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Due to the deposition of amyloid A (AA) fibrils in the glomeruli, unprovoked inflammation in AIDs frequently affects renal health. In fact, secondary AA amyloidosis is the most common form of amyloidosis in children. It is caused by the extracellular deposition of fibrillar low\u2010molecular weight protein subunits resulting from the degradation and accumulation of serum amyloid A (SAA) in numerous tissues and organs, primarily the kidneys. The molecular mechanisms underlying AA amyloidosis in AIDs are the elevated levels of SAA, produced by the liver in response to pro\u2010inflammatory cytokines, and a genetic predisposition due to specific SAA isoforms. Despite the prevalence of amyloid kidney disease, non\u2010amyloid kidney diseases may also be responsible for chronic renal damage in children with AIDs, albeit with distinct characteristics. Glomerular damage can result in various forms of glomerulonephritis with distinct histologic characteristics and a different underlying pathophysiology. This review aims to describe the potential renal implications in patients with inflammasomopathies, type\u2010I interferonopathies, and other rare AIDs in an effort to improve the clinical course and quality of life in paediatric patients with renal involvement.<\/jats:p>","DOI":"10.1111\/nep.14166","type":"journal-article","created":{"date-parts":[[2023,5,4]],"date-time":"2023-05-04T23:39:42Z","timestamp":1683243582000},"page":"363-371","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["Renal involvement in monogenic autoinflammatory diseases: A narrative review"],"prefix":"10.1111","volume":"28","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1244-0789","authenticated-orcid":false,"given":"Saverio","family":"La Bella","sequence":"first","affiliation":[{"name":"Department of Pediatrics University of Chieti\u2010Pescara \u201cG. d'Annunzio\u201d  Chieti 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