Anaemia of Chronic Disease (Anaemia of Inflammation)

Meet the patient

A 62-year-old man with active rheumatoid arthritis is sent to the ward with a mild normocytic anaemia and a "low iron" result the GP read as deficiency. He has taken oral iron for six weeks and feels no better. The iron studies arrive on the round: serum iron low, transferrin low, ferritin normal-to-high — the textbook rheumatoid-anaemia picture, not deficiency.[7]

The question that decides this admission is the one every registrar gets wrong first: is this iron deficiency, or iron the body is refusing to release? Six weeks of oral iron have failed for a reason — hepcidin is blocking the gut. Read the TIBC and the ferritin together and the trap closes behind you.[1][2]

What it actually is — the anaemia of the unwell patient

It is a hypoproliferative, usually normocytic anaemia that arrives within weeks of any sustained inflammatory insult. Not one disease but a stereotyped haematological response to chronic immune activation — and at the bedside its value is diagnostic, not therapeutic.[1]

The pattern that earns the mark: low serum iron with a LOW TIBC and a normal or raised ferritin. That single combination separates it from iron-deficiency anaemia (low iron, high TIBC, low ferritin) at a glance and stops a pointless course of oral iron before it starts.[1][2][18]

Two bedside realities frame every consultation. First, the anaemia itself is usually mild — the classic reviews put it plainly: it "seldom requires treatment" and is ameliorated by treating the underlying disease — so an anaemia disproportionate to the chronic illness should push you to hunt for something riding on top. Second, ACD often coexists with true iron deficiency (and with the anaemia of renal insufficiency) — which is exactly why the diagnosis becomes difficult when the ferritin sits in the middle range.[15][2]

How common, and who carries it

This is the commonest anaemia in hospitalised and chronically ill patients — the label attaches to almost every ward round, because the diseases that drive it are the diseases of the ward.[2][15]

Prevalence tracks the underlying disease: AI is prevalent in patients with diseases that cause prolonged immune activation — infection, autoimmune diseases and cancer — and the modern list has grown to include chronic kidney disease, congestive heart failure, chronic pulmonary diseases and obesity.[2]

[2] [16]

The risk factors are simply the causes: any chronic infection, autoimmune disease, malignancy, CKD, heart failure or chronic inflammatory state — with obesity and critical illness on the same list; the ICU's "anaemia of critical illness" is ACD in its purest form.[2]

The four-hit mechanism — 'iron is plentiful but locked away'

One sentence holds the whole topic: iron is abundant in the body but unavailable to the marrow. Four overlapping mechanisms produce that state, and a candidate who recites them in order owns the viva. Remember them as HITS.[1][2]

Hit one — hepcidin and ferroportin. This is the rate-limiting mechanism. Inflammation — through interleukin-6 — stimulates hepcidin gene transcription, most notably in the hepatocytes. Hepcidin binds ferroportin — an iron exporter present on absorptive enterocytes, macrophages, hepatocytes and placental cells — and triggers its internalisation and degradation.[3][7]

The body's iron stores are intact or increased, but iron cannot leave the storage cells to reach the marrow. This is functional iron deficiency: iron-restricted erythropoiesis despite adequate stores — the molecular definition of ACD established by Nemeth and colleagues in 2004.[3][14]

The molecular detail examiners love

Hepcidin is a peptide hormone secreted by the liver in response to iron loading and inflammation. IL-6 stimulates hepcidin gene transcription most notably in the hepatocytes, and hepatic hepcidin expression depends on the protein hemojuvelin. Ferroportin is an iron exporter present on absorptive enterocytes, macrophages, hepatocytes and placental cells. When hepcidin binds it, ferroportin is internalised and degraded — so dietary iron absorption falls and recycled iron is trapped in macrophages. Reticuloendothelial iron stores are therefore increased, the opposite of iron deficiency.

