Zusammenfassung
Im Jahr 2012 war für die diabetische Nephropathie in vielerlei Hinsicht ein Schlüsseljahr. Die ersten Daten der Studie German Chronic Kidney Disease (GCKD) als ein Register des Verlaufs von Nephropathien in den CKD-Stadien 2 bis 5 wurden veröffentlicht. Demnach scheint die hypertensive Nephropathie mittlerweile die diabetische Nephropathie als Hauptursache für die Aufnahme in das chronische Dialyseprogramm abzulösen. Genetische Studien zur Aufklärung eines erblichen Hintergrunds werden immer weniger und beschränken sich auf hypothesenfreie genomweite Assoziationsstudien. Hier zeigt sich mehrfach, wie kritisch die Definition der Phänotypen und auch der Kontrollen hinsichtlich der ernüchternden Ergebnisse zu sehen ist. Nach wie vor werden keine biologischen Effekte nachgewiesen. Podocalyxin im Urin könnte sich als Marker der frühen Podozytenschädigung bei Diabetikern etablieren. Des Weiteren wurde der Abbruch der Aliskiren Trial in Type 2 Diabetes Using Cardiovascular and Renal Disease Endpoints (ALTITUDE), die sich mit der dualen Blockade des Renin-Angiotensin-Aldosteron-Systems [RAAS; Aliskiren plus Angiotensinkonversionsenzym(ACE)-Hemmer oder Sartan] beschäftigte, endlich mit Daten unterfüttert. Die sich zunächst abzeichnende Vermehrung von Schlaganfällen konnte nicht bestätigt werden. Allerdings traten signifikant mehr Hyperkaliämien auf, die u. a. auf gravierende Studienfehler zurückzuführen waren.
Abstract
The year 2012 was a key year for diabetic nephropathy. First data from the German chronic kidney disease-study (GCKD) as a register of the course of nephropathy with CKD stages 2–5 were published. According to this study hypertensive nephropathy has replaced diabetic nephropathy as the main reason for initiating chronic hemodialysis treatment. Genetic studies for unraveling the genetic background became rarer and the focus was on hypothesis-free genome-wide association studies. The study results indicated how critical the definition of the phenotype including the controls is to be seen in the face of the disillusioning results. Just as always no biological effects were demonstrated. Urinary podocalyxin could become a marker for the early impairment of podocytes in diabetic patients. Furthermore, the premature termination of the “aliskirin trial in type 2 diabetes using cardiovascular and renal disease endpoints” (ALTITUDE) trial which tested the dual blockade of the renin-angiotensin-aldosterone (RAAS) system and aliskirin plus angiotensin conversion enzyme (ACE) inhibitor or sartan, has been relined by published data. The initial increase of strokes could not be confirmed; however, there were significantly more episodes of hyperkalemia, which can be attributed to serious flaws in the study design.
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Der korrespondierende Autor weist auf folgende Beziehung hin: Der Autor Prof. Dr. T.H. Lindner ist als Referent für die Fa. Novartis tätig.
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Lindner, T. Diabetes und Nieren. Diabetologe 9, 387–394 (2013). https://doi.org/10.1007/s11428-012-1015-x
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DOI: https://doi.org/10.1007/s11428-012-1015-x