What is the diagnosis and treatment for a patient with anemia (low RBC, hemoglobin, hematocrit), thrombocytosis (high platelet count), immature granulocytes, impaired renal function (low eGFR), and abnormal liver function tests (low calc globulin, high calc A/G ratio)?

Anemia of Chronic Kidney Disease with Inflammatory Features

The most likely diagnosis is anemia of chronic kidney disease (CKD) with concurrent inflammation, and the primary remedy is to address the underlying renal dysfunction while initiating erythropoiesis-stimulating agent (ESA) therapy with iron supplementation once iron deficiency is excluded. 1, 2

Primary Diagnosis

The constellation of findings points definitively to CKD-related anemia:

• Low eGFR directly causes decreased erythropoietin production, leading to normocytic anemia with low RBC, hemoglobin, and hematocrit 1, 2
• Chronic renal failure characteristically produces these exact hematologic changes: decreased HCT, hemoglobin, and RBC counts as toxic metabolites accumulate 2
• The elevated RDW suggests a mixed anemia picture, which is common in CKD where both EPO deficiency and inflammation coexist 1

Inflammatory Component

The elevated immature granulocytes and thrombocytosis indicate active inflammation:

• Immature granulocytes are elevated in CKD patients with inflammation and correlate with inflammatory markers like hs-CRP 3
• Thrombocytosis (high platelet count) is a reactive phenomenon to chronic inflammation, though severe iron deficiency can rarely cause thrombocytopenia instead 4
• The low absolute lymphocytes with elevated immature granulocytes reflects the inflammatory shift in white cell populations seen in CKD 3

Protein Abnormalities

The low globulin with high A/G ratio suggests:

• Decreased globulin production or increased protein loss through damaged kidneys (proteinuria should be assessed) 1
• This pattern is consistent with chronic kidney disease where protein metabolism is disrupted 1

Diagnostic Workup Required

Before initiating treatment, obtain:

• Complete iron studies (serum iron, TIBC, ferritin, transferrin saturation) to determine if functional or absolute iron deficiency exists, as iron is critical for hemoglobin synthesis and 25-37.5% of CKD patients have iron deficiency 1
• Reticulocyte count to assess bone marrow response and degree of erythropoietic suppression 1, 5
• Peripheral blood smear review to evaluate red cell morphology and confirm normocytic pattern versus microcytic changes 1
• Urinalysis for proteinuria and hematuria to assess degree of kidney damage 1
• Stool guaiac test to exclude occult gastrointestinal bleeding as a contributor to anemia 1

Treatment Algorithm

Step 1: Optimize Hemoglobin Target

• Hemoglobin should be used as the primary monitoring parameter rather than hematocrit, as it has superior precision with lower coefficient of variation 1
• Transfuse RBCs only if symptomatic or to achieve hemoglobin 7-8 g/dL in stable patients, avoiding over-transfusion 1, 6
• For patients with comorbidities worsened by anemia, target hemoglobin of 9-10 g/dL to limit chronic anemia effects on quality of life 1

Step 2: Iron Repletion

• If transferrin saturation <20% or ferritin <100 ng/mL, initiate iron supplementation before or concurrent with ESA therapy 1
• Higher iron parameters are required to support ESA-stimulated erythropoiesis compared to baseline requirements 1
• Monitor iron studies every 2-4 weeks initially to prevent iron overload while ensuring adequate stores 7

Step 3: Erythropoiesis-Stimulating Agent

• Initiate EPO therapy once iron stores are adequate to stimulate red cell production in the setting of EPO deficiency 1
• Monitor hemoglobin weekly during dose titration, then less frequently once stable 1, 8

Step 4: Address Inflammation

• Identify and treat underlying inflammatory triggers (infection, uremia, other comorbidities) as inflammation blunts ESA response 3
• Consider short-term corticosteroids if inflammatory component is severe and refractory, though this is not first-line 1, 6

Critical Pitfalls to Avoid

• Do not assume microcytic anemia without checking MCV, as CKD anemia is typically normocytic; microcytosis would suggest iron deficiency or genetic disorders requiring different management 1, 8
• Do not initiate iron therapy in thalassemia or genetic microcytic anemias without confirmed deficiency, as this accelerates iron overload and organ damage 7
• Do not transfuse platelets prophylactically despite thrombocytosis being present; this is reactive and does not require intervention 1
• Do not delay nephrology referral, as the low eGFR requires specialist management to slow CKD progression and optimize anemia treatment 1
• Monitor for iron overload if multiple transfusions become necessary, considering chelation if ferritin exceeds 1000-2500 μg/L 7

Monitoring Schedule

• Weekly CBC with differential during initial treatment phase to assess response 1, 8, 7
• Iron studies every 2-4 weeks until stable, then monthly 7
• Renal function (creatinine, eGFR) monthly to track CKD progression 1
• Inflammatory markers (CRP, immature granulocytes) periodically to assess inflammation control 3