[3] [7]

Hit two — direct marrow suppression. Inflammatory mediators inhibit the differentiation of erythroid cells, and erythroid progenitors respond poorly to erythropoietin — fewer precursors mature, which is why the reticulocyte count is inappropriately low, a hypoproliferative marrow that cannot even keep up with a mild shortfall.[2][1]

Hit three — a blunted EPO response. The kidney should answer anaemia with more erythropoietin; in inflammation, production of the hormone is impaired and erythroid progenitors respond poorly to it — abnormalities attributed to the effects of inflammatory cytokines. In CKD this compounds absolute loss of EPO-producing cells as nephrons die.[1][2]

Hit four — a shorter red-cell life. Survival is mildly shortened as slightly damaged cells are cleared early. The marrow would normally compensate — but with erythropoiesis already suppressed it cannot, and the balance tips into anaemia.[1][2]

Why the ferritin is high and the TIBC is low — the two acute-phase tricks. Ferritin doubles as a storage protein and an acute-phase reactant: serum ferritin climbs in inflammation — hyperferritinaemia is part of the characteristic iron-homeostasis pattern — even when stores are normal. Transferrin falls with it: a decreased serum transferrin is a characteristic feature of ACD, while in iron deficiency total iron-binding capacity increases significantly. These two behaviours are the entire biochemical signature of the disease.[1][2][18]

The mantra — say it on every round. Iron is plentiful but locked away. It predicts the iron studies, explains the failed oral iron, and points you to IV iron and the underlying cause.[1]

The iron-study pattern that decides the question

This is the single most testable element of the topic, and the discriminator is the direction of the TIBC. It is LOW in ACD and HIGH in iron deficiency — decreased serum transferrin is a characteristic ACD feature, and total iron-binding capacity increases significantly in iron-deficiency anaemia. Pair it with the ferritin (normal or high in ACD, low in deficiency) and most normocytic and microcytic anaemias resolve without a marrow.[1][2][18]

Learn the four iron-study moves as ITFH:[1]

The face-off that earns the mark — the two anaemias that must be separated before any iron is prescribed, with the wider differential behind them:[1]

[1] [7] [13]

The one-line discriminator: the TIBC. Low points to ACD, high points to iron deficiency — and thalassaemia sits in the wider microcytic differential when the film does not fit either. Ferritin is the confirmatory second line; the soluble transferrin receptor is the tie-breaker when the picture is mixed.[1][2][18]

The recurring trainee error. A "normal" ferritin in an inflamed, anaemic patient is read as excluding iron deficiency — it does not. Ferritin's test properties differ in inflammatory disease, and in patients with inflammation a ferritin under 100 mcg per litre is diagnostic of iron deficiency. Reach for the soluble transferrin receptor (raised in true deficiency, normal in pure ACD) and the sTfR-to-log-ferritin ratio.[2][16][19][14]

[2] [14]

Causes — group them as ACID

The same hepcidin mechanism runs through every trigger, so group the causes memorably as ACID.[1]

By morphology, ACD is normochromic and normocytic or, less often, microcytic — the rheumatoid-anaemia template — and aregenerative. Red cells are normochromic, not the markedly hypochromic film of established deficiency.[7][2]

[1] [2] [15] [18] [19]

Read the patient, not the number — clinical presentation

The presentation is the underlying disease, not the anaemia. The anaemia is mild, builds over weeks, and the patient blames the chronic illness — so you are recognising the haematological limb of someone already known to have, or being investigated for, a chronic inflammatory, infectious, malignant or renal condition.[1]

The anaemia develops against the backdrop of the driver disease, and it is the underlying condition — infection, autoimmune disease, cancer, CKD, heart failure, chronic lung disease — that dominates the picture: the anaemia is mild, builds slowly and seldom needs treatment in its own right, so symptoms are usually attributed to the chronic illness itself. When the anaemia does demand attention it is because the patient has become symptomatic from it, or the driver disease has decompensated.[2][15]

The features of the driver disease dominate. Rheumatoid arthritis gives symmetrical small-joint swelling, morning stiffness and deformity; IBD gives diarrhoea, weight loss and perianal disease; SLE gives malar rash, arthralgia and renal impairment; chronic infection gives fever, night sweats or a focus (cavity, abscess, endocarditis); malignancy gives weight loss and a mass; CKD gives hypertension, oedema and uraemia. The anaemia is one clue among many.[1]

