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Functional renal stress and electrolyte shifts in type 2 diabetes: isolated urea elevation and a hypernatremic
Ahmed Zeyad Rahemmah1, Hamid Choobineh1, Fariba Nabatchian1
1Department of Medical Laboratory Sciences, School of Allied Medical Sciences, Tehran University of Medical Sciences, Tehran, Iran.
Background:
Type 2 diabetes mellitus (T2D) disrupts fluid and electrolyte homeostasis through hyperglycemia-induced osmotic diuresis and insulin resistance, yet the interplay between electrolyte shifts, renal stress, and environmental context remains incompletely characterized-particularly in arid regions. To investigate the impact of T2D on serum electrolytes and renal function markers, and to explore their associations with metabolic and hemodynamic parameters in an Iraqi outpatient cohort.
Methods:
In this case-control study, 100 T2D patients and 100 age- and sex-matched non-diabetic controls were recruited from Baghdad, Iraq. Serum levels of potassium (K⁺), sodium (Na⁺), calcium (Ca²⁺), magnesium (Mg²⁺), chloride (Cl⁻), urea, creatinine, and cystatin C were measured. Comprehensive correlations with age, blood pressure, glycemic indices (HbA1c, fasting glucose), and C-peptide were analyzed.
Results:
Although mean electrolyte concentrations did not differ significantly between groups, hyperkalemia (8.8% vs. 2.7%; p < 0.05) was significantly more prevalent, while hypernatremia (27.0% vs. 18.0%; p = 0.277) showed a non-significant trend toward higher prevalence among T2D patients. Serum urea was significantly elevated in T2D (1.71 ± 0.07 vs. 1.60 ± 0.06 mmol/L; p = 0.038), while creatinine and cystatin C-sensitive markers of glomerular filtration-remained unchanged, indicating functional, pre-renal stress rather than structural kidney injury. Key correlations included: age-potassium (r = - 0.214, p = 0.032), C-peptide-calcium (r = - 0.196, p = 0.049), systolic blood pressure-creatinine (r = - 0.234, p = 0.018), and creatinine-calcium (r = 0.260, p = 0.008).
Conclusion:
T2D in hot climates is associated with a potential tendency toward a hypernatremic, hyperkalemic pattern, driven by chronic free water deficit and insulin resistance-mediated electrolyte redistribution-not overt nephropathy. While hyperkalemia reached statistical significance, the higher prevalence of hypernatremia did not, though it may reflect subclinical dehydration in this arid environment. Isolated urea elevation-despite normal cystatin C and creatinine levels-underscores urea's utility as an early indicator of volume depletion. These findings advocate for routine electrolyte and urea monitoring in T2D management, especially in resource-limited, high-temperature settings, to prevent subclinical complications before irreversible renal damage occurs.
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