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BACKGROUND Acute kidney injury predicts adverse outcomes after cardiac surgery. OBJECTIVES To determine whether ultra-short-term changes (within 120 min) in serum creatinine (SCrea) levels after cardiac surgery predict clinical outcomes (30-day mortality). DESIGN Observational cohort study. SETTING Austrian tertiary referral centre. PATIENTS A total of 7651 patients scheduled to undergo elective cardiac surgery. MAIN OUTCOME MEASURES We analysed SCrea levels measured pre-operatively (baseline) and within 120 min after surgery. We also adjusted the postoperative SCrea levels for fluid balance. Patients were grouped according to the difference between the pre and postoperative SCrea levels (ΔSCreaAdmICU). We performed univariable and multivariable analyses to determine the association between changes in SCrea levels and 30-day mortality. RESULTS After cardiac surgery, the SCrea level decreased in 5923 patients and increased in 1728 patients. Increased SCrea levels were associated with a 21% increase in 30-day mortality. Even minimal increases in SCrea (0 to

Acute kidney injury (AKI) is a clinical syndrome evolving from a broad spectrum of etiologies, which is often associated with manifold short- and long-term complications, and with a pronounced impairment of outcome. To avoid these profound consequences, prevention and therapy of AKI are of utmost importance. Within this context the metabolic management and nutrition must play an important role. AKI, also from a metabolic/nutritional point of view, is an extremely heterogeneous clinical syndrome, which often is a systemic disease process with prooxidative, proinflammatory, and hypercatabolic characteristics. Metabolism and nutrient requirements are not only determined by the acutely uremic state/the stage of AKI and by the type and intensity of renal replacement therapy (RRT) but also by the underlying disease process leading to AKI and associated complications. Nutrient requirements may differ widely between individual patients but may also vary in the same patient during the course of disease, and nutrition therapy must be coordinated with RRT. In sicker AKI patients a more holistic metabolic management is required that, in addition to general nutrition support and infusion of fluids and electrolyes, must include maintenance of electrolyte and acid–base balance, glucose control, and a stage-specific and individualized approach adapted for each patient at each phase of disease. Nevertheless, many patients with AKI are not critically ill and may be treated on open wards. They can be nourished orally with food or nutritional supplements. These patients also need a stage-adapted nutrition program. Because of the limited tolerance to fluids, electrolytes, and also many nutritional substrates and products, metabolic derangements frequently occur. Thus even more than in other clinical conditions, metabolic support in the more seriously ill AKI patients must not only be individualized but must be monitored more closely than patients with most other disease states.

Ubertherapie – als eine nicht indizierte oder vom Patienten nicht gewunschte Therapie und Diagnostik („non-beneficial therapy“) – ist ein inharentes und schwerwiegendes Problem der modernen Medizin und insbesondere der Intensivmedizin. Ubertherapie zieht sich durch alle Bereiche der Intensivmedizin, kann schon am Notfallort beginnen, betrifft (ungerechtfertigte) Aufnahmen auf die Intensivstation, die Uberdiagnostik und vor allem die Blutabnahmen, eine uberhohte Invasivitat oder den inadaquaten Einsatz maschineller Verfahren. Sie manifestiert sich an einem „Zuviel“ an Sedierung, Relaxation, Volumengabe, Sauerstoff, Kreislauftherapie, an Blutprodukten, Antibiotika und anderen Medikamenten und Ernahrung. Ubertherapie betrifft aber insbesondere auch das Lebensende, wenn ein kuratives Therapieziel nicht mehr erreicht werden kann. Ubertherapie hat wesentliche ethische Implikationen, missachtet alle 4 medizinethischen Grundsatze, die Autonomie, Wurde und Integritat der Patienten, ist mit keiner Benefizienz verbunden, steigert Schmerz, Leid, verlangert Sterben, vermehrt das Leid von Angehorigen, fuhrt zu Frustrationen im Team, missachtet die Verteilungsgerechtigkeit und schadigt bei prinzipiell limitierten Ressourcen die Gesellschaft insgesamt. Sie ist auch ein rechtliches Problem geworden und kann als Verursachung ungerechtfertigten Leides juristisch geahndet werden. Ubertherapie ist schlechte Medizin, kein Kavaliersdelikt; alle mussen kontinuierlich daran arbeiten, eine nichtgerechtfertigte Therapie zu vermeiden.

The central role of the organ system "gut" for critically ill patients has not been acknowledged until the last decade. The gut is a crucial immunologic, metabolic and neurologic organ system and impairment of its functions is associated with morbidity and mortality. The gut has a central position in the cross-talk between organs and dysfunction of the gut may result in impairment of other intra-abdominal and extra-abdominal organ systems. The intestinal tract is the most important source of endogenous infections and determines the inflammatory status of the organism. Gut failure is an element of the multiple organ dysfunction syndrome (MODS). The leading mechanism in the evolution of endogenous infections is the intestinal translocation of microbes. A dysbiosis and damage of the intestinal mucosa leads to a disorder of the mucosal barrier function, increases the permeability and promotes translocation (leaky gut hypothesis). A further crucial mechanism of organ interactions is the increase in intra-abdominal pressure. Intra-abdominal hypertension promotes further injury of the gut, increases translocation and inflammation and causes dysfunction of other organ systems, such as the kidneys, the cardiovascular system and the lungs. Maintaining and/or restoring intestinal functions must be a priority of any intensive care therapy. The most important measure is early enteral nutrition. Other measures are the preservation of motility and modulation of the intestinal microbiome. Intra-abdominal hypertension must be reduced by an individually adapted infusion therapy, positioning of the patient, administration of drugs (abdominal compliance) and decompression (by tubes, endoscopically or in severe cases surgically).

