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| Journal of Vascular Access 2005; 6: 45 - 46 |
| Vasculorama |
G. Dunea1
1Cook County Hospital, Chicago, Illinois, USA
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ABSTRACT
No abstract
AV fistulae hard to establish
It is widely recognized that in spite of practice guidelines fistula access is often difficult to achieve in patients starting dialysis. According to the DOPPS study of practice patterns, fistulae were used in only 43% of patients in the US and 67% in Europe. Difficulties arising from poor vasculature are common, especially in the aged, in diabetics, and in patients with calcified blood vessels. Targets set by national guidelines with respect to primary fistula use are therefore difficult to meet (Nephrol Dial Transplant 19: 2816).
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Tesio-Cath safe and effective
One type of central venous catheter used as a long term alternative to a functioning fistula is the Tesio-Cath. This consists of two parallel polyurethane lines, each with its own cuff and side holes. Used in London at St Mary’s Hospital in a series of 623 patients, it was effective and provided safe long term access. Catheter survival was 77% at one year and 44% at three years. Access related hospital admissions for infection were 0.28/1000 catheter days and sepsis related deaths 9.6/1000 patient years at risk (ibid).
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Timely fistula insertion desirable
For best results with arteriovenous fistulae, these should be created early and allowed to mature. According to a Canadian study, patients receiving a fistula at least four months before starting dialysis had less sepsis, fewer hospital admissions, and reduced mortality compared to patients receiving fistula within one month of starting dialysis. This difference was attributed to using fewer central venous catheters; but diabetes, inpatient start, graft use, and second access creation were also independently associated with hospitalization for sepsis (J Am Soc Nephrol 15: 1936).
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Vascular calcification occurs even before dialysis started
Italian investigators used spiral computed tomography in a group of patients with chronic renal failure not yet on dialysis to evaluate the extent of coronary atherosclerosis. They found that vascular calcification was present even in the early phases of chronic renal failure, a long time before dialysis was required. Coronary artery calcification was present in 40% of patients but in only 13% of controls. Metabolic factors such as calcium and phosphorus and parathyroid hormone concentrations, as well as inflammation markers, did not seem to pay a role in causing this calcification, and calcification of atherosclerotic plaques was deemed a more likely explanation (Am J Kidney Dis 44: 1024).
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Two types of vascular calcification
The vascular calcification seen in dialysis patients may take two forms. It may affect (1) the vascular media, as in Monckeberg’s sclerosis, or (2) the intima, as result of calcification of arteriosclerotic plaques. The plaques in the coronary arteries are less prone to rupture acutely but rather tend to narrow the arterial lumen, eventually causing myocardial ischemia, fibrosis, and left ventricular hypertrophy. Accordingly, dialysis patients are more likely to suffer sudden death or congestive heart failure than acute coronary syndromes (Kidney Int 66: 1315).
Calcium and vitamin D harmful in large doses?
Of more immediate concern to the vascular surgeon is the calcification present in the peripheral blood vessels used for establishing vascular access. Recently there has been intense interest in this subject, in particular in the possibility that nephrologists have put the interests of the bones ahead of those of the heart and blood vessels vasculature by prescribing large doses of calcium and vitamin D derivatives to suppress parathyroid hormone secretion. New strategies may be called for, including a reevaluation of the use of phosphate binders and vitamin D and the more widespread prescription of calcimimetic agents (Kidney Int 66: 1315).
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Middle molecules and vascular damage
A host of uremia retention products could also contribute to vascular damage and arteriosclerosis in dialysis patients. Some of these compounds cause oxidative or carbonyl stress by releasing harmful enzymes or generating advanced glycation products. Elevated homocysteine levels have been suspected to increase the risk of cardiovascular disease, as has impaired endothelium-dependent vasodilatation due to the inhibition of nitric oxide generation by excessive accumulation of ADMA (asymmetrical dimethylarginine) (Kidney Int 66: 1719).
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Sympathetic hyperactivity from functioning fistulae in transplant patients
In transplant recipients with functioning arteriovenous fistulae sympathetic activity is increased, as determined by hemodynamic studies and measurements of muscle sympathetic traffic (by microneurography) during acute fistula occlusion. It is not clear, however, if these functioning fistulae are so harmful as to require their closure (Nephrol Dial Transplant 19:1606).
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Antiproliferative depot to prevent venous stenosis
Prevention rather than mechanical revascularization is clearly a more desirable approach to the stenosis occurring at the venous end of arteriovenous grafts. One approach would be to inhibit the proliferation of the vascular smooth muscle cells that initiates the occlusive and thrombotic changes. Such inhibition in experimental animals was achieved by inserting at the time surgery a sustained release depot of the antiproliferative agent paclitaxel. (Kidney Int 66: 2061).
George Dunea, MD FRCP, FACP
Associate Editor
Address for correspondence:
Cook County Hospital
1825 West Harrison Street
Chicago, Illinois 60612 - USA geodunea@aol.com
REFERENCES
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G. Dunea
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