Dtsch Med Wochenschr 2013; 138(21): 1123-1129
DOI: 10.1055/s-0033-1343113
Übersicht | Review article
Angiologie, Nephrologie
© Georg Thieme Verlag KG Stuttgart · New York

Thromboembolische Komplikationen bei nephrotischem Syndrom

Thromboembolic complications in nephrotic syndrome
N. Maurin
1   KfH Nierenzentrum Neuwied
› Author Affiliations
Further Information

Publication History

29 August 2012

10 December 2012

Publication Date:
15 May 2013 (online)

Zusammenfassung

Zu den wichtigsten extrarenalen Folgen eines nephrotischen Syndroms (NS) zählen thromboembolische Komplikationen. Neben tiefer Beinvenenthrombose und Lungenembolie zeigt sich bei NS sehr häufig eine Nierenvenenthrombose. Aufgrund einer Vermehrung des prokoagulatorischen und antifibrinolytischen sowie einer Verminderung des antikoagulatorischen Potenzials führt eine multifaktorielle Störung des hämostatischen Gleichgewichts zu einer Hyperkoagulabilität bei NS, die durch eine Erhöhung der Blutviskosität und eine endotheliale Dysfunktion aggraviert wird. Zirkulierende Antikörper gegen α-Enolase, einem Plasmin(ogen)-bindenden Protein, sowie die Möglichkeit, dass in spezifischer Weise bestimmte Moleküle renal eliminiert werden, werden als Ursache für die besondere Häufigkeit von thromboembolischen Komplikationen bei idiopathischer membranöser Nephropathie diskutiert. Die Serum-Albuminkonzentration stellt ein indirektes Maß für die Thrombosegefährdung bei NS dar. In Anwendung der aktuellen Glomerulonephritis-Leitlinie von KDIGO (Kidney Disease: Improving Global Outcomes) empfiehlt sich bei NS mit einer Serum-Albumkonzentration < 25 g/l und dem Vorhandensein von mindestens einem zusätzlichen thrombogenen Risikofaktor eine primärprophylaktische Antikoagulation („konditionierte Prophylaxe“) mit einem oralen Vitamin K-Antagonisten (Zielbereich: INR 2–3), solange die Serum-Albuminkonzentration < 30 g/l ist.

Abstract

Thromboembolic complications are among the most important extrarenal consequences of nephrotic syndrome (NS). In addition to deep vein thrombosis in the legs and pulmonary embolism, NS is very frequently accompanied by renal vein thrombosis. Due to enhanced procoagulatory and antifibrinolytic potential and reduced anticoagulatory potential, multifactor disruption of hemostatic equilibrium leads to hypercoagulability in NS patients, which is aggravated by an increase in blood viscosity and endothelial dysfunction. Circulating antibodies against α-enolase, a plasmin(ogen)-binding protein, and the possibility of certain molecules being renally eliminated in specific manner are discussed as reasons for the particular frequency of thromboembolic complications in patients with idiopathic membranous nephropathy. Serum albumin concentration is an indicator for the risk of thrombosis in NS patients. When applying the current KDIGO (Kidney Disease: Improving Global Outcomes) clinical practice guideline for glomerulonephritis to NS patients with a serum albumin concentration of less than 25 g/l and at least one additional thrombogenic risk factor, primary prophylactic anticoagulation (“conditioned prophylaxis”) with an orally administered vitamin K antagonist (target INR 2–3) is recommended as long as the serum albumin concentration is less than 30 g/l.

 
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