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Post-transplant proteinuria is a biomarker of renal injury with a multifactorial etiology, negatively affecting graft function and survival. Renal allograft damage manifesting as proteinuria may involve aldosterone, and its blockade can potentially benefit kidney transplant recipients. This study aimed to evaluate the effect of spironolactone treatment on proteinuria and graft function in kidney transplant recipients.
This is a retrospective unicentric cohort study including kidney transplant recipients over 18 years old with persistent post-transplant proteinuria (urine protein-to-creatinine ratio > 0.5) who were treated with spironolactone. Clinical and laboratory data were collected retrospectively at the beginning of the treatment, at the 3rd and 6th months, and every year of therapy during a 5-year follow-up. Patients were grouped according to initial proteinuria: mild (<1), moderate (1-3) and severe (>3).
A total of 167 patients fulfilled the inclusion criteria, with most being male (n=122, 73%) and a mean age of 40.7 ± 14.5 years. The main etiology of chronic kidney disease was unknown (n=38, 23%), followed by chronic glomerulonephritis (n=37, 22%) and hypertensive nephrosclerosis (n=33, 20%). The patients were grouped according to the initial proteinuria in mild (n=47, 28%), moderate (n=90, 54%), and severe (n=30, 18%). Patients from the severe proteinuria group showed a significant reduction of proteinuria in the 6th month post-treatment (5.5 ± 1.9 to 3.2 ± 2.6, p <0.05), with progressive decline until the 5th year of treatment (1.4 ± 1.2, p <0.05). In the other groups, proteinuria remained stable during the follow-up, indicating effective control of proteinuria with the treatment. Renal function remained stable throughout the period in all groups.
The treatment with spironolactone effectively reduced proteinuria in kidney transplant recipients during a 5-year follow-up, mainly in patients with initial severe proteinuria. The graft function remained stable during the follow-up in all groups.