Document Detail

Effects of renin-angiotensin system blockade on macrophage infiltration in patients with hypertensive nephrosclerosis.
MedLine Citation:
PMID:  17785932     Owner:  NLM     Status:  MEDLINE    
The mechanisms of hypertensive nephrosclerosis are not fully understood. In experimental models of the disease, inflammatory reactions such as macrophage infiltration play an important role. In human hypertensive nephrosclerosis, however, there have been few studies examining the role of inflammation histologically. We investigated whether the number of infiltrating macrophages was increased in human hypertensive nephrosclerosis, and evaluated the effects of a blockade of the renin-angiotensin system on clinical and histological findings. We examined macrophage infiltration using immunohistochemistry in renal biopsy specimens obtained from 16 patients with hypertensive nephrosclerosis, 5 patients with IgA nephropathy, 5 patients with membranous nephropathy, and 5 patients with minimal change nephrotic syndrome. The number of infiltrating macrophages in glomeruli was significantly larger in the patients with hypertensive nephrosclerosis than in those with minimal change nephrotic syndrome. The patients with hypertensive nephrosclerosis were divided into groups based on their use of antihypertensive agents at the time of renal biopsy. We investigated the effects of antihypertensive agents on clinical findings, macrophage infiltration, and monocyte chemoattractant protein-1 expression. There was no difference in clinical findings between the hypertensive groups. The numbers of infiltrating macrophages and monocyte chemoattractant protein-1-positive cells in glomeruli were significantly smaller in patients treated with an angiotensin-converting enzyme inhibitor or angiotensin II type 1 receptor blocker, whereas calcium channel blockers had no influence on histological findings. In conclusion, inflammation is involved in the progression of human hypertensive nephrosclerosis and the inflammatory process is inhibited by blocking the renin-angiotensin system.
Toshihiko Imakiire; Yuichi Kikuchi; Muneharu Yamada; Taketoshi Kushiyama; Keishi Higashi; Naomi Hyodo; Kojiro Yamamoto; Takashi Oda; Shigenobu Suzuki; Soichiro Miura
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Hypertension research : official journal of the Japanese Society of Hypertension     Volume:  30     ISSN:  0916-9636     ISO Abbreviation:  Hypertens. Res.     Publication Date:  2007 Jul 
Date Detail:
Created Date:  2007-09-05     Completed Date:  2007-09-27     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9307690     Medline TA:  Hypertens Res     Country:  Japan    
Other Details:
Languages:  eng     Pagination:  635-42     Citation Subset:  IM    
Department of Internal Medicine, National Defense Medical College, Tokorozawa, Japan.
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MeSH Terms
Angiotensin II Type 1 Receptor Blockers / pharmacology
Angiotensin-Converting Enzyme Inhibitors / pharmacology
Cell Movement / drug effects,  physiology*
Chemokine CCL2 / metabolism
Glomerulonephritis, IGA / etiology,  pathology,  physiopathology
Glomerulonephritis, Membranous / etiology,  pathology,  physiopathology
Hypertension / complications*,  physiopathology
Kidney Glomerulus / metabolism,  pathology,  physiopathology
Macrophages / drug effects,  pathology*
Middle Aged
Nephrosclerosis / etiology*,  pathology*,  physiopathology
Nephrosis, Lipoid / etiology,  pathology,  physiopathology
Renin-Angiotensin System / drug effects,  physiology*
Retrospective Studies
Reg. No./Substance:
0/Angiotensin II Type 1 Receptor Blockers; 0/Angiotensin-Converting Enzyme Inhibitors; 0/CCL2 protein, human; 0/Chemokine CCL2

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