Managing Anemia in Non-dialysis CKD as per KDIGO– Via Case Study

Patient Information:

Name: Mr. Khalid Mehmood
Age: 61 years
Gender: Male
Diagnosis: Chronic Kidney Disease (Stage 4) secondary to long-standing diabetes mellitus and hypertension
Dialysis Status: Not yet on dialysis (non-dialysis CKD)
Chief Complaint: Persistent fatigue, dizziness, and reduced exercise tolerance over the past two months

  Current Medications:

• Losartan 50 mg once daily
• Metformin 500 mg twice daily
• Furosemide 40 mg once daily
• Calcium carbonate 500 mg twice daily with meals
• Multivitamin (renal formula (without iron) once daily
• Erythropoietin alfa 6,000 IU subcutaneously once weekly (started 6 weeks ago)

Laboratory Results:

Clinical Notes:

• No evidence of active bleeding or recent blood transfusion
• Reports adherence to medications, including EPO
• Complains of constipation after meals
• No history of gastrointestinal disease
• Appetite is fair but reports metallic taste occasionally
• Mild pedal edema present
• Ferritin has gradually increased from 85 µg/L (3 months ago) to 120 µg/L
• TSAT has remained below 20%
• Hb has improved only slightly despite ESA therapy

  Questions for the Pharmacist:

1. Based on these findings, what type of iron abnormality is most likely — absolute, functional, or mixed iron deficiency?
2. How does elevated CRP help explain this patient’s iron and ferritin pattern?
3. According to KDIGO 2025 guidelines, would you recommend initiating, continuing, or withholding iron therapy in this case?
4. Which route of iron administration (oral vs IV) would be more suitable here and why?
5. How might the use of phosphate binders (like calcium carbonate) influence iron absorption or therapy outcomes?
6. Would switching to ferric citrate be beneficial in this case? Explain pharmacological rationale.
7. How can the pharmacist help manage the patient’s constipation while ensuring adequate iron absorption?

 PHARMACIST/PHYSICIAN WORKUP:

1. Based on these findings, what type of iron abnormality is most likely — absolute, functional, or mixed iron deficiency?

Let’s first look at the difference between the absolute and functional iron deficiency

 Now Let’s look at the lab report findings:

 So, after comparing the above-mentioned criteria with the lab report of the patient, we came to the conclusion that it is functional iron deficiency in this patient.

2.      How does elevated CRP help explain this patient’s iron and ferritin pattern?

 As we can see in this patient the level of C-reactive protein (CRP) is elevated. CRP signs toward the presence of inflammation which involves the induction of hepcidin via IL-6. Hepcidin act as a guard or gate keeper to the iron stores and inhibit the release of iron in the blood. It also hinders the absorption of oral iron from the intestine.

 As the release of iron from the iron stores to the blood decreases due to hepcidin, ferritin level goes up and serum iron level and Transferrin Saturation (TSAT) goes down.

Its is also noteworthy that ferritin is an acute phase reactant of inflammation, meaning the level of ferritin goes up falsely during the inflammation, while in reality the iron stores are not that much high. Which makes Serum ferritin level a non-reliable indicator of iron deficiency during inflammation.

3.      According to KDIGO 2025 guidelines, would you recommend initiating, continuing, or withholding iron therapy in this case?

As per KDIGO guidelines: In people with anemia and CKD not receiving dialysis or treated with peritoneal dialysis (CKD G5PD), we suggest initiating iron if (2D):

·        Ferritin <100ug/l (<100ng/ml) and transferrin saturation (TSAT) <40% or

·        Ferritin ≥100 ng/ml (≥100 µg/l) and <300ug/l (<300ng/ml) and TSAT <25%

Thus, according to KDIGO guidelines and the lab reports of this patient, it is evident that the patient need iron therapy, as he is not receiving hemodialysis and his ferritin level is >100ug/L but <300ug/L and his TSAT level is <25%

Consequently, the initiation of iron therapy will be recommended in this patient.

4.      Which route of iron administration (oral vs IV) would be more suitable here and why?

In the lab report of the patient, we observe that the level of CRP is high, which as mentioned above signs toward the inflammation and during inflammation due to the elevation in the level of hepcidin induced by IL-6, the oral absorption of the iron decreases. Thus, the use of oral iron supplement will be of no use and we have to consider I.V iron therapy as it by-passes the intestinal route.

Along with I.V iron therapy, treatment of inflammation should also be started

I.V iron therapy will be initiated and maintained keeping in view the KDIGO guidelines which are mentioned as below:

·        In people with CKD treated with iron, it is reasonable to withhold iron if ferritin ≥700 ng/ml (≥700 µg/l) or TSAT ≥40%

·        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 people with CKD treated with iron, certain circumstances may warrant more frequent iron testing as shown in Table below:

·        In people with CKD treated with iron, consider temporarily suspending iron therapy during systemic infection.

·        In people with CKD treated with intravenous iron, considerations pertaining to hypersensitivity reactions to intravenous iron include the following:

a.      Intravenous iron should only be administered if there is capability to manage acute hypersensitivity and hypotensive reactions,

b.      Intravenous doses of iron should not exceed the maximum dose/administration for the compound (Table),

c.      Pretreatment with corticosteroids or antihistamines is not routinely necessary (type 1 histamine [H1]-channel blockers), and

d.      Test doses of intravenous iron are not usually required, because lack of response does not predict the risk of hypersensitivity

5.      How might the use of phosphate binders (like calcium carbonate) influence iron absorption or therapy outcomes?

The patient is taking calcium carbonate twice daily with meal as a phosphate binder. And we know that the such phosphate binders can also binds to the dietary iron as well. Which further impairs the absorption of the dietary iron.

It also increases gastric pH, further decreasing iron solubility and absorption.
So, on one hand though it helps in the correction of phosphate level but on the other hand it decreases the iron level which can aggravate the patient’s symptoms.

Secondly, calcium-based binders can also increase the level of calcium in the serum so careful monitoring is required while giving calcium-based binders.

📌Read Also: CKD Case Study – Iron Deficiency in Hemodialysis Patient

6.      Would switching to ferric citrate be beneficial in this case? Explain pharmacological rationale.

Ferric citrate possesses the properties of iron restoration as well as phosphate binding. Though it will help decreasing the phosphate level but it’s use for the purpose of restoration iron level will of no benefit in this case, as the patient’s CRP level is elevated.

However, if in a case the CRP level is normal and patient is having iron deficiency as well as hyperphosphatemia then ferric citrate can be considered.

7.      How can the pharmacist help manage the patient’s constipation.

 Stool softener (docusate) or bulk former laxative like psyllium can be given to such patient. They are safer than osmotic and stimulant laxative in CKD patients.

Along with the laxative, lifestyle modification like 30 min walk and appropriate fluid (if not restricted) and fiber intake will be recommended to such patient

👩‍⚕️Watch also: Clinical Points of Laxatives