Malignant hypertension in IgA nephropathy was not associated with background pathological phenotypes of glomerular lesions.
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.
Jiang
Lei
L
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.
Zhang
Jun-jun
JJ
Lv
Ji-cheng
JC
Liu
Gang
G
Zou
Wan-zhong
WZ
Zhao
Ming-hui
MH
Zhang
Hong
H
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
D001323:Autoantibodies; D001324:Autoantigens; D007070:Immunoglobulin A; D007074:Immunoglobulin G