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猫饮食的营养结构管理与慢性肾病的关系研究进展

肾脏是一个用来过滤毒素的重要器官,主要的功能是排泄废物及调节水分与电解质,维持机体电解质平衡,此外还有内分泌功能。当肾脏发生病变,就可能诱发尿毒症、贫血及酸中毒等一系列严重危害机体健康的问题。慢性肾病(chronic kidney disease,CKD)是一种肾功能障碍,可导致较高的病死率和致残率[1]。CKD的发病因素复杂多样,肾小球硬化、肾间质纤维化和肾小管萎缩是CKD的主要病理基础。CKD由全身性疾病或慢性中毒所引起,如心力衰竭、原发性全身性高血压、高血压肾动脉硬化症、糖尿病、痛风、低钾血症肾病、肝硬化及慢性中毒等[2]。

患CKD的猫存在3个月以上的单侧或双侧肾脏结构和功能异常的慢性疾病,该病会造成动物永久性肾脏损伤,且不可逆[3]。猫CKD在不同年龄阶段都有可能发生[4],但常发于老龄猫[5]。CKD是持续性的疾病,临床调查显示,CKD患病率随着年龄的增加而增大,12岁以上的猫患病率高达28%[6],并且该病是造成猫死亡的主要疾病之一。在所有年龄阶段的猫中,CKD的患病率为1.0%~3.0%,且CKD严重时可发展为慢性肾衰竭(chronic renal failure,CRF)。由于CKD是一种慢性进行性疾病,一旦发病只能通过饮食营养管理和对症治疗来减缓病程进展,延长宠物寿命。猫饮食的营养结构与CKD直接相关,本文就猫饮食的营养结构管理对CKD患猫的影响及相关研究进展进行综述,以期为猫CKD的科学研究提供参考,为今后猫CKD的预防和治疗提供思路。

1 水分与猫CKD

猫是天生的肉食性动物,天生具有低口渴感,喝水的欲望低,猫的天然食物包括小型哺乳动物、鸟类和小型爬行动物等,这些食物80%的重量都是水。猫在野外猎取食物时也会摄取大量的水,所以野猫能通过捕猎获取足够的水分,也不容易得慢性肾病、尿道结石等疾病。对于家养猫,现在大多数猫都以干猫粮为主[7],干粮的含水量不会超过整体的10%。猫采食干粮易使机体长期处于慢性脱水状态,使肾脏的负担增加,因此患肾脏疾病的宠物猫越来越多[8],尤其是老年猫以及一些易患CKD的猫品种,设法让猫多饮水是预防CKD最好的方式之一。

猫作为起源于沙漠的耐旱性动物,肾脏可以浓缩尿液来保存水分,而CKD导致肾脏不能对水分进行充分的再吸收,所以患有CKD的猫更容易脱水[9]。由于猫习惯从食物中获取水分,而不是额外喝水,所以患有CKD的猫也应该尽可能采用湿性饮食而不是干性饮食,在猫充分进食的基础上应尽量饲喂含水量高的食物,可以大大增加水的摄入量[10]。

因此,猫CKD的预防和治疗都需要让猫保持充分的水分摄入。让猫多喝水能降低猫因缺水而生病的概率,可以在日常管理中常换新鲜水,多个地点摆放水,以及在饮食中增加罐头、生骨肉等湿粮的饲喂频率。

