High post-dexamethasone cortisol levels linked to lower eGFR independent of CV factors
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Key takeaways :
- Patients with mild autonomous cortisol secretion had higher CKD prevalence vs. nonfunctioning adrenal adenomas.
- Researchers observed a negative correlation between post-dexamethasone cortisol level and eGFR.
SEATTLE — Higher post-dexamethasone cortisol was associated with lower estimated glomerular filtration rate independent of cardiovascular risk factors, researchers reported at the AACE Annual Scientific and Clinical Conference.
“The findings of this study have significant clinical implications for the management of patients with mild autonomous cortisol secretion. First, we identified [chronic kidney disease] as a clear mild autonomous cortisol secretion-associated comorbidity, and as such CKD should be screened for and monitored in patients with conservatively followed mild autonomous cortisol secretion. Second, we showed that cortisol was an independent factor associated with worse kidney function,” Irina Bancos, MD, associate professor of medicine and associate program director of the Endocrinology Fellowship Program in the division of endocrinology, metabolism and nutrition at Mayo Clinic, and Leili Rahimi, MD, from the division of endocrinology, diabetes, metabolism and nutrition and the department of medicine at the Mayo Clinic, told Healio. “This means that addressing hypertension, dyslipidemia and diabetes will not be enough to prevent CKD in patients with mild autonomous cortisol secretion. Finally, our findings raise a question whether adrenalectomy in patients with mild autonomous cortisol secretion may reverse or stop progression of CKD.”
Bancos, Rahimi and colleagues conducted a retrospective single-center study with data from 972 adults with nonfunctioning adrenal adenomas (56%) and mild autonomous cortisol secretion (44%) from 1999 to 2022. All patients were diagnosed based on a post-dexamethasone cortisol cutoff of 1.8 µg/dL.
The primary outcomes were an eGFR and advanced CKD with an eGFR of less than 30 mL/min/1.73 m2 consistent with stage 4 or 5 CKD.
Overall, researchers noted a high proportion of women, with 66% among those with mild autonomous cortisol secretion and 63% among those with nonfunctioning adrenal adenomas (P = .32). Patients with mild autonomous cortisol secretion were older compared with patients with nonfunctioning adrenal adenomas (median age, 62.8 vs. 59.4 years; P < .001). Both hypertension (58% vs. 49%; P = .005) and smoking (71% vs. 63%; P = .02) prevalence were higher among patients with mild autonomous cortisol secretion compared with patients with nonfunctioning adrenal adenomas, but diabetes (25% vs. 20%, respectively; P = .13) and dyslipidemia (44% vs. 44%, respectively; P = .86) prevalence were similar between the two groups.
Patients with mild autonomous cortisol secretion had lower BMI (median, 30.7 vs. 31.4 kg/m3; P = .04) and eGFR (median, 79.6 vs. 83.8 mL/min/1.73 m2; P < .001) but had higher advanced CKD prevalence (17.6% vs. 11.7%; P < .001) compared with patients with nonfunctioning adrenal adenomas.
Researchers observed a negative correlation between post-dexamethasone cortisol level and eGFR (P < .001). When researchers adjusted for age, sex, BMI, hypertension, dyslipidemia, diabetes and smoking status, this correlation decreased but remained statistically significant (P = .027). Patients with mild autonomous cortisol secretion also had a higher risk for developing stage 4 and 5 CKD compared with patients with nonfunctioning adrenal adenomas (adjusted OR = 3.38; 95% CI, 1.1-12.4).
The only other independent risk factor for advanced CKD was hypertension (OR = 11.8; 95% CI, 2.1-220.8).
According to Bancos and Rahimi, further research on the impact of adrenalectomy on kidney function change should be assessed in patients with adrenal adenoma and mild autonomous cortisol secretion.
“In addition, further research is needed to identify nonsurgical effective strategies for managing kidney function decline in patients with adrenal adenoma, such as mineralocorticoid receptor antagonists or sodium-glucose transporter 2 inhibitor,” Bancos and Rahimi said.
For more information:
Irina Bancos, MD, can be reached at bancos.irina@mayo.edu.
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Bancos I, et al. Abstract #1402092. Presented at: American Association of Clinical Endocrinology Annual Scientific and Clinical Conference; May 4-6, 2023; Seattle.
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