De novo collapsing glomerulopathy after kidney transplantation: Description of two cases.

Autor:	Cutruzzulà R; Nephrology Unit, Careggi University Hospital, and., Laudicina S; Department of Experimental and Clinical Medicine, University of Florence, Florence, Italy., Bagalà A; Department of Experimental and Clinical Medicine, University of Florence, Florence, Italy., Caroti L; Nephrology Unit, Careggi University Hospital, and., Bartiromo M; Nephrology Unit, Careggi University Hospital, and., Gianassi I; Nephrology Unit, Careggi University Hospital, and., Moscarelli L; Nephrology Unit, Careggi University Hospital, and., Di Maria L; Nephrology Unit, Careggi University Hospital, and., Larti A; Nephrology Unit, Careggi University Hospital, and., Allinovi M; Nephrology Unit, Careggi University Hospital, and., Antognoli G; Nephrology Unit, Careggi University Hospital, and., Cirami CL; Nephrology Unit, Careggi University Hospital, and.
Jazyk:	angličtina
Zdroj:	Clinical nephrology. Case studies [Clin Nephrol Case Stud] 2023 Apr 19; Vol. 11, pp. 66-71. Date of Electronic Publication: 2023 Apr 19 (Print Publication: 2023).
DOI:	10.5414/CNCS110887
Abstrakt:	Background: Among different forms of de novo focal segmental glomerulosclerosis (FSGS), which can develop after kidney transplantation (KTx), collapsing glomerulopathy (CG) is the least frequent variant, but it is associated with the most severe form of nephrotic syndrome, histological findings of important vascular damage, and a 50% risk of graft loss. Here, we report two cases of de novo post-transplant CG. Clinical Presentation: A 64-year-old White man developed proteinuria and worsening of renal function 5 years after KTx. Before the KTx, the patient was affected by an uncontrolled resistant hypertension, despite multiple antihypertensive therapies. Blood levels of calcineurin inhibitors (CNIs) were stable, with intermittent peaks. Kidney biopsy showed the presence of CG. After introduction of angiotensin receptor blockers (ARBs), urinary protein excretion progressively decreased in 6 months, but subsequent follow-up confirmed a progressive renal function decline. A 61-year-old White man developed CG 22 years after KTx. In his medical history, he was hospitalized twice to manage uncontrolled hypertensive crises. In the past, basal serum cyclosporin A levels were often detected above the therapeutic range. Low doses of intravenous methylprednisolone were administered due to the histological inflammatory signs shown on renal biopsy, followed by a rituximab infusion as a rescue therapy, but no clinical improvement was seen. Discussion and Conclusion: These two cases of de novo post-transplant CG were supposed to be mainly caused by the synergic effect of metabolic factors and CNI nephrotoxicity. Identifying the etiological factors potentially responsible for de novo CG development is essential for an early therapeutic intervention and the hope of better graft and overall survival. Competing Interests: The authors have no conflict of interest to declare. Figure 1.Light microscopy of patient A. Two glomeruli show segmentary sclerosis of the flocculus. Focal aspect of collapse of glomerular capillaries is shown in a glomerulus with some hyperplastic epithelial cells containing drops of protein reabsorption (collapsing lesion). No signs of endocapillary hypercellularity or glomerulitis.Figure 2.Clinical course after transplantation. eGFR = estimated glomerular filtration rate; KTx = kidney transplantation; RBx = renal biopsy. (© Dustri-Verlag Dr. K. Feistle.)
Databáze:	MEDLINE
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