An association of body mass index (BMI) and outcome, the "obesity paradox," has been described in patients with chronic kidney disease (CKD) and end-stage renal disease. We sought to assess whether a potential beneficial effect of a high body mass is also seen in CKD patients with critical illness.In a retrospective analysis of a prospectively collected database of 123,416 patients from 107 Austrian intensive care units (ICUs) in whom BMI was available, the association of 6 groups of BMI and hospital mortality was assessed in 12,206 patients with CKD 3-5 by univariate and multivariate logistic regression analyses.Patients with CKD were sicker, had a longer ICU stay, and had a higher ICU and hospital mortality than those without. The association of BMI and outcome in CKD patients indicated a U-shaped curve with the highest mortality in patients with BMI20 and ≥40, and the lowest with a BMI between ≥25 and40. This relationship was also significant in a multivariate analysis adjusted for severity of illness assessed by Simplified Acute Physiology Score III score, age, gender, admission diagnosis, and pre-existing comorbidities. It was not found in patients with CKD 5 on renal replacement therapy, in patients below 60 years of age, and those with diabetes mellitus requiring insulin treatment.BMI is associated with better outcomes in CKD 3-5 patients who have acquired acute intermittent diseases and are admitted to an ICU, but not those requiring renal replacement therapy. This higher tolerance to acute disease processes may in part explain the "obesity paradox" observed in CKD patients.

Background and objectives A knowledge of baseline serum creatinine (bSCr) is mandatory for diagnosing and staging AKI. With often missing values, bSCr is estimated by back-calculation using several equations designed for the estimation of GFR, assuming a “true” GFR of 75 ml/min per 1.73 m 2 . Using a data set from a large cardiac surgery cohort, we tested the appropriateness of such an approach and compared estimated and measured bSCr. Moreover, we designed a novel data-driven model (estimated serum creatinine [eSCr]) for estimating bSCr. Finally, we analyzed the extent of AKI and mortality rate misclassifications. Design, setting, participants, & measurements Data for 8024 patients (2833 women) in our cardiac surgery center were included from 1997 to 2008. Measured and estimated bSCr were plotted against age for men and women. Patients were classified to AKI stages defined by the Kidney Disease Improving Global Outcomes (KDIGO) group. Results were compared with data from another cardiac surgery center in Zurich, Switzerland. Results The Modification of Diet in Renal Disease and the Chronic Kidney Disease Epidemiology Collaboration formulae describe higher estimated bSCr values in younger patients, but lower values in older patients compared with the measured bSCr values in both centers. The Pittsburgh Linear Three Variables formula correctly describes the increasing bSCr with age, however, it underestimates the overall bSCr level, being in the range of the 25% quantile of the measured values. Our eSCr model estimated measured bSCr best. AKI stage 1 classification using all formulae, including our eSCr model, was incorrect in 53%–80% of patients in Vienna and in 74%–91% in Zurich; AKI severity (according to KDIGO stages) and also mortality were overestimated. Mortality rate was higher among patients falsely classified into higher KDIGO stages by estimated bSCr. Conclusions bSCr values back-estimated using currently available eGFR formulae are inaccurate and cannot correctly classify AKI stages. Our model eSCr improves the prediction of AKI but to a still inadequate extent.

All types of renal replacement therapies (RRTs), intermittent and continuous treatment modalities, are associated with a broad spectrum of untoward side effects on metabolism and nutrient balances. One group of side effects affects nutrient balances. On the one hand, this represents the loss of various nutrients (e.g., amino acids, water-soluble vitamins) and of peptides and proteins. On the other hand, the modality of RRT and the type of anticoagulation, respectively, can be associated with the uptake of relevant amounts of energy substrates such as lactate and citrate or glucose. From a metabolic view, even more relevant is the induction of an inflammatory reaction caused by the extracorporeal circuit and the sustained contact of blood and artificial surfaces. This can contribute to protein catabolism and the generation of reactive oxygen species and potentially may promote distant organ injury and impair immunocompetence. Because of the prolonged treatment time and associated high fluid turnover, the evolution of electrolyte derangements is most pronounced during continuous RRT. Metabolically most important is the risk of inducing hypophosphatemia, which increases the evolution of complications and mortality. Knowledge of these additional effects of RRTs on metabolism and nutrient balances is relevant in the care of critically ill patients, because they can be associated with serious complications and have fundamental implications for designing nutritional programs. Nutrition therapy has to be coordinated with RRT and must take into consideration the losses of several nutrients and the uptake of energy substrates such as lactate or citrate.

Fluid overload and oedema are signs of excess extracellular fluid volume. The underlying pathomechanism is, in most cases, an increase of extracellular sodium which binds water and subsequently expands the extracellular space. Although sodium and water retention is a physiologic response to disease, trauma and stress, a significant proportion of fluid overload in the critically ill patient occurs as a result of liberal infusion of fluids containing high sodium amounts. Therefore, oedema is not only an indicator of disease severity but also reflects iatrogenic sodium and fluid overload. In critically ill patients, oedema is either already present at hospital admission (e.g. due to a cardiac, hepatic, renal or inflammatory condition) or develops/aggravates during the disease course. Depending on the type of critical illness, the speed of fluid accumulation and the presence of organ dysfunction, fluid overload can occur after a variable time and amount of fluid infused. Oedema is most frequently encountered in patients with capillary leak (e.g. sepsis, major surgery) or acute on chronic organ (e.g. heart or liver) dysfunction. Organs mainly compromised by fluid overload are the heart and lungs, the gastrointestinal tract, the kidneys and wound healing.

