Table 1 AIM and kidney diseases

AKI

Ischemia–

reperfusion

Abrupt impairment of kidney filtration function

Dead cell debris in the lumen

AIM removes cellular debris in the systemic circulation

[4, 17, 27, 29, 35]

CKD

AKI, obesity, nephrosclerosis, diabetes

The blood, the urine, and GFR were abnormal

Dead cell debris, lipid droplets, oxLDL level, and glycosylation

IgM-free AIM cleans the lumen-obstructing debris, decreases triacylglycerol deposition within adipocytes, and facilitates oxLDL uptake

[9, 15, 17, 29, 36, 42, 44, 45, 49, 52,53,54,55]

DN

Metabolics, genetic, hemodynamic and environmental factors

High blood pressure, edema, foam uria, proteinuria

Microvascular lesions, morphological and structural changes in the kidney

Free AIM is limited to release, and AIM is elevated in whole plasma

[62, 63]

Glomerular Inflammation in IgAN

Infection, unbalanced immunity, genetics

Glular mesangial cell hyperplasia, and mesangial matrix hyperplasia

IgA with aberrant glycosylations and the deposition of an immune complex which consists of IgA1, IgM, variable IgG, and complement 3 at the glomerular mesangial region

IgA and IgM/IgG immune complexes linked by AIM cause severe inflammatory immune responses

[64, 66, 67]

Delayed graft function of kidney transplantation

Cold and warm IRI

Minuria, anuria, and elevated blood creatinine

Apoptosis and/or necrosis of the renal TECs. Intracellular DAMPs are set free, potentiating allo- and non-alloimmune injury

AIM eliminates necrotic cell debris, limits DAMP release from the damaged tissue, and decreases alloimmunity

[68, 70]