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Rocktaeschel, Jens; Morimatsu, Hiroshi; Uchino, Shigehiko; Goldsmith, Donna; Poustie, Stephanie J; Story, David A; Gutteridge, Geoffrey A; Bellomo, Rinaldo

doi:10.1186/cc2333

Cited by 115 publications

(17 citation statements)

References 21 publications

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“…In the past there have been studies which demonstrated that kidney injury can influence morbidity and mortality directly by causing water and salt retention leading to hyperkalemia, acidosis [17–18]and fluid overload. However, AKI has been associated with increased insulin resistance and protein breakdown that can lead to immune system dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Outcome of critically ill patients with acute kidney injury using the Acute Kidney Injury Network criteria*

Mandelbaum

Scott

Lee

et al. 2011

Critical Care Medicine

152

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Objective Acute kidney injury (AKI) affects 5–7% of all hospitalized patients with a much higher incidence in the critically ill. The Acute Kidney Injury Network proposed a definition in which serum creatinine rises (>0.3mg/dl) and/or oliguria (<0.5/ml/kg/h) for a period of 6 hours are used to detect AKI. Accurate urine output measurements as well as serum creatinine values from our database were used to detect patients with AKI and calculate their corresponding mortality risk and length of stay. Design Retrospective cohort study. Setting 7 intensive care units at, a large, academic, tertiary medical center. Patients Adult patients without evidence of end stage renal disease, with more than 2 creatinine measurements and at least a 6 hours urine output recording, who were admitted to the ICU between 2001 and 2007. Interventions Medical records of all the patients were reviewed. Demographic information, lab results, charted data, discharge diagnoses, physiological data and patient outcomes were extracted from the MIMIC-II database using a SQL query. Measurements and main results From 19,677 adult patient records, 14,524 patients met the inclusion criteria. 57% developed AKI during their ICU stay. In-hospital mortality rates were: 13.9%, 16.4%, 33.8% for AKI 1, 2 and 3 respectively compared to only 6.2% in patients without AKI (p<0.0001). After adjusting for multiple covariates AKI was associated with increased hospital mortality (OR 1.4 and 1.3 for AKI1 and AKI2 and 2.5 for AKI3; p<0.0001). Using multivariate logistic regression, we found that in patients who developed AKI, urine output alone was a better mortality predictor than creatinine alone or the combination of both. Conclusions More than 50% of our critically ill patients developed some stage of AKI resulting in stage-wise increased mortality risk. However, the mortality risk associated with AKI stages 1 and 2 does not differ significantly. In light of these findings reevaluation of the AKIN staging criteria should be considered.

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Section: Discussionmentioning

confidence: 99%

Outcome of critically ill patients with acute kidney injury using the Acute Kidney Injury Network criteria*

Mandelbaum

Scott

Lee

et al. 2011

Critical Care Medicine

152

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“…However, preliminary results of our group showed that sequential analysis of some urinary biochemical parameters has a potential role in detect AKI even before increases in creatinine [14,15]. In addition, a physicochemical acid–base analysis of blood [16] and urine [17,18] has also been previously used to describe some of the alterations that occur when renal function is impaired. However, these studies were limited to patients with established AKI: none has focused on a sequential evaluation of these physicochemical parameters in the course of AKI, including the days preceding AKI diagnosis.…”

Section: Introductionmentioning

confidence: 99%

Physicochemical analysis of blood and urine in the course of acute kidney injury in critically ill patients: a prospective, observational study

2013

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BackgroundSequential physicochemical alterations in blood and urine in the course of acute kidney injury (AKI) development have not been previously described. We aimed to describe these alterations in parallel to traditional renal and acid–base parameters.MethodsOne hundred and sixty eight consecutive critically ill patients with no previous kidney disease, who had an indwelling urinary catheter at ICU admission and who remained with the catheter for at least two days without dialysis were included. A sample of blood and spot urine were collected simultaneously, once daily, until catheter removal or dialysis requirement. Traditional acid–base and renal parameters were sequentially evaluated in parallel to blood and urinary physicochemical parameters. Patients were classified during this period as having or not AKI and, for patients with AKI, duration (transient or persistent) and severity (creatinine-based AKIN stage) were evaluated.ResultsOne hundred and thirteen patients (67.3%) had AKI: 92 at ICU admission and 21 during the observation period. AKI development was characterized in blood by increased values of phosphate and unmeasured anions (SIG), decreased albumin, and in urine by decreased values of sodium (NaU), chloride (ClU) as well as high urinary strong ion difference (SIDu). These alterations began to occur before AKI diagnosis, and they reverted in transient AKI but remained in persistent AKI. NaU, ClU and albumin decreased, and phosphate, SIG and SIDu increased with AKI severity progression. NaU and ClU values increased again when AKIN stage 3 was reached.ConclusionsSimultaneous physicochemical analysis of blood and urine revealed standardized alterations that characterize AKI development in critically ill patients. These alterations paralleled AKI duration and severity. Future studies should consider including sequential evaluation of urine biochemistry as part of the armamentarium for AKI diagnosis and management.

