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Dyschloremia Is a Risk Factor for the Development of Acute Kidney Injury in Critically Ill Patients.
Shao, M, Li, G, Sarvottam, K, Wang, S, Thongprayoon, C, Dong, Y, Gajic, O, Kashani, K
PloS one. 2016;(8):e0160322
Abstract
INTRODUCTION Dyschloremia is common in critically ill patients, although its impact has not been well studied. We investigated the epidemiology of dyschloremia and its associations with the incidence of acute kidney injury and other intensive care unit outcomes. MATERIAL AND METHODS This is a single-center, retrospective cohort study at Mayo Clinic Hospital-Rochester. All adult patients admitted to intensive care units from January 1st, 2006, through December 30th, 2012 were included. Patients with known acute kidney injury and chronic kidney disease stage 5 before intensive care unit admission were excluded. We evaluated the association of dyschloremia with ICU outcomes, after adjustments for the effect of age, gender, Charlson comorbidity index and severity of illness score. RESULTS A total of 6,025 patients were enrolled in the final analysis following the implementation of eligibility criteria. From the cohort, 1,970 patients (33%) developed acute kidney injury. Of the total patients enrolled, 4,174 had a baseline serum chloride. In this group, 1,530 (37%) had hypochloremia, and 257 (6%) were hyperchloremic. The incidence of acute kidney injury was higher in hypochloremic and hyperchloremic patients compared to those with a normal serum chloride level (43% vs.30% and 34% vs. 30%, respectively; P < .001). Baseline serum chloride was lower in the acute kidney injury group vs. the non-acute kidney injury group [100 mmol/L (96-104) vs. 102 mmol/L (98-105), P < .0001]. In a multivariable logistic regression model, baseline serum chloride of ≤94 mmol/L found to be independently associated with the risk of acute kidney injury (OR 1.7, 95% CI 1.1-2.6; P = .01). DISCUSSION Dyschloremia is common in critically ill patients, and severe hypochloremia is independently associated with an increased risk of development of acute kidney injury.
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Determinants of Urinary Output Response to IV Furosemide in Acute Kidney Injury: A Pharmacokinetic/Pharmacodynamic Study.
Silbert, BI, Ho, KM, Lipman, J, Roberts, JA, Corcoran, TB, Morgan, DJ, Pavey, W, Mas, E, Barden, AE, Mori, TA
Critical care medicine. 2016;(10):e923-9
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OBJECTIVES This study assessed the determinants of urinary output response to furosemide in acute kidney injury; specifically, whether the response is related to altered pharmacokinetics or pharmacodynamics. DESIGN Prospective cohort. SETTING Tertiary ICU. PATIENTS Thirty critically ill patients with acute kidney injury without preexisting renal impairment or recent diuretic exposure. INTERVENTION A single dose of IV furosemide. MEASUREMENTS AND MAIN RESULTS Baseline markers of intravascular volume status were obtained prior to administering furosemide. Six-hour creatinine clearance, hourly plasma/urinary furosemide concentrations, and hourly urinary output were used to assess furosemide pharmacokinetics/pharmacodynamics parameters. Of 30 patients enrolled, 11 had stage-1 (37%), nine had stage-2 (30%), and 10 had stage-3 (33%) Acute Kidney Injury Network acute kidney injury. Seventy-three percent were septic, 47% required norepinephrine, and 53% were mechanically ventilated. Urinary output doubled in 20 patients (67%) following IV furosemide. Measured creatinine clearance was strongly associated with the amount of urinary furosemide excreted and was the only reliable predictor of the urinary output after furosemide (area under the receiver-operating-characteristic curve, 0.75; 95% CI, 0.57-0.93). In addition to an altered pharmacokinetics (p < 0.01), a reduced pharmacodynamics response to furosemide also became important when creatinine clearance was reduced to less than 40 mL/min/1.73 m (p = 0.01). Acute kidney injury staging and markers of intravascular volume, including central venous pressure, brain-natriuretic-peptide concentration, and fractional urinary sodium excretion were not predictive of urinary output response to furosemide. CONCLUSIONS The severity of acute kidney injury, as reflected by the measured creatinine clearance, alters both pharmacokinetics and pharmacodynamics of furosemide in acute kidney injury, and was the only reliable predictor of the urinary output response to furosemide in acute kidney injury.
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Regional citrate versus systemic heparin anticoagulation for continuous renal replacement in critically ill patients.
