The endoplasmic reticulum (ER) stress response is a critical cellular mechanism involved in maintaining protein homeostasis and ensuring proper folding of newly synthesized proteins. Under conditions of ER stress, unfolded or misfolded proteins accumulate within the ER lumen, triggering a series of signaling pathways collectively known as the unfolded protein response (UPR). While the UPR is initially adaptive, prolonged or unresolved ER stress can lead to cellular dysfunction and contribute to the pathogenesis of various diseases. This review explores the intricate molecular mechanisms underlying the ER stress response and its implications for disease pathogenesis and pathophysiology. We examine the role of ER stress in the pathophysiology of diverse diseases, including neurodegenerative disorders, metabolic syndromes, cardiovascular diseases, and cancer. Furthermore, we discuss potential therapeutic strategies targeting the ER stress response to mitigate disease progression and improve clinical outcomes. A comprehensive understanding of the ER stress response and its contributions to disease pathology is essential for the development of novel therapeutic interventions and the advancement of personalized medicine approaches.

Pediatric renal tubular acidosis (RTA) is a group of disorders characterized by impaired acid-base regulation in the renal tubules, leading to metabolic acidosis. This comprehensive review provides an overview of the etiology, pathophysiology, clinical manifestations, diagnosis, and management of pediatric RTA. Etiologies of pediatric RTA include genetic mutations, autoimmune disorders, drug-induced causes, and systemic diseases affecting renal function. Pathophysiologically, RTA involves defects in renal tubular transport mechanisms, leading to impaired reabsorption of bicarbonate and/or impaired secretion of hydrogen ions. Clinical manifestations of pediatric RTA vary depending on the underlying subtype and may include failure to thrive, growth retardation, polyuria, dehydration, nephrocalcinosis, and electrolyte disturbances. Diagnosis of pediatric RTA involves clinical evaluation, laboratory tests, and specialized renal function studies, including measurement of urinary electrolytes, blood gas analysis, and assessment of acid-base status. Management of pediatric RTA aims to correct metabolic acidosis, restore electrolyte balance, prevent complications such as nephrocalcinosis and bone demineralization, and address the underlying cause. Treatment modalities include alkali therapy, potassium supplementation, and avoidance of medications that exacerbate acidosis. This review highlights the importance of early recognition and appropriate management of pediatric RTA to optimize outcomes and prevent long-term complications.