Pseudo-Bartter Syndrome: A Hidden Medical Risk in Eating Disorders

Pseudo-Bartter Syndrome is a serious and often overlooked medical complication of eating disorders, particularly in those who engage in purging behaviors such as self-induced vomiting or laxative misuse. Though it mimics features of Bartter Syndrome—a rare genetic kidney disorder—Pseudo-Bartter Syndrome is acquired and reversible, yet it can lead to life-threatening electrolyte imbalances if not properly recognized and managed.

This post explores what Pseudo-Bartter Syndrome is, how it develops in the context of eating disorders, and why medical providers and caregivers must be vigilant in monitoring and treating it.

What Is Pseudo-Bartter Syndrome?

Pseudo-Bartter Syndrome refers to a set of biochemical abnormalities that resemble Bartter Syndrome, particularly hypokalemia (low potassium), hypochloremic metabolic alkalosis, and elevated renin and aldosterone levels. Unlike Bartter Syndrome, which is a congenital defect in the kidneys’ ability to regulate electrolytes, Pseudo-Bartter Syndrome is caused by external losses of fluids and electrolytes, most commonly through purging behaviors.

It is most frequently observed in individuals with bulimia nervosa, anorexia nervosa binge-purge subtype, or ARFID with purging behaviors.

How Does It Develop?

The syndrome develops due to chronic fluid and electrolyte loss, typically from:

• Self-induced vomiting

• Laxative misuse

• Diuretic abuse

These purging behaviors lead to significant loss of sodium, potassium, chloride, and hydrogen ions. In response, the body compensates by activating the renin-angiotensin-aldosterone system (RAAS) to conserve sodium and water. This hormonal response results in renal retention of sodium and excretion of potassium, causing persistent hypokalemia and alkalosis.

When purging suddenly stops—especially during inpatient treatment or refeeding—fluid retention may rebound dramatically due to persistently elevated aldosterone levels, leading to edema and rapid weight gain.

Key Features of Pseudo-Bartter Syndrome

Clinical Feature Explanation Hypokalemia Low potassium from renal losses due to aldosterone overactivity Hypochloremic metabolic alkalosis Loss of gastric acid (HCl) via vomiting leads to elevated blood bicarbonate Edema after purging cessation Sodium retention and fluid rebound after sudden stop of diuretics or vomiting Normal blood pressure Distinguishes it from other causes of hyperaldosteronism High aldosterone and renin levels Secondary response to volume depletion, not a primary endocrine disorder

Source: Mehler et al., 2015; Birmingham & Treasure, 2010

Risk Factors

• Frequent or long-term vomiting

• Chronic laxative or diuretic use

• Rapid cessation of purging behaviors during treatment

• Poor medical monitoring during refeeding or outpatient recovery

• Inadequate electrolyte supplementation or fluid balance assessment

Why It Matters in Eating Disorder Treatment

Pseudo-Bartter Syndrome is particularly dangerous during the early stages of recovery, especially when purging behaviors are abruptly stopped. Patients may experience:

• Sudden, dramatic fluid retention (2–10 kg or more in a few days)

• Painful peripheral edema (hands, feet, face)

• Electrolyte instability (especially low potassium)

• Emotional distress or renewed urges to purge due to rapid weight gain

Without understanding this syndrome, clinicians and families may interpret the weight gain as “fat gain,” which can increase psychological resistance to treatment and hinder recovery.

Diagnosis and Lab Findings

Diagnosis is clinical but supported by lab testing:

• Serum electrolytes: Low potassium, low chloride, elevated bicarbonate

• Urine electrolytes: Inappropriately high sodium and potassium in the setting of volume depletion

• Elevated plasma renin and aldosterone levels

• Normal kidney function (unless complicated)

Differentiating Pseudo-Bartter from Bartter Syndrome requires history-taking and the absence of congenital renal disease.

Treatment and Management

1. Correct Electrolytes Carefully

• Replace potassium orally or IV depending on severity

• Monitor magnesium and chloride

• Address acid-base imbalance as needed

• Avoid overly aggressive fluid administration

2. Gradual Rehydration and Monitoring

• Monitor for signs of fluid overload

• Daily weight and input/output assessments

• Use of spironolactone (a potassium-sparing diuretic) may be considered to block aldosterone temporarily and mitigate edema

Source: Mehler & Andersen, Eating Disorders: A Guide to Medical Care and Complications, 2015

3. Psychological Support During Refeeding

• Anticipate emotional distress related to fluid-related weight gain

• Educate patients and families about the biological and temporary nature of edema

• Validate body discomfort while reinforcing the importance of medical stabilization

4. Prevent Relapse

• Discuss the consequences of purging resumption after edema subsides

• Set expectations about temporary weight fluctuations

• Reassure that pseudo-weight gain is not permanent fat gain

Provider Considerations

• Always screen for purging behaviors in patients with unexplained hypokalemia or alkalosis

• Educate interdisciplinary teams about Pseudo-Bartter risk before initiating refeeding

• Recognize that fluid shifts can destabilize recovery and must be handled with empathy

• In outpatient care, provide anticipatory guidance about symptoms and labs during recovery

Final Thoughts

Pseudo-Bartter Syndrome may be invisible to the untrained eye, but it carries real medical and psychological risks. For individuals in eating disorder recovery, understanding this syndrome is key to safe refeeding, electrolyte management, and emotional stabilization.

By identifying and managing Pseudo-Bartter Syndrome with compassion and clinical precision, we help patients build a safer and more sustainable foundation for recovery.

References

• Mehler, P. S., & Andersen, A. E. (2015). Eating Disorders: A Guide to Medical Care and Complications. Johns Hopkins University Press.

• Birmingham, C. L., & Treasure, J. (2010). Medical complications of eating disorders. European Eating Disorders Review, 18(6), 408–414.

• Kaye, W., et al. (2013). Anorexia nervosa and bulimia nervosa. Nature Reviews Disease Primers, 2, 16074.

• Westmoreland, P., Krantz, M. J., & Mehler, P. S. (2016). Medical complications of anorexia nervosa and bulimia. American Journal of Medicine, 129(1), 30–37.

• Sawyer, S. M., Whitelaw, M., Le Grange, D., Yeo, M., & Hughes, E. K. (2016). Physical and psychological recovery in adolescents. Journal of Adolescent Health, 58(3), 237–243.