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Mechanisms of glomerular crescent formation

Pierre Ronco, MD, PhD
Section Editors
Richard J Glassock, MD, MACP
Fernando C Fervenza, MD, PhD
Deputy Editor
John P Forman, MD, MSc


Cellular glomerular crescents are defined as two or more layers of proliferating cells in Bowman's space (picture 1 and picture 2) and are a hallmark of inflammatory glomerulonephritis and a histologic marker of severe glomerular injury. In general, the severity of the renal failure and other clinical manifestations of glomerulonephritis (eg, hypertension, edema) correlates with the percentage of glomeruli that exhibit crescents [1-5]. The duration and potential reversibility of the underlying disease correspond with the relative predominance of cellular or fibrous components in the crescents. (See 'Course of crescents' below.)

Crescentic glomerulonephritis is typically associated with the syndrome of rapidly progressive glomerulonephritis, which can occur in most forms of inflammatory glomerular injury, including postinfectious glomerulonephritis, IgA nephropathy, lupus nephritis, renal vasculitis, membranoproliferative glomerulonephritis, and anti-glomerular basement membrane (GBM) antibody disease. (See "Differential diagnosis and evaluation of glomerular disease", section on 'Moderate to severe glomerulonephritis'.)

This topic will review the mechanisms of glomerular crescent formation. The classification, clinical presentation, evaluation, diagnosis, and treatment of crescentic glomerulonephritis, as well as the mechanisms and pathogenesis of glomerular injury, are discussed elsewhere. (See "Overview of the classification and treatment of rapidly progressive (crescentic) glomerulonephritis" and "Mechanisms of immune injury of the glomerulus".)


Glomerular crescent formation appears to represent a nonspecific response to severe injury to the glomerular capillary wall [5]. The initiating event is the development of physical gaps (also called rents or holes) in the glomerular capillary wall, glomerular basement membrane, and Bowman's capsule (picture 2 and picture 3) [6,7]. These gaps permit the entry into Bowman's space of coagulation factors, which lead to fibrin formation (due to conversion of fibrinogen to fibrin polymers and delayed fibrinolysis) and cellular elements (such as monocytes and lymphocytes), both of which promote crescent formation (picture 3) [5,8].

Based upon experimental murine studies, crescent formation is believed to be primarily mediated by a T helper 1 (Th1) nephritogenic immune response involving CD4+ T cells, macrophages, and fibrin as effectors of cell-mediated immunity [9]. Th17 CD4 effector cells also appear to play an important role [10,11] with a potential cytokine-chemokine-driven cross-regulation of Th1 and Th17 subpopulations [12]. Recruitment of Th1 is also controlled by regulatory T cells [13]. (See "T helper subsets: Differentiation and role in disease".)


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Literature review current through: Sep 2016. | This topic last updated: Jan 22, 2013.
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