The ability of the human immune system to discriminate between self and nonself molecules is one of its key roles. Class I antigens, which aid the immune system in recognizing self-molecules, are present in the majority of nucleated cells in the human body. There is a light chain that goes along with the heavy chain in these antigens. This light-protein chain is known as β2-microglobulin, and it can be excreted into serum. Midway through the 1960s, β2-microglobulin (β2M) was identified as a urine protein in the urine of patients suffering from cadmium poisoning or Wilson's disease. Primarily, glomerular filtration is used to remove β2M from serum; however, the proximal convoluted tubule reabsorbs and catabolizes over 99.9% of the filtered protein, leaving urine with a low β2M concentration (often less than 360 µg/l). Megalin–cubilin complex is thought to be the mechanism of β2M removal from the tubular fluid based on ligand blotting experiments, megalin animal knockouts, and human illness. Due to mutations in the LRP2 megalin gene, this condition is linked to developmental delay, tubular proteinuria, and multisystemic disorders. We came to the conclusion that, when patients in the intensive care unit (ICU) have intracerebral haemorrhage (ICH), B2-MG can be used as a predictive marker of the onset of AKI. highlighting the most recent guidelines for the diagnosis and treatment of these patients while taking into account the evaluation of β2-MG as a tool to achieve early detection of AKI in individuals with ICH. More research is required to fully examine this problem.