Acute kidney injury (AKI) is a frequent and serious event associated with a high rate of complications, with an increased risk of progression to multiple organ dysfunction and excessive 'attributable' mortality. AKI affects all physiologic functions and organ systems with interrelated mechanisms, including the 'classical' consequences of the uremic state, the inflammatory nature of AKI per se and resulting systemic effects, the modulating effect of AKI in the presence of an (inflammatory) underlying disease process and the multiple untoward effects induced by renal replacement therapy (RRT) and anticoagulation.A rapidly increasing body of evidence is clarifying these systemic effects that are the reflection of a broad common pathology that ultimately results in an 'augmented' inflammation and impairment of immunocompetence. This includes the release of cytokines and inflammatory mediators, increase in oxidative stress, activation of various immune cells, neutrophil extravasation, generalized endothelial injury, increased vascular permeability and tissue oedema formation.These systemic phenomena associated with AKI induce distant organ injury affecting all organ systems with clinically the most relevant effects being exerted on the lungs, the intestines and liver and the heart and predispose the progression to multiple organ dysfunction syndrome and death. Currently available renal replacement therapy modalities are incapable of compensating for these systemic consequences of AKI.

Summary Purpose The nomenclature in clinical nutrition differs locally, among (para)medical disciplines, and both nationally and internationally. The inconsistencies hamper public, professional and scientific discussions. A working group of the German Society of Nutritional Medicine (DGEM) was established to work out definitions for the relevant terms used in nutritional support within Germany. Methods Terms were searched in (inter)national hard print technical literature (medical dictionaries, text books, (inter)national guidelines and online (PubMed, Embase, CINAHL, Google Scholar, general internet). (Inter)nationally agreed definitions published by Clinical Nutrition Societies were preferred to other reports. Results The terms were organised into four categories totaling 53 definitions: 1. Fields and structure: medical nutrition, clinical nutrition, nutrition steering committee, nutritional care, care catering, dietetics (dietary advice), obesity as part of clinical nutrition (obesity team), nutritional support (nutrition support team, malnutrition screening, nutritional support therapy), functional nutrition, nutritional assessment, nutrition therapy plan, nutritional therapy, 2. Nutritional conditions: disease-related malnutrition (starvation induced malnutrition, chronic disease-related malnutrition, acute disease-related malnutrition), cachexia, sarcopenia, specific nutrient deficiencies, refeeding syndrome, 3. Forms of nutrition: diet (regular diet, therapeutic diet, fortified food), artificial nutritional support (oral nutritional supplementation, enteral nutrition, parenteral nutrition) 4. Products: oral nutritional supplements and enteral formulas (whole protein formula, peptide-based formula, free amino acid formula, standard formula), parenteral solutions (total nutrient admixtures, multi-chamber systems, multiple bottle systems). Conclusion A comprehensive list of definitions for terms in nutritional support has been established for the first time and is made available to the international community for further development and discussions.

Glomerular filtration rate (GFR) in patients with chronic kidney disease (CKD) identifies patients at risk for death or end-stage renal disease (ESRD). CKD staging by GFR should incorporate proteinuria to augment risk stratification. We therefore tested the predictive power of the combination of GFR with proteinuria in patients with different histologically-diagnosed types of glomerulonephritis (GN).In a retrospective analysis, 2,687 patients with different forms of GN from 123 Austrian centres were investigated. Full data sets were available from 1,892 subjects. Classes of CKD on the basis of estimated GFR (eGFR) and of proteinuria grouped as1, 1-3.5, and3.5 g/24 h were tested for their association with all-cause mortality and ESRD.During a median follow-up of 130 months [interquartile range (IQR) 90; 178] 478 patients (25.3 %) died. Median eGFR was 49 ml/min/1.73 m(2) (IQR 24; 81) and proteinuria 3.8 g/24 h (IQR 1.7; 8.0). Adjusted multivariate Cox regression indicated that renal survival but not overall survival is related to proteinuria3.5 g/24 h [as opposed to1 g/24 h; hazard ratio (HR) 1.91] and shows progression to ESRD. However, subgroup analyses revealed that this risk with proteinuria3.5 g/24 h exists only in patients with immunoglobulin (Ig)A GN (HR 4.93), miscellaneous GN (HR 1.74), and CKD stage 5 (HR 2.50). Additionally, proteinuria is a risk factor for renal survival in males more than in females with GN and proteinuria3.5 g/24 h (HR 1.91).Proteinuria is a strong risk factor for renal survival particularly in patients with proteinuria3.5 g/24 but not for all types of GN, nor for all CKD stages. Proteinuria is not a risk factor for overall survival in patients with GN.

Summary Background Infusion therapy is one of the most frequently prescribed medications in hospitalized patients. Currently used crystalloid solutes have a variable composition and may therefore influence acid-base status, intracellular and extracellular water content and plasma electrolyte compositions and have a major impact on organ function and outcome. The aim of our study was to investigate whether use of acetate-based balanced crystalloids leads to better hemodynamic stability compared to 0.9% saline. Methods We performed a sub-analysis of a prospective, randomized, controlled trial comparing effects of 0.9% saline or an acetate-buffered, balanced crystalloid during the perioperative period in patients with end-stage renal disease undergoing cadaveric renal transplantation. Need for catecholamine therapy and blood pressure were the primary measures. Results A total of 150 patients were included in the study of which 76 were randomized to 0.9% saline while 74 received an acetate-buffered balanced crystalloid. Noradrenaline for cardiocirculatory support during surgery was significantly more often administered in the normal saline group, given earlier and with a higher cumulative dose compared to patients receiving an acetate-buffered balanced crystalloid (30% versus 15%, p = 0.027; 68 ± 45 µg/kg versus 75 ± 60 µg/kg, p = 0.0055 and 0.000492 µg/kg body weight/min, ±0.002311 versus 0.000107 µg/kg/min, ±0.00039, p = 0.04, respectively). Mean minimum arterial blood pressure was significantly lower in patients randomized to 0.9% saline than in patients receiving the balanced infusion solution (57.2 [SD 8.7] versus 60.3 [SD 10.2] mm Hg, p = 0.024). Conclusion The use of an acetate-buffered, balanced infusion solution results in reduced need for use of catecholamines and cumulative catecholamine dose for hemodynamic support and in less occurrence of arterial hypotension in the perioperative period. Further research in the field is strongly encouraged.

