Morphological abnormalities and variants

Microcytic RBCs

Fe deficiency, thalassaemia trait & syndromes, congenital sideroblastic anaemia, anaemia of chronic disorders

Macrocytic RBCs

Alcohol/liver disease (round macrocytes), MDS, pregnancy and newborn, haemolysis, B12 or folate deficiency, hydroxyurea and antimetabolites (oval macrocytes), acquired sideroblastic anaemia, hypothyroidism, chronic respiratory failure, aplastic anaemia

Dimorphic RBCs

Fe deficiency responding to iron, mixed Fe and B12/folate deficiency, sideroblastic anaemia, post-transfusion

Polychromatic RBCs

Response to bleeding or haematinic Rx, haemolysis, BM infiltration


HS, haemolysis e.g. warm AIHA, delayed transfusion reaction, ABO HDN, DIC and MAHA, post-splenectomy

Pencil/rod cells

Fe deficiency anaemia, thalassaemia trait & syndromes, PK deficiency


Hereditary elliptocytosis, MPD and MDS

Fragmented red cells

MAHA, DIC, renal failure, HUS, TTP

Teardrop RBCs

Myelofibrosis, metastatic marrow infiltration, MDS

Sickle cells

Sickle cell anaemia, other sickle syndromes (not sickle trait)

Target cells

Liver disease, Fe deficiency, thalassaemia, HbC syndromes.

Crenated red cells

Usually storage or EDTA artifact. Genuine RBC crenation may be seen post-splenectomy and in renal failure

Burr cells

Renal failure


Hereditary acanthocytosis, a-ß-lipoproteinaemia, McLeod red cell phenotype, PK deficiency, chronic liver disease (esp. Zieve's)

Bite cells

G6PD deficiency, oxidative haemolysis

Basophilic stippling

Megaloblastic anaemia, lead poisoning, MDS, haemoglobinopathies


Chronic inflammation, paraproteinaemia, myeloma

t Reticulocytes

Bleeding, haemolysis, marrow infiltration, severe hypoxia, response to haematinic therapy

Heinz bodies

Not seen in normals (removed by spleen), small numbers seen post-splenectomy, oxidant drugs, G6PD deficiency, sulphonamides, unstable Hb (Hb Zurich, Köln)

Howell-Jolly bodies

Made of DNA, generally removed by the spleen, dyserythropoietic states e.g. B12 deficiency, MDS, post-splenectomy, hyposplenism

H bodies

HbH inclusions, denatured HbH (ß4 tetramer), stain with methylene blue, seen in HbH disease (--/- a), less prominent in a thalassaemia trait, not present in normals

Hyposplenic blood film Howell-Jolly bodies, target cells, occasional nucleated RBCs, lymphocytosis, macrocytosis, acanthocytes

Anaemia is consistently found in the presence of chronic renal failure. Severity generally relates to the degree of renal impairment. The dominant mechanism is inadequate production of erythropoietin. Other contributory factors include (i) suppressive effects of uraemia and (ii) 5 in RBC survival. Uraemia impairs platelet function leading to blood loss and Fe deficiency. Small amounts of blood are inevitably left in the tubing following dialysis so that blood loss and Fe deficiency are further contributory factors in dialysis patients. Folate is lost in dialysis and supplementation is required to avoid deficiency. Aluminium toxicity (from trace amounts in dialysis fluids) and osteitis fibrosa from hyperparathyroidism are rare contributory factors.

Laboratory features

• Blood film — mostly normochromic RBCs; schistocytes and acantho-cytes present. No specific abnormalities in WBC or platelets.

• Microangiopathic haemolytic changes present in vasculitic collagen disorders with renal failure and classically in HUS and TTP.


• Short term treatment with RBC transfusion, based on symptoms (not Hb).

• Correction of Fe and folic acid deficiencies.

• Erythropoietin (Epo) will correct anaemia in most patients. Start at 50-100units/kg SC x 3/week. Give IV iron at same time. Response apparent <10 weeks; reduced doses required as maintenance. Renal Association guidelines have been produced for application and monitoring of Epo therapy. Although expensive it improves quality of life and avoids transfusion dependency and iron overload.

Side effects of Epo

• Thrombotic tendency.

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