On a retrospective study, Sangle et al. syndrome, hypertension and renal failure. Antiphospholipid syndrome nephropathy is usually a vascular disease that affects glomerular tuft, interstitial vessels, and peritubular vessels; histopathology characterizes the renal lesions as acute or chronic, the classic finding is usually thrombotic microangiopathy, that leads to fibrosis, tubule thyroidization, focal cortical atrophy, and glomerular sclerosis. Antiphospholipid syndrome nephropathy can also complicate patients with systemic lupus erythematosus, and there is vast information supporting the worse renal prognosis in this group of patients with the classic histopathologic lesions. Treatment consists of anticoagulation, as for other thrombotic manifestations of antiphospholipid syndrome. There is some evidence of glomerulonephritis as an isolated lesion in patients with antiphospholipid syndrome. The most frequently reported glomerulonephritis is usually membranous; with some reports suggesting that immunosuppressive treatment may be effective. Patients with end stage renal disease commonly are positive for antiphospholipid antibodies, but it is not clear what is the role of aPL in this setting. Patients with vascular access may have complications in the presence of antibodies so that anticoagulation is recommended. Patients ongoing renal transplant with persistent antiphospholipid antibody positivity may have early and late graft failure. Keywords: antiphospholipid syndrome, systemic lupus erythematosus, renal disease in antiphospholipid antibody syndrome, antiphospholipid antibody syndrome nephropathy, renal thrombotic microangiopathy Introduction Antiphospholipid antibody syndrome (APS) is usually a complex autoimmune systemic disease, characterized by the presence of circulating antibodies directed against anionic phospholipids, and the proteins Tiotropium Bromide bound to them (aPL) in the serum of patients with thrombosis or pregnancy complications. There are classic manifestations of APS, including thrombosis involving arterial and venous territories and obstetric morbidity, that are considered as classification criteria (1). Moreover, there are many other manifestations of APS, the non-criteria manifestations that include livedo reticularis, hematologic manifestations (thrombocytopenia and hemolytic anemia), cardiac valve disease, and renal involvement. Renal involvement was not mentioned in the first description of APS (2). Kidney compromise in APS represents a vast and complex myriad of syndromes that are a consequence of the vascular dysfunction and the coagulation dysregulation characteristic of the syndrome. Kidney disease associates with aPL is not an inflammatory condition in contrast with lupus nephritis. Recently, many groups are interested in this frequent complication of APS (3C5). All the vessels, veins, and arteries, from the renal arteries to the glomerular tuft capillaries can be involved. Table ?Table11 shows the renal syndromes that Tiotropium Bromide are related to APS. Table 1 Renal involvement in antiphospholipid antibody syndrome (APS). a) Hypertension b) Renal artery stenosis, thrombosis, and infarction c) Renal vein thrombosis d) Intrarenal vasculopathy [APS nephropathy (APSN)] e) Glomerular disease f) APS in kidney transplant g) APS in end stage renal disease and hemodialysis h) APSN in patients with systemic lupus erythematosus i) APSN in catastrophic APS Open in a separate window The Tiotropium Bromide real prevalence of renal involvement in APS is very difficult to establish, mainly due to the limitation of histopathology research, biopsy contraindications, and its association with lupus INF2 antibody (SLE). Retrospective series have mentioned a prevalence Tiotropium Bromide of 9C10% (6), but in series where APS renal disease has been intentionally studied the prevalence ranges from 10C40% (7C9). Hypertension Hypertension is usually a fairly common health problem in the adult population. Depending on the definitions used for classifying patients with high blood pressure (JNC8 or ACC/AHA 2017), 32C46% of adults has hypertension (7, 8). According to the last ACC/AHA definitions, a normal blood pressure is usually <120/<80?mmHg, elevated blood pressure 120C129/<80?mmHg, stage 1 hypertension 130C139/80C89?mmHg, and stage 2 hypertension >140/>90?mmHg (10, 11). Since the initial descriptions of APS, hypertension was one of the frequent signs related to the disease. Hughes in 1983, described patients with livedo reticularis in association with elevated blood pressure, suggesting a renovascular etiology. In 1986, he described a group of patients with APS and hypertension, which ranged from moderate elevation to malignant hypertension (2, 12). The etiology of the elevated blood pressure within this group of patients is usually thought to be renovascular in origin, since there are case reports (13, 14), and series where intrarenal vascular lesions exhibited in biopsies, were the only physiopathologic explanation. In a large series of renal biopsies in patients with APS, Nochy et al. found systemic hypertension on 93% of their patients, this being the most common clinical manifestation of APS nephropathy (APSN). Hypertension was severe in 31% of the patients and malignant in 12% (15). Taking into account the high prevalence of hypertension in APSN, elevation of blood pressure is considered one of the most important signs that suggest renal activity. Some studies have suggested that the presence of aPL is usually related.
On a retrospective study, Sangle et al
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