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Caveolin-1 as a Marker of Endothelial Damage in Primary Antiphospholipid Syndrome Nephropathy
Savino Sciascia1, Massimo Radin1, Irene Cecchi1
1University Center of Excellence on Nephrologic, Rheumatologic and Rare Diseases (ERK-Net, ERN-Reconnet and RITA-ERN Member) with Nephrology and Dialysis Unit and Center of Immuno-Rheumatology and Rare Diseases (CMID), Coordinating Center of the Interregional Network for Rare Diseases of Piedmont and Aosta Valley, San Giovanni Bosco Hub Hospital, ASL Città di Torino, Department of Clinical Biological Science, University of Turin, Turin, Italy.
Rationale & Objective:
Thrombotic microangiopathy (TMA) as seen in antiphospholipid syndrome nephropathy (APSN) is associated with poor kidney outcomes. Caveolin-1 (Cav-1) has emerged as a potential marker of endothelial damage and microvascular injury.
Study Design:
This retrospective study investigates the diagnostic potential value of Cav-1 immunohistochemistry in APSN-related TMA.
Setting & Participants:
Patients were retrieved from the Piedmont and Aosta Valley Rare Disease Registry, from which a total of 771 APS cases had been recorded.
Exposure:
Only case with biopsy-proven renal involvement were included.
Outcomes:
Cases were classified into three histopathological clusters: TMA (APSN-TMA), hyperplastic vasculopathy, and subendothelial edema. Immunohistochemical staining for Cav-1 was performed and graded based on expression in peritubular and glomerular capillaries.
Analytical Approach:
Clinical and laboratory data, including antiphospholipid antibody profiles, were correlated with Cav-1 expression.
Results:
Out of 771 patients with APS, a total of 11 patients with primary APS and renal involvement were retrieved (1.43%). APSN-TMA was identified in 7 (63.3%) cases, hyperplastic vasculopathy in 2 (18.1%), and subendothelial edema in 2 (18.1%). Cav-1 expression was significantly higher in APSN-TMA cases in both glomerular (P < 0.001) and peritubular (P < 0.05) capillaries compared with other clusters, with 5 of 7 APSN-TMA cases exhibiting diffuse (grade III) staining. Triple antiphospholipid antibody positive testing was more prevalent in APSN-TMA cases, reinforcing their distinct pathophysiological profile.
Limitations:
The small sample size warrants validation in larger cohorts, and Cav-1 expression, although associated with APSN, might not be disease-specific.
Conclusions:
APSN-TMA is a rare manifestation of a rare disease. Cav-1 is strongly associated with APSN-TMA and may serve as a novel marker for its diagnosis and stratification. Given the poor renal prognosis of APSN-TMA, identifying affected patients is crucial for optimizing management strategies.
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