General examination in isolated ACD shows pallor and the signs of the driver — and nothing else. No organomegaly, no jaundice, no lymphadenopathy, no bony tenderness, no neurological deficit. Splenomegaly with jaundice means haemolysis or a primary haematological disorder; bruising with infection means marrow failure; a mass means malignancy. Any of these redirects the diagnosis.[1]

Investigations — staged, iron studies first

The diagnosis is pattern recognition on iron studies, staged in four steps. First, full blood count and film; second, iron studies and inflammatory markers; third, a targeted work-up for the cause; fourth, specialist tests only when the picture is mixed or atypical.[1][2]

Full blood count. A normocytic normochromic anaemia in the majority, less often microcytic — an aregenerative picture. Reticulocytes are low — hypoproliferative. White cells are usually normal; thrombocytosis accompanies active inflammation.[7][1]

Blood film. Unremarkable — normocytic, normochromic. There is no specific marker of ACD; the film excludes the mimics (microcytosis of deficiency, target cells of thalassaemia, schistocytes of microangiopathy, blasts of leukaemia).[1]

Iron studies — the discriminator. The pattern, learned as ITFH:[1]

[1] [13] [1] [18] [19]

Inflammatory markers. AI is a diagnosis of exclusion, supported by the characteristic iron-homeostasis pattern — hypoferraemia with hyperferritinaemia — interpreted alongside evidence that the underlying disease is active. The harder question is never "is there inflammation?" but "is there coexisting iron deficiency hiding behind an acute-phase ferritin?" — precisely the setting where the soluble transferrin receptor and, if truly needed, marrow iron earn their keep.[2][13]

Work-up for the cause. Directed by the history — the drivers are the chronic infections, autoimmune diseases, malignancies and kidney disease above, and underlying causes should be investigated wherever the story points.[19][2]

Specialist tests for the mixed picture. When ACD coexists with true deficiency, the soluble transferrin receptor is raised (it increases significantly in iron-deficiency anaemia and is not increased in ACD); the sTfR divided by log(ferritin) sharpens this; and the reticulocyte haemoglobin content flags iron-restricted erythropoiesis — Thomas's diagnostic plot combines the sTfR/log-ferritin ratio with reticulocyte haemoglobin to separate classic deficiency, ACD and the combined state. Bone marrow examination remains the definitive test when the picture stays indeterminate.[14][18][13]

Bone marrow examination is reserved for the indeterminate case — when ferritin sits in the middle and the soluble transferrin receptor has not settled it, marrow examination may be necessary for a definitive diagnosis. In ACD the marrow shows increased reticuloendothelial iron stores — iron is present but cannot be used.[13][17][1]

Management — treat the cause, then IV iron and ESA

Step zero — treat the underlying disease, always and first. Control the infection, suppress the autoimmunity, treat the malignancy, manage the CKD, optimise the heart failure. As inflammation settles, hepcidin falls, iron is released from macrophages, and the Hb recovers. A patient whose anaemia does not recover despite good disease control has a second cause; go find it.[1][2]

Step one — iron, and when the gut is blocked, intravenously. Oral iron is often ineffective in ACD because raised hepcidin blocks its absorption from the intestine. Intravenous iron bypasses the blocked gut — and it is the route with the randomised evidence in heart failure with iron deficiency.[2][4]

Dosing and the phosphate trap. In FAIR-HF the studied regimen was 200 mg of IV iron as ferric carboxymaltose against saline placebo. In two head-to-head randomised trials in iron-deficiency anaemia, ferric carboxymaltose 750 mg on days 0 and 7 caused biochemical hypophosphataemia (phosphate under 2.0 mg/dL) in roughly three quarters of patients by day 35 — an FGF23-mediated effect — versus under 10 percent with iron isomaltoside 1000 mg as a single dose. Check phosphate after ferric carboxymaltose.[4][12]

Step two — erythropoiesis-stimulating agents: useful, but never chase a normal haemoglobin. The combination of iron therapy and ESAs improves anaemia in many patients with AI. The ceiling is trial-written: CHOIR targeted 13.5 versus 11.3 g/dL in CKD and the high-target arm accumulated more composite events (hazard ratio 1.34) with no incremental quality-of-life gain; TREAT targeted 13 g/dL and doubled stroke. Titrate to the lowest haemoglobin that keeps the patient off transfusion, repleting iron alongside.[2][9][5]

