| Literature DB >> 28679995 |
Saki Ameda1, Hiroyuki Kuroda1, Michiko Yamada1, Ken Sato1, Shogo Miura1, Hiroya Sakano1, Takanori Shibata1, Naoki Uemura1, Tomoyuki Abe1, Shigeyuki Fujii1, Masahiro Maeda1, Miri Fujita2, Masayoshi Kobune3, Junji Kato3.
Abstract
A 47-year-old man presented at a local ophthalmological hospital with blurred vision. He had been diagnosed with hypertensive retinopathy and renal failure and was referred to our hospital for treatment. A renal biopsy was done to evaluate pathology of high proteinuria, hematuria, and rapidly progressive glomerulonephritis. Blood pressure remained high despite antihypertensive therapy; anemia and thrombocytopenia gradually progressed. Thrombotic microangiopathy (TMA) was suspected based on red blood cell fragmentation due to hemolytic anemia, thrombocytopenia, and renal failure. However, plasma exchange resolved neither thrombocytopenia nor renal failure, and anemia gradually progressed. Backache suddenly developed 13 days later, and CT findings indicated a retroperitoneal hematoma secondary to bleeding from the kidney. Selective renal artery embolization via angiography stopped the bleeding, but the patient went into hemorrhagic shock. Pathological findings on renal biopsy were identical to those in malignant hypertension, namely an edematous membrane lining, thickened arterioles, and stenosis. We diagnosed thrombotic microangiopathy due to malignant hypertension, without decrease in activities of ADAMTS13 (a disintegrin and metalloprotease with thrombospondin type 1 motif) or its antibodies. Renal failure did not improve, and continuous hemodiafiltration was needed. This procedure stabilized blood pressure and improved the TMA.Entities:
Keywords: Malignant hypertension; Thrombotic microangiopathy (TMA)
Mesh:
Year: 2017 PMID: 28679995 DOI: 10.11406/rinketsu.58.637
Source DB: PubMed Journal: Rinsho Ketsueki ISSN: 0485-1439