New diagnostic and treatment strategies in renal artery stenosis: a promising pursuit or disappointment foretold?

Clinical management of renal artery stenosis has seen a major shift, after randomised clinical trials have shown no group benefit of endovascular intervention relative to optimal medical control. However, the inclusion criteria of these trials have been criticised for focusing on a subset of patients with atherosclerotic renal artery stenosis where intervention was unlikely to be beneficial. Moreover, new imaging and computational techniques have become available, which have the potential to improve identification of patients that will respond to interventional treatment. This review addresses the challenges associated with clinical decision making in patients with renal artery stenosis. Opportunities for novel diagnostic techniques to improve patient selection are discussed, along with ongoing Dutch studies and network initiatives that investigate these strategies.

[Premature cardiovascular disease: no indication for the determination of antiphospholipid antibodies or lupus anticoagulant as a possible risk factor]. / Vroegtijdige hart-vaatziekte: geen indicatie voor het bepalen van antifosfolipideantilichamen of lupusanticoagulans als mogelijke risicofactor.

In patients with premature atherothrombotic disease, the antiphospholipid syndrome (APS, defined as any thrombosis plus the repeated presence ofantiphospholipid antibodies) is sometimes looked for, as observational studies have suggested a link between APS and premature atherothrombosis. However, recent reviews that evaluated the prognostic value of antiphospholipid antibodies have concluded that the prognostic significance ofAPS for recurrent thrombotic disease is, at best, unclear and that its presence has no therapeutic consequences. A study that compared high- versus standard-dosage warfarin in patients with APS found no additional benefit from high-dosage warfarin. A study in patients with a recent ischaemic stroke found no additional benefit from warfarin (standard dosage) versus aspirin in patients with or without antiphospholipid antibodies. Therefore, on the basis of the evidence at hand, screening for APS in patients with premature atherosclerosis is not considered to be useful.

Acetylcholine-induced vasodilatation in the human hypertensive kidney: inhibition by muscarinic receptor antagonism.

OBJECTIVE: To evaluate the vascular response of the human hypertensive kidney to endothelial stimulation with acetylcholine (ACh) and to assess whether this effect can be inhibited by the non-specific muscarinic receptor antagonist atropine. PATIENTS AND METHODS: Three stepwise increasing doses of ACh (0.3, 1.0 and 3.0 microg/kg per min) in combination either with placebo or with 100 or 300 ng/kg per min atropine were infused into the right renal artery of 20 hypertensive patients. Renal blood flow was determined using the 133Xe wash-out technique. RESULTS: Infusion of ACh induced a dose-dependent increase in renal blood flow (P= 0.02). Both doses of atropine attenuated the ACh-induced renal vasodilatation (P < 0.05). CONCLUSIONS: Administration of ACh to the human hypertensive kidney induces a dose-dependent increase in renal blood flow. This effect is, at least partially, mediated by muscarinic receptors.

Adenosine-induced renal vasodilatation is prolonged in renal artery stenosis.

OBJECTIVE: The objective of this study was to determine whether the response of renal blood flow (RBF) to adenosine infusions differs between hypertensive patients with and without renal artery stenosis (RAS). DESIGN AND METHODS: Twenty-one hypertensive patients who underwent diagnostic angiography of the renal arteries were studied. Nine patients (median age 51 years; 45-61 interquartile ranges) were diagnosed as having essential hypertension (EH). Twelve patients (median age 52 years; 50-58) had hypertension and renal artery stenosis. In all patients three stepwise increasing doses of adenosine (1, 3 and 10 (microg/kg/min) were infused into the renal artery. RBF was measured before and during infusions by means of the 133xenon wash-out method. Arterial and venous plasma samples for renin concentration were obtained from the renal artery and renal vein. Intraarterial blood pressure and heart rate were monitored continuously. RESULTS: Both groups were similar with respect to age, body mass index, mean arterial pressure and baseline RBF (EH: median 428; RAS 343 ml/min/100 g). Both groups showed a similar dose-related increase in RBF during adenosine infusions (normal kidneys: 9, 21 and 34% change vs baseline; stenotic kidneys: 16, 39 and 52% change vs baseline). Ten minutes after discontinuation of the adenosine infusion, RBF returned to baseline in the normal kidney group, but increased further in the stenotic kidney group (71% vs baseline; P = 0.033). Adenosine infusion did not affect the renin secretion in either group. CONCLUSION: Both essential hypertensive patients and patients with renal artery stenosis show a dose-dependent vasodilatation following adenosine infusion. This vasodilatation is sustained after discontinuation of the adenosine infusion in patients with renal artery stenosis, suggesting a potentiated mechanism for vasodilatation induced by adenosine.