Published in:
Open Access 01-12-2013 | Research article
Zinc-alpha2-glycoprotein in patients with acute and chronic kidney disease
Published in: BMC Nephrology | Issue 1/2013
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Background
Zinc-alpha2-glycoprotein (AZGP1) is a secreted protein which is synthesized in a variety of cell types. AZGP1 has functionally been implicated in lipid metabolism, the regulation of cell cycling and cancer progression. Previous studies have shown increased circulating AZGP1 levels in patients with chronic kidney disease but AZGP1 has not been investigated in acute kidney injury (AKI). In this study, serum AZGP1 levels were measured in acute and chronic kidney disease to test for a correlation to renal function and other clinical parameters.
Methods
We performed ELISA based measurements of AZGP1 serum levels in 21 patients suffering from grade 3 AKI and in 20 chronic hemodialysis patients. In AKI patients, AZGP1 was first measured before initiation of acute renal replacement therapy and a second measurement was done during renal functional recovery. Sera of healthy blood donors served as controls. The association of AZGP1 with acute and chronic renal dysfunction was analysed, as well as the correlation with clinical parameters, body composition and biochemical variables.
Results
Levels of circulating AZGP1 were significantly elevated in AKI patients. High initial levels of AZGP1 correlated with extra-renal complications but not with parameters of renal function. At follow-up, AZGP1 levels were still increased but now correlated significantly with creatinine, eGFR and urea. Circulating AZGP1 in chronic hemodialysis patients was higher than in AKI patients. An association to parameters of lipid metabolism was not found.
Conclusions
This study illustrates that circulating AZGP1 is not only elevated in chronic hemodialysis patients but also sharply increases during the early phase of AKI. The unexpected association with extra-renal complications during AKI needs further exploration as it might point to unknown biological effects of AZGP1.