Hemodynamic effects of hemodialyzer pump speed on arteriovenous fistulas
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AIM: Arteriovenous fistulas (AVF) are the optimal vascular access for hemodialysis although many fistulas fail. The impetus to increase hemodialyzer blood flow (QB) in order to maximize solute clearances may be counterbalanced if AVF suffer adverse hemodynamic effects from accelerated pump flows. The optimal QB to maintain adequate hemodialysis without potentially contributing to AVF dysfunction is unknown. The aim of this study was to measure the hemodynamic effects of increased QB on AVF. MATERIALS AND METHODS: A prospective cohort of 14 patients with primary brachiocephalic AVF underwent venous Doppler measurements prior to cannulation (QB0) and during hemodialysis with QB of 350 mL/min at a standardized anatomical location over 3 - 16 consecutive months. Measurements included vein diameter, blood flow velocity, and volumetric flow. RESULTS: 163 paired Doppler measurements (QB0 and QB350) were made in 14 subjects. There were no significant differences in venous diameter, but significant increases in blood flow velocity and volumetric flow (p < 0.001). Mean blood flow velocity increased from 86.6 ± 35.0 cm/s at QB0 to 105.7 ± 35.0 cm/s at QB350. Mean volumetric flow increased from 849 mL/min at QB0 to 1,059 mL/min at QB350. Vein diameters increased linearly over time, with no significant changes in blood velocity or volumetric flow, suggesting AVF maturation may improve tolerance of pumped blood flow. CONCLUSION: Blood flow velocity and volumetric flow increased when hemodialyzer blood pump was applied to an AVF, creating a situation in which increased turbulence and shear stress might be plausible. Further study is needed to determine if increased QB affects clinical outcomes of AVF.
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Medullary Microvascular Thrombosis and Injury in Sickle Hemoglobin C Disease.

Sickle cell nephropathy is a common complication in patients with sickle cell hemoglobinopathies. In these disorders, polymerization of mutated hemoglobin S results in deformation of red blood cells, which can cause endothelial cell injury in the kidney that may lead to thrombus formation when severe or manifest by multilayering of the basement membranes (glomerular and/or peritubular capillaries) in milder forms of injury. As the injury progresses, the subsequent ischemia, tubular dysfunction, and glomerular scarring can result in CKD or ESRD. Sickle cell nephropathy can occur in patients with homozygous hemoglobin SS or heterozygous hemoglobin S (hemoglobin SC, hemoglobin S/ß(0)-thalassemia, and hemoglobin S/ß(+)-thalassemia). Clinical manifestations resulting from hemoglobin S polymerization are often milder in patients with heterozygous hemoglobin S. These patients may not present with clinically apparent acute sickle cell crises, but these milder forms can provide a unique view of the kidney injury in sickle cell disease. Here, we report a patient with hemoglobin SC disease who showed peritubular capillary and vasa recta thrombi and capillary basement membrane alterations primarily involving the renal medulla. This patient highlights the vascular occlusion and endothelial cell injury in the medulla that contribute to sickle cell nephropathy.