Renal failure
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Hypocalcemia is very common in critically ill patients. While the effect of ionized calcium (iCa) on outcome is not well understood, manipulation of iCa in critically ill patients is a common practice. We analyzed all-cause mortality and several secondary outcomes in patients with acute kidney injury (AKI) by categories of serum iCa among participants in the Acute Renal Failure Trial Network (ATN) Study. ⋯ Severe hypocalcemia with iCa<1 mmol/L independently predicted mortality in patients with AKI needing renal replacement therapy.
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Sepsis is a common and important cause of mortality in critically ill patients. Acute kidney injury (AKI) is one of the most important factors determining morbidity and mortality in the prognosis of sepsis. Recent studies have indicated that the pathogenetic mechanism in septic AKI is totally different from that in non-septic AKI. ⋯ Among the existing methods of treatment, usage of arginine, which is a vasopressor agent, ventilation with a low tidal volume, and hemofiltration methods cleaning toxic mediators from the circulation should be considered in the first place. Hyperglycemia treatment is of major importance, since, besides its anti-inflammatory effect, it has a protective role on the kidney. Regarding pathogenesis, rates of morbidity and mortality are aimed to be reduced through the new agents of therapy that have been studied on.
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Comparative Study
Early initiation of peritoneal dialysis after arterial switch operations in newborn patients.
We investigated the clinical outcome of early initiated peritoneal dialysis (PD) use in our newborn patients who underwent arterial switch operation (ASO) for transposition of the great arteries (TGA) and had routine intraoperative PD catheter implantation. We determined the risk factors for PD, factors associated with prolonged PD, morbidity, and mortality. The aim of the present study was to describe our experience of using PD in this patient cohort. ⋯ We advocate routine implantation of PD catheters to patients with TGA-VSD, coronary artery anomaly, and open sternum in which we have determined high rate of postoperative PD need.
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To assess the utility of neutrophil gelatinase-associated lipocalin (NGAL) in both urine and serum as a follow-up marker for the discrimination of prerenal acute kidney injury (AKI) from intrinsic AKI in critically ill pediatric patients with established AKI at the time of patient presentation. ⋯ In a heterogeneous group of critically ill children with established AKI, we found that NGAL in both urine and serum at the time of patient presentation discriminated intrinsic AKI from prerenal AKI.
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We investigated the protective effect and mechanism of neutrophil gelatinase-associated lipocalin (NGAL) on rats ischemia/reperfusion (I/R) renal injury. Eighteen Sprague-Dawley male rats were randomly divided into three groups. ⋯ Rats with NGAL displayed an attenuated renal damage and a decreased number of tubular epithelial cell apoptosis compared to the I/R + NS group (Scr 63.400 ± 11.908 vs. 121.857 ± 17.151 μmol/L, Bun 14.840 ± 2.868 vs. 28.557 ± 6.434 mmol/L, apoptosis cell number 7.800 ± 1.924 vs. 15.400 ± 3.049/high power field (HPF), p < 0.05), the values were lower in the control group (24.000 ± 3.829 μmol/L, 5.814 ± 1.961 mmol/L, 1.800 ± 0.837/HPF, p < 0.05) compared to two groups above; NGAL-treated rats showed down-regulated Cleaved caspase-3 protein (0.284 ± 0.066 vs. 0.409 ± 0.073, p < 0.05), Bax protein (0.346 ± 0.055 vs. 0.443 ± 0.041, p < 0.05), Bax mRNA (1.423 ± 0.187 vs. 2.550 ± 0.217, p < 0.05) compared to I/R + NS group, but the values were higher in both of the two groups than those in the control group (Cleaved caspase-3 protein 0.104 ± 0.029, Bax protein 0.155 ± 0.027, Bax mRNA 1.000 ± 0.000, p < 0.05). We supposed that exogenous NGAL can inhibit the activation of caspase-3, reduce the expression of Bax, and thus reduce renal tubular cell apoptosis and protect renal function in I/R injury rats.