Y. Konishi et al., Relationship of renal histological damage to glomerular hypertension in patients with immunoglobulin A nephropathy, J HYPERTENS, 18(1), 2000, pp. 103-109
Citations number
33
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Objective Studies of experimental animals show glomerular hypertension to b
e important in the progression of glomerular disease. We evaluated this con
nection clinically by examining the relationship between glomerular hemodyn
amics and histological changes in patients with immunoglobulin (Ig)A nephro
pathy.
Methods The subjects were 23 patients with IgA nephropathy. All patients un
derwent renal biopsies. Glomerular hemodynamics, in terms of glomerular cap
illary hydraulic pressure (PGC) and the whole-kidney ultrafiltration coeffi
cient, were calculated from the renal clearance, plasma total protein conce
ntration, and pressure-natriuresis relationship. The severity of glomerulos
clerosis, tubulointerstitial damage and mesangial matrix expansion was eval
uated semiquantitatively.
Results PGC ranged from 33-69 mm Hg, and the mean arterial pressure (MAP) f
rom 79-112 mm Hg. Their correlation was not significant (r = 0.29, P = 0.18
), PGC was significantly correlated with the glomerulosclerosis score, and
also with the score for tubulointerstitial damage (r = 0.65, P < 0.001 and
r(s) = 0.59, P = 0.007, respectively), but not with the score for mesangial
matrix expansion (r = 0.08, P = 0.72). MAP was significantly correlated on
ly with the score for tubulointerstitial damage (r(s) = 0.63, P = 0.004). I
n multiple linear regression analysis of the histological changes and hemod
ynamics, the glomerulosclerosis score and the score for tubulointerstitial
damage were correlated with PGC, but not with MAP.
Conclusion These clinical results support the speculation that glomerular h
ypertension is involved in the glomerulosclerosis and tubulointerstitial da
mage that occurs in IgA nephropathy. J Hypertens 2000, 18:103-109 (C) Lippi
ncott Williams & Wilkins.