Clinical features of glomerulopathies in children with iodine deficiency: a literature review

Abstract

Intraduction. This study aims to systematically analyze the clinical features, pathophysiological mechanisms, and progression patterns of glomerulopathies in children with iodine deficiency based on current literature. The aim of the study is to conduct a systemic analysis of the clinical features, pathophysiological mechanisms and nature of the progression of glomerulopathies in children with iodine deficiency based on data from modern scientific literature. Methods. A narrative literature review approach was applied using published data from peer-reviewed journals, including studies on thyroid–kidney interactions, pediatric glomerular diseases, and iodine deficiency-related metabolic and immunological alterations. Relevant clinical, experimental, and epidemiological studies were analyzed and synthesized. Results and discussion. Iodine deficiency leads to a reduction in the synthesis of thyroid hormones (T3, T4), which slows down metabolic processes, causes endothelial dysfunction, and activates the renin-angiotensin-aldosterone system. These changes result in a decrease in glomerular filtration rate, the development of proteinuria, and the progression of renal insufficiency. In addition, the activation of the immune system, an increase in pro-inflammatory cytokines (IL-2, IL-6, TNF-α), oxidative stress, and the activation of the complement system exacerbate glomerular damage. Clinically, these children are characterized by severe progression of glomerulopathies, stable proteinuria, edema syndrome, arterial hypertension, decreased glomerular filtration rate, and poor response to treatment. The results of the study confirm that iodine deficiency affects not only the endocrine system but also renal function. These findings are consistent with studies by Zimmermann, Pearce, and other authors, who have shown that iodine deficiency leads to systemic metabolic disorders. Iodine deficiency, as shown, exacerbates the development of glomerulopathies, proteinuria, and reduces kidney function. Conclusion. Iodine deficiency significantly influences both the development and progression of glomerulopathies in children through combined endocrine, immunological, and hemodynamic mechanisms. Early detection and correction of iodine deficiency, along with integrated nephrological and endocrinological monitoring, are essential for improving renal outcomes and preventing disease progression.