Acute renal failure (ARF) is a common and dangerous complication in intensive care medicine. Especially critical ill patients, who are suffering from major burns, have a high risk to develop ARF as a consequence of their trauma. Many factors, including the trauma itself, the damage of soft tissue and consecutive rhabdomyolysis, the development of the burn illness and therapeutic interventions play also a major role in this context. These circumstances have a major impact on the morbidity and mortality of severely burned patients. The aim of this manuscript is to review the reasons for the development of an ARF in burn patients as well as its consequences; moreover it highlights potential strategies to avoid ARF in critically ill burned patients.

Background Hypernatremia is a serious electrolyte disturbance and an independent risk factor for mortality in critically ill patients. In many cases, hypernatremia is an iatrogenic problem that develops in the intensive care unit (ICU). Study Design Case series. Setting & Participants 45 patients were studied in a medical ICU. For inclusion in the study, patients needed to show an increase in serum sodium concentration to greater than 149 mEq/L from an initial concentration of less than 146 mEq/L. Outcomes Solute balance, fluid balance, and both. Causes of hypernatremia. Measurements The daily mass balance of sodium, potassium, and water over 1- to 3-day intervals was measured while serum sodium levels were increasing. Results During the study period, 69 of 981 patients (7%) acquired hypernatremia after admission to the ICU. Of these, 45 had sufficient data for evaluation. Maximum serum sodium levels were 150 to 164 mEq/L. The average duration of hypernatremia was 2 days (range, 1 to 10 days), with an average onset on day 5.9 ± 4.3 of the ICU stay. Patients were classified as having a positive solute balance (n = 17; 38%), negative fluid balance (n = 20; 44%), or both (n = 8; 18%). The most important extrarenal factors contributing to hypernatremia were fever (45%) and diarrhea (18%). Polyuria was observed in 38% of patients and 35% had acute renal failure. Hypertonic solutions were administered to 27% of patients. Limitations Retrospective analysis; lack of daily measurement of body weight. Conclusion ICU-acquired hypernatremia is associated with multiple factors associated with negative fluid and positive solute balance.

Acute kidney injury (AKI) is associated with significantly increased morbidity and mortality. To provide a uniformly accepted definition, the RIFLE classification was introduced by the Acute Dialysis Quality Initiative, recently modified by the Acute Kidney Injury Network (AKIN), suggesting staging of AKI based on dynamic changes within 48 h. This study compares these two classification systems with regard to outcome. Cohort analysis of SAPS 3 database. Sixteen thousand seven hundred and eighty-four ICU patients from 303 ICUs were analysed. Classification was performed according to RIFLE (Risk, Injury, Failure) or according to AKIN (stage 1, 2, 3) without including a requirement of renal replacement therapy in the analysis. Changes of serum creatinine as well as urinary output were assessed for both AKIN and RIFLE during the first 48 h of ICU admission. Primary endpoint was hospital mortality. Incidence of AKI in our population of critically ill patients was found to range between 28.5 and 35.5% when applying AKIN and RIFLE criteria, respectively, associated with increased hospital mortality averaging 36.4%. Observed-to-expected mortality ratios revealed excess mortality conferred by any degree of AKI increasing from 0.81 for patients classified as non-AKI up to 1.31 and 1.23 with AKIN stage 3 or RIFLE Failure, respectively. AKIN misclassified 1,504 patients as non-AKI compared to RIFLE which misclassified 504 patients. Acute kidney injury classified by either RIFLE or AKIN is associated with increased hospital mortality. Despite presumed increased sensitivity by the AKIN classification, RIFLE shows better robustness and a higher detection rate of AKI during the first 48 h of ICU admission.

OBJECTIVE: Traditional cutoff values of serum creatinine considered to define postoperative acute renal failure have been challenged recently. In a previous investigation we demonstrated that minimal changes in serum creatinine concentration were associated with a substantial decrease in survival after cardiac surgery. In this investigation, we assessed the impact of minimal absolute increases in serum creatinine in a second institution, and we analyzed whether relative changes, as in the RIFLE classification and, partially, in Acute Kidney Injury Network (AKIN) classification, confer a different prognostic potential. DESIGN: Prospective analysis. SETTING: University hospital. PATIENTS: All consecutive patients undergoing cardiac surgery in the University Hospital of Zurich (Center USZ) over a 46-month period. INTERVENTIONS: Patients were prospectively documented. We analyzed maximal changes in serum creatinine in the first 48 hrs postoperatively (DeltaCrea) regarding death within 30 days. Results were compared with those of the University Hospital Vienna (Center AKH). Moreover, the prognostic potential of DeltaCrea within 48 hrs vs. serum creatinine elements according to RIFLE and AKIN classifications was assessed. MEASUREMENTS AND MAIN RESULTS: A total of 3,123 patients were evaluated from USZ. The majority of patients had decreased postoperative serum creatinine values (negative DeltaCrea) and the lowest mortality (1.8%). Minimal increases, [0, 0.5) mg x dL(-1), were associated with a more than doubled mortality in both centers (5%/6%). Mortality, according to RIFLE and AKIN classifications for both populations combined, was as follows: 7,023 (3.6%), 160 (29%), 43 (19%), and 15 (33%) for RIFLE Normal, Risk, Injury, and Failure; 6,644 (2.8), 463 (16.4), 3 (66.7), and 131 (1.8) for AKIN stage 0, 1, 2, and 3. CONCLUSIONS: Measuring repeat serum creatinine concentrations within 48 hrs and determining DeltaCrea were the most effective discrimination method to find patients at risk for adverse postoperative outcome after cardiac surgery, better than application of this sole criterion to the RIFLE (least discriminatory) or the AKIN classification.

