Abstract

This study is the first to evaluate protein glycooxidation products, lipid oxidative damage and nitrosative stress in non-stimulated (NWS) and stimulated whole saliva (SWS) of children with chronic kidney disease (CKD) divided into two subgroups: normal salivary secretion (n = 18) and hyposalivation (NWS flow < 0.2 mL min−1; n = 12). Hyposalivation was observed in all patients with severe renal failure (4–5 stage CKD), while saliva secretion > 0.2 mL/min in children with mild-moderate CKD (1–3 stage) and controls. Salivary amylase activity and total protein content were significantly lower in CKD children with hyposalivation compared to CKD patients with normal saliva secretion and control group. The fluorescence of protein glycooxidation products (kynurenine, N-formylkynurenine, advanced glycation end products), the content of oxidative damage to lipids (4-hydroxynonneal, 8-isoprostanes) and nitrosative stress (peroxynitrite, nitrotyrosine) were significantly higher in NWS, SWS, and plasma of CKD children with hyposalivation compared to patients with normal salivary secretion and healthy controls. In CKD group, salivary oxidation products correlated negatively with salivary flow rate, α-amylase activity and total protein content; however, salivary oxidation products do not reflect their plasma level. In conclusion, children with CKD suffer from salivary gland dysfunction. Oxidation of salivary proteins and lipids increases with CKD progression and deterioration of salivary gland function.

Highlights

  • Chronic kidney disease (CKD) is a multi-symptomatic syndrome resulting from a reduction in the number of active nephrons

  • In our earlier studies we have shown that oxidative stress in CKD children affects the kidneys and the oral cavity [3,22,23]

  • Hyposalivation was observed in all patients with severe renal failure (4–5 stage CKD), while saliva secretion >0.2 mL/min in children with mild-moderate CKD (1–3 stage) and controls

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Summary

Introduction

Chronic kidney disease (CKD) is a multi-symptomatic syndrome resulting from a reduction in the number of active nephrons. The most common causes of CKD in children are urological defects, glomerulopathies, congenital nephropathies, and kidney dysplasia [2,3]. Their effect is the reduction of active nephrons, leading to intraglomerular hypertension in the remaining nephrons and their hypertrophy. CKD complications can affect just about every organ [1] These include cardiovascular disease (hypertrophy of the left ventricle, coronary heart disease), respiratory system (pulmonary edema, “uremic lung”), endocrine disorders (glucose intolerance, dyslipidemia), hematological (normochromic anemia, hemorrhagic diathesis) or mineral and bone disorders (vitamin D deficiency, hypoparathyroidism) [1,4]. In the CKD pathogenesis, the key role of oxidative stress has recently been stressed [5,6,7]

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