ArticlePediatric nephrology (Berlin, Germany)2026
Birth characteristics and growth outcome in children with nephropathic cystinosis compared with other chronic kidney disease entities prior to kidney replacement therapy.
Article in Pediatric nephrology (Berlin, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundInfantile nephropathic cystinosis (INC) is characterized by progressive short stature and low body fat. Although birth size is typically normal, early growth data are limited.
methodsIn this prospective multicenter observational study, 77 conservatively treated children with INC and 527 congenital and hereditary CKD controls, stages 1-5, were analyzed. We investigated birth characteristics and linear body growth (length/stature), weight, and head circumference from birth up to 18 years. Linear mixed-effects models were applied to identify pre- and postnatal predictors of statural growth.
resultsNewborns with INC exhibited normal birth morphology, whereas CKD controls showed significantly reduced, disproportionate characteristics (each p < 0.01). Despite preserved birth morphology, born small for gestational age prevalence in INC was nearly twofold higher than in the general population, and CKD peers had an approximately 1.7 times higher prevalence than INC (p < 0.05). In INC, a weight-length dissociation emerged at approximately 6 months of age, followed by marked impairments in both characteristics within the first 2 years, persisting into adulthood. CKD peers showed only mild further decline and more favorable long-term growth. Statural growth in INC was associated with biochemical features of Fanconi syndrome and with birth weight in adolescence, whereas in CKD, birth weight remained the only consistent predictor.
conclusionsIn INC, growth deterioration begins around 6 months with weight-length dissociation and progresses to sustained deficits in stature and weight. This pattern resembles early postnatal disturbances that durably constrain somatic development and are driven more by disease-specific disturbances than by reduced glomerular filtration.
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