Pigment nephropathy

Pigment nephropathy occurs as a special form of acute kidney injury (AKI), triggered by hemolysis (e.g. transfusion incident) or rhabdomyolysis (myoglobinuria in rhabdomyolysis). This is caused by severe trauma (e.g. crush syndrome - He Q et al. 2011), drug abuse, acolohol withdrawal delirium, excessive physical stress, lipid-lowering drugs, etc.).

Heme pigments such as myoglobin and hemoglobin are filtered by glomeruli and absorbed by proximal tubules. Myoglobin-induced renal toxicity plays a key role in rhabdomyolysis-associated nephropathy.

Myoglobulins cause renal vasoconstriction, tubular obstruction, increased oxidative stress and inflammation. In this regard, heme is a signaling molecule capable of activating the inflammasome signaling pathway. Apparently, inflammasome-mediated inflammatory response occupies a central pathogenetic position in pigmentary nephropathy (Giuliani KTK et al. 2019).

Clinical symptoms of acute renal failure. Acute pigment nephropathies are also described in association with hemolysis in cardiopulmonary bypass (Haase M et al. 2007), occur in severe physical taumata such as accidents after earthquakes (He Q et al. 2011). Acute pigment nephropathy due to hemolysis is also observed in various tropical infections. However, it can also occur in the relatively rare genetic causes of hemolytic anemia, such as glucose-6-phosphate dehydrogenase (G6PD) deficiency (Kaul A et al. 2018).

1. Giuliani KTK et al (2019) Pigment Nephropathy: Novel Insights into Inflammasome-Mediated Pathogenesis. Int J Mol Sci 20:1997.
2. Haase M et al (2007) Cardiopulmonary bypass-associated acute kidney injury: a pigment nephropathy? Contrib Nephrol 156: 340-353.
3. He Q et al. (2011) Crush syndrome and acute kidney injury in the Wenchuan Earthquake. J Trauma 70:1213-1217
4. Kaul A et al (2018) G6PD deficiency is not an uncommon cause of pigment nephropathy. Saudi J Kidney Dis Transpl 29:1371-1375.