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We report a young patient with malignant hypertension (HTN) and multiorgan damage due to microangiopathy.

Design and method:

A 26-year old previously healthy man with family history of HTN developed acute symptoms related to long-standing unrecognized HTN. The patient presented with impaired consciousness, tonic-clonic seizures, high blood pressure (BP), jaundice, epigastric pain, vomiting, complete right eye blindness and partial left eye blindness. On admission, the patient was conscious but obtunded, with marked cognitive dysfunction, BP 240/130 mmHg, heart rate 120 bpm, breathing rate 30/min, temperature 37°C, oxygen saturation 94%. Following admission, a transient loss of consciousness with eyes turning to the left was observed upon sitting up, without any arrhythmia seen in ECG monitoring. Fundoscopy showed grade IV changes with papilledema, numerous hemorrhages and cotton wool spots. Neurological examination was unremarkable except for increased reflexes and triple flexion response on the right side.


Laboratory test abnormalities included elevated leukocyte count (14.7 × 103/μL), macrocytic anemia (Hb 12.87 g/dL, Hct 36.9%, MCV 100 fL), low platelet count (73 × 103/μL), elevated serum bilirubin (9.76 mg/dL) and creatinine (3.03 mg/dL), and slightly elevated AspAT and troponin I. Brain CT was unremarkable. BP was gradually normalized using intravenous/oral antihypertensive drugs. Clinical symptoms and laboratory abnormalities resolved, except for left eye blindness and serum creatinine (2.27 mg/dL at discharge). Secondary HTN was excluded. The final diagnosis was malignant HTN, acute hypertensive encephalopathy with seizures, acute liver damage, acute hemolytic anemia due to hypertensive microangiopathy, chronic kidney disease, and permanent left eye blindness. Due to hemolysis and low platelet count, differential diagnosis included hemolytic-uremic syndrome which was excluded. The clinical presentation resembled that of HELLP syndrome in pregnant women with eclampsia, with evidence of target organ damage, liver and kidney dysfunction, hemolytic jaundice, and low platelet count.


Young patients with essential HTN rarely present with such fulminant malignant HTN manifesting with neurological symptoms, with evidence of multiorgan damage due to microangiopathy. Similarly, microangiopathic hemolytic anemia rarely complicates malignant HTN. Initial clinical presentation was challenging due to neurological symptoms and evidence of multiorgan failure.

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