Takaya Sasaki 1 , Nobuo Tsuboi 1 , Yusuke Okabayashi 1 , Kotaro Haruhara 1 , Go Kanzaki 1 , Kentaro Koike 1 , Hiroyuki Takahashi 2 , Masahiro Ikegami 2 , Akira Shimizu 3 , Takashi Yokoo 1 . Show Affiliations »
Abstract
BACKGROUND: Diabetes and hypertension share renal histopathological features, such as arterial lesions and glomerular hypertrophy, that have not been investigated in relation to the blood pressure status of diabetic subjects. The severity of glomerular lesions varies across locations of the renal cortex, which may be further affected by diabetes and/or hypertension. METHODS: Histopathological lesions in different parts of the renal cortex of autopsy kidneys were evaluated and analyzed based on medical histories of diabetes and hypertension. RESULTS: This study included a total of 82 Japanese autopsies composed of normotensive nondiabetics (n = 31), hypertensive nondiabetics (n = 28), normotensive diabetics (n = 14), and hypertensive diabetics (n = 9). There were no differences in age, sex, renal function, or body size among groups. In both the superficial and juxtamedullary cortices, increased glomerular volume (GV) was significantly associated with either diabetes or hypertension. In addition, diabetes and hypertension showed a significant interaction with GV regardless of the cortical location. Values for global glomerulosclerosis (GGS) and arteriolar hyalinosis (AH) were associated with diabetes but not with hypertension. Only values for GGS consistently showed cortical surface superiority. The zonal distribution of AH, GV, or other diabetic glomerular lesions differed among the lesions depending on the presence or absence of hypertension. CONCLUSIONS: These results imply that diabetes and hypertension synergistically enhance glomerular hypertrophy across all layers of the human renal cortex. The process is closely associated with the severity of GGS and AH predominantly associated with diabetes. © American Journal of Hypertension, Ltd 2019. All rights reserved. For Permissions, please email: journals.permissions@oup.com.
BACKGROUND: Diabetes and hypertension share renal histopathological features, such as arterial lesions and glomerular hypertrophy , that have not been investigated in relation to the blood pressure status of diabetic subjects. The severity of glomerular lesions varies across locations of the renal cortex, which may be further affected by diabetes and/or hypertension . METHODS: Histopathological lesions in different parts of the renal cortex of autopsy kidneys were evaluated and analyzed based on medical histories of diabetes and hypertension . RESULTS: This study included a total of 82 Japanese autopsies composed of normotensive nondiabetics (n = 31), hypertensive nondiabetics (n = 28), normotensive diabetics (n = 14), and hypertensive diabetics (n = 9). There were no differences in age, sex, renal function, or body size among groups. In both the superficial and juxtamedullary cortices, increased glomerular volume (GV ) was significantly associated with either diabetes or hypertension . In addition, diabetes and hypertension showed a significant interaction with GV regardless of the cortical location. Values for global glomerulosclerosis (GGS) and arteriolar hyalinosis (AH ) were associated with diabetes but not with hypertension . Only values for GGS consistently showed cortical surface superiority. The zonal distribution of AH , GV , or other diabetic glomerular lesions differed among the lesions depending on the presence or absence of hypertension . CONCLUSIONS: These results imply that diabetes and hypertension synergistically enhance glomerular hypertrophy across all layers of the human renal cortex. The process is closely associated with the severity of GGS and AH predominantly associated with diabetes . © American Journal of Hypertension , Ltd 2019. All rights reserved. For Permissions, please email: journals.permissions@oup.com.
Entities: Chemical
Disease
Species
Keywords:
autopsy; blood pressure; diabetic nephropathy; glomerular capillary; hypertension; nephrosclerosis; renal cortex
Year: 2019
PMID: 31044221 DOI: 10.1093/ajh/hpz059
Source DB: PubMed Journal: Am J Hypertens ISSN: 0895-7061 Impact factor: 2.689