In a 78‑year‑old patient with mild normocytic anemia (hemoglobin 10.7 g/dL, hematocrit 34.1 %, mean corpuscular volume 90.7 fL) and markedly elevated red‑cell distribution width (RDW‑SD 49.7 fL, RDW‑CV 15 %) but otherwise normal complete blood count, renal function (estimated glomerular filtration rate 66 mL/min/1.73 m²), electrolytes, and liver enzymes, what is the most likely etiology and what work‑up and management are recommended?

Medical Advisory BoardAll articles are reviewed for accuracy by our Medical Advisory Board
Educational purpose only • Exercise caution as content is pending human review
Article Review Status
Submitted
Under Review
Approved

Last updated: February 25, 2026 • View editorial policy

Personalize

Help us tailor your experience

Which best describes you? Your choice helps us use language that's most understandable for you.

Mild Normocytic Anemia with Elevated RDW in a 78-Year-Old

This patient most likely has early or evolving iron deficiency anemia that has not yet progressed to microcytosis, and the immediate next step is to obtain serum ferritin, transferrin saturation, and C-reactive protein to confirm the diagnosis and guide investigation for the underlying source of iron loss. 1

Key Diagnostic Clues

The combination of normocytic anemia (MCV 90.7 fL) with markedly elevated RDW (RDW-SD 49.7 fL, RDW-CV 15%) is the critical finding that points toward iron deficiency rather than other causes of normocytic anemia. 1, 2

  • An elevated RDW in normocytic anemia strongly suggests underlying iron deficiency because it reflects a mixed population of older normocytic red cells produced when iron stores were adequate and newer microcytic cells produced after iron depletion began. 1, 2

  • In early iron deficiency, circulating red cells remain normocytic because they were manufactured before iron stores became critically low; microcytosis develops only after sustained iron-deficient erythropoiesis. 2

  • The borderline-low total protein (5.8 g/dL) and albumin (3.7 g/dL) raise concern for chronic gastrointestinal blood loss with protein-losing enteropathy, malabsorption (celiac disease), or occult malignancy—all of which can cause iron deficiency. 1

  • Stage 3a chronic kidney disease (eGFR 66 mL/min/1.73 m²) contributes to anemia via erythropoietin deficiency, but CKD-associated anemia typically shows a normal RDW, making isolated CKD an insufficient explanation. 2, 3

Immediate Laboratory Work-Up

First-Line Iron Studies

Order serum ferritin, transferrin saturation (TSAT), and C-reactive protein together as the initial diagnostic panel. 1

  • Ferritin < 30 µg/L confirms iron deficiency in the absence of inflammation. 1, 2

  • Ferritin < 45 µg/L provides optimal sensitivity and specificity for iron deficiency in routine practice and warrants gastrointestinal investigation even when inflammation is present. 1

  • TSAT < 16–20% confirms iron-deficient erythropoiesis, particularly when ferritin may be falsely elevated by inflammation, malignancy, or liver disease in elderly patients. 1

  • C-reactive protein must be measured concurrently because ferritin is an acute-phase reactant; in inflammatory states, ferritin up to 100 µg/L may still represent true iron deficiency. 1, 2

Additional Baseline Tests

  • Vitamin B12 and folate levels should be checked because combined deficiencies can produce a normal MCV with elevated RDW, mimicking this presentation. 1, 2

  • Reticulocyte count helps differentiate decreased production (low reticulocyte index < 2.0, consistent with iron deficiency or CKD) from increased destruction or loss (high index > 2.0, suggesting hemolysis or acute bleeding). 2

  • Peripheral blood smear may reveal hypochromic cells despite the normal MCV, confirming evolving iron deficiency. 1, 2

Investigation of the Underlying Cause

Once iron deficiency is confirmed, a systematic search for the source of iron loss is mandatory rather than treating with iron supplementation alone. 1

Gastrointestinal Evaluation (Highest Priority in Elderly Patients)

  • In elderly males with confirmed iron deficiency, gastrointestinal blood loss is the most common cause and must be investigated urgently, as occult malignancy is a critical concern in this age group. 1

  • Upper endoscopy with duodenal biopsies should be performed to detect:

    • Peptic ulcer disease, gastric cancer, NSAID-induced gastropathy, or angiodysplasia 1
    • Celiac disease, which accounts for 2–3% of iron-deficiency anemia cases and may present with isolated anemia 1

  • Colonoscopy is essential because colonic carcinoma, adenomatous polyps, and angiodysplasia are frequent findings in patients > 75 years with iron-deficiency anemia. 1

  • Stool guaiac testing should be performed immediately, though a negative result does not exclude intermittent or proximal GI bleeding. 1, 2

Renal Contribution

  • The eGFR of 66 mL/min/1.73 m² places the patient in CKD stage 3a, where erythropoietin deficiency begins to contribute to anemia. 3

  • However, CKD alone does not explain the elevated RDW, which points to a superimposed nutritional deficiency (most likely iron). 2

  • Among CKD patients, 25–37.5% have concurrent iron deficiency, making dual pathology common in this population. 2

Differential Diagnosis and What to Exclude

Anemia of Chronic Disease (Less Likely)

  • Anemia of chronic disease typically shows ferritin > 100 µg/L, TSAT < 20%, and a normal or low RDW—not the elevated RDW seen here. 2