The line you do not cross. The TREAT trial (4038 patients with type 2 diabetes and CKD) targeted a Hb of 13 g/dL with darbepoetin (the placebo arm was rescued only below 9.0 g/dL) and found no reduction in death or cardiovascular events, no reduction in death or end-stage renal disease, and a doubled stroke risk (101 versus 53 patients, HR 1.92). In cancer, a meta-analysis of 53 trials in 13,933 patients found ESAs increased mortality during the active study period (HR 1.17). This is the single most important safety rule in the topic.[5][10]

[2] [4] [5] [8] [9] [10] [12] [17]

What juniors write vs what gets marks

Juniors write "start oral iron for low iron". Marks go to: confirm with TIBC and ferritin, recognise hepcidin-blocked absorption, treat the underlying cause, and choose IV iron when deficiency coexists. Oral iron in pure ACD is the recurring trainee error — it fails, delays diagnosis, and annoys the gut.

[1] [6]

Resuscitation — when to transfuse

ACD is rarely a haematological emergency. The anaemia is mild and gradual, so there is time for a measured work-up. Transfusion is reserved for the symptomatic or decompensating patient, not for routine correction of a number.[1]

The trigger is clinical, not numerical — but the trial numbers exist and are decisive. TRICC randomised 838 euvolaemic critically ill patients to a restrictive strategy (transfuse below 7.0 g/dL, maintain 7.0 to 9.0 g/dL) versus a liberal 10.0-to-12.0 g/dL strategy: 30-day mortality was at least as low (18.7 versus 23.3 percent), in-hospital mortality was significantly lower (22.3 versus 28.1 percent), and the exception was acute myocardial infarction and unstable angina. Transfuse the symptomatic patient; do not correct numbers.[8]

Specific subtypes — CKD, heart failure, cancer, the ICU

Anaemia of CKD is the prototype "ACD plus" — AI mechanisms riding on absolute loss of erythropoietin as nephrons die; relative EPO deficiency has been central to ACD pathophysiology since the classic reviews. The KDIGO 2026 guideline covers exactly this territory: diagnosis and evaluation, iron, ESAs and HIF-PHI inhibitors, and transfusion. Its treatment caution is trial-written — CHOIR's 13.5 g/dL target harmed (HR 1.34), TREAT's 13 g/dL doubled stroke — so ESA use in CKD is an iron-replete, lowest-effective-dose affair.[15][6][9][5]

Anaemia of heart failure is a recognised entity — Weiss and colleagues add congestive heart failure to the causes of AI, alongside CKD, chronic lung disease and obesity. FAIR-HF randomised 459 patients with NYHA class II to III heart failure and iron deficiency (ferritin under 100 micrograms per litre, or 100 to 299 with TSAT under 20 percent, with or without anaemia) to IV ferric carboxymaltose against saline, and improved symptoms, NYHA class, exercise capacity and quality of life, with an acceptable side-effect profile.[2][4]

Anaemia of cancer and chemotherapy stacks inflammation on marrow suppression, renal impairment and blood loss — cancer is a named driver of AI. The caution is stark: a meta-analysis of 53 randomised trials in 13,933 patients with cancer found ESAs increased mortality during the active study period (HR 1.17) and worsened overall survival (HR 1.06). Balance harm against benefit, treat genuine iron deficiency on its own merits, and remember that combined iron therapy and ESAs can improve anaemia — the art is choosing who.[2][10]

Anaemia of critical illness (ICU). In the ABC study of 3534 critically ill patients, the mean admission haemoglobin was 11.3 g/dL with 29 percent under 10, diagnostic phlebotomy averaged 41.1 mL in the first 24 hours, and the 37 percent transfused had higher ICU and overall mortality. The AI mechanisms — hepcidin-driven sequestration, blunted EPO response, shortened red-cell survival — operate here in their purest form; TRICC's restrictive trigger (below 7.0 g/dL) is the transfusion answer, and minimising phlebotomy is the first move.[11][2][8]

