Incidence of type 2 diabetes is increasing rapidly. It accounts for up to half of all cases of new-onset diabetes in young people. Dysfunction in glucose homeostasis impacts acid-base regulation. In addition, injury to organs as a result of diabetes and antidiabetic drugs contribute to this dysregulation.
Hyponatremia is associated with increased plasma glucose concentrations. Higher glucose concentration results in an osmotic force that draws water to the extracellular space. This dilutes extracellular sodium and leads to lower plasma sodium levels. This is why measured sodium levels need to be altered with a correctional factor during hyperglycemic crises. Sodium levels can fluctuate wildly during treatment of hyperglycemic crises due to osmotic diuresis and fluid intake, as well. Many medications commonly used in the management of diabetes result in hyponatremia as well. Tricyclic antidepressants, used in the treatment of diabetic neuropathy, stimulate vasopressin and lead to lower levels. First-generation sulfonylureas and insulin are also known to cause hyponatremia by augmenting the effects of vasopressin at the renal collecting ducts.
Potassium levels are also altered in diabetes. High plasma glucose concentrations lead to potassium efflux to the extracellular space, causing hyperkalemia.
Diabetic ketoacidosis is a clinically significant acid-base disturbance in diabetes. It occurs due to an increase in the rate of hepatic ketoacid generation. Bicarbonate degrades to carbon dioxide and water, and anion-gap acidosis results. It is typically treated with insulin and volume resuscitation. Alkali therapy is not typically appropriate; bicarbonate will regenerate upon administration of insulin and the oxidation of ketoanions. Rarely, metformin can lead to acidosis. The incidence of metformin-induced acidosis increases in renal dysfunction due to decreased clearance.
Hyperkalemic renal tubular acidosis can occur in diabetic patients with nephropathy. Nephron dysfunction leads to impaired excretion of potassium and hydrogen, resulting in hyperkalemia and acidosis with hyperchloremia. It can even occur in patients with have mild nephropathy. It usually does not require treatment in the absence of comorbidities that worsen acidosis. When this occurs, the primary treatment goal should be to correct hyperkalemia, which results in correction of acidosis.
Divalent-cation and phosphorous homeostasis disruptions are also significant in diabetic patients. Magnesium is a common thread here. Low intake of magnesium is associated with increased risk of diabetes; low serum magnesium levels disrupt glucose uptake and contribute to microvascular complications and end-organ damage.
Overall, diabetic patients are at increased risk of acid-base disorders and electrolyte disturbances. The increased risk is due to the disease state of diabetes itself and the associated disruptions in glucose homeostasis, the drugs used to treat diabetes, and the organ damage associated with diabetes. Practitioners of many different specialties will therefore be exposed to more diabetic patients as they treat these conditions.
- Sodium levels may be depressed in diabetic patients. Sodium levels should be corrected when treating hyperglycemic crises.
- Potassium levels may be increased in diabetic patients. This results from several mechanisms.
- Drugs used to treat diabetes can cause electrolyte and acid-base disturbances, including mainstays of therapy like metformin and sulfonylureas, along with tricyclic antidepressants used to treat neuropathy.
Palmer BF, Clegg DJ. “Electrolyte and Acid-Base Disturbances in Patients with Diabetes Mellitus.” N Engl J Med. 2015;373(6):548-59.