The role of senescence of bone marrow cells in acute kidney injury

BACKGROUND: The prevalence of acute kidney injury (AKI) in elderly patients has grown considerably. Age-associated changes in the immune system can be one of the critical factors determining AKI outcomes. This study aimed to investigate the role of senescence of bone marrow (BM)-derived cells in the development of AKI, focusing on the immune response. METHODS: Female 7-week-old C57BL/6 mice were irradiated and treated with BM cells from either 48-week-old or 8-week-old male mice. Ischemia-reperfusion injury (IRI) was induced, and their functional deterioration, histological tubular damage, and inflammatory responses were compared. For the in-vitro study, lipopolysaccharide (LPS)-stimulated cytokine production by BM cells from old and young mice were examined. RESULTS: At 24 hours after IRI, there was no significant difference in the number of circulating immune cells between the mice transplanted with old or young BM cells. However, the mice with old BM cells showed less functional deterioration and histological tubular injury than those with young BM cells. Moreover, macrophage infiltration and renal cytokine interleukin (IL)-12 levels were lower in the mice with old BM cells at 24 hours post-IRI. Consistently, the in vitro study showed that LPS-induced production of cytokines interferon-γ, monocyte chemoattractant protein-1, and IL-10 was attenuated in cultured old BM cells, suggesting that age-related functional changes in these cells may lead to reduced inflammation in IRI. CONCLUSION: Immunosenescence could affect the susceptibility and response to renal IRI. Further studies specifically addressing age-related alterations can help in the development of treatment strategies for elderly patients with AKI.

A Case of Acute Carbon Monoxide Poisoning Resulting in an ST Elevation Myocardial Infarction

Carbon monoxide (CO) is a well-known chemical asphyxiant, which causes tissue hypoxia with prominent neurological and cardiovascular injury. After exposure to CO, several cardiac manifestations have been reported, including arrhythmias, acute myocardial infarction, and pulmonary edema. However, an ST elevation myocardial infarction (STEMI) due to CO poisoning is a very rare presentation, and the treatment for STEMI due to CO poisoning is not well established. Here, we report a rare case of STEMI complicated by increased thrombogenicity secondary to acute CO poisoning and complete revascularization after antithrombotic treatment.

Expression of Aquaporin-1, Vascular Endothelial Growth Factor and Vascular Endothelial Growth Factor Receptor-1 in the Peritoneal Tissues of Peritoneal Dialysis Patients / 대한신장학회지

PURPOSE: AQP-1 (Aquaporin-1) and VEGF (vascular endothelial growth factor) are known to play an important role in ultrafiltration in peritoneal dialysis. The aim of this study was to evaluate the expression of AQP-1 and VEGF and VEGFR-1 (VEGF type 1 receptor) in peritoneums obtained from uremic non-dialyzed patients and peritoneal dialysis patients and to see if expression of these molecules are correlated with each other and with pathological findings in peritoneum. METHODS: Peritoneal expressions of AQP-1, VEGF and VEGFR-1 were examined by immunohistochemistry using specific antibody to each molecule. The degree of vascular proliferation and inflammation in peritoneal tissues were assessed semi-quantitatively by a single pathologist. RESULTS: AQP-1, VEGF and VEGFR-1 were mainly expressed in the vascular endothelial cells in the peritoneum. No significant difference in peritoneal expression of these molecules was found according to the clinical situations in which peritoneal tissues were obtained. The degree of expression of AQP-1 and VEGF were related to each other but not related to expression of VEGFR-1. The expressions of AQP-1 and VEGF were related to the vascular proliferation. The expression of AQP-1 was also related to inflammation. CONCLUSION: In end-stage renal disease patients before and after initiation of peritoneal dialysis, the peritoneal expressions of AQP-1 and VEGF were related to vascular proliferation. Inflammation might have some influence in expression of AQP-1.