Complications, pitfalls and preventable harm

The disease-related complications are those of chronic anaemia on top of the driver disease — and the modern framing is a balancing act: treatment decisions require "a balanced consideration of the contribution of anemia to each patient's morbidity and the impact of anemia treatment on the patient's prognosis" across disease settings.[2]

The preventable-harm list is short and worth memorising:[2]

1. Misdiagnosing ACD as iron deficiency — both run with a low serum iron; the decreased transferrin and the normal-to-high ferritin stop a pointless, failed course of oral iron.[1][7]
2. Reading a "normal" ferritin as excluding deficiency in an inflamed patient — ferritin's test properties are demonstrably different in inflammatory disease; the soluble transferrin receptor remains the separator.[16][13]
3. Treating the Hb number, not the patient — the anaemia itself seldom requires treatment and is ameliorated by successful treatment of the underlying disease.[15]
4. Using oral iron where hepcidin blocks it — switch to the intravenous route.[2]
5. Missing coexisting deficiency behind a "typical" ACD picture — coexistence with iron deficiency is common and is precisely what makes the diagnosis hard.[15][2]
6. Over-shooting the ESA target — stroke in TREAT (HR 1.92), harm in CHOIR (HR 1.34), increased cancer mortality in meta-analysis (HR 1.17).[5][9][10]
7. Transfusing a stable patient for a number — TRICC's restrictive strategy was at least as effective, with lower in-hospital mortality.[8]
8. Failing to investigate the cause — ACD follows an underlying infectious, inflammatory or neoplastic disease in most patients (though a quarter have none identified); find it, treat it.[15]

[2] [5]

Prognosis and disposition

The prognosis of ACD is the prognosis of the underlying disease. The anaemia itself is usually mild — the classic reviews are plain that it seldom requires treatment in its own right and is ameliorated by treating the driver — but whether and how to treat it is a disease-by-disease judgement of the anaemia's contribution to morbidity against the treatment risks the trials above documented.[15][2]

Disposition follows the driver more than the haemoglobin. The anaemia itself seldom requires treatment and is ameliorated by successful treatment of the underlying disease — most patients are investigated and managed as outpatients while the driver is treated. Admit for symptomatic decompensation, rapid decline or diagnostic red flags; critical care is rarely needed for the anaemia itself.[15]

Safety-net on discharge: a documented plan for the underlying cause; a clear reason for any iron or ESA; a date to repeat the blood count and iron studies; and explicit advice to return if symptoms worsen or bleeding occurs. On ESA, monitor haemoglobin and iron status through titration; after ferric carboxymaltose, check phosphate — hypophosphataemia was tracked to day 35 in trials.[2][12]

Special populations

Chronic kidney disease. Two inseparable mechanisms — inflammation-driven iron sequestration and falling erythropoietin production. KDIGO 2026 addresses CKD anaemia across diagnosis and evaluation, iron, ESAs/HIF-PHIs and transfusion; the trial ceiling on enthusiasm is TREAT (13 g/dL doubled stroke) and CHOIR (13.5 g/dL harmed against 11.3 g/dL).[6][5][9]

Chronic heart failure. Iron deficiency here was defined operationally by FAIR-HF — ferritin under 100, or 100 to 299 with TSAT under 20 percent, with or without anaemia — and intravenous ferric carboxymaltose (200 mg of IV iron, 2:1 against saline) improved symptoms, functional capacity and quality of life with an acceptable side-effect profile. The ferric carboxymaltose phosphate caveat applies.[4][12]

Pregnancy. The same immune-activating causes operate, and ferritin means what it means anywhere else: its test properties differ in inflammatory disease, and in inflammation a ferritin under 100 mcg per litre remains diagnostic of iron deficiency.[16][19]

Elderly patients. The diseases that drive AI — CKD, heart failure, chronic lung disease, cancer, chronic infection — accumulate with age. Ferritin interpretation shifts in inflammatory and neoplastic disease, so hunt the treatable driver and any coexisting deficiency rather than accepting "anaemia of old age" as a diagnosis.[2][16]