  • The absence of elevated inflammatory markers (if CRP is normal) would effectively rule out anemia of chronic disease. 2

Combined Iron and B12/Folate Deficiency

  • When iron deficiency coexists with vitamin B12 or folate deficiency, the opposing effects on cell size can keep the MCV normal while the RDW remains elevated. 1, 2

  • This scenario is recognizable by elevated RDW in normocytic anemia and should be excluded by measuring B12 and folate. 1

Hemolysis (Unlikely)

  • A high reticulocyte count would be expected in hemolysis, whereas iron deficiency and CKD both produce a low reticulocyte index. 2

  • If the reticulocyte count is elevated, order lactate dehydrogenase, indirect bilirubin, haptoglobin, and a direct antiglobulin (Coombs) test to confirm or exclude hemolysis. 2

Bone Marrow Failure (Premature to Consider)

  • Bone marrow examination is not indicated at this stage because the anemia is mild, other cell lines are normal, and the elevated RDW points toward a nutritional cause. 2

  • Reserve bone marrow aspiration and biopsy for unexplained pancytopenia, progressive anemia despite treatment, or dysplastic features on peripheral smear. 2

Management Algorithm

Step 1: Confirm Iron Deficiency

  • Obtain ferritin, TSAT, and CRP within 24–48 hours. 1

  • If ferritin < 45 µg/L or TSAT < 16–20%, iron deficiency is confirmed. 1

Step 2: Initiate Oral Iron While Investigating the Source

  • Begin ferrous sulfate 325 mg (65 mg elemental iron) once daily to minimize gastrointestinal side effects in elderly patients. 1

  • A hemoglobin rise ≥ 10 g/L within 2 weeks confirms iron-deficiency anemia even when initial iron studies are equivocal. 1

  • Do not delay gastrointestinal investigation while waiting for a therapeutic trial; the bleeding source must be identified promptly to prevent recurrent hemorrhage. 1

Step 3: Urgent GI Referral

  • Fast-track upper endoscopy with duodenal biopsies and colonoscopy should be scheduled within 1–2 weeks for elderly patients with confirmed iron deficiency. 1

  • Do not attribute iron deficiency solely to dietary insufficiency in adults; mandatory GI evaluation is essential to exclude malignancy. 1

Step 4: Address CKD-Related Anemia (If Iron Deficiency Is Corrected)

  • Do not start erythropoiesis-stimulating agents (ESAs) until hemoglobin falls below 10 g/dL in asymptomatic patients. 2, 4

  • If ESAs are eventually required, use the minimal dose to lessen transfusion needs rather than targeting a specific hemoglobin level. 2

  • Provide supplemental iron only if ferritin is < 100 µg/L or TSAT is < 20% while on ESA therapy. 2, 4

Critical Pitfalls to Avoid

  • Do not assume normocytic anemia in the elderly is solely due to CKD or "anemia of aging"; the elevated RDW mandates investigation for iron deficiency and its underlying cause. 1, 2

  • Do not rely on ferritin alone when inflammation, malignancy, or liver disease may be present; add TSAT to confirm iron deficiency. 1

  • Do not postpone endoscopic evaluation to "optimize" the patient with iron therapy alone; occult GI malignancy must be excluded promptly. 1

  • Do not overlook combined nutrient deficiencies; iron deficiency can coexist with B12 or folate deficiency, recognizable by elevated RDW. 1

  • Do not order bone marrow examination at this stage; it is premature when a nutritional cause is likely and other cell lines are normal. 2

References

1
Guideline

Management of Microcytic Hypochromic Anemia

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2026

2
Guideline

Normocytic Anemia Diagnosis and Management

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2026

3
Research

Pathophysiology of renal anemia.

Clinical nephrology, 2000

Related Questions

What causes normocytic anemia?
What is the initial step in managing a patient with normocytic anemia?
What is the appropriate management for a patient with normocytic normochromic anemia, hyperuricemia, and a high reticulocyte count?
What are the causes of normochromic normocytic anemia?
What are the causes of normocytic normochromic anemia?
What is the most likely diagnosis in a middle‑aged male with coronary artery disease status post percutaneous transluminal coronary angioplasty, hypertension, five‑year history of gout, rising serum creatinine (1.5‑1.55 mg/dL) with estimated glomerular filtration rate 45‑50 mL/min/1.73 m², moderate proteinuria (urine protein‑creatinine ratio 0.43), bilateral cortical renal scarring, and incidental moderate splenomegaly?
What is the role of upadacitinib (Rinvoq) for a patient with ulcerative colitis, anterior uveitis, and ankylosing spondylitis who has failed conventional therapy?
Will tinea versicolor spread to other skin areas or be contagious to others?
In a patient without peptic ulcer disease, renal impairment, or heart failure, are meloxicam and naproxen both effective for mechanical joint, muscle, or ligament pain and stiffness, and which is preferred?
What are the clinical features, diagnostic criteria, treatment, and secondary prophylaxis for acute rheumatic fever?
What is the pathophysiological basis for gynecomastia?

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

Have a follow-up question?

Our Medical A.I. is used by practicing medical doctors at top research institutions around the world. Ask any follow up question and get world-class guideline-backed answers instantly.

Ask Question