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“…Inadequate renal H ϩ secretion caused, for example, by mutations to acid-base transporters (1)(2)(3)(4) or carbonic anhydrases (5), or by renal failure (6,7), can lead to a life-threatening decrease in blood pH. Moreover, to maintain a stable blood pH, the kidney must appropriately increase H ϩ secretion in response to metabolic acidosis (a decrease in blood pH caused by a decrease in [HCO 3 Ϫ ] at a fixed CO 2 ) or to respiratory acidosis.…”

mentioning

confidence: 99%

Evidence from renal proximal tubules that \documentclass[12pt]{minimal}\usepackage{amsmath}\usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy}\usepackage{mathrsfs}\setlength{\oddsidemargin}{-69pt}\begin{document}\begin{equation}{\mathrm{HCO}}_{3}^{-}\end{equation}\end{document} and solute reabsorption are acutely regulated not by pH but by basolateral \documentclass[12pt]{minimal}\usepackage{amsmath}\usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackag

Zhou

Zhao

Bouyer

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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Respiratory acidosis, a decrease in blood pH caused by a rise in [CO 2], rapidly triggers a compensatory response in which the kidney markedly increases its secretion of H ؉ from blood to urine. However, in this and other acid-base disturbances, the equilibrium CO 2 kidney ͉ out-of-equilibrium solution ͉ acid-base disturbances ͉ volume reabsorption A major task of the kidney is to secrete H ϩ into the urine.Inadequate renal H ϩ secretion caused, for example, by mutations to acid-base transporters (1-4) or carbonic anhydrases (5), or by renal failure (6, 7), can lead to a life-threatening decrease in blood pH. Moreover, to maintain a stable blood pH, the kidney must appropriately increase H ϩ secretion in response to metabolic acidosis (a decrease in blood pH caused by a decrease in [HCO 3 Ϫ ] at a fixed CO 2 ) or to respiratory acidosis. However, a half century after the classical observation that respiratory acidosis rapidly stimulates renal H ϩ secretion (8, 9), we still have little insight into how the kidney senses acute acid-base disturbances.The renal proximal tubule (PT) reabsorbs (from lumen to blood) a liquid that contains Ϸ80% of the HCO 3 Ϫ filtered by the glomerulus. The PT cell does this reabsorbtion by secreting H ϩ into the PT lumen and using this H ϩ to titrate luminal HCO 3 Ϫ to CO 2 and H 2 O. After entering the cell across the apical membrane, the CO 2 and H 2 O recombine to produce H ϩ and HCO 3 Ϫ . The cell extrudes the H ϩ into the lumen across the apical membrane through Na-H exchangers (10-12) and H ϩ pumps (13) and moves the HCO 3 Ϫ out across the basolateral membrane via the electrogenic Na͞HCO 3 cotransporter NBCe1-A (14, 15). Carbonic anhydrases catalyze the interconversions between CO 2 and H 2 O on the one hand and HCO 3 Ϫ and H ϩ on the other (5). Because blood pH is the parameter regulated by these acid-base transport processes, blood pH or, more likely, intracellular pH (pH i ), has been thought to be the parameter sensed by renal cells. However, because of the interconversion CO 2 ϩ H 2 O^HCO 3 In the present study, we perfused single, isolated S2 segments of rabbit PTs and collected the fluid that had passed along the PT lumen. Analysis of this collected fluid allowed us to compute volume reabsorption (J V ); HCO 3 Ϫ reabsorption (J HCO 3 ), which is virtually the same as the H ϩ -secretion rate under the conditions of our experiments; and the reabsorption of solutes other than NaHCO 3 (J Other ). We made the surprising observation that, at least in the short term, J HCO 3 and J Other do not respond to changes in basolateral or intracellular pH. The most straightforward hypothesis is that PT cells have sensors for basolateral HCO 3 Ϫ and a parameter related to CO 2 . Materials and MethodsExcept for the compositions of most of the OOE CO 2 ͞HCO 3 Ϫ solutions, our methods are described in detail in ref. 17.Tubule Perfusion. We hand dissected kidneys from ''pathogenfree'' female New Zealand White rabbits (1.4-2.0 kg) to yield individual segments of midcortical S2 PTs in accorda...

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Untitled

Cited by 115 publications

References 21 publications

Outcome of critically ill patients with acute kidney injury using the Acute Kidney Injury Network criteria*

Outcome of critically ill patients with acute kidney injury using the Acute Kidney Injury Network criteria*

Physicochemical analysis of blood and urine in the course of acute kidney injury in critically ill patients: a prospective, observational study

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