No abstract

Rapidly progressive glomerulonephritis (RPGN), characterized by rapid kidney dysfunction caused by aggressive glomerulonephritis, is usually associated with crescentic glomerulonephritis (CrGN). In the present study, the data from patients with CrGN were retrospectively analyzed at a tertiary medical center in China with the aim of investigating the clinicopathological features and the association of the type of CrGN with the prognosis. The renal biopsies of 49 patients diagnosed with CrGN were obtained between December 2011 and July 2016. Of the 49 patients, 11 patients (22.45%) had type I CrGN, 19 (38.78%) had type II CrGN and 19 (38.78%) had type III CrGN. The majority of CrGN patients exhibited multiple-system involvement and 28 patients (57.14%) had kidney enlargement. Proportions of patients with acute kidney injury (AKI), acute kidney diseases without AKI, and chronic kidney disease were 28.57, 46.94 and 24.49%, respectively. Among the 3 types of CrGN, patients with type I CrGN tended to have a higher proportion of AKI with more cellular crescent formation, and higher serum creatinine and retinol binding protein. Circulating anti-GBM antibodies were present in all type I CrGN patients and anti-neutrophilic cytoplasmic autoantibodies were detected in 84.21% of patients with type III CrGN. Type III CrGN patients had a superior kidney survival, whereas type I CrGN patients had the worst kidney prognosis (P<0.001). There was no significant difference in overall patient survival among the 3 types of CrGN. CrGN remains the primary cause of critical illness in RPGN patients. There was much heterogeneity between the different subtypes of CrGN. Patients with type I tended to have an acute onset and had the poorest kidney survival.

No abstract

IgA nephropathy (IgAN), the most common glomerulonephritis, has an unclear pathogenesis. The role of Th22 cells, which are intimately related to proteinuria and progression in IgAN, in mediating infection-related IgAN is unclear. This study aimed to characterize the association between intrinsic renal cells (tubular epithelial cells and mesangial cells) and Th22 cells in immune regulation of infection-related IgAN and to elucidate the impact of Th22 lymphocytosis; the proinflammatory cytokines IL-1, IL-6, and TNF-α; and CCL chemokines on kidney fibrosis. Hemolytic streptococcus infection induced an increase in IL-1, IL-6, and TNF-α, resulting in Th22 cell differentiation from T lymphocytes obtained from patients with IgAN, and the CCL20-CCR6, CCL22-CCR4, and/or CCL27-CCR10 axes facilitated Th22 cell chemotaxis. The increased amount of Th22 cells caused an increase in TGF-β1 levels, and anti-CD80, anti-CD86, and CTLA-4Ig treatment reduced TGF-β1 levels by inhibiting Th22 lymphocytosis and secretion of cytokines and chemokines, thus potentially relieving kidney fibrosis. Our data suggest that Th22 cells might be recruited into the kidneys via the CCL20-CCR6, CCL22-CCR4, and/or CCL27-CCR10 axes by mesangial cells and tubular epithelial cells in infection-related IgAN. Th22 cell overrepresentation was attributed to stimulation of the B7-CTLA-4Ig antigen-presenting pathway and IL-1, IL-6, and TNF-α.

Tonsil infection may aggravate the renal pathological lesions of IgAN by exacerbating Th22 cell accumulation. Our data suggested a collaboration between HMC and Th22 cells in IgAN with tonsillitis underlying the effects of CCL20, CCL22, and CCL27.