Pathological influence of obesity on renal structural changes in chronic kidney disease.

BACKGROUND: Role of obesity in renal pathological and structural changes remains poorly investigated, and this study was designed to examine the pathological effects of obesity on renal structural components in patients with chronic kidney diseases (CKD). METHODS: The study subjects were obese (body mass index, BMI > or = 25 kg/m2) patients with nonglomerulonephritis (non-GN, n = 26), IgA nephropathy (IgAN, n = 19), benign nephrosclerosis (BNS, n = 15), and thin basement membrane disease (TMD, n = 6), and 65 nonobese controls (n = 20, 20, 10, and 15, respectively). Patients were evaluated for glomerular lesions (mesangial proliferation and focal segmental/global glomerulosclerosis), glomerular size, and thickness of glomerular basement membrane (GBM). RESULTS: Urinary protein was higher in obese non-GN, IgAN, and BNS groups than in the respective controls. Focal segmental glomerulosclerosis (FSGS) lesions were noted in all obesity groups. The glomeruli were larger in size in obese than in nonobese patients of the non-GN and IgAN groups. The glomeruli of nonobese TMD and BNS patients were significantly larger in size than those of nonobese non-GN patients. GBM were thicker in obese than in nonobese patients irrespective of types of glomerular diseases, but only significantly so in non-GN and BNS groups. CONCLUSION: In non-GN, IgAN, and BNS, obesity worsens proteinuria and is associated with structural changes such as glomerulomegaly and GBM thickening, similar to changes observed in obesity-related nephropathy. Obesity seems to worsen the renopathological state in CKD

Vasculites dos médios e grandes vasos Medium and large vessel vasculitis

As vasculites são constituídas por um grande grupo de síndromes caracterizadas por inflamação e necrose da parede dos vasos sangüíneos, resultando em estreitamento ou oclusão do lúmen. A distribuição dos vasos envolvidos varia consideravelmente e serve de base para a classificação das síndromes vasculíticas: grandes vasos (arterite de Takayasu, arterite temporal); pequenos e médios vasos (poliarterite nodosa, síndrome de Churg-Strauss, granulomatose de Wegener, vasculites nas doenças reumáticas); e pequenos vasos (vasculite de hipersensibilidade, púrpura de Henoch-Schonlein, poliangeíte microscópica, crioglobulinemia). Este artigo revisa as vasculites dos médios e grandes vasos e opções terapêuticas atuais; além de oferecer orientação sobre abordagem diagnóstica e tratamento dos pacientes com suspeita de vasculite cutânea.<br>Vasculitis comprises a broad group of syndromes characterized by inflammation and necrosis on the walls of blood vessels, resulting in narrowing or occlusion of the lumen. The distribution of involved blood vessel varies considerably and serves as the basis for one classification of vasculitic syndromes: large vessels (Takayasu arteritis, giant cell arteritis); medium and small muscular arteries (polyarteritis nodosa, Churg-Strauss syndrome, Wegener's granulomatosis, vasculitis in rheumatic diseases); and small vessels ("hypersensitivity" vasculitis, Henoch-Schonlein purpura, microscopic polyangiitis, cryoglobulinemia). This article reviews medium and large vessel vasculitis and current treatment options; it also presents a comprehensive approach to diagnosing and treating patients with suspected cutaneous vasculitis