To study the glomerular morphological abnormalities in congestive hear
t failure (CHF), we analyzed 27 autopsy cases without other causes of
renal disease. Their mean age was 59 years, and they showed mild prere
nal azotemia. They had generally been treated with digitalis and diure
tics, and a few Of them with captopril or nifedipine. The abnormal glo
merular findings of enlargement, hyperemia, and mesangial thickening w
ere observed at high frequencies (61%, 64%, and 57%, respectively). Th
ey characteristically showed mesangiolysis (ML) by the findings of mic
roaneurysms (81%) and mesangial degeneration (70%) such as loose retic
ular matrix and poor matrix area. In addition, glomerular infiltration
of mononuclear leukocytes including macrophages was noted in 70% of t
he cases. Glomerular enlargement was not correlated with the grade of
hyperemia, but it was correlated with the grade of ML index of % glome
ruli with microaneurysms (F = 7.22, p < 0.004). There was an inverse r
elationship between the grades of mesangial thickening and of the ML i
ndex (P < 0.005). The number of glomerular leukocytes was positively c
orrelated with mean glomerular size (P < 0.002) and with the ML index
(P < 0.03). Notably, the glomerular macrophage-positive cases showed a
prominently higher mean ML index than the negative cases (P < 0.005).
There was an inverse correlation between the mean glomerular size and
the partial oxygen pressure in arterial blood (PaO2; P < 0.01), and a
positive correlation between the mean glomerular size and hematocrit
(Hct) levels (P < 0.02. The cases positive for mesangiolytic mesangial
degeneration showed significantly lower PaO2 values than the cases ne
gative for this lesion (P < 0.04). In the analysis; of the various cau
ses of CHF, the patients with congenital cardiac anomalies showed mean
levels of the lowest PaO2 (P < 0.02) and the highest Hct (P < 0.03) a
nd histologically the largest mean glomerular size (P < 0.04). There w
as no difference in the ML index and tile glomerular leukocyte number
among the subgroups classified by the causes. These results indicate t
hat ML associated with glomerular enlargement is the major glomerular
abnormality characteristic in patients with severe CHF and suggest tha
t glomerular infiltration of leukocytes, especially of macrophages, sh
ould play an important rule in the progression of both ML and glomerul
omegaly. The contributions of persistent hypoxia and up-regulated angi
otensin II as the causative factors of these glomerular abnormalities
in congestive heart failure are discussed.