AKI after TAVR is associated with worse outcomes. Blood transfusion should be administered restrictively in TAVR. Patients with CKD, PAD, prior CABG, and TA approach require close surveillance as they are at risk for AKI through seven days after TAVR. doi: 10.1111/jocs.12768 (J Card Surg 2016;31:416-422).

Trough levels of MPA do not show a strong correlation with AUC. In clinical situations where MPA levels are essential to guide therapy, an AUC0-4 would be a better indicator of the adequacy of treatment.

We investigated the ability of serum uric acid (SUA) to predict laboratory tumor lysis syndrome (LTLS) and compared it to common laboratory variables, cytogenetic profiles, tumor markers and prediction models in acute myeloid leukemia patients. In this retrospective study patients were risk-stratified for LTLS based on SUA cut-off values and the discrimination ability was compared to current prediction models. The incidences of LTLS were 17.8%, 21% and 62.5% in the low, intermediate and high-risk groups, respectively. SUA was an independent predictor of LTLS (adjusted OR 1.12, CI95% 1.0–1.3, p = 0.048). The discriminatory ability of SUA, per ROC curves, to predict LTLS was superior to LDH, cytogenetic profile, tumor markers and the combined model but not to WBC (AUCWBC 0.679). However, in comparisons between high-risk SUA and high-risk WBC, SUA had superior discriminatory capability than WBC (AUCSUA 0.664 vs. AUCWBC 0.520; p <0.001). SUA also demonstrated better performance than the prediction models (high-risk SUAAUC 0.695, p<0.001). In direct comparison of high-risk groups, SUA again demonstrated superior performance than the prediction models (high-risk SUAAUC 0.668, p = 0.001) in predicting LTLS, approaching that of the combined model (AUC 0.685, p<0.001). In conclusion, SUA alone is comparable and highly predictive for LTLS than other prediction models.

The metabolism of a typical Western diet generates 50-100 mEq of acid (H + ) per day, which must be excreted in the urine for the systemic acid-base to remain in balance. The 2 major mechanisms that are responsible for the renal elimination of daily acid under normal conditions are ammonium (NH 4 + ) excretion and titratable acidity. In the presence of systemic acidosis, ammonium excretion is intensified and becomes the crucial mechanism for the elimination of acid. The impairment in NH 4 + excretion is therefore associated with reduced acid excretion, which causes excess accumulation of acid in the body and consequently results in metabolic acidosis. Chronic kidney disease (CKD) is associated with the impairment in acid excretion and precipitation of metabolic acidosis, which has an adverse effect on the progression of CKD. Recent studies suggest that the progressive decline in renal ammonium excretion in CKD is an important determinant of the ensuing systemic metabolic acidosis and is an independent factor for predicting the worsening of kidney function. While these studies have been primarily performed in hypertensive individuals with CKD, a closer look at renal NH 4 + excretion in non-hypertensive individuals with CKD is warranted to ascertain its role in the progression of kidney disease.