Faculty of Medicine, Department of Medical Physiology, Laboratory for Cellular Physiology, University of Belgrade, Visegradska 26/II, 11129, Belgrade, Serbia.
University of Haifa, 199 Abba Hushi Blvd, Mount Carmel, 3498838, Haifa, Israel.
Sci Rep. 2023 Mar 10;13(1):4025. doi: 10.1038/s41598-023-31205-7.
Acute kidney injury (AKI) relates to an abrupt reduction in renal function resulting from numerous conditions. Morbidity, mortality, and treatment costs related to AKI are relatively high. This condition is strongly associated with damage to proximal tubule cells (PTCs), generating distinct patterns of transcriptional and epigenetic alterations that result in structural changes in the nuclei of this epithelium. To this date, AKI-related nuclear chromatin redistribution in PTCs is poorly understood, and it is unclear whether changes in PTC chromatin patterns can be detected using conventional microscopy during mild AKI, which can progress to more debilitating forms of injury. In recent years, gray level co-occurrence matrix (GLCM) analysis and discrete wavelet transform (DWT) have emerged as potentially valuable methods for identifying discrete structural changes in nuclear chromatin architecture that are not visible during the conventional histopathological exam. Here we present findings indicating that GLCM and DWT methods can be successfully used in nephrology to detect subtle nuclear morphological alterations associated with mild tissue injury demonstrated in rodents by inducing a mild form of AKI through ischemia-reperfusion injury. Our results show that mild ischemic AKI is associated with the reduction of local textural homogeneity of PTC nuclei quantified by GLCM and the increase of nuclear structural heterogeneity indirectly assessed with DWT energy coefficients. This rodent model allowed us to show that mild ischemic AKI is associated with the significant reduction of textural homogeneity of PTC nuclei, indirectly assessed by GLCM indicators and DWT energy coefficients.
急性肾损伤(AKI)与多种情况导致的肾功能突然下降有关。与 AKI 相关的发病率、死亡率和治疗成本相对较高。这种情况与近端肾小管细胞(PTC)的损伤密切相关,导致特定的转录和表观遗传改变模式,从而导致该上皮细胞核的结构变化。迄今为止,PTC 中与 AKI 相关的核染色质重分布知之甚少,也不清楚在轻度 AKI 期间是否可以使用常规显微镜检测到 PTC 染色质模式的变化,而轻度 AKI 可能会进展为更具破坏性的损伤形式。近年来,灰度共生矩阵(GLCM)分析和离散小波变换(DWT)已成为识别核染色质结构中离散结构变化的潜在有价值方法,这些变化在常规组织病理学检查中不可见。在这里,我们提出的研究结果表明,GLCM 和 DWT 方法可成功用于肾脏病学,以检测与通过缺血再灌注损伤诱导轻度 AKI 在啮齿动物中表现出的轻度组织损伤相关的细微核形态改变。我们的结果表明,轻度缺血性 AKI 与通过 GLCM 定量的 PTC 核局部纹理均匀性降低以及通过 DWT 能量系数间接评估的核结构异质性增加有关。该啮齿动物模型使我们能够证明轻度缺血性 AKI 与 PTC 细胞核纹理均匀性的显著降低有关,这是通过 GLCM 指标和 DWT 能量系数间接评估的。