慢性肾脏疾病(CKD)是一种多因素病理,逐渐导致代谢功能恶化,并导致肾小球滤过不足和电解质失衡。它对公共卫生的经济影响具有挑战性。墨西哥的CKD患病率很高,与一些最常见的代谢紊乱如糖尿病和高血压密切相关。肾功能的逐渐丧失引起炎症状态和影响若干系统的内分泌改变。高血清催乳素水平与CKD进展有关,炎症,和嗅觉功能。此外,营养状况因肾功能受损而改变。卡路里和蛋白质摄入量的减少往往伴随着营养不良,在疾病的晚期阶段可能很严重。营养和嗅觉功能紧密相连,CKD患者经常抱怨嗅觉缺陷,这最终会导致食物摄入不足。CKD患者存在广泛的嗅觉缺陷,如气味辨别,identification,和检测阈值。CKD中的慢性炎症状态会损害嗅觉上皮,导致气味分子的化学检测不足。此外,认知功能的下降削弱了气味分化的能力。目前尚不清楚腹膜透析和血液透析是否能改善嗅觉缺陷,但是肾移植有很强的积极作用。在本次审查中,我们讨论由CKD引起的嗅觉缺陷是否是诱导的炎症状态的结果,高催乳素血症,或两者的组合。
Chronic kidney disease (CKD) is a multifactorial pathology that progressively leads to the deterioration of metabolic functions and results from deficient glomerular filtration and electrolyte imbalance. Its economic impact on public health is challenging. Mexico has a high prevalence of CKD that is strongly associated with some of the most common metabolic disorders like diabetes and hypertension. The gradual loss of kidney functions provokes an inflammatory state and endocrine alterations affecting several systems. High serum levels of prolactin have been associated with CKD progression, inflammation, and olfactory function. Also, the nutritional status is altered due to impaired renal function. The decrease in calorie and protein intake is often accompanied by malnutrition, which can be severe at advanced stages of the disease. Nutrition and olfactory functioning are closely interconnected, and CKD patients often complain of olfactory deficits, which ultimately can lead to deficient food intake. CKD patients present a wide range of deficits in olfaction like odor discrimination, identification, and detection threshold. The chronic inflammatory status in CKD damages the olfactory epithelium leading to deficiencies in the chemical detection of odor molecules. Additionally, the decline in cognitive functioning impairs the capacity of odor differentiation. It is not clear whether peritoneal dialysis and hemodialysis improve the olfactory deficits, but renal transplants have a strong positive effect. In the present review, we discuss whether the olfactory deficiencies caused by CKD are the result of the induced inflammatory state, the hyperprolactinemia, or a combination of both.