ABSTRACT
The term thrombotic microangiopathy (TMA) was first introduced by Symmers in 1952 (1). It defines a pathological lesion characterized by thickened walls of small arteries and arterioles with mucinous swelling of the intima and endothelial cells, which at times detach from the basement membrane. Poorly defined material accumulates in the subendothelial space and together, with intraluminal platelet and fibrin thrombi, can cause obstruction of vessels. The kidney appears to be an organ particularly vulnerable to TMA injury, with characteristic morphological alterations involving the glomeruli and microvasculature; this organ is the particular focus of this review. TMA occurs in a variety of clinical settings as a result of multiple types of initiating injuries (Table 1). Among these, two important and closely related syndromes-which have as their basis the pathological lesions of TMA-are referred to as thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS). The classical symptom constellation of these entities consists of microangiopathic hemolytic anemia, thrombocytopenia, fever, neurological abnormalities, and renal insuffiency. Patients with TTP primarily present with neurological symptoms, whereas renal involvement is the hallmark of HUS (2). The association between TMA and infection with the human immune deficiency virus (HIV) was first described by Boccia et al. in 1984 (3). Since then, thrombotic microangiopathy, typically manifest as HUS or TTP, has been established as a common form of HIV associated disease (4).