2 蛋白质与猫CKD

蛋白质进入身体转化为能量的过程会产生含氮废物氨,这一有潜在毒性的废物由肾脏负责过滤,经尿液排出,因此许多宠物主人和医生对“高蛋白质会造成肾脏负担”这一概念深信不疑。猫蛋白质需求是通过氮平衡试验研究的,即氮的丢失与摄入是平衡的。对于健康猫,基于干物质计算饲粮的粗蛋白质含量,美国饲料管理协会(AAFCO)建议生长期或繁殖期的猫饲粮中粗蛋白质含量最低为30%,成年期最低为26%。摄入蛋白质的种类和数量是否是发生肾脏疾病的危险因素在过去的一个世纪有很大争议。但对于健康的猫而言,高蛋白质可以诱发猫肾脏疾病的假设并没有科学依据,食用高蛋白质饮食并不会对健康的宠物肾脏产生负面效果[11]。并且研究表明,年龄较大(>13岁)的猫能量需求可能会增加,严重的蛋白质限制可能会导致肌肉组织的丧失;所以健康猫预防CKD不是限制猫饮食中蛋白质的含量,而是要根据猫实际年龄阶段和身体需求给予适量高品质的蛋白质[12]。对于患有CKD的猫,有动物模型显示低蛋白质摄入量会导致入球小动脉的收缩,降低肾小球内压力;而高蛋白质饮食会扩张入球小动脉,增加肾小球内压力。而长时间的肾小球高滤过会损伤残余肾功能[13]。因此,低蛋白质饮食可以通过影响肾素对入球小动脉的调节降低肾小球内压力,减轻尿毒症相关代谢并发症和保护残存肾单位功能,延缓CKD病程,减轻症状[14]。但盲目的给患有CKD的猫减少蛋白质摄入是不可取的,CKD老年患猫对蛋白质和脂肪的消化率降低[15],这时蛋白质摄入不足可能会导致肌肉质量的大量损失,使CKD老年猫丧失大量体组织,进而增加早亡几率。猫CKD病例中,总是建议限制饮食中蛋白质含量,限制蛋白质的最初原因是减少血液中氨的产生以及肾小球性蛋白尿,控制氨的产生可以防止血氨症的出现,并且一定程度延缓尿毒症的进程。当血氨维持在安全范围内,高质量的蛋白质对病患是有益的,蛋白质的质量标准可以参考其生物学价值即“BV值”。当猫血氨指标超过80 mg/dL(28.6 mmol/L),同时肌酐指标超过2.5 mg/dL(221 μmol/L)时,控制蛋白质的摄入可以减少肾脏的负担,限制蛋白质的主要目的是为了降低血氨指标,目标是将血氨降低到60 mg/dL(21.4 mmol/L)以下[16]。猫肾脏饮食通常每100 kcal含有6~7 g蛋白质(高于成年猫建议的每100 kcal含有5 g蛋白质[17],但低于维持饮食中常见的每100 kcal含有9~10 g蛋白质)。限制蛋白质含量并不等于给予的蛋白质含量可以低于NRC的最低标准。蛋白质限制应随着肾脏机能的丧失逐步的进行[18]。

3 磷与猫CKD

磷是身体必须的重要矿物质元素之一,许多食物都含有磷,身体可以通过肾脏有效调节体内的磷水平。高膳食磷含量是包括人类在内,很多物种的死亡危险因素,在对猫的研究中,大量证据表明,过度摄入磷是成年猫患CKD的原因之一。一项持续4周的研究中,13只健康成年猫被喂食过量磷(860 mg/MJ代谢能)与喂食平衡对照组饮食的猫(5.6 g/kg DM)进行比较,结果证明,摄入过量可利用磷会导致猫肾脏损害或功能障碍[19]。另一项持续了28周的试验中,同样给成年猫喂食高磷含量,低钙磷比的食物,甚至直接出现了B超肾回声的改变,肾滤过率降低,血清肌酐浓度上升和肾结石的形成[20]。虽然高无机磷的摄入和猫CKD的因果关系尚未达成共识,但是多项试验表明,过度的摄入磷元素,可能对猫患CKD造成决定性影响。所以在猫日常饮食中严格控制磷的摄入是预防猫CKD的手段之一,成年猫的磷安全上限为2.5~3.5 g/Mcal[21]。

研究表明,如果一只猫患上了CKD,肾脏调节磷元素的能力就会逐渐丧失,所以大多数慢性肾衰猫会出现高磷血症[22],高磷血症与肾脏疾病发病风险呈正相关。减缓身体的磷负担是治疗CKD的首要目标[23]。猫如果被确诊为CKD,就需要限制食物中磷的摄入,减轻肾脏负担,并预防病情进一步发展为继发性甲状旁腺亢进及高磷酸盐血症。随着肾脏过滤磷能力的降低,CKD猫血液中的磷元素大量聚积,长此以往,就可能诱发甲状旁腺亢进。当血液中的磷不断升高,破坏钙磷平衡后,为了使得身体内钙磷比例保持平衡,甲状腺旁腺会释放激素,把骨骼中的钙质抽出以保持钙、磷比例平衡。这一结果不仅会造成猫骨骼疏松,并且分解离析出的矿物质会进一步增加肾脏的负担[24]。

饮食调整是控制磷摄入的重要手段,在猫CKD的早期就需要限制摄入相对高磷含量的食物来控制血磷水平,磷广泛存在于动物体内,尤其是骨骼和内脏的矿物质,如肉制品、奶制品和鱼都有很多的磷(

