title: Impact of hypertension and hypertension-related vascular lesions in IgA nephropathy.
abstract: It remains poorly understood whether vascular pathology plays an important role in the progression of renal parenchymal disease in humans. Moreover, in the case of hypertensive patients with mild proteinuria, nephrologists tend to make a diagnosis of benign nephrosclerosis without renal biopsy. Among 172 patients who were treated at our hospital for biopsy-proven IgA nephropathy, we performed quantitative histopathological analysis in 38 patients with mild proteinuria of less than 0.5 g/day. We related these histopathological parameters with clinical data at biopsy and also with follow-up data. The percentage of glomeruli showing global sclerosis exceeded 10% of total glomeruli in 15 of the patients (39.5%) and exceeded 20% in 9 (23.7%). Arteriosclerosis and tubulointerstitial changes significantly correlated with glomerular sclerosis, but mesangial cell proliferation did not. Among the 38 patients, the 12 with hypertension showed more severe glomerular sclerosis, tubulointerstitial changes and arteriosclerosis compared with the 26 without hypertension, but the mesangial cell proliferation was identical between the two groups. Stepwise multiple regression analysis revealed that hypertension and urinary protein excretion (UPE) were independent risk factors for arteriosclerosis. The follow-up data of a mean period of 27.6 months showed that 9 of the 38 patients (23.7%) had an increase in UPE. Hypertension, arteriosclerosis, age, and UPE at biopsy were selected as the important risk factors for an increase in UPE in the follow-up. Our results provide not only clinical but histopathological evidence that hypertension affects the prognosis of mild proteinuric nephropathy through vascular lesions.
authors.affiliation: Second Department of Internal Medicine, National Defense Medical College, Tokorozawa, Japan. ryota.ikee@tokushukai.jp
authors.forename: Ryota
authors.initials: R
authors.lastname: Ikee
authors.forename: Shuzo
authors.initials: S
authors.lastname: Kobayashi
authors.forename: Takamitsu
authors.initials: T
authors.lastname: Saigusa
authors.forename: Tamehachi
authors.initials: T
authors.lastname: Namikoshi
authors.forename: Muneharu
authors.initials: M
authors.lastname: Yamada
authors.forename: Noriaki
authors.initials: N
authors.lastname: Hemmi
authors.forename: Toshihiko
authors.initials: T
authors.lastname: Imakiire
authors.forename: Yuichi
authors.initials: Y
authors.lastname: Kikuchi
authors.forename: Shigenobu
authors.initials: S
authors.lastname: Suzuki
authors.forename: Soichiro
authors.initials: S
authors.lastname: Miura
mesh_terms: D000293:Adolescent; D000328:Adult; D000367:Age Factors; D000368:Aged; D050197:Atherosclerosis / Q000209:etiology / Q000473:pathology; D002648:Child; D005260:Female; D005920:Glomerular Mesangium / Q000473:pathology; D005922:Glomerulonephritis, IGA / Q000150:complications* / Q000473:pathology*; D006801:Humans; D006977:Hypertension, Renal / Q000209:etiology* / Q000473:pathology*; D007668:Kidney / Q000473:pathology; D007678:Kidney Glomerulus / Q000473:pathology; D008297:Male; D008875:Middle Aged; D011507:Proteinuria / Q000209:etiology; D012044:Regression Analysis; D012307:Risk Factors; D014652:Vascular Diseases / Q000209:etiology* / Q000473:pathology*