Study of Serum Aldosterone, Serum, and Urinary Electrolytes in Type 2 Diabetes Mellitus Patients (>5 Years) and Their Correlation with Microvascular Complications

Background: Diabetes Mellitus is characterized by a shared phenotype of chronic hyperglycemia and bears a disproportionate burden in India with particularly high microvascular complication rates. While Renin-Angiotensin-Aldosterone System (RAAS) dysfunction and electrolyte imbalances are known to exacerbate microvascular injury, their specific roles remain underexplored in cases of type 2 diabetes mellitus (T2DM), despite the documented prevalence of both hypoaldosteronism and hyperaldosteronism. Aims and Objectives: The primary aim of this study was to assess the levels of serum aldosterone, serum electrolytes, and urinary electrolytes in T2DM patients with a disease duration of more than 5 years. The objective was to correlate these biochemical findings with the presence of microvascular complications, specifically retinopathy, nephropathy, and neuropathy. Materials and Methods: This cross-sectional, observational, and analytical study was conducted at a tertiary care center in Western Maharashtra between September 2023 and February 2026. The study enrolled 120 adult participants aged 18 years or older who had T2DM for at least 5 years. Serum aldosterone levels were measured using a fully automated chemiluminescent immunoassay (CLIA), while serum and urinary electrolytes alongside osmolality were measured using ion-selective electrodes and osmometry. Microvascular complications were assessed using standard clinical criteria, which included dilated fundoscopy for diabetic retinopathy, urine albumin-to-creatinine ratio (UACR) for diabetic nephropathy, and clinical symptoms along with the Michigan Neuropathy Screening Instrument (MNSI) score for diabetic neuropathy. Results: The key finding of the study was a statistically significant inverse relationship between low serum aldosterone (<1.17 ng/dL) and the prevalence of diabetic neuropathy ( p =0.023), suggesting hyporeninemic hypoaldosteronism as a novel risk factor. Patients with diabetic nephropathy exhibited classical tubular dysfunction parameters, including significantly elevated serum osmolality ( p =0.010), reduced urine osmolality ( p =0.001), and reduced urinary potassium ( p =0.006). Both the diabetic nephropathy and diabetic retinopathy groups showed elevated serum osmolality ( p =0.010 and p =0.031 respectively), indicating osmotic stress-induced microvascular injury. There was a statistically significant positive correlation between the duration of diabetes and microvascular complications, though HbA1c and overall serum aldosterone levels did not show statistically significant direct correlations with complications or electrolyte levels. Conclusion: The study identifies aldosterone deficiency as a novel, potentially modifiable, and early predictive marker for diabetic neuropathy. Furthermore, tubular dysfunction parameters such as elevated serum osmolality, reduced urine osmolality, and reduced urinary potassium can serve as early markers for nephropathy. These findings highlight the critical importance of integrating routine aldosterone and electrolyte testing in the diabetic population to enable earlier interventions and mitigate microvascular complications.