表1

)。通常,食品中磷的构成,主要由3部分组成,分别是有机磷、无机磷以及植物中含有极少部分的磷。尽管各个饲料协会规定了商业食品中磷的最低含量和钙磷比(1:1~2:1),却没有规定钙磷的上限具体是多少,包括对于有机磷与无机磷的占比的规定及信息的披露也是缺乏相关要求的,不同饲料原料制作的猫粮含磷量大不相同,如果猫粮中使用过于富含磷但廉价的原材料,如低质量肉骨粉或是大量动物内脏,这时候饲粮中磷含量则会飙升。所以,在日常管理中,CKD猫要减少高磷含量的食材,如内脏、生骨骼。

表1 磷元素和蛋白质含量简表

Table 1 Brief table of phosphorus and protein contents

项目
Items 磷
Phosphorus/
(mg/g) 蛋白质
Protein/% 蛋清 Albumen 0.15 10.90 蛋黄 Yolk 3.90 15.86 鸡肉 Chicken 1.78 17.44 瘦牛肉 Lean beef 1.92 20.85 猪里脊 Pork tenderloin 2.16 21.20 三文鱼 Salmon 2.00 19.84

如果猫是处于CKD的晚期,想要达到理想的血磷指标,靠低磷饮食远远不够,还需要使用磷元素结合剂。磷元素结合剂不仅可以进一步控制血磷,防止身体吸收太多的磷[25],中和身体各部分的磷,减低肾脏压力;还可以让没有尿毒症危险的CKD猫放心摄入一些优质、高利用率的动物蛋白质,这对整体健康非常重要,可有效避免肌肉组织萎缩、体重下降以及内源性蛋白质丧失等引起的早亡并发症。

4 维生素D与猫CKD

维生素D是犬、猫和人体内矿物质代谢最重要的调节因子之一,对矿物质的调节代谢本质上和骨骼疾病相关[26]。研究表明,CKD-矿物质和骨异常(CKD-MBD)可发生于CKD的早期阶段,且与人类、狗和猫的高死亡率相关[27⇓-29]。CKD的治疗策略旨在延缓矿物质和骨骼疾病的发生,从而避免CKD的进展。目前,在CKD患者中补充维生素D类似物已被广泛应用,以预防或减弱CKD-MBD的发展[30⇓⇓⇓⇓⇓-36]。有些研究显示,维生素D除了治疗肾性骨病以外还可以减少蛋白尿[37]。合理的活性维生素D水平对于控制继发性甲状腺旁腺素至关重要[38]。

猫在CKD过程中缺乏维生素D,同样会导致肾脏继发性甲状旁腺功能亢进症(secondary hyperparathyroidism,SHPT),这是猫CKD晚期最常见的矿物质疾病[26],肾功能下降引起1,25-二羟基-维生素D缺乏,降低胃肠道对钙的吸收。在对人的研究中,SHPT可以导致钙从骨骼中释放增加,尿钙排泄减少[39]。猫不能通过阳光照射在体内合成足够的维生素D,必需从食物中获取[40⇓-42]。对于维生素D缺乏的慢性肾衰竭患者,建议提供维生素D补充物,如钙剂和维生素D合剂。对动物有价值的维生素D一般为维生素D2和维生素D3,前者存在于一些真菌中,后者广泛存在于动物性食物中[29,38],而猫只能利用维生素D3转化[30,43]。纵观人类医学,肾病患者补充维生素D类似物已经被广泛应用,希望以后在猫CKD诊疗研究中,补充维生素D疗法能带来惊喜。基于干物质计算饲粮的维生素D含量,AAFCO建议,生长期或繁殖期含量最低为750 IU/kg,成年期含量最低为500 IU/kg,最高不超过10 000 IU/kg。健康猫可以根据日常饮食中摄入的维生素D含量决定是否额外补充富含维生素D的食物、宠物保健品等,CKD猫需要根据宠物医生根据病情设计的肾病饮食管理进行治疗,注意基于干物质计算饲粮的维生素D含量最高不超过10 000 IU/kg。

5 盐与猫CKD

高钠饮食摄入会对人体健康产生有害影响,所以对猫粮中钠含量增加或减少的潜在影响表示担忧。没有足够的数据来确定患有心脏病或肾病的猫的适当钠摄入量,此外,对健康的青年猫和老年猫的研究表明,在中长期内摄入高达740 mg/MJ代谢能的膳食钠水平,没有出现肾或心脏功能损害的迹象[44]。严重的钠限制可能会增加肾素-血管紧张素-醛固酮系统(RAAS)的激活,增加钾的排泄,这可能对CKD患者有害。盐的主要成分是氯化钠,钠、氯、钾是体液中的关键电解质,猫需要经食物摄入才能维持正常的生理机能。根据AAFCO建议,以干物质为基础计算猫饲粮中的钠含量最低为0.2%,氯含量最低为0.3%,钾含量最低为0.6%。

