Endocrine Abstracts

JOINT2318

Background: Diabetic nephropathy (DN) is the most common cause of Hyporeninemic Hypoaldosteronism (HH), which often presents as hyperkalemia. Most of these patients are on Renin-Angiotensin-Aldosterone inhibitors (RAASi) to slow the progression of kidney disease. However, these medications can cause hyperkalemia as a side effect, which can complicate the disease management.

Case presentation: A 65-year-old female with Hypertension and Type 2 Diabetes Mellitus, currently on Lisinopril and Metformin, was brought from the clinic for elevated potassium levels. She denied chest pain, dyspnea, oliguria, or peripheral edema. No family history of hyperkalemia. Vital signs were normal. Physical examination was unremarkable. Laboratory tests showed Potassium 8 mEq/l without EKG changes, Sodium 131mEq/l, Creatinine 1.4 mg/dL (baseline 1.3 mg/dL), urine Protein/Creatinine ratio 4.5 g/g (ref <3.5 g/g), HbA1c 13%. Lisinopril was temporarily held, and the patient received calcium gluconate, and dextrose with insulin but remained hyperkalemic. The nephrology team suggested emergent hemodialysis (HD). Because of unexplained hyperkalemia, hormonal testing was added which showed Cortisol 20 mg/dL (ref 5-25 mg/dL), plasma Renin activity 0.4 ng/mL/hr (ref 0.7-3.3 ng/mL/hr), Aldosterone 2 mg/d (ref 3-25 mg/d). After one session of HD, repeat potassium was 3.9mEq/l. She was restarted at a lower dose of lisinopril with daily electrolyte monitoring and her glucose regimen was optimized. She was subsequently discharged with strict outpatient follow-up.

Discussion: DN causes autonomic dysfunction, resulting in decreased renal sensitivity to renin stimulation factors, causing HH and hyperkalemia. RAASi are effective in preventing progression to end-stage kidney disease but are a known cause of hyperkalemia. Withdrawing RAASi based on a diagnosis of HH alone may deprive patients of the cardiorenal benefits of these medications. Therefore, initiation of low-dose RAASi with gradual titration combined with a low potassium diet and avoidance of nephrotoxic medications can be done with close outpatient monitoring. However, the best treatment remains to be the optimization of glucose control.

Conclusion: HH is a complication of DN, and the optimization of glucose control plays a central role in the management. In addition, RAASi are effective means of slowing disease progression, and the benefits of continuing RAASi in patients who develop correctable side effects outweigh the risks, provided that proper patient education with close monitoring of laboratory tests and follow-up can be done.

Reference: Sousa AG, Cabral JV. Hyporeninemic hypoaldosteronism and diabetes mellitus: Pathophysiology assumptions, clinical aspects and implications for management. World J Diabetes. 2016 Mar 10;7(5):101-11. doi: 10.4239/wjd.v7.i5.101. PMID: 26981183; PMCID: PMC4781902.