Renal involvement in familial Mediterranean fever in an Algerian population

Khellaf, G.; Benziane, A.; Kaci, L.; Ait-Idir, Djouher; Missoum, Soumia; Benabadji, M.

doi:10.5414/cn110930

Cited by 2 publications

(3 citation statements)

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“…42 In this cohort of patients with FMF and renal involvement, less than 35% avoided haemodialysis or death. 42 However, the prevalence of NAKD may vary across nations because of variations in affordability, adherence to therapy, and other environmental variables. 15 Large epidemiological studies investigating the frequency of NAKD in FMF patients are lacking, probably due to the poor use of renal biopsies and the satisfactory improvement with medical therapy.…”

Section: Familial Mediterranean Fevermentioning

confidence: 81%

“…Differently, other results suggest a lower frequency of NAKD in FMF patients 38 . In a recent study, 58 FMF patients underwent renal biopsy due to the presence of chronic kidney disease, with an AKD rate of approximately 89.6% 42 . In this cohort of patients with FMF and renal involvement, less than 35% avoided haemodialysis or death 42 .…”

Section: Inflammasomopathiesmentioning

confidence: 99%

“…In a recent study, 58 FMF patients underwent renal biopsy due to the presence of chronic kidney disease, with an AKD rate of approximately 89.6% 42 . In this cohort of patients with FMF and renal involvement, less than 35% avoided haemodialysis or death 42 . However, the prevalence of NAKD may vary across nations because of variations in affordability, adherence to therapy, and other environmental variables 15 .…”

Section: Inflammasomopathiesmentioning

confidence: 99%

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Renal involvement in monogenic autoinflammatory diseases: A narrative review

et al. 2023

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Autoinflammatory diseases (AIDs) are mostly caused by dysfunctions in single genes encoding for proteins with a prominent role in the regulation of innate immunity, such as complement factors, inflammasome components, tumour necrosis factor (TNF)-α, and proteins belonging to type I-interferon (IFN) signalling pathways. 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-molecular 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-inflammatory cytokines, and a genetic predisposition due to specific SAA isoforms. Despite the prevalence of amyloid kidney disease, non-amyloid 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-I interferonopathies, and other rare AIDs in an effort to improve the clinical course and quality of life in paediatric patients with renal involvement.

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Section: Familial Mediterranean Fevermentioning

confidence: 81%

Section: Inflammasomopathiesmentioning

confidence: 99%