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Abstract: PUB235

Hemodynamic and Infectious Challenges in a Kidney Transplant Recipient with Severe Pulmonary Hypertension and Arteriovenous Fistula-Induced High-Output Heart Failure

Session Information

Category: Transplantation

  • 2002 Transplantation: Clinical

Authors

  • Younis, Sherif Elbaz, Tilman J. Fertitta Family College of Medicine, University of Houston, Kingwood, Texas, United States
  • Chand, Ranjeeta, Texas Transplant Institute, San Antonio, Texas, United States
Introduction

High-output heart failure (HOHF) from persistent arteriovenous fistula (AVF) is an underrecognized complication after kidney transplantation. Chronic high flow states may result in pulmonary hypertension and impaired renal allograft perfusion, particularly in patients with delayed graft function (DGF). Management becomes more challenging during sepsis when standard fluid resuscitation protocols can precipitate cardiopulmonary decompensation.

Case Description

A 59-year-old woman with end-stage kidney disease secondary to diabetic nephropathy underwent deceased donor kidney transplantation, complicated by DGF requiring hemodialysis. Kidney biopsy demonstrated acute tubular necrosis with mild interstitial fibrosis and vascular disease. Persistent dyspnea and severe pulmonary hypertension prompted right heart catheterization, which confirmed HOHF due to a high-flow aneurysmal left upper extremity AVF. AVF ligation resulted in marked improvement in urine output and renal allograft perfusion, with recovery to a baseline creatinine of 1.0 mg/dL.
Six months later, she presented with sepsis secondary to extended-spectrum beta-lactamase Escherichia coli urinary tract infection. Initial management included rapid administration of 1 liter of normal saline for hypotension. Shortly after fluid resuscitation, the patient developed acute hypoxic respiratory failure with pulmonary edema requiring noninvasive ventilation and ICU admission. Laboratory evaluation showed acute kidney injury with creatinine increase to 1.81 mg/dL and supratherapeutic tacrolimus trough level of 15.2 ng/mL. She was treated with intravenous meropenem, aggressive diuresis, and adjustment of immunosuppression. Respiratory status and kidney function improved, and creatinine returned to baseline before discharge.

Discussion

This case demonstrates the persistent hemodynamic vulnerability of kidney transplant recipients with prior AVF-induced HOHF and pulmonary hypertension, even after AVF ligation. Standardized high-volume fluid resuscitation in sepsis may precipitate acute right ventricular decompensation and pulmonary edema in this population. Careful individualized fluid administration with close hemodynamic monitoring is essential. In addition, sepsis-associated tacrolimus toxicity may further worsen allograft dysfunction.

Acknowledgment

We acknowledge our college in the internal medicine departments.