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The Arteriovenous Fistula

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The Arteriovenous Fistula DISEASE OF THE MONTH J Am Soc Nephrol 14: 1669–1680, 2003 Eberhard Ritz, Guest Editor The Arteriovenous Fistula KLAUS KONNER,* BARBARA NONNAST-DANIEL,† and EBERHARD RITZ† *Merheim Hospital, Medical Faculty, University of Cologne, Germany; †Department of Nephrology, Med. Klinik IV, Erlangen-Nu¨rnberg, Germany; and ‡Department Internal Medicine, Ruperto Carola University, Heidelberg, Germany. The ground-breaking article by Brescia and Cimino in 1966 (1) side fistula. Flow increased from 21.6 Ϯ 20.8 ml/min to 208 Ϯ revolutionized the creation of the vascular access, and the 175 ml/min immediately after operation. In well-developed fistu- Cimino fistula was soon used in almost all dialysis patients. lae, flow rates may ultimately reach values of 600 to 1200 ml/min. Unfortunately, subsequent wide-spread use of PTFE grafts Flow increases as a result of both vasodilation and vascular instead of AV fistulae occurred because of the ease of the remodeling. The latter has been studied using echo-tracking surgical technique, the immediate availability of the graft for techniques (8). It was found that the diameter of the proximal puncture, the need of high blood flow for high-efficiency, antecubital vein increased progressively while the intima me- short-duration hemodialysis sessions, and because of financial dia thickness remained unchanged. Venous dilation caused disincentives against the AV fistula. PTFE grafts currently reduction of mean shear stress, which had returned to normal account for 80% of primary vascular accesses created in the values by 3 mo. The venous limb of the AV fistula underwent United States (2,3), but they are less frequently used in other excentric hypertrophy as documented by increased wall cross- countries. It has been increasingly recognized that outcomes of sectional area. In parallel, remodeling of the radial artery was PTFE grafts are poorer. In the DOQI guidelines (4), this has led seen without arterial hypertrophy, despite a marked increase in to the recommendation that AV fistulae should be the first diameter and blood flow (9). option; however, this advice has not been followed uniformly. The changes in blood flow after creation of an AV fistula One impediment may be the astonishingly high rate of primary initiate compensatory responses that have been elegantly eluci- failures of AV fistulae, up to 50% in some centers (4). The dated in experimental models (10). Apart from primarily NO- DOPPS study (Figure 1) documented substantial differences be- mediated vasodilation, adaptive remodeling of the vessel wall is tween survival of PTFE grafts and AV fistulae and differences of induced by reorganization of cellular and extracellular compo- survival of AV fistulae between the United States and other nents, ultimately altering wall geometry. Elevated flow after cre- countries (3). On the basis of our experience, we are of the opinion ation of an AV fistula enlarges the arterial diameter (10). Kamiya that primary failure rates can be substantially improved by atten- and Togawa (11) documented that after creation of a carotid to tion to small but important details of surgical technique. The jugular anastomosis the flow-loaded artery enlarged until wall DOQI guidelines state that AV fistulae are feasible only in 50% of shear stress had returned to baseline values. This response usually the patients, but we (5) and others (6) found that construction of occurred rapidly, but when extremely high shear stress was in- native AV fistulae is feasible in up to 90%. duced, it required up to 6 mo (12), for example in the monkey iliac It is the purpose of this article (a) to provide some insights into artery subjected to a 10-fold increase of flow. the fascinating cellular biology and pathophysiology underlying Endothelial cells play a central role in adaptive remodeling the vascular adaptation to the creation of an AV fistula and (b) to (13). Shear stress, i.e., the frictional force generated by blood describe some small, often neglected, but important technical flow, acts on the apical cell surface to deform the cell in the details that determine the success of the procedure. It is the direction of blood flow, thus eliciting rapid cytoskeletal re- intention to improve results and to influence patterns of practice. modeling and activating signaling cascades with the conse- quent acute release of nitric oxide (NO) and prostacyclin Vascular Remodeling and Adaptation to High Flow followed by activation of transcription factors, including NF- Wedgewood et al. (7) measured flow rates in the radial artery ␬B, c-fos, c-jun, and SP-1. The mediators of the adaptive before and immediately subsequent to the creation of an end-to- response include integrins, focal