2026.101502