Can Post-transplant Congestive Nephropathy from Hypervolemia Cause Slow Graft Function?

Introduction: Low cardiac output alone does not define renal dysfunction in cardiorenal syndrome (CRS). Congestive nephropathy (CN) depicts the role of renal venous hypertension in CRS. Our understanding of CN is evolving. Furthermore, we do not have any known reports of CN in renal allografts. Case Description: A 48-yo female with ESRD from Fabry's disease, who started hemodialysis in February 2020 was on Midodrine to sustain hemodialysis due to hypotension. She made about a cup of urine. She received a deceased donor kidney transplant in late April 2024. Due to peri-operative hypotension with systolic blood pressure in the 70s, she received multiple liters of IVF therapy perioperatively and post-operatively (Figure). She received IV albumin boluses and was restarted on oral Midodrine post-operatively. There was evidence of hypervolemia and fluid retention. She had slow graft function and subsequently responded well to combination IV Furosemide + IV Chlorothiazide infusions and subsequent switch to oral Torsemide 100 mg daily + oral Metolazone 5 mg daily with later fall in serum creatinine. She was discharged on post-op day #8 for outpatient management and monitoring of improving renal allograft function (Figure). Discussion: To our knowledge, this is the first report of CN in a new renal allograft. The serum creatinine trajectory supports the speculation that both native kidneys and the newly transplanted renal allograft were simultaneously impacted by CN. The subsequent falling creatinine with decongestive diuresis supports this hypothesis. Further investigation is warranted.