AKI is a common and serious complication of cardiac surgery that has a significant impact on patient morbidity and mortality. The Kidney Disease Improving Global Outcomes definition of AKI is widely used to classify and identify AKI associated with cardiac surgery (cardiac surgery–associated AKI [CSA-AKI]) on the basis of changes in serum creatinine and/or urine output. There are various preoperative, intraoperative, and postoperative risk factors for the development of CSA-AKI which should be recognized and addressed as early as possible to expedite its diagnosis, reduce its occurrence, and prevent or ameliorate its devastating complications. Crucial issues are the inaccuracy of serum creatinine as a surrogate parameter of kidney function in the perioperative setting of cardiothoracic surgery and the necessity to discover more representative markers of the pathophysiology of AKI. However, except for the tissue inhibitor of metalloproteinase-2 and insulin-like growth factor binding protein 7 ratio, other diagnostic biomarkers with an acceptable sensitivity and specificity are still lacking. This article provides a comprehensive review of various aspects of CSA-AKI, including pathogenesis, risk factors, diagnosis, biomarkers, classification, prevention, and treatment management.

Aim: Diabetic nephropathy (DN) is a devastating complication of diabetes mellitus (DM). Therefore, screening strategies in order to prevent its development and/or retard its progression are of paramount importance. We investigated if monocyte chemoattractant protein‐1 (MCP‐1) was associated with new onset microalbuminuria‐the earliest sign of the albuminuric phenotype of DN‐ in patients with type 2 DM and normoalbuminuria.Methods: We measured MCP‐1 in serum and urine samples from patients of the Randomized Olmesartan And Diabetes Microalbuminuria Prevention (ROADMAP) study and its Observational Follow‐up (OFU) cohort. A case control design was used with inclusion of 172 patients who developed microalbuminuria (MA) and of 188 well matched controls who remained normoalbuminuric.Results: The median duration of follow‐up for the ROADMAP cohorts was 6.5 years, whereas the mean time until occurrence of MA was 53.2 months. In the multivariate analysis, serum and urine MCP‐1 remained significant predictors of new onset MA. The risk for MA increased continuously with increasing serum and urine MCP‐1 levels but reached statistical significance only in the highest quartiles. The risk associations were stronger with serum MCP‐1.Conclusions: MCP‐1 is a marker and possibly a mediator of early diabetic nephropathy. Further prospective studies are necessary to test whether diabetic patients with elevated MCP‐1 levels would benefit from specific therapeutic interventions.

Aim: It is important to know which factors predict the development of microalbuminuria in patients with diabetes mellitus type II. Material: Data from the Randomized Olmesartan and Diabetes Microalbuminuria Prevention Study were used to identify predictors for the new onset of microalbuminuria. Furthermore, the interaction of baseline albuminuria and baseline estimated glomerular filtration rate (eGFR) and the effects of treatment with olmesartan were investigated. Results: A total of 4447 patients were randomized to receive 40-mg olmesartan or placebo for a median of 3.2 years. Baseline urinary albumin–creatinine ratio (UACR) was the most important predictor of microalbuminuria, followed by age, weight, glycosylated hemoglobin type A1C, blood glucose, total cholesterol, SBP number of antihypertensive drugs and heart rate. The development of microalbuminuria was not affected by hemodynamic factors. The incidence of microalbuminuria increased from the lower to the higher UACR tertile at all baseline eGFR tertiles. The effects of olmesartan on prevention of new onset microalbuminuria were more obvious in those with the highest baseline UACR at all baseline eGFR tertiles. The eGFR declined more significantly in the olmesartan group (from 85.0 to 80.1 ml/min per 1.73 m²), whereas the decrease in the placebo group was smaller (from 84.7 to 83.7 ml/min per 1.73 m²). The highest rate of eGFR decline in the olmesartan group was in patients with the highest baseline eGFR (>95 ml/min per 1.73 m²) at all baseline UACR tertiles. The transition from normoalbuminuria to microalbuminuria in the olmesartan treated patients was not accompanied by preservation of renal function. Conclusion: Predictors of new onset microalbuminuria are the classical cardiovascular risk factors. Microalbuminuria development was associated with baseline UACR but not baseline eGFR, whereas eGFR decrease after introduction of olmesartan was dependent on baseline eGFR but not on baseline UACR. The effects of olmesartan on microalbuminuria development and on eGFR decrease are probably mediated by different mechanisms. Clinical Trials.gov number, NCT00185159.

Zusammenfassung: Die akute Pankreatitis (AP) stellt die häufigste gastrointestinale Ursache für Krankenhausaufnahmen dar. Die Mortalität liegt bei 5 %, kann jedoch in Abhängigkeit vom Schweregrad auf bis zu 40 % ansteigen. Insbesondere schwere Verlaufsformen sind mit einem Multiorganversagen vergesellschaftet und haben eine schlechte Prognose. In diesem Zusammenhang kann es bei bis zu 10 % der Patienten zum akuten Nierenversagen (Acute kidney injury, AKI) kommen, das sich meistens spät nach dem Versagen anderer Organe entwickelt, aber auch initial oder isoliert auftreten kann. Darüber hinaus bestimmt das AKI als Komplikation der schweren Pankreatitis maßgeblich die Prognose, da die Mortalität, vor allem bei dialysepflichtigem AKI, auf bis zu 75 % dramatisch ansteigen kann.Im Vergleich zu anderen intensivmedizinisch assoziierten AKIs (z. B. Volumenmangel, kardiales Pumpversagen, Sepsis oder Intoxikationen) weist das mit einer AP assoziierte AKI (AP-AKI) viele Gemeinsamkeiten, aber auch deutliche Unterschiede auf. Die zwei existierenden Formen des AP-AKI (initiale prärenale Schädigung aufgrund eines Volumenmangels, intrarenale Schädigung in der Spätphase) können aufeinander folgend, aber auch unabhängig voneinander auftreten. Obwohl die Pathophysiologie gänzlich unverstanden ist, scheint eine systemische und lokale entzündliche Reaktion eine wichtige Rolle zu spielen. Die frühe Diagnose und die rechtzeitige Einleitung einer effektiven supportiven und ätiopathogenetisch gerichteten Therapie kann die Prognose deutlich verbessern. Ungeachtet dessen finden sich derzeit nur wenige Studien, die sich explizit mit AKI und Pankreatitis befassen.In der vorliegenden Übersicht konzentrieren wir uns – unter Verwendung der aktuellsten Literatur – auf die zugrunde liegenden pathophysiologischen Mechanismen des AP-AKI, untersuchen in dieser Hinsicht den diagnostischen und prognostischen Stellenwert alter und neuer Serum- und Urinmarker und diskutieren die für die AP-AKI empfohlenen Behandlungsansätze inklusive möglicher Nierenersatzverfahren.