KIDNEY LIMITED THROMBOTIC MICROANGIOPATHY (TMA) and AUTOIMMUNE DISEASE

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KIDNEY LIMITED THROMBOTIC MICROANGIOPATHY (TMA) and AUTOIMMUNE DISEASE

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Co-author 1

ARCHANA VASHISHT archana_vashisht18@yahoo.co.in Essen Health Care Nephrology Newyork United States *

Co-author 2

Petras Lohana petrasd2@nychhc.org North Central Bronx Hospital Internal medicine Newyork United States -

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Introduction

TMA describes a specific pathologic lesion involving microvascular thrombosis and is characterized by hemolytic anemia and thrombocytopenia. While TTP and HUS are primary forms, secondary TMAs can occur with pregnancy, medications, malignancy, infections and systemic autoimmune diseases, often affecting the kidneys.

Methods

A woman in her mid-40s with Chronic kidney disease (CKD) 3A (baseline S.Cr 1.3mg/dl), morbid obesity, well-controlled HIV, prior cervical SCC (stage IIB, post-chemotherapy 2021–2022), and left ovarian teratoma admitted with c/o abdominal bloating, leg edema, and hypotension (80/52 mmHg). Labs showed S.Cr 2.2 mg/dl, platelets 135000/µL, Hemoglobin 7.3 g/dl, UPCR 1.4 g/g. Urine microscopy showed granular cast with RBCs. FeNa 2%, FeUrea 23.8%. Echo showed small pericardial effusion with EF 55%. Patient underwent large volume paracentesis for ascites. Workup revealed non–portal hypertensive ascites (SAAG <1.1), negative malignancy and infection evaluation. Hepatitis B core antibody was positive but other Hepatitis serology were negative. Follow up labs showed ANA 1:1280, Anti-RNP 100 CU, aPTT 30.7s, PT 13.7s, INR 1.2, D-dimer 5010 ng/mL, LDH 232 U/L, ESR 141 mm/hr, ADAMTS13 activity 54%, C4 levels were normal, C3 levels were variable. Given renal abnormalities, serositis, cytopenia and positive autoimmune antibodies, renal biopsy was performed to explore possible underlying systemic autoimmune disorder. Renal biopsy demonstrated chronic TMA and moderate Focal Segmental Glomerulosclerosis (FSGS) with mild fibrosis. She was treated with pulse steroids, azathioprine, and hydroxychloroquine, resulting in marked improvement in ascites, cytopenia and proteinuria. S.cr trended back to 1.3 mg/dl post hemodynamic stability. Bilateral leg edema was likely secondary to hypoalbuminemia (Serum albumin 2.2 gm/dl).

Results

Despite normal coagulation studies, the markedly elevated D-dimer suggested ongoing microvascular thrombosis and endothelial injury. Absence of schistocytes, normal bilirubin and normal haptoglobin was consistent with chronic biopsy findings, and indicating a more chronic or smoldering process rather than acute microangiopathic hemolysis. Patient was diagnosed with kidney-limited chronic TMA as a concurrent cause of CKD, alongside obesity-related FSGS. The TMA etiology was presumed to be Lupus spectrum autoimmune disease despite negative dsDNA and normal complements. On Rheumatology follow up patient was diagnosed with quiescent SLE. Patient remains on immunosuppression. AKI was deemed secondary to pre renal etiology.

Conclusion

This case highlights kidney-limited TMA, an often overlooked diagnosis requiring kidney biopsy. Unlike systemic TMA, it may present without hemolysis and reflects a chronic form with high risk of End Stage Kidney Disease, emphasizing the need for early recognition and timely treatment of underlying etiology for TMA.

References

1) Kidney Res Clin Pract. 2022;41(5):524–532. doi:10.23876/j.krcp.22.010
2) Mod Pathol. 2024;100690. doi:10.1016/j.modpat.2024.100690
3) Am J Hematol. 2022;97(11):E426–E429.
4) J Clin Med. 2022;11(11):3124. doi:10.3390/jcm11113124

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