对人来说,长期的高盐饮食与高血压、心脏疾病、肾脏疾病、胃黏膜损伤乃至胃部肿瘤的产生都有联系。但有研究表明,对于猫而言,提高盐份摄入对猫结石有何具体影响还不确定,但结果来看得结石的几率会下降。高盐饮食有利于猫多饮水,反而减少了一些疾病的发生。患有肾病的人类饮食建议低钠,但这方面对于猫而言一直饱受争议,甚至有研究发现低盐不利于猫肾脏健康,并且会加剧猫CKD的风险[45]。研究表明,给猫吃低盐饮食会刺激醛固酮激素的分泌,会让RAAS持续活跃[46],这是一个调节体液平衡,保持电解质平衡的复杂系统,其中的醛固酮,作用之一就是保留体内的钠,排出体内的钾。RAAS长期活跃会增加肾脏负担,诱发肾损伤,让已有的肾损伤加剧。也有研究表明,提高盐摄入对减少肾病猫RAAS刺激有益,在没有出现高钠血症的前提下,猫得了CKD,增加盐的摄入也许有益[38],但CKD猫具体该摄入多少盐比较理想目前还没有答案。美国NRC猫饲养标准中的安全上限是每1 000 kcal含0.3 g钠,换算为猫粮,每千克含盐2.66~2.90 g都算是安全范围,所以对于健康猫而言,在控制量的前提下摄入盐也是预防CKD的途径之一。

6 ω-3脂肪酸与猫CKD

ω-3脂肪酸作为必需脂肪酸主要从饮食中获得,特别是鱼油,它们是健康饮食的重要组成部分,还可能对炎症和心血管疾病高风险患者具有治疗作用[47]。研究表明,CKD患者血液中的ω-3脂肪酸水平明显低于普通人群,这可能是由于食物摄入量较低以及炎症、营养物质吸收不良和代谢变化造成的[48]。有人提出,鱼油中的二十碳五烯酸(eicosapentaenoic acid,EPA)改变了类二十碳烯酸的代谢,导致血管舒张介质的产生增加,促炎性类二十碳烯酸的产生减少,这些变化有利于肾功能[49]。Valle Flores等[52]研究发现,口服补充ω-3脂肪酸可以显著降低血液透析CKD患者的炎症标志物浓度,并且能够证明,在CKD患者的日常饮食中包含天然来源或ω-3脂肪酸补充剂可以改善他们的总体状况。有试验证明,每天服用1.8 g EPA和1.2 g二十二碳六烯酸(DHA)治疗2年,对抑制肾脏疾病恶化有重要作用[51]。

脂肪酸是机体长时间运动所消耗的主要能量。猫饮食中的脂肪也是必需脂肪酸的来源[52],EPA作为鱼油的主要成分是最常见的猫饮食补剂。Plantinga等[53]研究表明,EPA的理想含量可能为200~1 000 mg。Plantinga等[54]研究表明,高浓度的ω-3脂肪酸是CKD猫的重要饮食管理,含有最高EPA脂肪酸浓度(200~1 000 mg)的饮食可能影响了CKD猫更长的生存时间。还有一研究结果[55]显示,提供给动物的饲粮中EPA+DHA含量(490 mg)与Plantinga等[53-54]的研究结果相似。

因此,健康猫为预防疾病的发生,在日常饮食中应保证必需脂肪酸的充分摄入,尤其是动物源性的必需脂肪酸,如鱼油中的多不饱和脂肪酸。对于CKD患猫,为改善患猫的生活质量并降低死亡率,ω-3补充剂也是CKD饮食治疗方案不可缺少的一部分。

7 小结

CKD作为老年猫的常见疾病,如今临床发病率越来越高,CKD的预防要从日常饲养管理做起,如让猫补充充足的水分,摄入充足的高质量蛋白质,防止摄入过量的磷,保证机体不缺乏维生素D和必需脂肪酸,保证摄入适量的盐等;除此之外,要保证每年给猫定期体检,尤其是老年猫,遵循预防大于治疗的原则,可以最大程度降低猫CKD的患病率。

