ArticleClinical and experimental nephrology2014
Cyclosporin A may cause injury to undifferentiated glomeruli persisting in patients with Alport syndrome.
Article in Clinical and experimental nephrology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- Clinical practice recommendations for the management of Alport syndrome: a joint statement of the Korean Society of Nephrology and the Korean Society of Pediatric Nephrology.Kidney research and clinical practice · 2026Article
- Clinicopathological characteristics and cyclosporine-responsive proteinuria in nail-patella syndrome with a novel LMX1B mutation.Pediatric nephrology (Berlin, Germany) · 2026Article
- Investigation of the current situation regarding diagnosis and treatment of Alport syndrome in Asian countries: results of survey of the Asian Paediatric Nephrology association (AsPNA) tubular and inherited working group.Clinical and experimental nephrology · 2023Article
- A review of clinical characteristics and genetic backgrounds in Alport syndrome.Clinical and experimental nephrology · 2019Review
- Renal, auricular, and ocular outcomes of Alport syndrome and their current management.Pediatric nephrology (Berlin, Germany) · 2018Article
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10 authors at 1 institution in 1 country.
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Abstract
BACKGROUND/
aimsAlport syndrome (AS) is a renal disorder caused by a genetic abnormality of type IV collagen α3 and α4, or α5 genes and shows a poor prognosis. Since the defect of type IV collagen synthesis disturbs the maturation process of the glomerular capillary loop, residual immature glomeruli persist after birth. The therapeutic efficacy of cyclosporin A (CyA) for AS patients seems to be controversial. We recently noted that renal specimens obtained from a child with AS who was treated with CyA and then developed CyA nephropathy included an increased number of undifferentiated embryonic-type glomeruli.
methodsWe analyzed renal histologic and immunohistologic findings in children with AS who did (n = 3) or did not (n = 2) develop CyA-induced nephropathy despite appropriately low serum CyA concentrations (<100 ng/mL) being maintained over a period of 2 years. To discriminate embryonic-type from mature glomeruli, staining for type IV collagen α1, laminin β1, and laminin β2 accompanied by light microscopic observation were employed. Staining patterns were used to semiquantitatively assess glomerular immaturity (glomerular immaturity index, or GII).
resultsIn initial biopsy specimens, residual embryonic-type glomeruli were observed in each patient. Patients with early-onset CyA nephropathy had a high GII (median value 2.91 vs 1.23 ± 0.62 normal kidney tissues). In the follow-up biopsy after CyA treatment, surviving embryonic-type, collapsing embryonic-type, and sclerotic glomeruli that had failed to differentiate were observed. Taken together, the number of these glomeruli essentially equaled the total number of embryonic-type glomeruli in specimens obtained before CyA treatment.
conclusionsOur findings indicate a need for caution in CyA therapy for patients with AS, even for a relatively short course of administration, because some patients may have an unexpected number of embryonic-type glomeruli that predispose to CyA nephropathy.
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