Conclusion: It appears that caspase-3 may play
a key role in the nephrotoxic injury resulting from PAP, PPD or its oxidized form.”
“Background: Hyperphosphatemia is associated with morbidity and mortality in hemodialysis patients. The use of calcium chelators is restricted by the risk of hypercalcemia VX-765 and vascular calcifications. Sevelamer, a non-calcium chelator, is associated with risks of metabolic acidosis and poor compliance. Lanthanum carbonate is a non-calcium chelator not associated with these issues. However, accumulation in liver and bone has been a reason for concern.
Methods: Adult patients (n=112) from 9 hemodialysis centers, with serum phosphorus >5.5 mg/dL and on hemodialysis for >1 year, were selected to switch to lanthanum carbonate (mean dosage: 2,189 +/- 491 mg/day); 103 completed the study. Laboratory assays for serum phosphate,
calcium, parathyroid hormone, alkaline phosphatase, gamma-glutamyl transpeptidase (gamma GT), aspartate transaminase, alanine transaminase and plasma bicarbonate were performed monthly. Seven patients underwent a bone biopsy for evaluation of lanthanum bone content.
Results: Switching to lanthanum carbonate led to a reduction in mean serum phosphate levels (-18.2%; p<0.001) and calcium x phosphorus product CX-4945 (-17.6%; p<0.0001). There were no important changes in other variables, except for an increase in transaminases in 2 patients with preexisting liver disease, who discontinued therapy. An increase in plasma bicarbonate concentration was observed (p=0.001). Although some
lanthanum was detected in bone, its distribution did not follow the mineralization front.
Conclusions: Lanthanum VX-680 clinical trial carbonate is effective and well tolerated, provided that recipients do not have preexisting liver disease. After 8 months of treatment, lanthanum was not detected in the mineralization front of bone. In hemodialysis patients, lanthanum carbonate does not seem to be involved in metabolic bone disease.”
“Background: We hypothesized that post-operative serum uric acid (SUA) may be associated with acute kidney injury (AKI).
Methods: In this prospective, observational study, the relationships between SUA, urine neutrophil gelatinase-associated lipocalin (uNGAL) and interleukin-18 (uIL-18), serum monocyte chemoattractant protein-1 (sMCP-1) and tumor necrosis factor-alpha (sTNF-alpha), and incidence of AKI were determined. SUA were divided into tertiles and their association with AKI investigated.
Results: A total of 100 cardiac surgery patients were included for analyses. The 1st, 2nd, and 3rd SUA tertiles were associated with 15.1%, 11.7%, and 54.5% incidence of AKI, respectively. The 3rd SUA tertile, compared to the referent 1st tertile, was associated with an eightfold (OR 8.38, CI95% 2.13-33.05, p=0.002) increased risk for AKI.