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Article Synopsis
  • This study aimed to explore the relationship between microvascular renal lesions and antiphospholipid antibodies (aPL) in patients with systemic lupus erythematosus (SLE).
  • Among the analyzed 35 studies, it was found that 31.3% of aPL-positive SLE patients had microvascular lesions, compared to only 10.4% of aPL-negative patients, which indicates a significant association.
  • The research showed a notably higher risk for these lesions in patients with lupus anticoagulant and IgG anticardiolipin antibodies, while no link was found between aPL and different types of lupus nephritis.
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Renal Involvement in Antiphospholipid Syndrome.

Front Immunol

July 2019

Internal Medicine Rheumatology Service, Centro Médico ABC, Mexico City, Mexico.

Antiphospholipid syndrome is a complex autoimmune disease, characterized by the presence of vascular thrombosis, obstetric, hematologic, cutaneous, and cardiac manifestations. Renal disease in patients with antiphospholipid syndrome was not recognized in the first descriptions of the disease, but later on, the renal manifestations of the syndrome have been investigated widely. Renal manifestations of antiphospholipid syndrome conform a wide spectrum of diverse renal syndromes.

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The effects of nephropathy risk variants in the apolipoprotein L1 gene (APOL1) on renal histopathology in African Americans with arterionephrosclerosis or putative 'hypertension-associated' nephropathy are unknown. APOL1 genotype-phenotype correlations were performed in a blinded manner from renal biopsies in 196 self-reported African Americans with arterionephrosclerosis on kidney biopsy at a large national nephropathology practice. Subjects had chronic kidney disease without nephrotic syndrome.

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Pituitary adenylate cyclase activating polypeptide (PACAP) is a neuropeptide with well-known cytoprotective effects. We have reported earlier that PACAP decreases mortality and the degree of tubular atrophy in a rat model of renal ischemia/reperfusion injury. Recently, we have shown that kidney cultures isolated from PACAP deficient mice show increased susceptibility to renal oxidative stress.

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Interstitial fibrosis and tubular atrophy (IF/TA) in kidney allografts are induced by multiple factors, and although much effort has been devoted on the classification of IF/TA, clarification of the causes of non-specific IF/TA is equally important for appropriate therapy. Tamm-Horsfall protein (THP) in renal tissue can be a useful marker for the histological expression of urine backflow and suspected vesicoureteral reflux (VUR). Here, we examined the presence of VUR in pediatric recipients with interstitial THP deposits in kidney allografts to clarify the cause of non-specific IF/TA.

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