title: Malignant hypertension in IgA nephropathy was not associated with background pathological phenotypes of glomerular lesions.
abstract: BACKGROUND
  It was reported that IgA nephropathy (IgAN) was the major cause of secondary malignant hypertension (MHT). However, the pathogenesis of MHT secondary to IgAN (IgAN-MHT) is unknown and its association with glomerular pathological phenotypes remains inconclusive. The present study aimed to investigate whether glomerular pathological phenotypes and anti-endothelial cell antibodies (AECA) were associated with the occurrence of IgAN-MHT.
  
  
  METHODS
  The glomerular pathological phenotypes of 45 patients with IgAN-MHT were analysed using Haas' histologic grading system of IgAN. Sera were collected from 34 of the 45 patients with IgAN-MHT, 19 patients with primary MHT, 41 patients with non-MHT IgAN and 10 healthy volunteers. AECA of both IgG and IgA isotypes were detected by western blot analysis using human umbilical vein endothelial cell lysate as antigen.
  
  
  RESULTS
  In the 45 patients with IgAN-MHT, 7 (15.56%), 5 (11.11%), 13 (28.89%), 9 (20%) and 11 (24.44%) patients were graded as Hass I, II, III, IV and V, respectively. Although the severity of non-ischaemic sclerosis, crescents and mesangial proliferation were significantly different between patients with different grades, the levels of blood pressure, SCr and proteinuria at presentation were comparable. Eleven and four protein bands of endothelial proteins could be blotted by AECA-IgG and AECA-IgA in sera from patients with IgAN-MHT. The prevalences of anti-121 kD AECA-IgG (15/34) and anti-92 kD AECA-IgA (10/34) in IgAN-MHT were significantly higher than that of primary MHT, non-MHT IgAN and normal controls, respectively. Patients with anti-92 kD AECA-IgA had more severe glomerular ischaemic sclerosis (6.25-92.86%, median 39.61%) than those without (0-91.67%, median 18.18%, P = 0.035). There was no significant difference in the prevalence of AECA between IgAN-MHT patients with different background glomerular lesions. Only one IgAN patient with MHT was found with both anti-121 kD AECA-IgG and anti-92 kD AECA-IgA. No particular manifestations were found.
  
  
  CONCLUSIONS
  The occurrence of IgAN-MHT was not associated with the background glomerular pathological phenotypes of IgAN. AECA might play a role in the pathogenesis of IgAN-MHT.
authors.affiliation: Renal Division of Peking University First Hospital, Institute of Nephrology, Peking University, Key Laboratory of Renal Disease, Ministry of Health of China, Beijing 100034, People's Republic of China.
authors.forename: Lei
authors.initials: L
authors.lastname: Jiang
authors.forename: Jun-jun
authors.initials: JJ
authors.lastname: Zhang
authors.forename: Ji-cheng
authors.initials: JC
authors.lastname: Lv
authors.forename: Gang
authors.initials: G
authors.lastname: Liu
authors.forename: Wan-zhong
authors.initials: WZ
authors.lastname: Zou
authors.forename: Ming-hui
authors.initials: MH
authors.lastname: Zhao
authors.forename: Hong
authors.initials: H
authors.lastname: Zhang
mesh_terms: D000368:Aged; D001323:Autoantibodies / Q000097:blood; D001324:Autoantigens / Q000302:isolation & purification; D016022:Case-Control Studies; D002478:Cells, Cultured; D042783:Endothelial Cells / Q000276:immunology; D005260:Female; D005922:Glomerulonephritis, IGA / Q000145:classification / Q000150:complications* / Q000276:immunology / Q000473:pathology*; D006801:Humans; D006974:Hypertension, Malignant / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D007070:Immunoglobulin A / Q000097:blood; D007074:Immunoglobulin G / Q000097:blood; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D011379:Prognosis
chemical_list: D001323:Autoantibodies; D001324:Autoantigens; D007070:Immunoglobulin A; D007074:Immunoglobulin G