Child Kidney Dis.  2024 Jun;28(2):51-58. 10.3339/ckd.24.006.

How to delay the progression of chronic kidney disease: focusing on medications

Affiliations
  • 1Department of Pediatrics, Chungnam National University Sejong Hospital, Sejong, Republic of Korea

Abstract

Patients with chronic kidney disease (CKD) bear a significant financial burden and face numerous complications and higher mortality rates. The progression of CKD is associated with glomerular injury caused by glomerular hyperfiltration and oxidative stress. Factors such as uncontrolled hypertension, elevated urine protein levels, anemia, and underlying glomerular disease, contribute to CKD progression. In addition to conservative treatment, several medications are available to combat the progression of CKD to end-stage kidney disease. Renin-angiotensin-aldosterone system blockers could slow the progression of CKD by reducing glomerular hyperfiltration, lowering blood pressure, and decreasing inflammation. Mineralocorticoid receptor antagonists inhibit the mineralocorticoid receptor signaling pathway, thereby attenuating inflammation and fibrosis. Sodium-glucose cotransporter 2 inhibitors exhibit protective effects on the kidneys and against cardiovascular events. Tolvaptan, a selective vasopressin V2-receptor antagonist, decelerates the rate of increase in total kidney volume and deterioration of kidney function in patients with rapidly progressive autosomal dominant polycystic kidney disease. The protective effects of AST-120 remain controversial. Due to a lack of evidence regarding the efficacy and safety of these medications in children, it is imperative to weigh the benefits and adverse effects carefully. Further research is essential to establish the efficacy and safety profiles in pediatric populations.

Keyword

Child; Renal insufficiency, chronic; Renin-angiotensin system; Sodium-glucose transporter 2 inhibitors

Figure

  • Fig. 1. The renin-angiotensin-aldosterone system. ACE, angiotensin-converting enzyme; ARB, angiotensin receptor blocker; AT1 receptor, angiotensin II type 1 receptor; MRA, mineralocorticoid receptor blocker.


Reference

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