Lymph Vessels of the Transplanted Kidney

Abstract

Lymph vessels were evaluated in 20 transplanted canine kidneys. Prior to the occurrence of morphological rejection changes, transplants with good blood flow rates show areas with dilated but, less frequently, also undilated lymph vessels. In transplants with the presence of a rejection infiltrate and a decrease of the blood flow rate of 21–50% the lymph vessels may be focally dilated or, in contrast, narrowed by the cells of the rejection infiltrate. Numerous vesicles and vacuoles can be seen within the cytoplasm of endothelial cells. Interendothelial junctions may be occasionally open, the walls of endothelial cells become attenuated, and disintegration of the cell membrane is followed by a focal destruction of the wall and the development of defects. Cells of the rejection infiltrate penetrate through the gaps in the wall of the lymph vessels. The possible mechanism of the disintegration is discussed in this paper.

Is defective lymphatic drainage a trigger for lymphoid neogenesis?

“…However, because the lymphatic vasculature of the graft originates from the donor and displays allogeneic antigens, it is one of the targets of the immune system of the recipient. Accordingly, previous ultrastructural studies have demonstrated that rejection episodes were associated with focal narrowing of the lumina of lymph vessels, disruption of lymphatic microvascular endothelial junctions and destruction of endothelial cells responsible for focal defects in the walls of the lymphatic vessels [25,26]. These alterations probably have functional repercussions because an interruption in the lymph flow from the graft to the draining lymph node of the recipient has been reported in a canine allograft lung rejection model [27].…”

Chronic allograft nephropathy: An update

“…During acute rejection, between recipient metabolic demands and graft renal mass explains chronic allograft nephropathy. The three-there is an increased production of lymph fluid and disruption of the lymphatic microvascular endothelial junc-year graft survival rates of transplants that come from female, black, very young, or very old donors are less tions, which retards lymphatic flow [102,103]. Obstruction of the lymphatics that drain the vessel wall causes compared with grafts from donors who are supposedly endowed with a larger nephron mass [90], but the studies vessel wall lesions, as observed in chronic allograft nephropathy [104].…”

The role of non-hematopoietic stromal cells in the persistence of inflammation

“…It is debatable whether newly formed lymphatic vessels are able to establish functional connections and deliver antigen, fluid, and cells to the draining lymph nodes. The inability of lymphatic vessels to deliver antigens to the draining lymph node could favor the persistence of TLOs, where an excess of antigen is presented in structures whose stroma component is potentially unable to exert the tollerogenic activity attributed to lymph node stroma (Kline and Thomas, 1976; Eliska et al, 1986; Joos et al, 1993; Ruggiero et al, 1994; Angeli et al, 2006; Angeli and Randolph, 2006; Thaunat et al, 2006; Li et al, 2011). In this context the ectopic expression of CCL21 on newly formed (but yet non-functional lymphatic vessels) might compete with the chemokine gradient established by pre-existent functional lymphatic vessels, thus contributing to the entrapment of leukocytes and DCs within the TLOs (Kerjaschki et al, 2004; Burman et al, 2005).…”