Chronic recurrent dehydration associated with periodic water intake exacerbates hypertension and promotes renal damage in male spontaneously hypertensive rats
Chronic recurrent dehydration associated with periodic water intake exacerbates hypertension and promotes renal damage in male spontaneously hypertensive rats
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DOI：
10.1038/srep33855
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发表时间：
2016-09-22
影响因子：
4.6
通讯作者：
Denton, Kate M.
中科院分区：
文献类型：
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作者：
Hilliard, Lucinda M.;Colafella, Katrina M. Mirabito;Denton, Kate M.
流行病学证据表明，周期性饮水引起的反复脱水与慢性肾脏疾病(CKD)有关。然而，对周期性摄水对慢性肾脏病进展的长期影响以及涉及的潜在机制的关注很少。因此，我们研究了反复脱水和周期性限水对雄性自发性高血压大鼠(SHR)动脉压、肾功能和形态的慢性影响。水受限自发性高血压大鼠动脉压升高，肾小球滤过率降低。这与尿液渗透压的周期性变化有关，表明反复脱水。此外，与对照组相比，水受限的自发性高血压患者表现出更大的肾脏纤维化和有利于促炎细胞因子产生的肾脏T细胞的失衡。此外，限水组的尿NGAL水平高于对照组。综上所述，我们的结果提供了重要的证据表明，与慢性周期性饮酒相关的反复脱水会加速CKD和高血压的进展，并表明在这种情况下，反复发作的急性肾损伤可能会推动肾脏炎症过程。需要进一步的研究来阐明驱动反复脱水引起的肾脏疾病进展的具体途径。
Epidemiological evidence links recurrent dehydration associated with periodic water intake with chronic kidney disease (CKD). However, minimal attention has been paid to the long-term impact of periodic water intake on the progression of CKD and underlying mechanisms involved. Therefore we investigated the chronic effects of recurrent dehydration associated with periodic water restriction on arterial pressure and kidney function and morphology in male spontaneously hypertensive rats (SHR). Arterial pressure increased and glomerular filtration rate decreased in water-restricted SHR. This was observed in association with cyclic changes in urine osmolarity, indicative of recurrent dehydration. Additionally, water-restricted SHR demonstrated greater renal fibrosis and an imbalance in favour of pro-inflammatory cytokine-producing renal T cells compared to their control counterparts. Furthermore, urinary NGAL levels were greater in water-restricted than control SHR. Taken together, our results provide significant evidence that recurrent dehydration associated with chronic periodic drinking hastens the progression of CKD and hypertension, and suggest a potential role for repetitive bouts of acute renal injury driving renal inflammatory processes in this setting. Further studies are required to elucidate the specific pathways that drive the progression of recurrent dehydration-induced kidney disease.