Case report reveals a frameshift HRG mutation causing recurrent thrombosis in an end-stage renal disease patient, highlighting the importance of genetic testing before kidney transplantation.
OBJECTIVE: To report a novel pathogenic frameshift mutation in the histidine-rich glycoprotein (HRG) gene causing hereditary thrombophilia, and to discuss its clinical implications for kidney transplantation decision-making. METHODS: A 42-year-old female with end-stage renal disease on maintenance hemodialysis presented with recurrent dialysis access thrombosis. Routine coagulation tests were normal, but decreased antithrombin and elevated D-dimer prompted genetic investigation. Whole-exome sequencing was performed to identify potential genetic etiologies. RESULTS: Whole-exome sequencing identified a previously unreported pathogenic frameshift mutation in the HRG gene: c.694delG (p.E232fs). This mutation explained the patient's prothrombotic phenotype. Given the significantly elevated risk of renal allograft thrombosis associated with this condition, a multidisciplinary risk assessment led to deferral of the planned kidney transplantation. CONCLUSIONS: This case highlights the critical role of early genetic testing in patients with unexplained recurrent thrombosis. Identifying a novel HRG mutation not only establishes a rare etiology of hereditary thrombophilia but also guides personalized management and high-stakes surgical decisions, such as deferral of organ transplantation to avoid graft loss.
No takes yet. Share an insight, caveat, or question.
Lin et al. (2026) studied this question.
Synapse has enriched 5 related papers. Consider them for comparative context: