Context Acute kidney injury(AKI) and renal tubular damage(RTD), especially if complicated by acute tubular necrosis (ATN), could increase the risk of later chronic kidney disease. No prospective studies on AKI and RTD in children with type1diabetes mellitus(T1DM) onset are available. Objectives to evaluate the AKI and RTD prevalence, and their rate and timing of recovery in children with T1DM onset. Design prospective study. Settings and patients: 185children were followed up after 14days from T1DM onset. The patients who did not recover from AKI/RTD were followed-up 30 and 60days later. Main outcome measures AKI was defined according to the KDIGO criteria. RTD was defined by abnormal urinary beta-2-microglobulin and/or neutrophil gelatinase-associated lipocalin and/or tubular reabsorption of phosphate<85% and/or fractional excretion of Na(FENa)>2%. ATN was defined by RTD+AKI, prerenal-(P-)AKI by AKI+FENa<1% while acute tubular damage(ATD) by RTD without AKI. Results Prevalence of diabetic ketoacidosis(DKA) and AKI were 51.4% and 43.8% respectively. Prevalence of AKI in T1DM patients with and without DKA was 65.2% and 21.1%. 33.3% reached AKI stage2 and 66.7% of patients reached AKI stage1. RTD was evident in 136/185(73.5%) patients (32.4% showed ATN; 11.4% P-AKI; 29.7% ATD). All patients with DKA or AKI presented with RTD. The physiological and biochemical parameters of AKI and RTD were normal again in all patients. The former within 14days and the latter within 2months, respectively. Conclusions Most patients with T1DM onset may develop AKI and/or RTD, especially if presenting with DKA. Over time the physiological and biochemical parameters of AKI/RTD normalize in all patients.

Summary Background PNPLA3 I148M polymorphism has an effect on modulation of estimated glomerular filtration rate (eGFR) in nonobese nondiabetic adults and in children with histologically confirmed nonalcoholic fatty liver disease (NAFLD). Objectives The objective of the study is to explore the impact of PNPLA3 I148M polymorphism on eGFR in children with obesity with and without NAFLD. Methods We genotyped 591 patients with obesity for PNPLA3 I148M polymorphism. Anthropometrical, biochemical, and instrumental data were collected. NAFLD was defined by the presence of ultrasound‐detected liver steatosis and/or ALT levels greater than 40 IU/L. Results Patients with NAFLD showed significantly lower eGFR levels compared with subjects without NAFLD. Children with PNPLA3 MM genotype showed lower eGFR levels compared with those with either PNPLA3 IM or II genotypes both in the presence and absence of NAFLD. A general linear model for eGFR variance, including gender, duration of obesity, PNPLA3 genotypes, HOMA, BMI‐SDS, LDL‐C, and triglycerides as covariates, confirmed an inverse association between eGFR and PNPLA3 genotype only in the presence of NAFLD. Conclusions Children with obesity and PNPLA3 MM genotype show lower eGFR levels compared with other genotypes, with a major effect of this polymorphism in the presence of NAFLD.

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BackgroundChronic recurrent multifocal osteomyelitis (CRMO), also known as chronic nonbacterial osteomyelitis, is a rare, noninfectious inflammatory disorder that causes multifocal bone lesions with swelling and pain. Lytic and sclerotic bone lesions could be found on X-ray. Short tau inversion recovery magnetic resonance imaging (STIR MRI) shows bone marrow oedema, bone expansion, lytic areas and periosteal reaction. CRMO is characterized by periodic exacerbations and remissions of unclear/unknown pathogenesis.Case presentationA 10 years old girl, suffering from pain in her right shoulder since the age of 9 years presented to our Department. Thanks to clinical data, laboratoristic and radiological findings and bone biopsy CRMO was diagnosed. So patient started anti-inflammatory treatment and her conditions improved.ConclusionsIn a child with bone pain should be considered also rare condition as CRMO to perform a correct diagnosis and start an adequate treatment avoiding complications such as bone damage. This condition should be suspected in a child with recurrent bone pain, modest increase of inflammatory indices, lytic or sclerotic bone lesion on X Ray. Typical CRMO localizations are metaphyses of long bones, pelvis, clavicle, vertebral column, sternum, ribs, jaw, but any bone can be involved. The most common CRMO differential diagnosis is represented by infections, malignant bone tumors, Langerhans Cells Histiocytosis (LCH).

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