The cardinal treatment modality for any glomerular disease is glucocorticoids. The glucocorticoids cause an imbalance in the hypothalamus–pituitary–adrenal axis by altering the endogenous cortisol levels. The low levels of cortisol result in a clinical syndrome called adrenal insufficiency (AI). The occurrence of iatrogenic AI by the glucocorticoids among glomerular disease is evaluated in this study by both biochemical cortisol assay and clinical evaluation, and also, the value of salivary cortisol over serum cortisol is correlated. Materials and methods: This cross-sectional study was done on 30 biopsy-proven glomerular disease patients on glucocorticoid treatment. Clinical implications were noted using a detailed questionnaire, and serum and salivary cortisol assays were analyzed by enzyme-linked immunosorbent assay (ELISA) technique. Results: On clinical evaluation, 78% of the study population did not show signs of AI. However, 15% of the patients exhibited cushingoid symptoms. Biochemical assay with serum cortisol showed 45% with low serum cortisol levels, suggesting AI and only 3% of the study population had low salivary cortisol levels. There was no linear correlation between serum and salivary cortisol levels. Conclusion: The evidence of AI among glucocorticoid-treated glomerular disease patients is established with serum cortisol assay. The value of salivary cortisol is not marked as the other confounding factors, such as drugs and cross-reactivity with antibodies, could alter the assay values. Overall, the suppression of the hypothalamic–pituitary–adrenal (HPA) axis is evident in our study, and a monitored glucocorticoid therapy is vital so as to prevent the tendency of AI and its complications.