Hypernatremia is common in the intensive care unit (ICU). We assessed the prevalence of hypernatremia and its impact on mortality and ICU length of stay (LOS).Retrospective analysis.All patients admitted to a medical ICU of a university hospital during a 35-month observation period.Hypernatremia (serum sodium149 mmol/L) after admission to the ICU.Main outcomes were 28-day hospital mortality and ICU LOS. Demographic factors, main diagnosis, and severity of illness. Cox proportional hazards regression models were used for data analysis.Of 981 patients, 90 (9%) had hypernatremia, on admission to the ICU in 21 (2%) and developed during the ICU stay in 69 patients (7%). Of these 981 patients, 235 (24%) died; LOS was 8 +/- 9 (SD) days. Mortality rates were 39% and 43% in patients with hypernatremia on admission or that developed after admission compared with 24% in patients without hypernatremia (P0.01). LOS was 20 +/- 16 days in patients with hypernatremia compared with 8 +/- 10 days in patients without hypernatremia (P0.001). In multivariable analysis, hypernatremia was an independent risk factor for mortality (relative risk, 2.1; 95% confidence interval, 1.4 to 3.3).Retrospective design, absence of data for long-term mortality.Most cases of hypernatremia in the ICU developed after admission, suggesting an iatrogenic component in its evolution. Hypernatremia is associated with increased mortality. Strategies for preventing hypernatremia in the ICU should be encouraged.

Background Acute kidney injury is frequently observed at the intensive care unit, after surgery, and after toxic drug administration. A rise in serum creatinine and a fall in urine output are consequences of much earlier injury to the most sensitive part of tubular cells located at the proximal tubule. The aim of the present study was to investigate the course of two cell-cycle arrest urinary biomarkers compared to serum creatinine in four clinical settings: ischemic reperfusion injury, cardiac failure, severe acute kidney injury, and chemotherapy-induced kidney injury. Methods A recently developed bedside test known as NephroCheck measures two urinary parameters: insulin-like growth factor binding protein 7 (IGFBP7) and tissue inhibitor of metalloproteinase-2 (TIMP-2). The test is based on a sandwich immunoassay technique. The final test output, labeled AKIRisk, is shown as a numeric result. Results This report revealed that [IGFBP7] · [TIMP-2] in urine rise rapidly prior to any change in serum creatinine. A unique feature of all four clinical settings is that a rapid decline predicts the recovery of kidney function. Besides, a subclinical kidney injury might be detected by the test. Conclusion This bedside test detects biomarkers of renal injury. A rapid decline in AKIRisk was associated with the restoration of kidney function, whereas a prolonged high AKIRisk score was associated with end-stage renal disease. However, the dynamics seem to differ, depending on the cause and the extent of injury. Further studies will be needed to clarify the issue. Electronic supplementary material The online version of this article (doi:10.1186/s12882-015-0203-5) contains supplementary material, which is available to authorized users.

More than 20 years ago we reported an analysis of a case series of elderly critically ill patients with acute kidney injury (AKI)—then termed acute renal failure. At that time, AKI was regarded as a “simple” complication, but has since undergone a fundamental change and actually has become one of the central syndromes in the critically ill patient. We have analyzed elderly patients above 65 years of age with an AKI defined as serum creatinine above 3 mg/dl corresponding to modern KDIGO stage 3, most of them requiring renal replacement therapy (RRT). Using an extremely complete data set the diagnosis differentiated the underlying disease entity, the dominant cause of AKI, acute and chronic risk factors (comorbidities). Special aspects such as severity of disease, early AKI at admission versus late AKI, early versus later start of RRT, AKI not treated by RRT in spite of indication for RRT, various measures of short-term and long-term prognosis, renal outcome, patients dying with resolved AKI, and causes of death were evaluated. Crude mortality was 61 % which corresponds to modern studies with gross variation among the different subgroups. Age per se was not a determinant of survival either within the group of elderly patients or as compared to younger age groups. Despite an increase in mean age and disease severity during the observation period prognosis improved. A total of 17 % of patients developed a chronic kidney disease. Long-term survival as compared to the general population was low. A look back at the last two decades illustrates a remarkable evolution or rather metamorphosis of a syndrome. AKI has evolved as a central syndrome in intensive care patients, a systemic disease process associated with multiple systemic sequels and extra-renal organ injury and exerting a pronounced effect on the course of disease and short- and long-term prognosis not only of the patient but also of the kidney. Moreover, the “non-renal-naive” elderly patient with multiple comorbidities has become the most frequent ICU patient in industrialized nations.

