Abstract
BackgroundWe have previously shown that dietary iron restriction prevents the development of renal damage in a rat model of chronic kidney disease (CKD). However, iron deficiency is associated with appetite loss. In addition, calorie restriction is reported to prevent the development of end-stage renal pathology in CKD rats. Thus, the beneficial effect of iron restriction on renal damage may depend on calorie restriction. Here, we investigate the effect of pair-feeding iron restriction on renal damage in a rat model of CKD.MethodsFirst, to determine the amount of food intake, Sprague-Dawley (SD) rats were randomly given an ad libitum normal diet or an iron-restricted diet, and the food intake was measured. Second, CKD was induced by a 5/6 nephrectomy in SD rats, and CKD rats were given either a pair-feeding normal or iron-restricted diet.ResultsFood intake was reduced in the iron-restricted diet group compared to the normal diet group of SD rats for 16 weeks (mean food intake; normal diet group and iron-restricted diet group: 25 and 20 g/day, respectively). Based on the initial experiments, CKD rats received either a pair-feeding normal or iron-restricted diet (20 g/day) for 16 weeks. Importantly, pair-feeding iron restriction prevented the development of proteinuria, glomerulosclerosis, and tubulointerstitial damage in CKD rats. Interestingly, pair-feeding iron restriction attenuated renal expression of nuclear mineralocorticoid receptor in CKD rats.ConclusionsPair-feeding iron restriction affected renal damage in a rat model of CKD.
Highlights
The prevalence of chronic kidney disease (CKD) is increasing, and this public health problem can lead to cardiovascular diseases and death
Management of CKD reduces the risk of cardiovascular diseases and death, controversies exist regarding the benefits of some recommended treatment targets in CKD patients [1]
A 5/6 nephrectomy induced proteinuria in both pair-feeding normal or iron-restricted diet groups compared to the Control-PF group, while proteinuria was attenuated in the CKD-IRPF group compared to the CKD-PF group (Fig 2B)
Summary
The prevalence of chronic kidney disease (CKD) is increasing, and this public health problem can lead to cardiovascular diseases and death. Iron deposits have been detected in proximal tubules in human CKD patients and animal models of CKD [2,3,4,5]. In this regard, we have previously reported that dietary iron restriction prevents the development of renal damage and further deterioration of preexisting renal damage in a rat model of CKD [6,7]. We have previously shown that dietary iron restriction prevents the development of renal damage in a rat model of chronic kidney disease (CKD).
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