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Mesangiolytic glomerulopathy in severe congestive heart failure
Insights
Glomerular abnormalities like enlargement and mesangiolysis are common in congestive heart failure (CHF). Leukocyte infiltration, particularly macrophages, may drive these changes and kidney damage in CHF patients.
Area of Science:
- Nephrology
- Cardiology
- Pathology
Background:
- Congestive heart failure (CHF) can lead to renal complications.
- Glomerular changes in CHF are not fully understood.
- Autopsy studies offer insights into organ damage in severe disease.
Purpose of the Study:
- To investigate glomerular morphological abnormalities in patients with congestive heart failure (CHF).
- To identify characteristic lesions and their correlation with clinical parameters.
- To explore the role of inflammation in CHF-related kidney damage.
Main Methods:
- Analysis of 27 autopsy cases with CHF and no other renal disease.
- Histopathological examination of glomeruli for enlargement, hyperemia, mesangial thickening, and mesangiolysis (ML).
- Correlation of glomerular findings with clinical data including azotemia, medications, partial oxygen pressure (PaO2), and hematocrit (Hct).
Main Results:
- High frequencies of glomerular enlargement (61%), hyperemia (64%), and mesangial thickening (57%) were observed.
- Mesangiolysis (ML), characterized by microaneurysms (81%) and mesangial degeneration (70%), was a key finding.
- Glomerular enlargement correlated with ML and leukocyte infiltration (especially macrophages), and inversely with PaO2.
- Patients with congenital heart anomalies showed the largest glomeruli and lowest PaO2.
Conclusions:
- Mesangiolysis associated with glomerular enlargement is a hallmark glomerular abnormality in severe CHF.
- Glomerular leukocyte infiltration, particularly macrophages, likely contributes to ML and glomerulomegaly.
- Hypoxia and angiotensin II may be causative factors in CHF-related glomerular pathology.
Abstract:
To study the glomerular morphological abnormalities in congestive heart failure (CHF), we analyzed 27 autopsy cases without other causes of renal disease. Their mean age was 59 years, and they showed mild prerenal azotemia. They had generally been treated with digitalis and diuretics, and a few of them with captopril or nifedipine. The abnormal glomerular findings of enlargement, hyperemia, and mesangial thickening were observed at high frequencies (61%, 64%, and 57%, respectively). They characteristically showed mesangiolysis (ML) by the findings of microaneurysms (81%) and mesangial degeneration (70%) such as loose reticular matrix and poor matrix area. In addition, glomerular infiltration of mononuclear leukocytes including macrophages was noted in 70% of the cases. Glomerular enlargement was not correlated with the grade of hyperemia, but it was correlated with the grade of ML index of % glomeruli with microaneurysms (F = 7.22, p < 0.004). There was an inverse relationship between the grades of mesangial thickening and of the ML index (P < 0.005). The number of glomerular leukocytes was positively correlated 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 negative for this lesion (P < 0.04). In the analysis of the various causes 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) and histologically the largest mean glomerular size (P < 0.04). There was no difference in the ML index and the glomerular leukocyte number among the subgroups classified by the causes. These results indicate that ML associated with glomerular enlargement is the major glomerular abnormality characteristic in patients with severe CHF and suggest that glomerular infiltration of leukocytes, especially of macrophages, should play an important role in the progression of both ML and glomerulomegaly. The contributions of persistent hypoxia and up-regulated angiotensin II as the causative factors of these glomerular abnormalities in congestive heart failure are discussed.