Managing malignant hypertension with renal TMA: a case for caution in blood-pressure reduction

Abstract

Malignant hypertension with renal thrombotic microangiopathy is a rare yet serious cause of acute kidney injury (AKI). Patients are often treated with antihypertensive therapy; however, managing their blood pressure is complex, with targets for initial treatment unclear. We report on a 55-year-old male with severe hypertension (blood pressure 210/140 mmHg), AKI (serum creatinine 9.27 mg/dL), anemia (hemoglobin 7.6 g/dL), thrombocytopenia (platelets 113 k/μL), and renal biopsy confirming malignant arteriolar nephrosclerosis and thrombotic microangiopathy. Previously prescribed 20-mg azilsartan daily, he lost consciousness the next day and was urgently admitted with a blood pressure of 118 mmHg and increased serum creatinine from 1.28 to 9.27 mg/dL over 6 months. Azilsartan was stopped; blood pressure managed with 12.5 mg of losartan daily, targeting systolic pressure between 150 and 160 mmHg. His creatinine peaked on day 14; however, treatment with 12.5 - 50 mg/day of losartan and 5 - 10 mg/day of amlodipine gradually improved renal function to 4.48 mg/dL by month ten without hemodialysis or further syncope. Our case suggests a gradual approach to blood-pressure management to avoid ischemic risks.

Keywords: Acute kidney injury (AKI); Antihypertensive therapy; Blood-pressure management; Malignant hypertension; Renal thrombotic microangiopathy (TMA).

Fig. 1

Time course. UPCR, urinary protein/urinary creatinine; SBP, systemic blood pressure; Hb, hemoglobin; PLT, platelet; sCre, serum creatinine

Fig. 2

Fundoscopy findings on Day 2. a. Right fundus image. b. Left fundus image. Fundus examination on Day 2 revealed retinal edema, cottony leukoplakia, hemorrhages, and moderately narrowing of arteries, indicating Keith–Wagener group 3 hypertensive retinopathy findings

Fig. 3

Renal histology. a. An interlobular arteriole shows an “onion skin” lesion (allow), indicative of concentric proliferation of smooth muscle cells and fibrous components within the intima. Stained with Azan, 400 × magnification. b. Mucoid-like intimal edema causing luminal narrowing is observed in the afferent arterioles (allow). Stained with Periodic acid-Schiff, 400 × magnification. c. Swelling of endothelial cells is noted (allow). Stained with Periodic acid-Schiff, 400 × magnification. d. Intimal edema with karyorrhexis and entrapment of red-blood cells is present (allow). Stained with Periodic acid-Schiff, 400 × magnification. e. Intimal edema with fibrin deposition is evident (allow). Stained with Periodic acid-Schiff, 400 × magnification. f. Mucoid intimal edema with entrapment of red-blood cells (yellow allow) and associated collapse of the glomerulus (blue allow) is seen. Stained with Periodic acid-methenamine-silver, 400 × magnification. g. Double contours of the glomerular basement membrane and endocapillary hypercellularity are observed (allow). Stained with Periodic acid-methenamine-silver, 400 × magnification. h. Partial deposition of C3 is seen in some glomeruli without specific deposition of other immune complexes. The immunofluorescence antibody assay revealed no specific immune complex deposition. Immunofluorescent staining, 400 × magnification. i. Wrinkled glomerular basement membranes and semidiffuse effacement of podocyte foot processes are observed. Viewed with electron microscopy, 1500 × magnification