More than tubular dysfunction: cystinosis and kidney outcomes.


Journal

Journal of nephrology
ISSN: 1724-6059
Titre abrégé: J Nephrol
Pays: Italy
ID NLM: 9012268

Informations de publication

Date de publication:
04 2022
Historique:
received: 10 02 2021
accepted: 20 05 2021
pubmed: 8 6 2021
medline: 13 4 2022
entrez: 7 6 2021
Statut: ppublish

Résumé

Cystinosis is a lysosomal storage disease that affects many tissues. Its prognosis depends predominantly on kidney involvement. Cystinosis has three clinical forms: nephropathic infantile, nephropathic juvenile and non-nephropathic adult. Proximal tubular dysfunction is prominent in the infantile form, whereas a combination of glomerular and tubular alterations are observed in the juvenile form. Thirty-six children with nephropathic cystinosis were included in the study. Clinical features, molecular genetic diagnoses, and kidney outcomes of the patients were evaluated. Twenty-one children (58.3%) were male. The median age at diagnosis was 18.5 months. Twenty-eight patients (77.8%) had infantile nephropathic cystinosis, while eight (22.2%) had juvenile nephropathic cystinosis. An acute rapid deterioration of the kidney function with proteinuria, hypoalbuminemia, and nephrotic syndrome, was observed in 37.5% of patients with the juvenile form. The mean estimated glomerular filtration rate (eGFR) was 82.31 ± 37.45 ml/min/1.73m Glomerulonephritis may be a frequent finding in addition to the well-known tubular dysfunction in patients with cystinosis. Furthermore, our results highlight that the presence of severe proteinuria at the time of diagnosis is a relevant prognostic factor for kidney survival.

Sections du résumé

BACKGROUND
Cystinosis is a lysosomal storage disease that affects many tissues. Its prognosis depends predominantly on kidney involvement. Cystinosis has three clinical forms: nephropathic infantile, nephropathic juvenile and non-nephropathic adult. Proximal tubular dysfunction is prominent in the infantile form, whereas a combination of glomerular and tubular alterations are observed in the juvenile form.
METHODS
Thirty-six children with nephropathic cystinosis were included in the study. Clinical features, molecular genetic diagnoses, and kidney outcomes of the patients were evaluated.
RESULTS
Twenty-one children (58.3%) were male. The median age at diagnosis was 18.5 months. Twenty-eight patients (77.8%) had infantile nephropathic cystinosis, while eight (22.2%) had juvenile nephropathic cystinosis. An acute rapid deterioration of the kidney function with proteinuria, hypoalbuminemia, and nephrotic syndrome, was observed in 37.5% of patients with the juvenile form. The mean estimated glomerular filtration rate (eGFR) was 82.31 ± 37.45 ml/min/1.73m
CONCLUSION
Glomerulonephritis may be a frequent finding in addition to the well-known tubular dysfunction in patients with cystinosis. Furthermore, our results highlight that the presence of severe proteinuria at the time of diagnosis is a relevant prognostic factor for kidney survival.

Identifiants

pubmed: 34097292
doi: 10.1007/s40620-021-01078-y
pii: 10.1007/s40620-021-01078-y
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

831-840

Informations de copyright

© 2021. Italian Society of Nephrology.

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Auteurs

Bahriye Atmis (B)

Department of Pediatric Nephrology, Cukurova University Faculty of Medicine, Adana, Turkey. bahriyeatmis@gmail.com.

Aysun K Bayazit (A)

Department of Pediatric Nephrology, Cukurova University Faculty of Medicine, Adana, Turkey.

Derya Cevizli (D)

Department of Pediatric Nephrology, Cukurova University Faculty of Medicine, Adana, Turkey.

Deniz Kor (D)

Department of Pediatric Metabolism and Nutrition, Cukurova University Faculty of Medicine, Adana, Turkey.

Hatice Busra Fidan (HB)

Department of Pediatrics, Cukurova University Faculty of Medicine, Adana, Turkey.

Atil Bisgin (A)

Department of Medical Genetics, Cukurova University Faculty of Medicine, Adana, Turkey.
Cukurova University AGENTEM (Adana Genetic Diseases Diagnosis and Treatment Center), Adana, Turkey.
Medical Genetics Department of Balcali Clinics and Hospital, Faculty of Medicine, Adana, Turkey.

Sebile Kilavuz (S)

Department of Pediatric Metabolism and Nutrition, Cukurova University Faculty of Medicine, Adana, Turkey.

Ilker Unal (I)

Department of Biostatistics, Cukurova University Faculty of Medicine, Adana, Turkey.

Kivilcim Eren Erdogan (KE)

Department of Pathology, Cukurova University Faculty of Medicine, Adana, Turkey.

Engin Melek (E)

Department of Pediatric Nephrology, Cukurova University Faculty of Medicine, Adana, Turkey.

Gulfiliz Gonlusen (G)

Department of Pathology, Cukurova University Faculty of Medicine, Adana, Turkey.

Ali Anarat (A)

Department of Pediatric Nephrology, Cukurova University Faculty of Medicine, Adana, Turkey.

Neslihan Onenli Mungan (N)

Department of Pediatric Metabolism and Nutrition, Cukurova University Faculty of Medicine, Adana, Turkey.

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