Abstract

Safety of living donors is paramount to the transplant community. Although rare, donor nephrectomy is associated with post-surgical problems. We present a case of adrenal insufficiency after laparoscopic left donor nephrectomy. A 28 year old Caucasian woman was evaluated as a kidney donor. She had no medical history and had an active lifestyle. Pre-operatively, her creatinine was 0.8 mg/dL with estimated GFR of 100.6 mL/min. All other testing including UA, urine protein, blood work, CXR, EKG were normal and blood pressure was 102/55 mmHg with HR of 74/min. Intraperative course was uneventful. Post-operatively she had persistent nausea and vomiting. Her creatinine was 1.0 mg/dL. She eventually tolerated oral intake and was discharged on post-op day 5 but readmitted on post-op day 12 for recurrent nausea, dehydration, hypotension (BP 70/60 mmHg). Non-contrast abdominal CT revealed post-op changes in the renal fossa, no fluid collection and normal adrenal glands. She received IV fluids and was discharged home. She continued to have nausea, vomiting, weight loss, and syncope. Extensive testing at outside hospital with CT scan of head, Holter monitor and 2-D echo did not reveal an etiology. She was re-evaluated at our center and found to have 20 lb weight loss and orthostatic hypotension (BP 103/71 mmHg lying, 94/62 mmHg sitting and 84/60 mmHg standing). Labs were unremarkable. An ACTH stimulation test (250 mcg) was abnormal with baseline value of 2.7 mcg/dL and 60-minute value of 17 mcg/dL. She was started on prednisone 20 mg daily with prompt improvement of symptoms and changed to hydrocortisone 20 mg per day with follow-up by endocrinology. Adrenal insufficiency has been reported after radical nephrectomy with resection of the unilateral adrenal gland. To our knowledge, this is the first case of proven adrenal insufficiency after living donor nephrectomy. Left nephrectomy requires ligation of the adrenal vein, which may produce vascular congestion and reduce function. Functional reserve in the contralateral gland should prevent adrenal insufficiency. In our patient, it appears that the right adrenal had decreased function as manifested by the abnormal ACTH stimulation test. Presentation of adrenal insufficiency is highly variable with symptoms ranging from vague and insidious to life-threatening. The diagnosis requires high index of clinical suspicion and demonstration of low cortisol production. Timely evaluation and treatment is crucial and potential kidney donors should be counseled regarding this rare complication.

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