Introduction and aims: Vascular calcification is common in patients suffering from advanced chronic kidney disease (CKD), yet little is known about vascular calcification and arterial stiffness in the early stages of renal dysfunction. We evaluated, in patients suffering from CKD 3, the arterial vascular damage by means of the measurement of arterial stiffness and the coronary calcium score. Methods: Eleven patients (7 M, 4 f, aged 64±7 years) with mild to moderate renal failure were enrolled. We deliberately excluded patients with diabetes and previous history of heart disease from this study; we did this in order to exclude the interference of other pathologies apart from functional kidney insufficiency in the genesis of vascular alterations. the causes of renal failure were nephroangiosclerosis (73%), membranous glomerulonephritis (18%), and interstitial nephritis (9%). all the patients underwent the assessment of coronary calcification by means of multi-detector Ct (expressed as calcium score [Cs] according to agatston score), arterial stiffness by pulse wave velocity (pWV) measurement, common carotid intima-media thickness (iMt) by B-mode Us scan, and left ventricular mass index by echocardiography. renal function (Gfr) was evaluated using the Cockroft and Gault formula. Blood samples were drawn for the measurement of serum creatinine, lipid profile, glycidic profile, electrolytes, hOMa index, etc. Results: the main results are summarized in the table. Whilst the calcium score (Cs) was abnormal in only one patient (the remaining patients had a Cs <50 hU), the pWV and iMt were high in all of them. No substantial alterations in the lipid profile and hOMa index were present. Conclusions: Our data, albeit obtained in a small number of patients, show that in the early stages of chronic renal failure, in the absence of diabetes and cardiac involvement, vascular calcification is only rarely present. On the contrary, arterial stiffening, as shown by pWV and iMt, starts very early, even in the presence of a normal lipid profile and insulin resistance. further studies in larger groups are needed to confirm this results, as well as to understand at which moment or which factors lead to the development of the extensive vascular calci-fication observable in the advanced stages of CKD. Table. Results Variable Mean±SD GFR, mL/min 40.6±10 Total cholesterol, mg/dL 198±35 LDL cholesterol, mg/dL 111±29 HDL cholesterol, mg/dL 53±16 Triglycerides, mg/dL 183±93 HOMA index, % 1.9±1.5 PWV, m/sec 10.5±1.6 ccIMT, mm 0.8± 1.2 LVM index, g/m 2 110±41 CS (HU)* 0-1074 *Expressed as range. increased pulse wave velocity (pWV), a marker of arterial stiffness, is considered a strong predictor of cardiovascular mortality both in general and in the renal-disease population. however, it is unknown whether it may be affected by the rapid variations in the fluid status induced by treatment in dialysis (hD) patients. We studied 13 patients (6 M, 7 f, 65±12 years) on thrice-weekly chronic hD treatment in a study session after the longest interdial...

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In 12 mechanically ventilated and anesthetized rabbits, we investigated whether the magnitude of respiratory changes in the aortic velocity time integral (VTI(Ao)), recorded by transthoracic echocardiography (TTE) during a stepwise blood withdrawal and restitution, could be used as a reliable indicator of volume depletion and responsiveness. At each step, left and right ventricular dimensions and the aortic diameter and VTI(Ao) were recorded to calculate stroke volume (SV) and cardiac output (CO). Respiratory changes of VTI(Ao) (maximal - minimal values divided by their respective means) were calculated. The amount of blood withdrawal correlated negatively with left and right ventricular diastolic diameters, VTI(Ao), SV, and CO and correlated directly with respiratory changes of VTI(Ao). Respiratory VTI(Ao) variations (but not other parameters) at the last blood withdrawal step was also correlated with changes in SV after blood restitution (r = 0.83, P < 0.001). In conclusion, respiratory variations in VTI(Ao) using TTE appear to be a sensitive index of blood volume depletion and restitution. This dynamic parameter predicted fluid responsiveness more reliably than static markers of cardiac preload.

Aims To test the existence of an association between reports of hypoglycaemia and angiotensin converting enzyme inhibitors, in a spontaneous reports database. Methods The French Pharmacovigilance database was examined for an association between adverse drug reaction reports mentioning hypoglycaemia, and angiotensin converting enzyme inhibitors (ACEI) using the case/non-case methodology, with reports of hypoglycaemia as cases and all other reports as comparators. The association between ACEI or other chosen drugs and hypoglycaemia was also tested in the subgroups of patients taking or not antidiabetic agents (ADA). Results 428 of 93338 reports mentioned hypoglycaemia (202/2227 with ADA (OR 40, 95% CI 33-48)). 46/5717 reports mentioned ACEI (OR 1.8 (1.25-2.54)). Other study drugs associated with hypoglycaemia were cibenzoline (OR 80 (57-112)), disopyramide (OR 32 (22-46)), nifedipine (OR 2.16 (1.32-3.51)), diltiazem (OR 1.76 (1.01-3.06)) nitrates (nitroglycerin, molsidomine) (OR 1.91 (1.16-3.16)) and frusemide (OR 1.89 (1.31-1.76)), but not nicardipine, amlodipine, felodipine or nitrendipine, diazepam, atenolol or combination thiazide diuretics. However, ACEI and other drugs were associated with ADA, so that in the subgroups of patients taking or not ADA, the association of ACEI with hypoglycaemia disappeared (OR 0.9 (0.5-1.4) and 1.2 (0.7-2.2), respectively). The same was found for other drugs except cibenzoline. Conclusion The association between reporting of hypoglycaemia and ACE inhibitors was related to concomitant use of antidiabetic agents. This was true also for other drugs used in arterial disease or renal failure, such as calcium channel blockers, nitrates, and frusemide.