Children. The same mechanisms operate at any age — chronic infection, autoimmune disease and kidney disease drive AI in children as in adults. Treat the underlying disease; iron therapy and ESAs have their place, with genuine deficiency the trigger for iron.[2]

Immunocompromised. Infection and cancer are named AI drivers, so immunocompromised patients carry the same inflammation-driven anaemia risk. Treat the underlying disease; the combination of iron therapy and ESAs can improve anaemia in many patients.[2]

Evidence, trials and regional differences

The whole modern topic rests on one molecular discovery: the hepcidin-ferroportin axis. Nemeth and colleagues showed in 2004 that hepcidin binds ferroportin and triggers its internalisation and degradation — completing the loop between iron availability and inflammation, and turning ACD from a descriptive label into a mechanistically understood disease.[3]

The framing reviews are Weiss and Goodnough's 2005 NEJM review and the 2019 Blood update by Weiss, Ganz and Goodnough — which renames the entity anaemia of inflammation and adds CKD, congestive heart failure, chronic pulmonary diseases and obesity to the causes.[20][2]

The landmark trials:[1]

[4] [5] [9]

Regional differences. KDIGO 2026 is the global reference for CKD anaemia — an update to the 2012 guideline, built on systematic evidence reviews appraised under GRADE, offering actionable recommendations plus practice points where systematic evidence is lacking, and written for a worldwide audience of healthcare providers, patients and stakeholders.[6]

On the horizon. Emerging therapeutics that antagonise hepcidin function and redistribute endogenous iron for erythropoiesis may offer additional options in pure ACD, and the KDIGO 2026 guideline now covers hypoxia-inducible factor-prolyl hydroxylase inhibitors alongside ESAs for CKD anaemia; their place in AI beyond CKD is still being defined.[2][6]

Ward-round test

Stem 1. A 62-year-old with active rheumatoid arthritis has a mild normocytic anaemia: serum iron low, transferrin low, ferritin high. What is the diagnosis, and which single iron-study feature splits it from iron deficiency?[7]

Answer — stem 1

Anaemia of chronic disease — the textbook rheumatoid anaemia. The low transferrin (TIBC), sitting beside a normal-to-high ferritin, is the discriminator from iron deficiency, where ferritin falls. Treat the rheumatoid disease — rheumatoid anaemia is best corrected by optimal control of systemic disease activity — and add iron only if coexisting deficiency is confirmed.

[7] [1]

Stem 2. A patient with active Crohn disease has a mild anaemia, a ferritin at the low end of what you would accept in an inflamed patient, and a low transferrin saturation. Is this pure ACD, and what do you give?[2]

Answer — stem 2

Probably not pure ACD — AI with coexisting iron deficiency is the difficult diagnosis the reviews warn about, and a ferritin that low in an inflamed patient puts deficiency on the table. Give intravenous iron — the gut is blocked by hepcidin — and treat the Crohn disease.

[2] [4]

Stem 3. A dialysis patient is started on an erythropoiesis-stimulating agent. What haemoglobin do you aim for, and what went wrong in the trials that pushed higher?[5][6]

Answer — stem 3

[5]

The lowest Hb that keeps the patient off transfusion. TREAT pushed darbepoetin toward 13 g/dL and saw no cardiovascular or renal benefit but a doubled stroke risk (101 versus 53 patients, HR 1.92); CHOIR's 13.5 g/dL arm accumulated more events than the 11.3 g/dL arm (HR 1.34) with no quality-of-life gain. Replete iron — the combination of iron therapy and ESA improves anaemia in many patients.

[5] [9] [2]

Stem 4. A 70-year-old with chronic heart failure has ferritin 85 mcg/L, TSAT 15 percent, Hb 105 g/L. What single treatment improves symptoms here, and does the anaemia matter for the choice?[4]

Answer — stem 4

IV ferric carboxymaltose — FAIR-HF showed symptom, NYHA-class and exercise benefit in heart failure with iron deficiency with or without anaemia. Oral iron is ineffective here. The iron deficiency, not the Hb, drives the prescription.

[4]

References

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