Case Presentation: A 33-year-old woman with stage 4 CKD, uncontrolled hypertension, obesity status post lap banding, and medication nonadherence presented with two days of worsening dyspnea, orthopnea, and PND. She denied chest pain or infectious symptoms but had missed antihypertensives for a week. Her blood pressure was 246/166 mmHg, and she was hypoxic. Chest X-ray showed pulmonary edema. Labs demonstrated leukocytosis, anemia, creatinine 8.8 mg/dL, BUN 84 mg/dL, eGFR 6 mL/min/1.73m², nephrotic-range proteinuria, hypoalbuminemia, and significant electrolyte abnormalities. NT-proBNP was 25,867. She was admitted to the ICU and started on nicardipine and bumetanide drips but had poor diuretic response and required hemodialysis. Renal function failed to recover, and she progressed to ESRD. Given the rapid decline, a kidney biopsy was performed, revealing chronic thrombotic microangiopathy (TMA) with 15 of 30 globally sclerotic glomeruli and >80% interstitial fibrosis and tubular atrophy, consistent with irreversible hypertensive nephrosclerosis and secondary FSGS. Secondary hypertension workup was negative. Her course was complicated by new blurry vision. MRI showed multiple T2/FLAIR hyperintensities in the periventricular and juxtacortical white matter and a small focus of diffusion restriction, attributed to hypertensive microvascular infarcts. Neurologic evaluation was otherwise unrevealing, and she was started on aspirin.
Discussion: TMA is a rare but severe complication of malignant hypertension, driven by endothelial injury and microvascular thrombosis. Hypertension-associated TMA carries a poor renal prognosis, with most patients progressing to ESRD despite therapy. This patient’s extensive glomerulosclerosis and >80% fibrosis reflected chronic, irreversible injury at presentation, limiting the potential for renal recovery even with aggressive blood pressure control. Preserved ADAMTS13 activity and the absence of severe thrombocytopenia supported hypertension-induced TMA rather than primary TMA. Malignant hypertension-related TMA carries the poorest prognosis among all TMA etiologies, with 83.3% of patients progressing to ESRD despite therapeutic intervention. Her neurologic findings highlight the systemic microvascular burden of chronic hypertension. White matter changes and small infarcts arise from sustained endothelial dysfunction and predict future stroke risk and cognitive decline. Early recognition and strict blood pressure control remain crucial to preventing these complications. This case underscores the importance of multidisciplinary care, close follow-up, and addressing medication nonadherence, which significantly decreases the risk of hypertensive emergencies. Given her young age and permanent ESRD, renal transplant evaluation will be necessary, though recurrent hypertensive injury remains a concern.
Conclusions: This case emphasizes the need to recognize chronic TMA as a severe complication of uncontrolled hypertension, particularly in patients with underlying CKD. The irreversible vascular and glomerular injury in this patient highlights the importance of early and aggressive blood pressure control and close follow-up to prevent catastrophic end-organ damage.