What could cause preserved renal function in a patient with heart failure and iron deficiency anemia?

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: December 12, 2025View editorial policy

Personalize

Help us tailor your experience

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

Preserved Renal Function in Heart Failure with Iron Deficiency Anemia

Direct Answer

An eGFR of 103 mL/min/1.73m² and creatinine of 0.56 mg/dL represent preserved—even supranormal—renal function that can occur in heart failure patients with iron deficiency anemia due to hyperfiltration, younger age, low muscle mass, or early disease stage before cardiorenal syndrome develops. 1

Understanding the Clinical Context

Why This Renal Function is Actually Normal or Hyperfiltration

  • Hyperfiltration state: An eGFR >90 mL/min/1.73m² with a low creatinine (0.56 mg/dL) suggests either true hyperfiltration or reduced creatinine production from decreased muscle mass, both common in heart failure patients. 1

  • Low muscle mass effect: Iron deficiency anemia contributes to muscle dysfunction and sarcopenia in heart failure, which reduces creatinine production independent of actual kidney function, artificially lowering serum creatinine and elevating calculated eGFR. 2, 3

  • Early disease stage: This patient may have heart failure that has not yet progressed to Type 2 cardiorenal syndrome (chronic heart failure causing chronic kidney disease), which typically develops over time with sustained neurohormoral activation. 1, 4

The Cardiorenal Relationship

  • Bidirectional deterioration takes time: While heart failure is strongly associated with renal dysfunction development, up to a quarter of patients with chronic kidney disease have heart failure symptoms before formal diagnosis, indicating the relationship is not immediate or universal. 1

  • Venous congestion is key: The dominant mechanism of worsening kidney function in heart failure is increased right-sided venous filling pressure and renal venous congestion, not low cardiac output in most patients. 1 If this patient lacks significant congestion, renal function may remain preserved.

  • Preserved perfusion pressure: Kidney perfusion pressure (mean arterial pressure minus central venous pressure) ideally should be >60 mmHg. 1 Without elevated central venous pressure or hypotension, renal perfusion can remain adequate despite cardiac dysfunction.

Iron Deficiency Anemia's Role

Impact on Renal Function Assessment

  • Iron deficiency is extremely common: In heart failure patients, iron deficiency occurs in 35-43% of cases in Western studies, often independent of anemia status. 5

  • Muscle dysfunction mechanism: Iron deficiency contributes to skeletal muscle dysfunction in heart failure, which reduces muscle mass and creatinine production, potentially making eGFR appear falsely elevated. 1, 2

  • Anemia definition: Anemia is defined as hemoglobin <13.0 g/dL in men and <12.0 g/dL in women, and is present in 30-50% of heart failure patients. 1, 5

Iron Deficiency Without Severe Anemia

  • Iron deficiency can exist without anemia: Iron deficiency is defined as ferritin <100 μg/L or ferritin 100-299 μg/L with transferrin saturation <20%, and can occur without causing anemia. 2, 5

  • Functional versus absolute deficiency: Functional iron deficiency (normal total body iron sequestered in storage) versus absolute iron deficiency (decreased total body iron) both occur in heart failure and may not immediately impact renal function. 3

Clinical Scenarios Explaining Preserved Function

Patient Characteristics That Maintain Normal eGFR

  • Younger patients: Age is a risk factor for both anemia and renal dysfunction in heart failure; younger patients may maintain preserved renal function longer. 5

  • Heart failure with preserved ejection fraction (HFpEF): If this patient has HFpEF rather than reduced ejection fraction, renal dysfunction may be less prominent early in disease course. 1

  • Adequate volume status: Patients who are euvolemic without significant congestion or dehydration maintain better renal perfusion pressure and function. 1

  • Early heart failure stage: NYHA Class I-II heart failure may not yet have activated sufficient neurohormonal compensatory mechanisms to cause renal decline. 1

Medications Preserving Renal Function

  • ACE inhibitors/ARBs: These medications, while causing predictable small increases in creatinine (up to 20% acceptable), have long-term renoprotective effects and may preserve function over time. 1

  • Beta-blockers: Bisoprolol continues to provide prognostic benefit even in renal decline and does not significantly affect overall eGFR, potentially stabilizing renal function. 1

  • Appropriate diuretic use: If diuretics are dosed appropriately to maintain euvolemia without excessive volume depletion, renal perfusion can be preserved. 1

Important Caveats and Pitfalls

Assessment Limitations

  • Creatinine-based eGFR limitations: In patients with low muscle mass from iron deficiency and heart failure, creatinine-based eGFR calculations may overestimate true kidney function. 1

  • Check for microalbuminuria: Even with preserved eGFR, microalbuminuria (30-300 mg/24h) indicates early kidney damage and increased cardiovascular risk. 1

  • Monitor for progression: While currently preserved, this patient remains at high risk for developing Type 2 cardiorenal syndrome with chronic renal hypoperfusion and sustained neurohormonal activation over time. 1, 4

Management Considerations

  • Address iron deficiency: Intravenous ferric carboxymaltose improves symptoms, NYHA class, exercise capacity, and quality of life in heart failure patients with iron deficiency (ferritin <100 μg/L or 100-299 μg/L with transferrin saturation <20%), regardless of anemia status. 1, 5

  • Avoid nephrotoxic agents: NSAIDs and certain antibiotics should be avoided as they increase risk of heart failure worsening and can precipitate acute kidney injury. 1

  • Continue guideline-directed medical therapy: Do not withhold ACE inhibitors, ARBs, or beta-blockers based on preserved renal function; these medications provide mortality benefit and long-term renoprotection. 1

  • Serial monitoring: Establish baseline and monitor renal function regularly, as the bidirectional relationship between cardiac and renal function means deterioration can occur as heart failure progresses. 1

References

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Guideline

Cardiorenal Syndrome: Definition, Pathophysiology, and Clinical Presentation

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

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.