Hyperleukocytosis (>100 x 10(9)/L) is an uncommon presentation of chronic leukemias. It can present with a variety of symptoms secondary to leukostasis, a syndrome caused by the sludging of circulating leukemic blasts in the microvasculature. The management includes hydration, cytoreduction, prevention of tumor lysis and, rarely, leukapheresis in cases complicated by leukostasis and hyperviscosity syndrome. We present a case of severe leukocytosis complicated by leukostasis in which leukapheresis was utilized to bring about a rapid reversal of microvascular sludging.

SummaryBackground and objectives Disseminated intravascular coagulation (DIC) is common in deceased kidney donors and is considered a relative contraindication to donation. The significance of donor DIC on recipient kidney function is poorly understood. Additionally, the significance of thrombocytopenia in recipients of kidneys from DIC-positive donors is understudied. Design, setting, participants, & measurementsIn a retrospective cohort of 162 kidney transplants, the presence of DIC in donors, the occurrence of thrombocytopenia in recipients, and risk factors for delayed or slow graft function (DGF/SGF) were assessed. The effects of DIC donor status on DGF/SGF in the study sample as a whole, and of thrombocytopenia on DGF/SGF in recipients of DIC-positive kidneys specifically, were examined using multiple logistic regression.Results DIC donor status was not associated with occurrence of DGF/SGF, but thrombocytopenia was significantly associated with DIC-positive donor status (P ϭ 0.008). Thrombocytopenia was independently associated with DGF/SGF only in the recipients of DIC-positive kidneys (P ϭ 0.005). Patient and graft survival at 1 year were not affected by donor DIC status or by thrombocytopenia status.Conclusions Donor DIC was not associated with short-term suboptimal graft function, defined as DGF/ SGF, nor with long-term patient or graft survival. However, thrombocytopenia appears to portend DGF/ SGF in recipients of DIC-positive kidneys and may be a clinical sign on which the basis of therapeutic decisions could be undertaken.

Atherosclerotic renal artery stenosis is the most common disease of the renal arteries and may lead to ischemic renal disease and hypertension. A close relationship exists between renal and cardiovascular disease, as they often occur concomitantly, and abnormalities in either system can cause disease and determine clinical outcome in the other. Renovascular disease is gaining recognition as a potentially important risk factor for cardiovascular morbidity and mortality. This article explores the association between atherosclerotic renal artery stenosis and the cardiovascular system.

3 Vascular calcification and systolic hypertension occur in rats given high doses of warfarin-a process presumed to be related to warfarin's inhibition of vitamin K regeneration and thus low levels of active MGP. 3,4 In humans, long-term warfarin therapy is associated with increased valvular and coronary calcification seen on computed tomography 5 and increased calcium deposition on histopathologic examination of aortic valves.6 It is therefore possible that warfarin-induced arterial calcification may lead to systolic hypertension in humans as well. We recently performed a post hoc analysis of a randomized clinical trial of warfarin in atrial fibrillation and demonstrated that there was no effect on blood pressure (BP) or pulse pressure (PP) after 24 months of warfarin therapy in all trial participants.7 A subgroup analysis suggested, however, that patients with underlying hypertension or diabetes mellitus (DM) receiving warfarin might have increased systolic BP and PP compared with controls. 7 In the present study, we tested these subgroups separately and hypothesized that long-term warfarin therapy leads to increased systolic BP and PP in older men with DM and hypertension. METHODSWe performed an historical cohort study of male patients with a diagnosis of DM and hypertension who were on warfarin therapy for 3 years or longer. Patients on dialysis or receiving anticoagulation for