Carbamylated Hemoglobin can Differentiate Acute Kidney Injury from Chronic Kidney Disease.

Carbamylated hemoglobin (CarHb) was found to have a potential role in the differentiation of patients with acute kidney injury (AKI) from chronic kidney disease (CKD). This study was aimed at the evaluation of the diagnostic performance and usefulness of CarHb in the differentiation of AKI from CKD. Forty patients with renal disease and twenty age- and sex-matched healthy controls were included in the study. Urea, creatinine, Hb, and CarHb were measured in all the subjects. Patients with AKI and CKD were found to have significantly increased levels of CarHb when compared to controls (P < 0.05 for both groups). Patients with CKD had significantly increased levels of CarHb when compared to patients with AKI (P < 0.05). CarHb showed significant positive correlation with urea in patients with renal disease (r = 0.776, P < 0.0001). Significant area under curve (AUC = 0.840, P < 0.0001) was obtained for CarHb and a cut-off value of 98.33 µg VH/g Hb resulted with the best combination of 85% sensitivity and 75% specificity. CarHb may provide clinical utility since patients with AKI and CKD have similar clinical presentation usually. A cut-off value of 98.33 µg VH/g Hb has been found to be useful to differentiate AKI from CKDs.

Evaluation of protein oxidation and its association with lipid peroxidation and thyrotropin levels in overt and subclinical hypothyroidism.

Both overt (OHT) and subclinical hypothyroid (SHT) disorders have been found to be associated with increased oxidative stress (OXS). Excess thyrotropin [thyroid stimulating hormone (TSH)] is known to directly produce OXS. Increased lipid peroxidation is known to facilitate protein carbonylation. However, the associations between lipid and protein oxidation and elevated TSH levels have not been studied. Thyroid profile, lipid peroxidation as malondialdehyde (MDA) levels and protein carbonylation as protein carbonyls (PCO) were estimated in OHT and SHT groups consisting of 36 patients each, in comparison to 39 euthyroid controls. We also determined the associations between TSH, MDA, and PCO levels in OHT and SHT groups. Increased oxidative damage was evidenced through significant elevations in the concentrations of MDA and PCO in OHT and SHT groups compared to controls (p < 0.01). Both TSH and MDA levels were positively associated with PCO in OHT group. Partial correlation analysis revealed that both excess TSH and increased MDA levels are mutually influencing elevated PCO. The results indicate that there is a simultaneous oxidative damage to lipids and proteins leading to increased MDA and PCO levels in both patient groups. Either of the excess TSH and increased MDA levels are combinably involved in the elevation of PCO in hypothyroidism.