Acute kidney injury (AKI) is a frequent complication after cardiac surgery with adverse short-term and long-term outcomes. Although prevention of AKI (PrevAKI) is strongly recommended, the optimal strategy is uncertain. The Kidney Disease: Improving Global Outcomes (KDIGO) guideline recommended a bundle of supportive measures in high-risk patients. In a single-centre trial, we recently demonstrated that the strict implementation of the KDIGO bundle significantly reduced the occurrence of AKI after cardiac surgery. In this feasibility study, we aim to evaluate whether the study protocol can be implemented in a multicentre setting in preparation for a large multicentre trial.
We plan to conduct a prospective, observational survey followed by a randomised controlled, multicentre, multinational clinical trial including 280 patients undergoing cardiac surgery with cardiopulmonary bypass. The purpose of the observational survey is to explore the adherence to the KDIGO recommendations in routine clinical practice. The second phase is a randomised controlled trial. The objective is to investigate whether the trial protocol is implementable in a large multicentre, multinational setting. The primary endpoint of the interventional part is the compliance rate with the protocol. Secondary endpoints include the occurrence of any AKI and moderate/severe AKI as defined by the KDIGO criteria within 72 hours after surgery, renal recovery at day 90, use of renal replacement therapy (RRT) and mortality at days 30, 60 and 90, the combined endpoint major adverse kidney events consisting of persistent renal dysfunction, RRT and mortality at day 90 and safety outcomes.
The PrevAKI multicentre study has been approved by the leading Research Ethics Committee of the University of Münster and the respective Research Ethics Committee at each participating site. The results will be used to design a large, definitive trial.
NCT03244514.

OBJECTIVE: To evaluate the prevalence, risk factors and outcome of acute kidney injury (AKI) in very low birth weight (VLBW) infants.
METHODS: In this retrospective study of VLBW infants, we analyzed the prevalence of AKI, as defined by changes in serum creatinine and urine output, associated risk factors and outcomes.
RESULTS: A total of 293 VLBW infants (mean gestational age 28.7 wk) were included, of whom 109 weighed less than 1000 g at birth. The overall prevalence of AKI was 11.6% (22% in infants with a birth weight under 1000 g and 5.4% those heavier). A total of 19 (55%) affected infants died, with a mortality rate of 58% in infant less than 1000 g and 50% in those heavier. After adjusting for confounding variables, only necrotizing enterocolitis (NEC) remained associated with AKI, with odds ratio of 4.9 (95%CI: 1.9-18.6). Blood pressure and glomerular filtration rate (GFR) were not different between affected infants and the others upon discharge from hospital. A normal GFR was documented in all affected infants at one year of age.
CONCLUSIONS: Using Kidney Disease Improving Global Outcomes definition of AKI, it occurred in over 10% of VLBW infants, more commonly in infants with lower birth weight. NEC was an independent associated risk factor. Renal function, as defined by GFR, was normal in all surviving affected infants 10 to 12 mo later.

OBJECTIVE: Use of small changes in serum creatinine to diagnose AKI allows for earlier detection but may increase diagnostic false-positive rates because of inherent laboratory and biologic variabilities of creatinine.
METHODS: We examined serum creatinine measurement characteristics in a prospective observational clinical reference cohort of 2267 adult patients with AKI by Kidney Disease Improving Global Outcomes creatinine criteria and used these data to create a simulation cohort to model AKI false-positive rates. We simulated up to seven successive blood draws on an equal population of hypothetical patients with unchanging true serum creatinine values. Error terms generated from laboratory and biologic variabilities were added to each simulated patient\'s true serum creatinine value to obtain the simulated measured serum creatinine for each blood draw. We determined the proportion of patients who would be erroneously diagnosed with AKI by Kidney Disease Improving Global Outcomes creatinine criteria.
RESULTS: Within the clinical cohort, 75.0% of patients received four serum creatinine draws within at least one 48-hour period during hospitalization. After four simulated creatinine measurements that accounted for laboratory variability calculated from assay characteristics and 4.4% of biologic variability determined from the clinical cohort and publicly available data, the overall false-positive rate for AKI diagnosis was 8.0% (interquartile range =7.9%-8.1%), whereas patients with true serum creatinine ≥1.5 mg/dl (representing 21% of the clinical cohort) had a false-positive AKI diagnosis rate of 30.5% (interquartile range =30.1%-30.9%) versus 2.0% (interquartile range =1.9%-2.1%) in patients with true serum creatinine values <1.5 mg/dl (P<0.001).
CONCLUSIONS: Use of small serum creatinine changes to diagnose AKI is limited by high false-positive rates caused by inherent variability of serum creatinine at higher baseline values, potentially misclassifying patients with CKD in AKI studies.

OBJECTIVE: Contrast-induced acute kidney injury or contrast-induced nephropathy (CIN) is a significant complication of intravascular contrast medium (CM). These guidelines are intended as a practical approach to risk stratification and prevention. The major risk factor that predicts CIN is pre-existing chronic kidney disease.
METHODS: Members of the committee represent radiologists and nephrologists across Canada. The previous guidelines were reviewed, and an in-depth up-to-date literature review was carried out.
RESULTS: A serum creatinine level (SCr) should be obtained, and an estimated glomerular filtration rate (eGFR) should be calculated within 6 months in the outpatient who is stable and within 1 week for inpatients and patients who are not stable. Patients with an eGFR of ≥ 60 mL/min have an extremely low risk of CIN. The risk of CIN after intra-arterial CM administration appears be at least twice that after intravenous administration. Fluid volume loading remains the single most important measure, and hydration regimens that use sodium bicarbonate or normal saline solution should be considered for all patients with GFR < 60 mL/min who receive intra-arterial contrast and when GFR < 45 mL/min in patients who receive intravenous contrast. Patients are most at risk for CIN when eGFR < 30 mL/min. Additional preventative measures include the following: avoid dehydration, avoid CM when appropriate, minimize CM volume and frequency, avoid high osmolar CM, and discontinue nephrotoxic medications 48 hours before administration of CM.

Partial EN (enteral nutrition) should always be aimed for in patients with renal failure that require nutritional support. Nevertheless PN (parenteral nutrition) may be necessary in renal failure in patient groups with acute or chronic renal failure (ARF or CRF) and additional acute diseases but without extracorporeal renal replacement therapy, or in patients with ARF or CRF with additional acute diseases on extracorporeal renal replacement therapy, haemodialysis therapy (HD), peritoneal dialysis (PD) or continuous renal replacement therapy (CRRT), or in patients on HD therapy with intradialytic PN. Patients with renal failure who show marked metabolic derangements and changes in nutritional requirements require the use of specifically adapted nutrient solutions. The substrate requirements of acutely ill, non-hypercatabolic patients with CRF correspond to those of patients with ARF who are not receiving any renal replacement patients therapy (utilisation of the administered nutrients has to be monitored carefully). In ARF patients and acutely ill CRF patients on renal replacement therapy, substrate requirements depend on disease severity, type and extent/frequency of extracorporeal renal replacement therapy, nutritional status, underlying disease and complications occurring during the course of the disease. Patients under HD have a higher risk of developing malnutrition. Intradialytic PN (IDPN) should be used if causes of malnutrition cannot be eliminated and other interventions fail. IDPN should only be carried out when modifiable causes of malnutrition are excluded and enhanced oral (like i.e. additional energy drinks) or enteral supply is unsuccessful or cannot be carried out.