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Right heart catheterization (RHC) was performed after 30?min of rest. After measuring the cardiac index (CI), the AVF was compressed with a blood pressure cuff until fistula flow was barely audible with a stethoscope. http://www.selleckchem.com/products/Adriamycin.html Mean pulmonary artery pressure (MPAP), CI and pulmonary capillary wedge pressure (PCWP) were re-evaluated under compression of the AVF. PH was diagnosed, wherever the MPAP was equal or >25?mmHg [8]. As RHC confirmed RHF resulting from high-flow AVF in the KTRs, closure of AVF was performed about 17?��?3?days post-transplant in our center to improve kidney allograft function. Duplex ultrasound detected high-flow AVF (>2.5?l/min fistula flow) as well as a pathologic biphasic flow pattern in the kidney allograft vein of all four KTRs. This was indicative for tricuspid regurgitation and iliac congestion (Fig.?1a). After AVF closure, normal linear flow patterns in the allograft and iliac vein were detected in these patients (Fig.?1b). Echocardiographic investigation revealed a moderately to severely dilated right ventricle with a flattened septum, paradoxical septal movements and http://www.selleckchem.com/products/obeticholic-acid.html severe tricuspid regurgitation associated with elevated pulmonary artery pressure (PAP) (Table?1, Fig.?1c). The measured ejection fraction was above 65% prior to and after AVF closure, demonstrating that left ventricular function was not impaired in any of the patients. RHC demonstrated a significant elevated MPAP and CI but normal PCWP, which confirmed the echocardiographic findings. After AVF obliteration, PAP and MPAP decreased significantly (P? http://www.selleck.cn/products/LY294002.html in the KTRs was associated with a significant reduction of total proteinuria, albuminuria and alpha1-microglobulinuria by 55%, 60% and 70% respectively within 24?h after intervention (Table?1). The results of our study show that KTRs with RHF, consecutive tricuspid regurgitation [2] and iliac congestion are at risk for the development of delayed and marginal graft function. We hypothesized, that reduction of venous efflux of the kidney allograft resulting from PH [2,3] represents the underlying mechanism for DGF in our patients. This is supported by our finding that successful treatment of PH significantly improved allograft function in KTRs within 24?h after intervention. This improvement of allograft function was associated with a decrease of ��congestion albuminuria��, and a reduction of alpha1-microglobulinuria reflecting the recovery of renal tubular function after AVF closure.
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