Gitelman syndrome is a rare hereditary disorder of the thiazide-sensitive NaCl transporter in the distal renal tubular cells, but mimicking of such hereditary tubular disorders has been described in different autoimmune diseases (Sjögren syndrome, SLE, ...). A 62-year-old woman with painful red eyes and sicca syndrome presented at the ophthalmological department. The diagnostic evaluation identified a Sjögren syndrome with early endophthalmitis as the reason for the red eyes. Results of laboratory examination indicated severe hypokalemia, metabolic alkalosis and hypomagnesemia, although this had not been seen years earlier. Together with the urine analysis, a rare case of an acquired Gitelman syndrome was diagnosed. Substitution with potassium and magnesium improved the initial symptoms of weakness, but renal electrolyte wasting persisted even after treatment of Sjögren syndrome. In patients with autoimmune disease, laboratory analysis of serum electrolytes should be performed because different acquired tubular disorders can lead to severe hypokalemia.

BACKGROUND Kidney transplant recipients with a current positive complement-dependent cytotoxicity crossmatch (CDCXM) are at high risk for hyperacute rejection and graft loss. Immunoadsorption (IA) represents an efficient strategy to remove donor-specific alloantibodies. In this analysis, we evaluated effectiveness of peritransplant IA as an anti-humoral strategy to overcome a current positive CDCXM in presensitized renal allograft recipients. METHODS Between 1999 and 2003, 40 high risk cadaveric kidney allograft recipients (median CDC panel reactive antibody [PRA] level, 77%; number of retransplants, n = 38) were subjected to peritransplant IA with protein A (one pretransplant IA session followed by a course of repeat posttransplant IA sessions) in addition to preemptive antilymphocyte antibody therapy. RESULTS In nine of these patients, a current positive CDCXM was rendered negative by a single pretransplant IA session. Thirty-one recipients had a negative CDCXM already before pretransplant IA. No difference in graft survival was found between CDCXM-positive and CDCXM-negative recipients (3-year graft survival, 78% vs. 71%, P = 0.6). Comparable rates of immunological graft loss at 3 years were observed (11% vs. 13%, P = 0.8). Patient groups did not significantly differ with respect to median serum creatinine at 1 year (1.23 mg/dL [CDCXM-positive] vs. 1.57 mg/dl [CDCXM-negative], P = 0.07) and at the end of follow-up (median 32 months; 1.19 mg/dL vs. 1.63 mg/dL, P = 0.06). Moreover, patient groups showed similar rates of biopsy-proven cellular rejection (11% vs. 20%) or C4d-positive graft dysfunction (33% vs. 32%). CONCLUSION Our results demonstrate that peritransplant IA enables successful cadaveric kidney transplantation in the context of a positive CDCXM.

Purpose of review This review will give an overview of current trends in diagnosis, treatment, and pathogenesis of ascites and intraabdominal infection in cirrhotic and noncirrhotic critically ill patients. Recent findings Single clone-bacterial DNA has been found in sterile ascites and serum, proving the concept of direct translocation. Activation of mesenteric macrophages can be induced by splanchnic vasodilatation but also by hypoxia. Carbon monoxide, an end product of heme catabolism, promotes splanchnic vasodilatation, representing a possible link between gastrointestinal hemorrhage and circulatory dysfunction. Colorimetric test strips and automated counters accurately diagnose spontaneous bacterial peritonitis. Vasopressin V2-antagonists have been introduced as novel therapy for impaired water excretion in hyponatremia. Summary Emerging pathophysiological concepts have modified the conventional view of hydrostatic and Starling forces in the evolution of ascites. Current data indicate that the dynamic sequence of bacterial translocation, mesenteric inflammation, splanchnic vasodilatation and intrahepatic vasoconstriction determines occurrence, severity, and outcome of ascites and intraabdominal infection.

Ileus refers to the partial or complete blockage of the small and/or large intestine either by functional (adynamic or paralytic ileus) or mechanical bowel obstruction. The diffuse gastrointestinal dysmotility during functional and mechanical ileus may result in intestinal dilatation, increased luminal pressure and gut wall ischaemia which may lead to increased intra-abdominal pressure (IAP). Any type of ileus may promote abdominal fluid sequestration with severe systemic hypovolaemia, intestinal bacterial overgrowth with the evolution of bacterial translocation and systemic invasive infections and inflammation of the intestinal wall with concomitant release of cytokines and the development of the systemic inflammatory response syndrome. The most serious complications of ileus are mediated by an increase in IAP. Intra-abdominal hypertension has been found in up to 20% of critically ill patients and may lead to a broad pattern of systemic consequences with multiple organ dysfunction, including cardiovascular, hepatic, pulmonary, renal and neurological function. The abdominal compartment syndrome is an emergency condition which is defined as elevation of IAP above 20 to 25 mmHg and the presence of systemic consequences. Therapeutic considerations include the maintenance of adequate hydration status, avoidance of drugs known to impair intestinal perfusion, stimulation of gastric and intestinal motility and various nutritional aspects. Colonic tube placement after decompressive colonoscopy may be effective in reducing intestinal dilatation. In the abdominal compartment syndrome the 'open abdominal approach' with decompressive laparotomy by opening the peritoneal cavity and temporary abdominal closure is the therapy of choice.

