Patient Information:

Name: Mrs. Shazia Khan
Age: 63 years
Gender: Female
Diagnosis: Stage 5 CKD secondary to diabetic nephropathy
Dialysis Status: Receiving maintenance hemodialysis (HD) three times weekly
Chief Complaint: Fatigue, weakness, and shortness of breath on exertion

Current Medications:

• Erythropoietin alfa (EPO) 8,000 units subcutaneously twice weekly
• Amlodipine 10 mg once daily
• Sevelamer carbonate 800 mg three times daily with meals
• Atorvastatin 20 mg nightly
• Calcium acetate 667 mg three times daily
• Furosemide 40 mg daily
• Multivitamin (renal formula) daily

Recent Laboratory Results:

Clinical Notes:

• The patient reports compliance with EPO and phosphate binder therapy.
• No recent transfusions.
• No active bleeding.
• Mild hypertension observed during dialysis.
• Complains of constipation and occasional nausea after meals.
• Ferritin trending upward over last 3 months (from 320 → 480 µg/L).
• Hb has remained around 9–9.5 g/dL despite ESA use.

Questions for the Pharmacist:

1. Based on these findings, what type of iron status abnormality does this patient have?
2. How would you differentiate whether this is absolute or functional iron deficiency?
3. According to KDIGO 2025 recommendations, should iron therapy be continued, held, or modified?
4. What are the potential causes of suboptimal ESA response in this case?
5. What role does hepcidin play in this patient’s iron metabolism?
6. Would you recommend switching the route or formulation of iron therapy? Why or why not?
7. How might hyperphosphatemia and phosphate binders influence iron absorption or availability?
8. What monitoring plan (parameters, frequency) would you propose for anemia management?

Pharmacist Workup:

Q.1. Based on these findings, what type of iron status abnormality does this patient have?

Based on the above finding, it is observed that the patient is having functional iron deficiency due to inadequate absorption of oral iron as a result of inflammation. Inflammation, manifested by elevated CRP level, signs towards the high level of hepcidin. Hepcidin inhibit the absorption of iron from the intestine and also inhibits the release of iron from the iron stores.

The is also manifested by the high level of ferritin-480 µg/L (stored iron) while the level of serum iron is low (45 µg/dL).

Q.2. How would you differentiate whether this is absolute or functional iron deficiency?

First, we need to recall the difference between absolute and functional iron deficiency:

 Now let’s observe the report of the patient:

 From the report of the patient, it is come to know that the patient is having functional iron deficiency, as iron store are adequate but the TSAT is less than minimum level. This is due to the high level of inflammation associated hepcidin which block iron release from storage sites and reduce intestinal absorption.

Q.3. According to KDIGO 2025 recommendations, should iron therapy be continued, held, or modified?

According to the KDIGO guidelines when the oral iron therapy doesn’t provide adequate results, then the patient should be shifted to the IV iron therapy. And as we can see that the patient is having inflammation and inflammation associated hepcidin will not let adequate absorption of oral iron from the intestine. So, there will no amply benefit of using oral iron Thus, here IV iron therapy will be recommended to this patient.

However, we will need to hold the iron therapy if ferritin level becomes >700 µg/L or TSAT >40% as per KDIGO guidelines. Thus, close monitoring of ferritin level and TSAT is required while giving IV iron therapy.

Along with giving the IV therapy, the inflammation manifested by elevate CRP, need to be treated on immediate basis.

Q.4. What are the potential causes of suboptimal ESA response in this case?

 The most basic cause of suboptimal results of ESA, is the inadequate serum level of iron. Which can be seen in the case under study. This inadequate iron level is due to:

·        Elevated hepcidin-which hinders the intestinal absorption of iron and also blocks the release of iron from iron stores.

·        Secondly, hyperphosphatemia also contributes to the suboptimal response of ESA, as it interferes with bone marrow and erythropoiesis.

Q.5. What role does hepcidin play in this patient’s iron metabolism?

As, we can see that the level of CRP is elevated in the current case. So, it is evident that inflammation associated hepcidin level will also be elevated. Which block iron release from storage sites (ferritin and reduce intestinal absorption. Due to this the serum level of iron has drop down (45 µg/dL) in this patient.

Q.6. Would you recommend switching the route or formulation of iron therapy? Why or why not?

The patient under study is taking multivitamin designed especially for renal patient, which sometimes consists of iron as well (RENAVIT®) and sometimes doesn’t consist of iron (FOLMINTA®). Here the formulation is not mentioned. Suppose the patient is taking RENAVIT® which does consist of iron, still there is no adequate benefits of this oral iron due to high level of inflammation associated hepcidin. So, it is recommended to switch the route of iron from oral to IV route along with shifting to some iron-free multivitamin designed for renal patients.

While using IV route for iron therapy, regular monitoring of ferritin and TSAT level is required.

📌 Watch also: CKD case study-Exposing Irrational use of Multivitamins

Q.7. How might hyperphosphatemia and phosphate binders influence iron absorption or availability?

High serum phosphate is common in CKD due to reduced renal excretion.

It stimulates FGF23 (fibroblast growth factor 23) release from bone, which in turn:

• Suppresses erythropoietin (EPO) production, impairing red blood cell formation.
• Increases hepcidin levels — the hormone that blocks intestinal iron absorption and traps iron in storage sites.
• Result → Functional iron deficiency and anemia resistance to ESA (erythropoiesis-stimulating agents).

Effect of Phosphate Binders on Iron Absorption

There are basically two categories to consider:

a. Non-iron-based binders

(e.g., calcium carbonate, calcium acetate, sevelamer, lanthanum carbonate)

•  These can bind dietary iron in the gut, reducing its absorption.
•  Sevelamer, in particular, can chelate iron and other micronutrients, further lowering iron availability.
• Long-term use may worsen iron deficiency in CKD patients who already have impaired absorption.

b. Iron-based binders

(e.g., Ferric citrate, Sucroferric oxyhydroxide)

•       These provide dual benefits: phosphate control and iron supplementation.
•     Ferric citrate, for example, increases serum ferritin and TSAT, improving iron stores.
•      However, careful monitoring is still needed to avoid iron overload.

In the case under study, the patient is taking non-iron based phosphate binder, which can bind dietary iron or iron supplements if taken together and can worsen iron deficiency in such patient.

(Suppose a patient need to take both iron supplement as well as non-iron based phosphate binders then either the administration time must by separated by 2 hrs or iron-based binders like ferric citrate can be consider instead of using iron supplement and phosphate binder separately)

Q.8. What monitoring plan (parameters, frequency) would you propose for anemia management?

As per KDIGO guidelines:

“In people with CKD treated with iron, it is reasonable to test hemoglobin, ferritin, and TSAT every 3 months for those not receiving dialysis or CKD G5PD and every month for those with CKD G5HD”.

 In the case under study, as we are looking towards starting IV therapy and patient is receiving dialysis, So, we will recommend monthly lab test of hemoglobin, ferritin, and TSAT.

Along with these, following parameters need to be assess regularly:

•    CRP level
•    Serum phosphate
•   Blood pressure