Renal transplant artery stenosis is a relatively frequent complication after transplantation, with an incidence of up to 23% being reported. The gold standard for the diagnosis still remains renal arteriography. Several imaging techniques are available to confirm the diagnosis (duplex-Doppler, nuclear magnetic resonance, spiral computerized tomography), and their use depends, in part, on the centre’s experience. The treatment can either be conservative (providing graft perfusion is not jeopardized) or by revascularization (surgical or percutaneous transluminal angioplasty). There are several unresolved questions concerning revascularization of the graft: whether and when to intervene? Is the stenosis progressive in the long term? Is hypertension alone an indication for angioplasty? How do we assess the haemodynamic significance of the stenosis? What is a significant stenosis—50, 60, 80 or 90%? Is stenosis ‘good’ for something? In Slovenia, since 1990, all renal transplant recipients are screened regularly for the presence of stenosis by duplex-Doppler (performed by nephrologists), and also in cases of deterioration of graft function or hypertension. In the majority of patients with a diagnosed stenosis, the latter was found to be stable over time (assessed by regular Doppler, graft function and hypertension control). In some patients, spontaneous regression of the stenosis was observed. Frequent Doppler assessment of these patients helps to be more conservative with angioplasty and angiography. Deterioration of graft function (with stenosis diagnosed by Doppler) is the main indication for angiography (and angioplasty). Better definition of significant stenosis and randomized studies comparing conservative treatment vs angioplasty are warranted. Duplex-Doppler seems to be the ideal screening and follow-up test.

Background: The majority of citrate protocols for hemodialysis (HD) use calcium (Ca)-free dialysate, a limited number use dialysate with Ca, aiming to simplify the procedure. This randomized clinical study sought to compare the anticoagulant effect of citrate using Ca-free dialysate and dialysate with Ca 1.25 mmol/L. Methods: Fifty HD procedures (in 5 chronic HD patients treated by chronic citrate anticoagulation) were randomly assigned to Ca-free dialysate (25 procedures) or Ca-1.25 dialysate (25 procedures), both with Mg 0.5 mmol/L, Na 138 mmol/L, and bicarbonate 28 mmol/L. Ca-free HD: 15% Na₃ citrate 80 ml/hour was infused into the arterial line, and 1 M CaCl₂, 14 ml/hour into the venous line. Ca-1.25 group: 15% Na₃ citrate 100 ml/hour, 1 M CaCl2 2–4 ml/hour. Polyflux H dialyzers were used. Antithrombotic effect was assessed visually after HD at 3 points: dialyzer, arterial, and venous bubble traps, using a score of 5 (no clotting) to 1 (total clotting). Results: Ca-free group: arterial bubble trap score 4.7 ± 0.5, dialyzer 4.5 ± 0.6, venous bubble trap 4.8 ± 0.6. Ionized calcium (iCa) at dialyzer inlet 0.34 ± 0.17, outlet 0.21 ± 0.06 mmol/L. All HDs were completed successfully. Ca-1.25 group: arterial bubble trap score 4.7 ± 0.5 (NS), dialyzer 2.6 ± 1.04 (p<0.01), venous bubble trap 2.4 ± 0.9 (p<0.01). Volume of clot in venous bubble trap was 1.9 ± 1.8 mL (range 0.5–6 mL). iCa at dialyzer inlet 0.24 ± 0.05 mmol/L (p<0.05), outlet 0.63 ± 0.11 mmol/L (p<0.01). Four of 25 HD procedures (16%) were prematurely terminated due to threatening dialyzer clotting, in 6/25 HD procedures (24%), the venous line was changed (p<0.01). Conclusion: Citrate anticoagulation with Ca-1.25 dialysate resulted in significantly worse anticoagulation of dialyzer and venous bubble trap compared with Ca-free dialysate, despite higher citrate dose.