Post-transplant
erythrocytosis (PTE) is defined as persistently elevated
hemoglobin > 17 g/dL or hematocrit levels > 51% following
kidney transplantation, independent of duration. It is a relatively common complication within 8 months to 24 months post-
transplantation, occurring in 8%-15% of kidney transplant recipients. Established PTE risk factors include male gender, normal
hemoglobin/hematocrit pre-transplant (suggestive of robust native kidney
erythropoietin production),
renal artery stenosis, patients with a well-functioning graft, and dialysis before
transplantation. Many factors play a role in the development of PTE, however, underlying endogenous
erythropoietin secretion pre-and post-transplant is significant. Other contributory factors include the renin-angiotensin- aldosterone system,
insulin-like growth factors, endogenous
androgens, and local renal
hypoxia. Most patients with PTE experience mild symptoms like malaise,
headache,
fatigue, and
dizziness. While prior investigations showed an increased risk of thromboembolic events, more recent evidence tells a different story-that PTE perhaps has lessened risk of thromboembolic events or negative graft outcomes than previously thought. In the evaluation of PTE, it is important to exclude other causes of
erythrocytosis including
malignancy before treatment.
Angiotensin converting enzyme inhibitors (ACE-I) and
angiotensin receptor blockers (ARBs) are the mainstays of treatment. Increased ACE-I/ARB use has likely contributed to the falling incidence of
erythrocytosis. In this review article, we summarize the current literature in the field of post-transplant
erythrocytosis after
kidney transplantation.