Refine
Has Fulltext
- no (7)
Document Type
- Other (7) (remove)
Language
- English (7)
Is part of the Bibliography
- yes (7)
Keywords
- Assays (1)
- Biological Assay (1)
- CKD (1)
- DPP-4 inhibitors (1)
- Dialysis patients (1)
- Dipeptidyl peptidase IV (1)
- Mortality (1)
- PTH (1)
- Serum intact-parathyroid hormone level (1)
- acute kidney injury (1)
- gliptins (1)
- ischemia reperfusion injury (1)
- oxidative stress (1)
DPP4 inhibition prevents AKI
(2017)
Preclinical studies in cell culture systems as well as in whole animal chronic kidney disease (CKD) models showed that parathyroid hormone (PTH), oxidized at the 2 methionine residues (positions 8 and 18), caused a loss of function. This was so far not considered in the development of PTH assays used in current clinical practice. Patients with advanced CKD are subject to oxidative stress, and plasma proteins (including PTH) are targets for oxidants. In patients with CKD, a considerable but variable fraction (about 70 to 90%) of measured PTH appears to be oxidized. Oxidized PTH (oxPTH) does not interact with the PTH receptor resulting in loss of biological activity. Currently used intact PTH (iPTH) assays detect both oxidized and non-oxPTH (n-oxPTH). Clinical studies demonstrated that bioactive, n-oxPTH, but not iPTH nor oxPTH, is associated with mortality in CKD patients.
New data from the LEADER trial show that the glucagon-like peptide 1 receptor agonist liraglutide protects against diabetic nephropathy in patients with type 2 diabetes mellitus. The renoprotective efficacy of liraglutide is not, however, as great as that reported for the sodium-glucose cotransporter 2 inhibitor emplagiflozin in the EMPA-REG OUTCOME trial.