Anemia is an almost constant result of chronic renal failure.
Erythropoietin deficiency is the primary cause. Accumulation of
toxic metabolic end products plays a secondary role in the pathogenesis
of the anemia; however, the effects of these end products largely
can be overcome by exogenous erythropoiesis-stimulating agents (ESAs).
Inflammatory cytokines lead to increased hepcidin levels in plasma,
which block iron absorption in the gut and iron release from macrophage
stores. If adequate iron sources are available, hemoglobin levels
of 11 to 12 g/dL can be maintained by subcutaneous or intravenous
ESA injections. Hemoglobin levels greater than 12 g/dL should
be avoided, as clinical trials have shown increased mortality if
that target hemoglobin is used. Approximately 95 percent of patients
respond to erythropoietin without significant side effects.
and abbreviations that appear in this chapter include: ADAMTS-13,
a disintegrin and metalloproteinase with thrombospondin domain 13;
EPO, erythropoietin; ESA, erythropoiesis-stimulating agent; HIF,
hypoxia-inducible factor; HUS, hemolytic uremic syndrome; Na+-K+,
sodium-potassium; PRCA, pure red cell aplasia; TTP, thrombotic thrombocytopenic
purpura; VHL, von Hippel-Lindau.
Anemia is one of the most common manifestations of chronic renal
failure. Untreated anemia can, depending on its severity, be associated
with a number of abnormalities, including decreased oxygen delivery
to the tissues; increased cardiac output and cardiomegaly; decreased
cognition and mental acuity; and overall decrease in patient welfare
(see Chap. 33). The degree of anemia appears
to be roughly proportional to the severity of renal failure, but
there is not a strict linear relationship between hematocrit and
creatinine clearance. At creatinine clearances of less than 20 mL/min,
the hematocrit (Hct) is frequently less than 30 mL/dL,
although there is great variability (Fig. 36–1).
In polycystic kidney disease the anemia is usually less severe for
the degree of renal failure, and patients who have undergone nephrectomy
are frequently more anemic than are patients being treated with
hemodialysis. Infectious, neoplastic, immunologic, and metabolic
disorders that can accompany renal disease can affect the degree
of anemia and its response to treatment.1
Relationship between hematocrit and creatinine clearance
in patients with chronic renal disease. Anemia
is inversely related to the degree of renal impairment in most patients
with chronic renal disease.
(Redrawn with permission from Radtke HW, Claussner
A, Erbes PM, et al.2)
Experimental and clinical observations on the effect of intensive
dialysis, bilateral-nephrectomy, and treatment with erythropoietin
(EPO) have clarified some of the pathophysiologic mechanisms responsible
for the anemia of chronic renal disease. The primary cause of the
anemia is decreased production of EPO by the diseased kidneys.2,3 A
diminished capacity to excrete potentially toxic metabolic end products may
contribute to the anemia by shortening the red cell life span, by
marrow suppression, and by increasing the risk of blood ...