Abstract: FR-PO0437
Hypertensive Emergency Unmasking Renal Thrombotic Microangiopathy in a Young Patient
Session Information
- AKI: Case Reports - TMA, Vasculitis, Immune-Mediated Injury, and Systemic Disease
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Ohonba, Nosagie, Icahn School of Medicine at Mount Sinai, New York, New York, United States
- Sanchez Trinidad, Jeanette Marie, Icahn School of Medicine at Mount Sinai, New York, New York, United States
Introduction
Hypertensive emergency can cause severe renal injury through endothelial dysfunction, arteriolar damage, and thrombotic microangiopathy (TMA). This presentation may mimic primary TMA, vasculitis, glomerulonephritis, or pulmonary-renal syndrome, particularly when accompanied by acute kidney injury, hematuria, proteinuria, and respiratory failure. Renal biopsy is critical in distinguishing hypertension-mediated vascular injury from immune-mediated kidney disease.
Case Description
A 39-year-old man with long-standing hypertension and CKD, baseline creatinine approximately 1.5 mg/dL, presented with hypertensive emergency complicated by acute hypoxemic respiratory failure, pulmonary edema, and severe oliguric AKI. Admission creatinine was 9.47 mg/dL. Urinalysis showed hematuria and proteinuria, prompting concern for pulmonary-renal syndrome or glomerulonephritis.
Extensive serologic evaluation was unrevealing, including ANA, ANCA, anti-GBM, anti-dsDNA, complements, hepatitis serologies, and SPEP. Renal artery imaging showed no stenosis. Blood pressure was initially controlled with intravenous antihypertensives, followed by transition to a multidrug oral regimen. Due to persistent renal failure with uremia, metabolic acidosis, and volume overload, he was initiated on hemodialysis. Renal biopsy demonstrated advanced chronic vascular injury consistent with TMA-pattern vascular injury and hypertensive nephrosclerosis, without evidence of active immune-complex glomerulonephritis or vasculitis or atypical HUS. He remained dialysis dependent on discharge.
Discussion
This case highlights hypertensive emergency as a cause of severe renal vascular injury and biopsy-proven TMA-pattern damage in a young patient. In malignant hypertension, abrupt pressure elevation can exceed renal autoregulatory capacity, causing endothelial injury, fibrinoid arteriolar damage, ischemia, and microvascular thrombosis. Renal ischemia may further activate the renin-angiotensin-aldosterone system, worsening hypertension and kidney injury.
Hypertension-associated TMA is uncommon but recognized, reported in approximately 20–30% of patients with malignant hypertension, with broader estimates ranging from 14–46% depending on diagnostic criteria and biopsy use. This case emphasizes the importance of distinguishing hypertension-mediated TMA from primary TMA, complement-mediated disease, vasculitis, and glomerulonephritis, as treatment and prognosis differ significantly.