Subject(s)
Cardiomyopathies , Hyperoxaluria, Primary , Kidney Failure, Chronic , Kidney Transplantation/methods , Myocardium/pathology , RNA, Small Interfering/administration & dosage , Transaminases/genetics , Adult , Biopsy/methods , Calcium Oxalate/blood , Cardiomyopathies/diagnosis , Cardiomyopathies/drug therapy , Cardiomyopathies/etiology , Cardiomyopathies/surgery , Humans , Hyperoxaluria, Primary/blood , Hyperoxaluria, Primary/genetics , Hyperoxaluria, Primary/physiopathology , Hyperoxaluria, Primary/therapy , Kidney Failure, Chronic/etiology , Kidney Failure, Chronic/therapy , Male , Mutation , Patient Care Management/methods , Patient Care Team , Renal Agents/administration & dosage , Renal Dialysis/methodsABSTRACT
We tested a new bedside method to determine the function of native arteriovenous fistula in 16 patients performed during hemodialysis without stopping the treatment. We initially measured vascular access flow (Q(a)) in each patient using the Transonic HD01(plus) device. We then measured the pressure in arterial and venous drip chambers at different blood pump flow rates (Q(bset)=0, 50, 100, 250, 300, 350 ml/min). The intravascular blood pressure gradient (P(f)) between arterial and venous puncture sites was estimated by a mathematical model. P(f) was positive for low Q(bset), but became negative when Q(bset) overcame the threshold value (Q(Inv)). Such critical flow showed a high correlation with Q(a), even if it was systemically lower. Computer analysis of fluid dynamics showed that when the blood pump flow overcame the Q(Inv) threshold, a critical transition from laminar flow to vortex circulation took place downstream of the venous needle, causing a dangerous shearstress on the vessel wall. Our results show that Q(Inv) provides an indication of the maximal blood pump flow rate needed to be reached to maximize blood flow supply in order to limit hemodynamic stress on the vascular access.