Acute renal failure is a complication in critically ill patients that has been associated with an excess risk of hospital mortality. Whether this reflects the severity of the disease or whether acute renal failure is an independent risk factor is unknown. The aim of this study was to analyze severity of illness and mortality in a group of critically ill patients with acute renal failure requiring renal replacement therapy in a number of Austrian intensive care units.Prospective, multicenter cohort study.A total of 17,126 patients admitted consecutively to 30 medical, surgical, and mixed intensive care units in Austria over a period of 2 yrs.Analyzed data included admission data, Simplified Acute Physiology Score, Logistic Organ Dysfunction system, Simplified Therapeutic Intervention Scoring System, length of intensive care unit stay, intensive care unit mortality, and hospital mortality. Of the admitted patients, 4.9% (n = 839) underwent renal replacement therapy because of acute renal failure (renal replacement therapy patients). These patients had a significantly higher hospital mortality (62.8% vs. 15.6%, p.001), which remained significantly higher even when renal replacement therapy patients were matched with control subjects for age, severity of illness, and treatment center. Since univariate analysis demonstrated further intensity of treatment to be an additional predictor for outcome, a multivariate model including therapeutic interventions was developed. Five interventions were associated with nonsurvival (mechanical ventilation, single vasoactive medication, multiple vasoactive medication, cardiopulmonary resuscitation, and treatment of complicated metabolic acidosis/alkalosis). In contrast, the use of enteral nutrition predicted a favorable outcome.The results of our study suggest that acute renal failure in patients undergoing renal replacement therapy presents an excess risk of in-hospital death. This increased risk cannot be explained solely by a more pronounced severity of illness. Our results provide strong evidence that acute renal failure presents a specific and independent risk factor for poor prognosis.

Background. Re-transplanted kidney allograft recipients with high levels of panel reactive antibodies (PRA) are at increased risk of early immunologic graft loss. In these patients, prophylactic peri-operative antibody depletion by immunoadsorption (IA) could prevent humoral graft injury and thus, in combination with anti-cellular rejection therapy, improve graft survival. Methods. Twenty re-transplanted and broadly immunized cadaver kidney recipients (median PRA reactivity 87%, range 55–100%) were treated with IA (protein A) immediately before transplantation and during the early post-transplantation period (median number of IA sessions 11, range 1–24). Patients received additional prophylactic anti-lymphocyte antibody therapy. Nineteen patients had a negative pre-transplant crossmatch. In one patient, a positive cross-match was rendered negative by the pre-transplant IA session. Results. One-year graft survival was 80% and patient survival 95%. Median (range) serum creatinine in functioning grafts was 1.6 (0.8–2.7) mgudl at discharge and 1.5 (1.0–5.8) mgudl at 1 year. Two grafts were lost due to acute vascular rejection, whereby one rejection occurred after withdrawal of immunosuppression due to septicaemia. One patient had acute cellular rejection, which was reversed by a second course of anti-lymphocyte antibody therapy. Thrombotic microangiopathy and surgical complications were the causes for one graft loss each. Retrospective immunohistochemistry revealed peritubular C4d staining, a presumed marker for humoral alloreactivity, in 12 out of 15 biopsies. Conclusions. These results suggest that prophylactic peri-operative IA and anti-lymphocyte antibody therapy might be an effective therapeutic strategy for the prevention of early graft failure in sensitized re-transplant recipients.

Preoperative renal insufficiency is an important predictor of mortality after cardiac surgery. This retrospective cohort study was designed to identify the optimal cut-off for baseline serum creatinine (bSCr) and estimated glomerular filtration rate (eGFR) to predict survival. Furthermore, we investigated the potential confounding effect of other perioperative risk indicators on short- and long-term survival.Data of 9490 cardiac surgical patients were prospectively collected between 1997 and 2008 (follow up to 2010) at the Medical University Vienna. We identified bSCr cut-off values and calculated uni- and multivariate hazard models for short- and long-term survival and compared the results with a validation set from Zurich. The estimated survival curves defined a distinct period of increased mortality until 150 days.Cut-off values of115 µmol litre(-1) for bSCr and ≤50 ml min(-1) for eGFR were identified. Increased bSCr, associated with higher mortality [hazard ratio (HR) 2.61, 95% confidence interval (CI) 2.43-2.80, P0.0001], was present in 19.5% of patients and remained predictive for short- (HR 1.59, 95% CI 1.38-1.83, P=0.0027) and long-term survival (HR 1.46, 95% CI 1.32-1.62, P0.0001) in the multivariate hazard models. A cut-off of120 µmol litre(-1) for bSCr was determined for the validation set. Decreased eGFR was present in 23.6% (HR 2.86, 95% CI 2.67-3.06, P0.0001).In our patients, increased bSCr was an independent predictor of mortality, which may critically influence risk evaluation and perioperative treatment guidance.

Background: Immunoadsorption (IAS) and therapeutic plasma exchange (TPE) are considered safe although fibrinogen is removed. To date no comparison of fibrinogen reduction and associated risk of bleeding in apheresis exists. Methods: Retrospective analysis of TPE, three IAS adsorbers, and combined TPE/IAS regarding fibrinogen reduction and bleeding incidence in 67 patients (1,032 treatments). Results: TPE and TPE/IAS reduced fibrinogen by 64 ± 11% and 58 ± 9%, leading to concentrations Conclusion: Hypofibrinogenemia occurs in 20% of patients after TPE and TPE/IAS, but rarely after IAS. IAS removes fibrinogen independently of volume processed. Overall, bleeding is rare in apheresis.

