Kidney Week

Abstract: PUB197

Cancer-Associated Thrombotic Microangiopathy (CA-TMA): A Case of Uvular Squamous Cell Carcinoma (SCC) with Multiorgan Involvement

Session Information

• Publication Only

Category: Onconephrology

• 1600 Onconephrology

Authors

• Huynh, Duong B., Wyckoff Heights Medical Center, New York, New York, United States

Duong B. Huynh, MD

• Abreu, July Mariam, Wyckoff Heights Medical Center, New York, New York, United States

July Mariam Abreu

• Nguyen, Khiet T., Spartanburg Regional Healthcare System, Spartanburg, South Carolina, United States

Khiet T. Nguyen, MD

• Munoz Peralta, Ramona I., Wyckoff Heights Medical Center, New York, New York, United States

Ramona I. Munoz Peralta, MD

• Mahankali, Bhavani, Wyckoff Heights Medical Center, New York, New York, United States

Bhavani Mahankali

• Bhat, Premila, Wyckoff Heights Medical Center, New York, New York, United States

Premila Bhat, MD, FASN

• Teferici, Stela, Wyckoff Heights Medical Center, New York, New York, United States

Stela Teferici, MD

Introduction

CA-TMA is a rare paraneoplastic complication often reported with adenocarcinomas (AC). We present biopsy-proven CA-TMA causing dialysis-dependent AKI, new-onset heart failure (HF), de novo hypertension (HTN) in a patient with uvula SCC

Case Description

A 59-year-old man (T2DM, alcohol/tobacco use) presented with right neck mass, dyspnea, weight loss. A month prior, pre-op exam for neck lymph node (LN) biopsy showed normal ejection fraction (EF), negative stress test, normal creatinine. On admission, he had refractory HTN (167/97, peak 180/110 mmHg), hypoxia (SpO2 91%) with pulmonary edema/pleural effusions. Echo: EF 45%, wall motion abnormalities; EKG: bigeminy PVC. CT/MRI neck: a 4.9×7.6 cm mass encasing carotid artery. Neck LN biopsy confirmed metastatic SCC. Labs: BNP 2777, platelets 57, Hgb 10.6, Cr 2.65 mg/dL, mild proteinuria; renal image: no hydronephrosis/artery stenosis. Over a week, Cr rose to 4.85 with hemolytic evidence (MAHA): haptoglobin <20, LDH 571, reticulocytes 8.7%, mild bilirubinemia, rare schistocytes. ADAMTS13 mildly reduced; coagulation labs normal. ANA 1:1280 but C-ANCA, Ds-DNA, Coombs, SPEP, Complement, ASO, Scleroderma Ab, Antiphospholipid: negative. Dialysis started on day 7 for worsening pulmonary edema not responding to diuretics. Hematology improved spontaneously–platelets/haptoglobin normalized, LDH/ret count declined–despite dialysis dependence. Laryngoscopy biopsies confirmed invasive SCC of the uvula (primary site). Renal biopsy showed severe TMA of glomerular and arteriolar compartments. Tumor was unresectable due to encased carotid; chemotherapy planned

Discussion

CA-TMA can occur with SCC, broadening the spectrum beyond AC. Not all TMA is TTP/DIC. Here, TTP was unlikely given nonsevere/resolved thrombocytopenia, mildly reduced ADAMTS13, and renal-predominant disease, so plasmapheresis was not pursued. CA-TMA is a systemic endothelial disorder, manifested here by MAHA, AKI, refractory HTN, pulmonary edema, new HF, conduction abnormality. Hematologic improvement despite dialysis dependence reflects quiescent TMA–extensive renal microvascular occlusion reduces platelet consumption, paradoxically signaling irreversible kidney injury, not resolution. Early nephrology involvement and kidney biopsy were critical in establishing the diagnosis and guiding management and avoiding unnecessary invasive treatments like plasmapheresis