adhesion–associated proteins, and stretch-sensitive calcium channels. The crucial importance of endothelial cells is illustrated by the observation (14) that Correspondence to Dr. Eberhard Ritz, Klinikum der Universita¨t/Heidelberg, Medizinische Klinik, Bergheimer Strasse 56A, 69115 Heidelberg, Germany. de-endothelialization eliminates the dilation resulting from an Phone: 49-622191120; Fax: 49-6221162476; E-mail: [email protected] increase of flow. Acute flow-induced endothelial release of 1046-6673/1406-1669 nitric oxide (NO) (15) as well as increased vessel wall cGMP Journal of the American Society of Nephrology content (16) have been documented in high flow models. Copyright © 2003 by the American Society of Nephrology Inhibition of NO by L-NAME interfered with flow-induced DOI: 10.1097/01.ASN.0000069219.88168.39 vascular enlargement (17). 1670 Journal of the American Society of Nephrology J Am Soc Nephrol 14: 1669–1680, 2003 Figure 1. Fistula versus graft survival in patients starting hemodialysis with a permanent vascular access comparing DOPPS results from Europe and United States. Reprinted with permission from reference 4. The first step of remodeling involves controlled removal of to low-flow conditions, and this was abrogated by endothelin preexistent vessel wall constituents. The arterial wall of an AV receptor antagonists. Under high-flow conditions, there was an fistula exhibits early tears and fragmentation of the internal increased number of PCNA-positive cells in the media, which elastic lamina (18) and enlarged fenestrae (19), increasing again was abrogated by endothelin receptor antagonists. Obvi- arterial distensibility. The loss of the internal elastic lamina ously the responses of the intima to low flow and of the media results from degradation by metalloproteinases, which are re- to high flow are exaggerated. Against this background, it is leased from endothelial cells (20). A role for oxidative stress is remarkable that remodeling is largely appropriate in uremic suggested by the observation that endothelial cells of flow- patients (8,9). loaded carotid arteries stain positive for nitrotyrosine, which is Although not directly related to uremia, the processes underly- indicative of the presence of peroxynitrite (21), and this is ing the development of stenoses in coronary saphenous vein grafts abrogated by administration of L-NAME. The urokinase type are of interest for understanding the development of fistula ste- of plasmin activator is also upregulated. This observation is noses. It is thought that the changes provoking delayed stenoses important, because the plasminogen-plasmin system activates are initiated during surgery and consist of denudation of the pro-metalloproteinases. It is therefore not surprising that non- surface endothelial cells and insudation of granulocytes and selective inhibitors of metalloproteinases diminish flow-medi- monocytes with deposition of fibrin and thrombocyte-containing ated arterial enlargement in a rat AV fistula model (22). thrombi (26). CRP induces a pro-inflammatory phenotype of The involvement of the above systems raises the issue saphenous vein endothelial cells, which is reversible with the whether remodeling is normal or not in uremia. It is well administration of endothelin receptor antagonists (27); of interest known that generation of NO is reduced in uremia (22), and in view of the microinflammatory state of uremia and the role of numerous specific abnormalities have been described in endo- endothelin receptor antagonists in experimental models of uremia thelial cell monolayer cultures (HUVEC) exposed to uremic (25). Interventions interfering with smooth muscle cell accumu- serum: increased ELAM-1 and VCAM expression, increased lation in the neointima further suggest a role of PDGF (28), presence of von Willebrand factor on the extracellular matrix angiotensin subtype AT-1 receptors (29), VEGF (30), and leptin (23), abnormal cell morphology, accelerated growth, and in- (31), among others. creased expression of tissue factor mRNA (24). Platelet dep- One important aspect in the evolution of the AV fistula of osition on extracellular matrix, which had been synthesized in uremic patients is iatrogenic remodeling resulting from punc- the presence of uremic serum, is also increased. Interestingly ture of the AV fistula (32). Puncture displaces tissue, and the an antibody to human tissue factor prevented the increase in defect caused by the cannulation is replaced by a thrombus platelet deposition observed on “uremic” extracellular matrix, causing a slight increase in tissue mass. Even after healing, the a finding potentially relevant for the genesis of fistula stenoses. edges of the puncture hole stay apart as shown by applying There are few formal analyses of vascular remodeling in ure- tattoo
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