Key result
Renal macrophage infiltration after fatal myocardial infarction varies by timing of death, with CD163+ and CD68+ cells predominating early and CD163+ cells predominating after 3 days.
Why the study?
The phenotypic heterogeneity of renal macrophage infiltration and its links to clinical characteristics across different post-myocardial infarction timepoints remained uncharacterized.
Observational (n=30)
p-value: p=<0.05
Renal macrophage infiltration exhibits significant phenotypic heterogeneity depending on the timing of death after myocardial infarction, suggesting a dynamic systemic inflammatory response.
Renal macrophage phenotypes post-MI may correlate with clinical features; leaves open prognostic value and therapeutic relevance.
Purpose. To characterise phenotypic heterogeneity of renal macrophage infiltration and its relationships with clinical and medical history data in patients who died at different times after myocardial infarction (MI). Material and Methods. We analyzed the material (kidney sections) collected from patients (n = 30) who died from type 1 MI. Renal macrophage infiltration was assessed by the immunohistochemistry method using antibodies to CD68, CD80, CD163, CD206, and stabilin-1. Results. The study included patients with MI aged 74.8 ± 9.8 years. ST-segment elevation myocardial infarction (STEMI) was diagnosed in 87% of patients; the creatinine level was 115.1 ± 79 μmol/L at admission to hospital. The study showed a significant heterogeneity of macrophage phenotypes in renal tissue: the counts of CD163+, CD68+, CD206+, CD80+, and stabilin-1+ cells were 55 (27; 55), 30 (27; 56), 4 (2; 6), 3 (2; 5), and 2 (1; 3) per field of view, respectively. The CD163+ and CD68+ macrophages were predominant cell types in patients who died within three days after MI onset (p < 0.05). In case of fatal outcome that occurred after three days of MI, the count of CD163+ cells was the highest and exceeded the number of СD68+ cells, which, nevertheless, prevailed over other cell phenotypes (p < 0.05). Starting from day 4 of MI, the counts of CD206+ cells decreased from 6 (5; 8) to 2 (1; 2) similarly to a decrease in CD80+ count from 5 (3; 5) to 2 (1; 2) (p < 0.05). The rate of adverse cardiovascular complications and the severity of coronary lesions were associated with CD80+ and CD206+ cell counts; the development of left ventricular aneurysm was associated with the numbers of stabilin-1+ and CD163+ cells. Conclusion. Renal macrophage infiltration was characterized by a pronounced cellular heterogeneity that depended on the timing of death after MI. The CD163+ and CD68+ cells predominated at the early stages of MI; the CD163+ cells were predominant at the later stages. The CD80+ and CD206+ cell counts changed quantitatively, decreasing from day 4 of MI. The presence of multiple correlation relationships between the cells of macrophage lineage in the kidneys and the development of adverse cardiovascular complications in patients with MI provides rationale for further studies.
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Керчева et al. (2021) conducted an observational in Myocardial infarction (n=30). Timing of death after myocardial infarction vs. Early (≤3 days) vs late (>3 days) death was evaluated on Renal macrophage infiltration phenotypes (CD163+, CD68+, CD206+, CD80+, and stabilin-1+ cell counts) (p=<0.05). Renal macrophage infiltration after fatal myocardial infarction varies by timing of death, with CD163+ and CD68+ cells predominating early and CD163+ cells predominating after 3 days.
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