What a Nephrologist Should Know about Eating Disorders

Anorexia nervosa is characterized by caloric restriction and pathologic behaviors to achieve weight loss, such as excessive exercising, dieting, or purging (e.g. abuse of laxatives or diuretics, surreptitious vomiting). Patients with bulimia nervosa engage in purging behaviors and binge eating. Consequently, patients with anorexia nervosa tend to present with a low body mass index, while those with bulimia nervosa often have a normal or high body mass index.

Recognition of eating disorders is important for optimal patient care. Eating disorders have several complications that a nephrologist might evaluate during inpatient or outpatient consultation. As eating disorders are underdiagnosed, these patients may present to nephrology for management of the kidney, electrolyte, or acid-base complications of their disease without a prior diagnosis. To recognize these entities, clinicians must distinguish between psychiatrically disordered eating and poor appetite in patients with chronic kidney disease (CKD) and end stage kidney disease (ESKD). This is accomplished by asking questions about a person’s psychological relationship to food, eating, and body weight (the SCOFF screening questionnaire is a good tool for this).

Pseudo-Bartter syndrome

One of the most pathophysiologically interesting complications of eating disorders is Pseudo-Bartter syndrome. Patients who engage in purging behaviors may present to healthcare attention with hypovolemia, hypokalemia, and metabolic alkalosis (hence the name Pseudo-Bartter syndrome). This can occur in the setting of diuretic abuse, but can also arise from other forms of purging such as vomiting or laxative/enema abuse. Such purging behaviors lead to a chronically volume depleted state, which stimulates the renin-angiotensin-aldosterone system, and this hyperaldosteronism can persist for up to three weeks after stopping purging behaviors and restoring euvolemia.

This becomes particularly relevant in patients admitted to the hospital, who are frequently administered IV crystalloid for volume depletion at the same time as the patient ceases their  purging behaviors. Hyperaldosteronism leads to a sodium-avid state by increasing sodium reabsorption in the distal nephron, so sodium-containing bolus intravenous fluids can lead to positive fluid balance with peripheral and pulmonary edema. At times this can be severe enough to require endotracheal intubation. Keep in mind that part of these psychiatric disorders is a fear of gaining weight, so fluid overload won’t do your psychiatry colleagues any favors in treating the underlying problem.

The management of Pseudo-Bartter syndrome includes potassium repletion, gradual fluid administration to correct the metabolic alkalosis over 1-2 days, and initiation of an mineralocorticoid receptor antagonist such as spironolactone for 2-3 weeks to manage edema and hypokalemia. Loop or thiazide diuretics should be avoided in such patients, as these will worsen intravascular volume depletion and continue the cycle of aldosterone stimulation, urinary potassium wasting, and sodium chloride reclamation in the distal nephron.

Associated electrolyte abnormalities

Chronic purging behaviors and volume depletion can lead to several electrolyte abnormalities. Purging behaviors themselves can lead to all kinds of metabolic abnormalities that might prompt nephrology consultation. Laxative abuse can cause extrarenal loss of bicarbonate and potassium. Diuretic abuse, vomiting, and chronic volume depletion can cause metabolic alkalosis with renal potassium wasting. Diuretics cause urinary sodium and chloride loss, while extrarenal causes of volume depletion such as vomiting and laxative abuse will lead to reclamation of sodium chloride in the nephron (Table 1). Hypovolemic hyponatremia may develop in the setting of laxative or diuretic abuse combined with low solute intake.

Table 1. Electrolyte derangements in the setting of vomiting, diuretics & laxative abuse

Purging behaviorVolume statusSerum potassiumSerum bicarbonateUrine sodiumUrine potassiumUrine chloride
Laxatives ↓↑

Refeeding syndrome

Patients with anorexia nervosa are at risk for developing refeeding syndrome in the setting of caloric reintroduction. Refeeding syndrome is characterized by hypokalemia, hypophosphatemia, and hypomagnesemia in the setting of increased protein intake after starvation. Patients with anorexia nervosa are in a catabolic state, using fat and protein for energy in the setting of caloric restriction. This leads to total body depletion of potassium, magnesium, and phosphorus and extracellular shift to maintain normal serum levels of these electrolytes. Re-introduction of nutrition will stimulate insulin secretion and cause intracellular shifts of these electrolytes, which can be fatal. Close monitoring and aggressive repletion of potassium, phosphorus, and magnesium is critical in these patients as they gradually increase their protein and carbohydrate intake.

Evolution of CKD and Kidney Stones

There are several other nephrology-related complications of eating disorders. Chronic kidney disease is common in patients with anorexia nervosa. This is thought to be multifactorial, due to the chronic volume depletion and increased prevalence of kidney stones. Electrolyte abnormalities may also play a role; for reasons that are less well understood, chronic hypokalemia is associated with the development of CKD. Low muscle mass may contribute to overestimation of the GFR with standard eGFR equations in patients with anorexia nervosa. Acute kidney injury can also arise from volume depletion or obstructing kidney stones. Eating disorders are also associated with ammonium urate and calcium oxalate kidney stones. Volume depletion can lead to low urine volume and highly concentrated urine, which can contribute to the precipitation of solutes. Ammonium urate stones may be more likely in those who abuse laxatives and develop a metabolic acidosis that increases urinary ammoniagenesis.

Keep an eye out for these disorders! You could make an immense difference if you understand the underlying pathophysiology and know how to manage these complications.

Post By:
L. Parker Gregg, MD, MSCS
UT Soutwestern Medical Center, Dallas, TX
NSMC Intern 2019

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