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It has recently been recognized that coronary plaques Suggested reading are not static obstructive lesions of the coronaries, but 1. Raine AEG, Margreiter R, Brunner FP. Report on management dynamic structures that can progress with time and of renal failure in Europe XXII, 1991. Nephrol Dial Transplant are susceptible to rupture and coronary thrombosis. 1992; [Suppl 2]: 7–35 Cell activation and ensuing proteolysis cause destabil2. Lindner A, Charra B, Sherrard DJ, Scribner BH. Accelerated atherosclerosis in prolonged maintenance hemodialysis. N Engl ization of the fibrous cap at the interface between J Med 1974; 290: 697–701 coronary lumen and the lipid deposits beneath the 3. Amann K, Schwarz U, Törnig J, Stein G, Ritz E. Abnormalies fibrous cap. Thus, the question arises whether the cardiaque au cours de urémie chronique. In: Grüngeld J.-P, morphology of the coronary lesion in the uraemic Bach J-F, Kreis H, eds. Actualités Néphrologique Jean patient with known high mortality from coronary Hamburger 1997. Medicine-Science Flammarion, Paris: 1–15 4. Ibels LS, Alfrey AC, Huffer WE, Craswell PW, Anderson JT, disease [1], and possibly more agressive atherogenesis Weil R. Arterial calcification and pathology in uremic patients [2] (although this point is controversial ) differs from undergoing dialysis. Am J Med 1979; 66: 790–796 the non-renal patient. The figures show three findings 5. Reusser LM, Osborn LA, White HJ, Sexson R, Crawford MH. which are characteristic of coronary arteries and the Increased morbidity after coronary angioplasty in patients in chronic hemodialysis. Am J Cardiol 1994; 73: 965–967 coronary plaque in the uremic patient [3]. Firstly, the thickening of the media and intima of the diseased coronary artery is certainly more conspicuous than in the non-renal patient (Figure 1a vs Figure 1b), and this is confimed by quantitative measurements. This finding is consistent with the previous observations of Ibels [4] in non-coronary vessels. Secondly, there is more pronounced calcification of the plaques (Figure 2) and this correlates with the mean serum phosphate concentration. X-ray diffraction analysis shows that the calcium containing deposits are hydroxylapatite. Thirdly, (Figure 3) the plaques are heavily infiltrated by activated macrophages, known forerunners of plaque destabilization and plaque rupture. For clinical nephrologists these findings are of interest since they may at least explain partly the malignant character of coronary plaques in the uraemic patient and the very frequent recurrence of coronary stenosis after percutaneous transluminal coronary arterioplasty (PTCA) [5].

Why are coronary plaques more malignant in the uraemic patient?