Kutsogiannis, DJ, Gibney, RT, Stollery, D, Gao, J
Kidney international. 2005;(6):2361-7
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BACKGROUND We determined the effect of regional citrate versus systemic heparin anticoagulation for continuous renal replacement therapy in critically ill subjects suffering from acute renal failure who were not at high risk for hemorrhagic complications. METHODS Between April 1999 and June 2002, 30 critically ill subjects requiring continuous renal replacement therapy and using 79 hemofilters were randomly assigned to receive regional citrate or systemic heparin anticoagulation. RESULTS The median hemofilter survival time was 124.5 hours (95% CI 95.3 to 157.4) in the citrate group, which was significantly longer than the 38.3 hours (95% CI 24.8 to 61.9) in the heparin group (P < 0.001). Increasing illness severity score, male gender, and decreasing antithrombin-III levels were independent predictors of an increased relative hazard of hemofilter failure. After adjustment for illness severity, antithrombin-III levels increased significantly more over the period of study in the citrate as compared to the heparin group (P= 0.038). Moreover, after adjustment for antithrombin-III levels and illness severity score, the relative risk of hemorrhage with citrate anticoagulation was significantly lower than that with heparin (relative risk of 0.14; 95% CI 0.02 to 0.96, P= 0.05). CONCLUSION Compared with systemic heparin anticoagulation, regional citrate anticoagulation significantly increases hemofilter survival time, and significantly decreases bleeding risk in critically ill patients suffering from acute renal failure and requiring continuous renal replacement therapy.
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Incidence of contrast nephropathy in patients receiving comprehensive intravenous and oral hydration.
Mueller, C, Seidensticker, P, Buettner, HJ, Perruchoud, AP, Staub, D, Christ, A, Buerkle, G
Swiss medical weekly. 2005;(19-20):286-90
Abstract
BACKGROUND Contrast-induced nephropathy (CIN) remains a major complication of percutaneous coronary interventions (PCI) and a common cause of acute renal failure. The most effective preventive strategy is unknown. OBJECTIVES This study sought to estimate the incidence of CIN in patients receiving comprehensive intravenous and oral volume supplementation for PCI during which iopromide (Ultravist 370, Schering, Berlin, Germany) was used. METHODS We prospectively studied the development of CIN in 425 consecutive patients undergoing PCI, applying comprehensive intravenous and oral hydration in all patients. Baseline renal function was assessed by calculating the glomerular filtration rate (GFR) with the use of the abbreviated Modification of Diet in Renal Disease Study equation. CIN was defined as an increase in serum creatinine of at least 0.5 mg/dl (44 mmol/l) within 48 hours. RESULTS Mean patients' age (mean +/- SD) was 64 +/- 10 years. A total of 133/425 patients (31%) were 70 years or older, 107 (25%) were women, 70 (16%) were diabetics, 218 (51%) had prior myocardial infarction, and 43 (10%) underwent PCI for an acute ST-segment elevation myocardial infarction. Mean GFR was 89 ml/min/1.73 m2. Glomerular filtration rate was below 60 ml/min/ 1.73 m2 in 43 patients (10%). During PCI 226 +/- 80 ml of iopromide were used. With the comprehensive hydration strategy used, CIN developed in only 6 of 425 (1.4%; 95% confidence interval 0.5-3.1%) patients. No patient required dialysis. CONCLUSIONS Applying the combination of intravenous and oral volume supplementation results in a very low incidence of CIN following PCI. Hydration remains the cornerstone for the prevention of CIN.
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Effects of lactate-buffered and lactate-free dialysate in CAVHD patients with and without liver dysfunction.
McLean, AG, Davenport, A, Cox, D, Sweny, P
Kidney international. 2000;(4):1765-72
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BACKGROUND Continuous modalities of renal replacement deplete patients of bicarbonate, which is traditionally replaced indirectly by lactate in dialysate or replacement fluids. We have compared a new lactate-free dialysate (unbuffered dialysate with separate bicarbonate replacement of dialytic bicarbonate loss) with standard lactate-buffered dialysate in terms of acid-base control, lactate accumulation, and hemodynamic stability in patients undergoing continuous renal replacement therapy in an intensive care unit. METHODS A nonrandomized crossover cohort study involving 54 patients with multi-organ failure (of whom 19 had significant hepatic dysfunction) was performed. All patients completed 24-hour continuous hemodiafiltration against both lactate-buffered and lactate-free dialysate. Arterial pH, blood gases, bicarbonate, and lactate, venous sodium, blood pressure, and inotrope requirements were measured before and at six hourly intervals during the first 24 hours of dialysis against each dialysate. RESULTS Lactate-free dialysate provided more rapid control of acidosis than lactate buffered with less total administration of buffer than that given during the lactate-buffered period (total mmol bicarbonate vs. total mmol lactate + bicarbonate). Lactate accumulation was slight in both periods, but was higher during lactate-buffered continuous venovenous hemodiafiltration (CVVHD). The mean arterial pressure rose during lactate-free dialysis with decreased inotrope doses and fell during lactate-buffered dialysis with increased inotrope requirement. Results in patients with liver dysfunction were not significantly different from those without it. CONCLUSIONS Over the time scale of 24 hours, lactate derived from continuous dialysis circuits is efficiently cleared from the blood of most patients with multi-organ failure, but with less effect on systemic acidosis than is produced by equivalent amounts of bicarbonate.