Orthostatic hypotension after kidney transplantation in a patient with diabetic kidney disease: an underrecognized and therapeutic challenge.

Orthostatic hypotension (OH) is characterized by an excessive drop in blood pressure upon standing, leading to impaired quality of life, increased fall risk, and potential cardiovascular complications. It is frequently associated with autonomic dysfunction in patients with neurodegenerative diseases, diabetes mellitus, and aging. Despite its potential impact, OH may be underrecognized in kidney transplant (KT) recipients, particularly in the early post-transplant period, when diuresis-induced hypovolemia may serve as a precipitating factor. We present a case of severe OH in a woman in her 50s who underwent living-donor KT for diabetic kidney disease. Pre-transplant therapy with a glucagon-like peptide-1 (GLP-1) receptor agonist led to significant weight loss, followed by post-transplant diuresis, ultimately resulting in volume depletion. One month postoperatively, the patient developed persistent dizziness and fatigue. Orthostatic testing confirmed neurogenic OH, and assessment of cardiac autonomic function using the coefficient of variation of R-R intervals (CVRR) revealed significant autonomic dysfunction. Despite initial treatment with midodrine, symptoms persisted. Given concurrent mild hyperkalemia, fludrocortisone was administered. Unfortunately, no improvement in OH was observed during the observation period. This case underscores the importance of considering OH in KT recipients, particularly in the early post-transplant period when diuresis may exacerbate autonomic dysfunction. OH would be more common than recognized in routine clinical practice and is potentially underdiagnosed. Given the increasing number of elderly and diabetic KT recipients, heightened awareness and appropriate diagnostic evaluation of OH are essential for timely intervention. Fludrocortisone should also be considered in cases where volume depletion coexists with hyperkalemia, although its effectiveness may be limited, highlighting the therapeutic challenge in managing OH after KT.