Kidney-limited thrombotic microangiopathy caused by relative hypertension in a hemodynamically vulnerable kidney allograft, mimicking malignant hypertension.

Malignant hypertension is traditionally defined as severe systemic blood pressure elevation accompanied by end-organ damage. In kidney transplant recipients, however, kidney allografts may be particularly vulnerable to hypertensive injury even at lower blood pressure levels, owing to impaired autoregulation associated with denervation and calcineurin inhibitor exposure. We report a 52-year-old kidney transplant recipient presenting with severe kidney injury (serum creatinine, 4.90 mg/dL) 16 months after transplantation. Although systemic blood pressure remained within the range of 140-170/90-105 mmHg-below the classical threshold of malignant hypertension-an allograft biopsy revealed the lesions suggestive of thrombotic microangiopathy (TMA), including mesangiolysis and edematous intimal thickening of the arteries. After exclusion of antibody-mediated rejection, calcineurin inhibitor toxicity, and primary TMAs, the patient was diagnosed with kidney-limited TMA attributable to relative hypertension producing a malignant hypertension-like phenotype in the setting of graft-specific vulnerability. Given the presumed contribution of the renin-angiotensin system (RAS)-mediated vascular injury, an angiotensin II receptor blocker was initiated despite severe kidney dysfunction, resulting in marked improvement in kidney function and proteinuria. This case illustrates that kidney allografts may develop a malignant hypertension-like pathophysiology with kidney-limited TMA at blood pressure levels below the classical malignant range. Awareness of this discrepancy may help clinicians recognize atypical hypertensive injury in transplant recipients, and early RAS blockade may be considered as a potential strategy to preserve allograft function, even in the setting of severe kidney injury.