Blood: Hemococotin deficiency promotes acute kidney damage in patients with sickle cell disease!

Center point: In sickle cell disease (SCD), the ratio of plasma alpha-1 microglobulin to hemacoglobin concentration is associated with AKI biomarkers.
in genetically modified SCD mice, the removal of circulating hemolystin to the kidneys could trigger AKI.
: Acute kidney injury (AKI) is one of the main clinical manifestations of sickle cell disease (SCD).
clinical evidence suggests that red blood cell albumin can cause SCD AKI, but its sterile inflammatory process is still unclear.
recently, researchers found that hemococotin deficiencies in SCD patients were associated with increased claims for alpha-1 microglobulin (A1M) compared to healthy control groups, resulting in a 10-fold increase in the ratio of A1M/hemoglobin in SCD patients.
A1M/hemococotin ratio was associated with hemolysis and AKI markers in people with SCD and mice.
experiments in mice showed that in SCD mice, excess hemorubin was directed to the kidneys, during which A1M could lead to AKI, while excess hemolystin in the control group was delivered to the liver as expected.
using genetic and bone marrow chifing techniques, the researchers confirmed that a lack of hemoglobin, stimulated by hemolytic stress, could promote AKI in sickle mice.
but AKI was blocked when a purified hemocoagulant protein was used to correct the lack of hemocoagulant protein in sickle mice before inducing hemolytic stress.
this study identified the deficiency of obtained hemocoagulants as a risk factor for the occurrence of AKI in SCD patients, and hecoagulant replacement therapy is a potential treatment option.
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