Outcome of Biopsy-Proven Kidney Thrombotic Microangiopathy (TMA) Based on Etiology and Management: A Case Series
Background: Thrombotic microangiopathy is a rare complex condition with a wide variety of etiologies. It is characterized by thrombocytopenia, anemia and organ dysfunction. There is limited data available that compares prognosis based on etiologies and management. Despite its rarity, we have seen a considerable number of cases in our institution. We conducted a retrospective analysis of those biopsy proven cases, their etiologies, differences in treatment plans and outcome. The study aims to identify patterns in TMA outcomes based on different causes and management strategies. Methods: Biopsy proven cases of TMA in AMC were identified between 2018-2024. Their etiology, management and clinical outcomes were reviewed as a part of retrospective case series. Specifically, the focus is on assessing changes in creatinine levels, the need for dialysis, and the utility of therapeutic agents, such as eculizumab, on renal function. Results: 11 patients out of the 33 were either hereditary or mixed (hereditary or acquired), indicating involvement of complement mediated-TMA. 10 pts were started on complement inhibitors. Improvement was seen in 70% of the patients with improvement in kidney function. Details in Table 5 Conclusion: Despite its infrequency, TMA presents a significant challenge in clinical practice due to its heterogenous etiology and variable response to treatment. Complement inhibitors have shown to improve outcome in biopsy proven complement mediated cases of TMA.
Authors
- Aman Pal
- Sameer Mehta (ORCID: https://orcid.org/0000-0002-5588-905X)
- Aliyah Audil (ORCID: https://orcid.org/0009-0000-9189-8941)
- Sidrah Abid
Institutions
- Albany Medical Center Hospital (US)
Publication Details
- Journal
- Journal of the American Society of Nephrology
- Published
- 2025-10-01
- DOI
- https://doi.org/10.1681/asn.2025gf13c21j
- Primary Topic
- Complement system in diseases
- Type
- article
- Field-Weighted Citation Impact
- 0.00