Neonatal hyperviscosity.

Erythropoietin was administered to five anemic azotemic diabetic subjects for 1 year to assess the effect of increasing red cell mass on clinical well-being and the course of renal functional decline. None of the subjects manifested worsened hypertension or cerebrovascular or cardiovascular complications despite an increase in mean hematocrit from a baseline mean of 29.6% to a mean of 39.5%. The serum creatinine concentration after 1 year of treatment with erythropoietin was 3.7 mg/dL, which was unchanged from the baseline value of 3.5 mg/dL. Plasma viscosity remained constant as red cell mass increased. Although the viscosity of whole blood rose as the hematocrit increased, it was within the range of normal blood viscosity for an equivalent hematocrit. The favorable impact of erythropoietin treatment on three diabetic subjects who had macular edema and anemia is described. One hypothesis to explain the benefit of a raised hematocrit on both diabetic nephropathy and retinopathy is that the metabolic, hormonal, and hemodynamic components of the diabetic syndrome, in concert, produce tissue and cellular hypoxia that is ameliorated in part by the greater oxygen-transporting capacity of a raised red cell mass. The pseudohypoxia of diabetes may be implicated in the pathogenesis of diabetic neuropathy, retinopathy, muscular dysfunction, and nephropathy.

Blood Viscosity↗

PubMed1995

Erythropoietin and systemic hypertension.

Systemic hypertension has been reported to develop, or to worsen, in 20-30% of patients treated with recombinant human erythropoietin (r-HuEPO) worldwide. The greatest increases in blood pressure affect day-time systolic and night-time diastolic blood pressure. Hypertension may develop in some patients as early as 2 weeks and in others as late as 4 months after the start of r-HuEPO treatment. In haemodialysis patients with systemic hypotension, r-HuEPO usually induces a 10% increase in blood pressure, with no significant change in the frequency of hypotensive episodes. Several risk factors for the development, or worsening, of hypertension after r-HuEPO therapy have been identified. They include the presence of pre-existing hypertension, rapid increase in haematocrit, a low baseline haematocrit before r-HuEPO administration, high doses and i.v. route of administration, the presence of native kidneys, a genetic predisposition to hypertension, and possibly a younger age. There are several potential mechanisms by which r-HuEPO therapy may increase blood pressure in haemodialysis patients. They include increased blood viscosity; the loss of hypoxic vasodilation; the activation of neurohumoral systems (catecholamines, the renin-angiotensin system); and especially a direct vascular effect. This last mechanism is supported by several data, and many factors may be involved in its pathogenesis (an increased cell calcium uptake; an imbalance in local vasoactive agents, with increased synthesis of ET-1; a mitogenic effect; and a platelet-dependent mechanism).

Blood Viscosity↗