Renal calcification in children with renal tubular acidosis:What a paediatrician should know

Renal tubular acidosis(RTA)can lead to renal calcification in children,which can cause various complications and impair renal function.This review provides pediatricians with a comprehensive understanding of the relationship between RTA and renal calcification,highlighting essential aspects for clinical manage-ment.The article analyzed relevant studies to explore the prevalence,risk factors,underlying mechanisms,and clinical implications of renal calcification in children with RTA.Results show that distal RTA(type 1)is particularly associated with nephrocalcinosis,which presents a higher risk of renal calcification.However,there are limitations to the existing literature,including a small number of studies,heterogeneity in methodologies,and potential publication bias.Longitudinal data and control groups are also lacking,which limits our understanding of longterm outcomes and optimal management strategies for children with RTA and renal calcification.Pediatricians play a crucial role in the early diagnosis and management of RTA to mitigate the risk of renal calcification and associated complications.In addition,alkaline therapy remains a cornerstone in the treatment of RTA,aimed at correcting the acid-base imbalance and reducing the formation of kidney stones.Therefore,early diagnosis and appropriate therapeutic interventions are paramount in preventing and managing renal calcification to preserve renal function and improve long-term outcomes for affected children.Further research with larger sample sizes and rigorous methodologies is needed to optimize the clinical approach to renal calcification in the context of RTA in the pediatric population.

Findings on intraprocedural non-contrast computed tomographic imaging following hepatic artery embolization are associated with development of contrast-induced nephropathy

BACKGROUND Contrast-induced nephropathy(CIN)is a reversible form of acute kidney injury that occurs within 48-72 h of exposure to intravascular contrast material.CIN is the third leading cause of hospital-acquired acute kidney injury and accounts for 12%of such cases.Risk factors for CIN development can be divided into patientand procedure-related.The former includes pre-existing chronic renal insufficiency and diabetes mellitus.The latter includes high contrast volume and repeated exposure over 72 h.The incidence of CIN is relatively low(up to 5%)in patients with intact renal function.However,in patients with known chronic renal insufficiency,the incidence can reach up to 27%.AIM To examine the association between renal enhancement pattern on non-contrast enhanced computed tomographic(CT)images obtained immediately following hepatic artery embolization with development of CIN.METHODS Retrospective review of all patients who underwent hepatic artery embolization between 01/2010 and 01/2011(n=162)was performed.Patients without intraprocedural CT imaging(n=51),combined embolization/ablation(n=6)and those with chronic kidney disease(n=21)were excluded.The study group comprised of 84 patients with 106 procedures.CIN was defined as 25%increase above baseline serum creatinine or absolute increase≥0.5 mg/dL within 72 h post-embolization.Post-embolization CT was reviewed for renal enhancement patterns and presence of renal artery calcifications.The association between noncontrast CT findings and CIN development was examined by Fisher’s Exact Test.RESULTS CIN occurred in 11/106(10.3%)procedures(Group A,n=10).The renal enhancement pattern in patients who did not experience CIN(Group B,n=74 with 95/106 procedures)was late excretory in 93/95(98%)and early excretory(EE)in 2/95(2%).However,in Group A,there was a significantly higher rate of EE pattern(6/11,55%)compared to late excretory pattern(5/11)(P<0.001).A significantly higher percentage of patients that developed CIN had renal artery calcifications(6/11 vs 20/95,55%vs 21%,P=0.02).CONCLUSION A hyperdense renal parenchyma relative to surrounding skeletal muscle(EE pattern)and presence of renal artery calcifications on immediate post-HAE noncontrast CT images in patients with low risk for CIN are independently associated with CIN development.