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Updated: Dec 30, 2025

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Published on: June 11, 2012
Dialysis-associated hyperglycemia: manifestations and treatment
Yijuan Sun1,2, Maria-Eleni Roumelioti2, Kavitha Ganta1,2
1Renal Section, Medicine Service, Raymond G. Murphy Veterans Affairs Medical Center, 1501 San Pedro, SE, Albuquerque, NM, 87108, USA.
Insights
Dialysis-associated hyperglycemia (DAH) involves unique fluid and electrolyte issues. Insulin infusion is key for management, but careful monitoring for hypoglycemia and other abnormalities is crucial.
Area of Science:
- Nephrology
- Endocrinology
- Internal Medicine
Background:
- Dialysis-associated hyperglycemia (DAH) presents unique pathophysiological challenges.
- Understanding fluid and electrolyte shifts is critical in managing DAH.
Purpose of the Study:
- To review the pathophysiology of DAH.
- To establish treatment guidelines for DAH.
Main Methods:
- Systematic review of published literature on DAH.
- Synthesis of evidence-based treatment guidelines.
Main Results:
- DAH involves hypoglycemia risk with insulin, elevated serum tonicity, and variable extracellular volume abnormalities (edema or hypovolemia).
- Insulin corrects hyperglycemia, hypertonicity, ketoacidosis, and hyperkalemia, but may worsen hypovolemia, requiring saline.
- Monitoring for hypoglycemia and electrolyte disturbances during treatment is essential.
Conclusions:
- Insulin infusion is the cornerstone of DAH management, addressing primary fluid and electrolyte derangements.
- Close patient monitoring is vital to detect and manage potential complications like hypoglycemia or further fluid/electrolyte imbalances.
Purpose:
Dialysis-associated hyperglycemia (DAH), is associated with a distinct fluid and electrolyte pathophysiology. The purpose of this report was to review the pathophysiology and provide treatment guidelines for DAH.
Methods:
Review of published reports on DAH. Synthesis of guidelines based on these reports.
Results:
The following fluid and solute abnormalities have been identified in DAH: (a) hypoglycemia: this is a frequent complication of insulin treatment and its prevention requires special attention. (b) Elevated serum tonicity. The degree of hypertonicity in DAH is lower than in similar levels of hyperglycemia in patients with preserved renal function. Typically, correction of hyperglycemia with insulin corrects the hypertonicity of DAH. (c) Extracellular volume abnormalities ranging from pulmonary edema associated with osmotic fluid shift from the intracellular into the extracellular compartment as a consequence of gain in extracellular solute (glucose) to hypovolemia from osmotic diuresis in patients with residual renal function or from fluid losses through extrarenal routes. Correction of DAH by insulin infusion reverses the osmotic fluid transfer between the intracellular and extracellular compartments and corrects the pulmonary edema, but can worsen the manifestations of hypovolemia, which require saline infusion. (d) A variety of acid-base disorders including ketoacidosis correctable with insulin infusion and no other interventions. (e) Hyperkalemia, which is frequent in DAH and is more severe when ketoacidosis is also present. Insulin infusion corrects the hyperkalemia. Extreme hyperkalemia at presentation or hypokalemia developing during insulin infusion require additional measures.
Conclusions:
In DAH, insulin infusion is the primary management strategy and corrects the fluid and electrolyte abnormalities. Patients treated for DAH should be monitored for the development of hypoglycemia or fluid and electrolyte abnormalities that may require additional treatments.
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