There is increasing evidence for an important pathogenetic role of alloantibodies in acute renal allograft rejection. Acute humoral rejection (AHR) has been reported to be associated with a poor transplant survival. Although treatment modalities for cellular rejection are fairly well established, the optimal treatment for AHR remains undefined. Ten of 352 kidney allograft recipients transplanted at the authors' institution between November 1998 and September 2000 were diagnosed as having AHR, supported by severe graft dysfunction, C4d deposits in peritubular capillaries (PTC), and accumulation of granulocytes in PTC. AHR was diagnosed 18.9 +/- 17.5 d posttransplantation. All patients were subjected to immunoadsorption (IA) with protein A (median number of treatment sessions, 9; range, 3 to 17). Seven recipients with additional signs of cellular rejection (according to the Banff classification) received also antithymocyte globulin. In nine of ten patients, AHR was associated with an increase in panel reactive antibody reactivity. A pathogenetic role of alloantibodies was further supported by a positive posttransplant cytotoxic crossmatch in all tested recipients (n = 4). In nine of ten recipients, renal function recovered after initiation of anti-humoral therapy. One patient lost his graft shortly after initiation of specific therapy. Another recipient with partial reversal of AHR returned to dialysis 8 mo after transplantation. Mean serum creatinine in functioning grafts was 2.2 +/- 1.2 mg/dl after the last IA session (n = 9) and 1.5 +/- 0.5 mg/dl after a follow-up of 14.2 +/- 7.1 mo (n = 8). In conclusion, this study suggests that AHR, characterized by severe graft dysfunction, C4d staining, and peritubular granulocytes, can be effectively treated by timely IA. In the majority of patients, IA treatment can restore excellent graft function over a prolonged time period.

Objective: To assess the frequency and independent predictors of severe acute renal failure in patients resuscitated from out-of-hospital ventricular fibrillation cardiac arrest. Design: A cohort study with a minimum follow-up of 6 months. Setting: Emergency department of a tertiary care 2200-bed university hospital. Patients and participants: Consecutive adult (>18 years) patients admitted from 1 July 1991 to 31 October 1997 after witnessed ventricular fibrillation out-of-hospital cardiac arrest and successful resuscitation. Measurements and results: Acute renal failure was defined as a 25% decrease of creatinine clearance within 24 h after admission. Out of 187 eligible patients (median age 57 years, 146 male), acute renal failure occurred in 22 patients (12%); in 4 patients (18%) renal replacement therapy was performed. Congestive heart failure (OR 6.0, 95% CI 1.6–21.7; p=0.007), history of hypertension (OR 4.4, 95% CI 1.3–14.7; p=0.02) and total dose of epinephrine administered (OR 1.1, 95% CI 1.0–1.2; p=0.009) were independent predictors of acute renal failure. Duration of cardiac arrest, pre-existing impaired renal function and blood pressure at admission were not independently associated with renal outcome. Conclusions: Severe progressive acute renal failure after cardiopulmonary resuscitation (CPR) is rare. Pre-existing haemodynamics seem to be more important for the occurrence of acute renal failure than actual hypoperfusion during resuscitation.

BACKGROUND In patients with sepsis and systemic inflammatory response syndrome, amino acid extraction by the liver is enhanced, resulting in decreased plasma amino acid concentrations. Systematic investigations of the elimination of intravenously infused amino acids have not been performed. OBJECTIVE The objective of this study was to compare the elimination of 17 amino acids in patients with sepsis and in healthy control subjects. DESIGN Elimination of amino acids was evaluated in 9 patients with sepsis and in 8 healthy control subjects by using a combined loading and maintenance infusion of 375 mg amino acids/kg body wt for 60 min. Pharmacokinetic variables were analyzed from plasma curves. RESULTS With the exception of lysine, methionine, glutamate, ornithine, phenylalanine, and tyrosine, plasma concentrations of amino acids were lower in the patients with sepsis than in the control subjects; phenylalanine was the only amino acid whose plasma concentration increased (P < 0.001). In patients with sepsis, whole-body clearance (Cl(tot)) of total amino acids was 74% higher than in control subjects (x +/- SEM: 13,161 +/- 1659 and 7566 +/- 91 mL/min, respectively; P < 0.01), the Cl(tot) of essential amino acids was 64% higher (P < 0.02), that of nonessential amino acids was 82% higher (P < 0.01), and that of both branched-chain amino acids and glucogenic amino acids was 97% higher (P < 0.001). With the exception of phenylalanine, ornithine, proline, and glutamate, the Cl(tot) of all amino acids was elevated. The Cl(tot) of phenylalanine and ornithine decreased slightly (NS). CONCLUSIONS In patients with sepsis, plasma concentrations of most amino acids are greatly decreased and the elimination of amino acids from the intravascular space during intravenous infusion is greatly enhanced.

The principles of nutritional therapy (ie, maintain lean body mass, stimulate immunocompetence, and repair functions, such as wound healing) are similar for patients with acute renal failure (ARF) and with other catabolic clinical conditions. However, if a patient with ARF requires nutritional support, the multiple metabolic consequences of acute uremia must be taken into account. These do not only affect fluid, electrolyte, and acid-base balance but also the metabolism of amino acids, proteins, carbohydrates, and lipids. In addition, these metabolic alterations are modified by the acute disease process per se, by associated complications (such as severe infections), and last but not least, by the type and intensity of renal replacement therapy. Whenever possible, enteral nutrition should be provided in patients with ARF because even small amounts of luminal nutrients will help to maintain intestinal functions. Nevertheless, in many patients a parenteral nutrition, at least supplementary and/or temporarily, will become necessary. Metabolic complications of nutritional support frequently occur in patients with ARF because tolerance to volume load and electrolytes is limited and the use of various nutrients is impaired. Despite the notorious difficulty to demonstrate clear-cut benefits of nutritional interventions and especially, of parenteral nutrition on prognosis in critically ill patients, there can be no doubt that nutritional therapy presents a cornerstone in the treatment of patients with ARF. Preexisting and/or hospital-acquired malnutrition have been identified as important factors contributing to the persisting high mortality in acutely ill patients with ARF.