Abstract
Background: Lung transplant recipients are prone to developing multifactorial hyponatremia from immunosuppressive therapies and posttransplant lymphoproliferative disorders.
Clinical Case: A 77-year-old male with a history of lung transplantation in 2017 presented for a 3-month history of confusion, decline in executive function and chronic abdominal pain. Vital signs were BP 137/81 mmHg, HR 81 bpm, RR 14 per minute, SPO2 99% and afebrile. The patient was clinically euvolemic with a presenting sodium was 129 mmol/L, and was treated with 2.5L IV 0.9% saline. Home immunosuppression with cyclosporine, azathioprine and prednisone 5 mg/d were continued. Sodium declined to 126 mmol/L on day 4 prompting endocrine consult. Labs prior to fluid administration were consistent with iso-osmolar hyponatremia: sOsm 283 mOsm/kg and uOsm 409 mOsm/kg. Pseudohyponatremia was suspected and electrophoresis and immunofixation revealed a free kappa light chain gammopathy. Evaluation when sodium was 126 mmol/L was now consistent with hypotonic hyponatremia: sOsm 273 mOsm/kg, uOsm 398 mOsm/kg, and urine sodium 56mmol/L. TSH was normal and AM cortisol was 11.9 ug/dL (3.7–19.4 ug/dL), drawn while on maintenance prednisone. Lab findings and improvement of abdominal pain after receiving high dose prednisone for CT contrast-allergy prophylaxis raised our suspicion for SIADH and undertreated secondary AI. Retrospective chart review revealed tacrolimus use after lung transplant before its discontinuation 9 months prior to admission. Chronic hyponatremia was noted a few months post lung transplantation, with a nadir of 120 mmol/L and only mild improvement despite tacrolimus discontinuation and empiric fludrocortisone use. The patient was treated with a 1L fluid restriction, doubling of prednisone to 10 mg/d and cessation of fludrocortisone for lack of concern for primary. Abdominal symptoms resolved, mental status improved, and serum sodium rose to 132 mmol/L over the next few days, later normalizing to 135–140 mmol/L on follow up. The patient was eventually diagnosed with Waldenström macroglobulinemia.
Conclusion: Hyponatremia in lung transplant recipients can be multifactorial. Calcineurin inhibitors and steroids are part of typical immunosuppressive regimens and can lead to hyponatremia through salt wasting nephropathy or SIADH(1), and undertreated secondary AI, respectively. Posttransplant lymphoproliferative disorders occur in up to 9% of cases(2) and must be suspected as an etiology of hyponatremia.
References: 1.Cowan AJ, Johnson CK, Libby EN. Plasma cell diseases and organ transplant: A comprehensive review. Am J Transplant. 2018;18(5):1046–58.2.Aris RM, Maia DM, Neuringer IP, Gott K, Kiley S, Gertis K, et al. Post-transplantation lymphoproliferative disorder in the Epstein-Barr virus-naïve lung transplant recipient. Am J Respir Crit Care Med. 1996;154(6 Pt 1):1712–7.
SARS-CoV-2 and Norovirus Co-Infection after Lung Transplantation