CKD确诊时宠物大多已经处于病程中后期,临床上尚无治疗CKD原发病的特效药物[56]。猫CKD治疗的目标是延缓肾功能受损的过程,延长寿命,提高生活质量。目前,猫CKD的治疗集中于对症治疗和饲养管理2方面,其中饲养管理与CKD预后效果紧密相关,所以CKD的饲养管理就更加重要。猫CKD饮食管理主要包括水分、蛋白质、磷、维生素D、盐的摄入量的控制以及ω-3脂肪酸的补充。合理的饮食营养结构有助于延缓CKD病程的进展,实施管理方案的过程中宠物主人扮演了重要角色。兽医必须与宠物主人进行良好的沟通,将CKD的病程特点和预后情况向宠物主人交代清楚,根据CKD的分期进行个体化饮食管理设计,饲养管理作为CKD管理的重要组成部分会越来越引起重视,如何建立更好的饲养管理体系,改善患猫生存质量和降低死亡率是未来研究的课题。

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=2" class="main_content_center_left_zhengwen_bao_erji_title main_content_center_left_one_title" style="font-size: 16px;">{{custom_sec.title}}{{custom_sec.content}}[1]HUNTER E

,

PERCIVAL B

,

AHMAD Z

, et al. NMR-based metabolomics associated with chronic kidney disease in humans and animals:a one health perspective[J]. Molecular and Cellular Biochemistry, 2021, 476(11):4133-4137.

Chronic kidney disease (CKD) is a renal dysfunction that can lead to high rates of mortality and morbidity, particularly when coupled with late diagnosis. CKD has become a major health problem due to its challenging detection at early stages when clear symptoms are yet to be presented. Thus, CKD is likely to be identified when the substantive conditions of the disease are manifest. In order to address the development of the disease and provide necessary treatments at the initial stage, the investigation of new biomarkers and metabolites associated with early detection of CKD are needed. Identified metabolites could be used to confirm the presence of the disease, obtain information on its mechanism and facilitate the development of novel pharmaceutical treatments. Such metabolites may be detected from biofluids and tissues using a range of analytical techniques. There are a number of metabolites that have been identified by mass spectrometry at high sensitivities, whilst the detection of metabolites directly from biofluids using NMR could present a more rapid way to expand our understanding of this disease. This review is focused on NMR-based metabolomics associated with CKD in humans and animals.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[2]DENNIS J

,

DIBARTOLA S P

,

SCHENCK P A

. Canine and feline nephrology and urology[M].2nd ed. Washington,D.C.: Saunders, 2010:143-144.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[3]

王巍, 刘耀川, 高锋. 猫慢性肾病概述[J]. 动物医学进展, 2017, 38(6):98-101.

WANG W

,

LIU Y C

,

GAO F

. Overview of chronic kidney disease in cats[J]. Progress in Veterinary Medicine, 2017, 38(6):98-101. (in Chinese)

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[4]BARTGES J W

. Chronic kidney disease in dogs and cats[J]. The Veterinary Clinics of North America Small Animal Practice, 2012, 42(4):669-692.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[5]CANEY M S

. An online survey of dietary and phosphate binder practices of owners of cats with chronic kidney disease[J]. Journal of Feline Medicine and Surgery, 2017, 19(10):1040-1047.

Objectives The objective of this study was to learn about owner experiences of chronic kidney disease (CKD), focusing on use of therapeutic renal diets (TRDs) and intestinal phosphate binders (IPBs). Methods An online survey was promoted to UK-based cat owners. Results In total, 859 owners participated. Most cats (n = 620; 72.18%) had two or more clinical signs at the time of their CKD diagnosis. Most common were polydipsia (n = 462; 53.78%) and weight loss (n = 426; 49.59%). In 94 cats (10.94%) CKD was only diagnosed as a result of wellness screening. In total, 371 participants (43.19%) reported that their cat's blood pressure had been measured; 100 of these (26.95% of those where blood pressure had been measured) subsequently received anti-hypertensive medication. In total, 90.80% of all participating owners had received a recommendation to feed a TRD. Five hundred and seventy-one owners (66.47%) reported that they were feeding a TRD as a component of their cat's diet. The most common reason for not feeding a TRD was that the cat did not like it (n = 123; 59.13%). Where a veterinary recommendation to feed a TRD had been received, 564 owners (72.31%) reported feeding a TRD as a component of their cat's diet vs seven owners (7.04%) who had not received a veterinary recommendation to feed a TRD. IPBs had been recommended to 321 owners (37.81%) and for 72 owners (8.38%) the recommendation came from a source other than a veterinary professional. Where used, IPBs were commonly added to a TRD (n = 136; 49.28%) and were generally accepted within 4 weeks (n = 178; 73.86%). Conclusions and relevance Awareness of TRDs was high but much lower for IPBs. A veterinary recommendation to feed a TRD was associated with higher compliance.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[6]BARTLETT P C

,

VAN BUREN J W

,

NETERER M

, et al. Disease surveillance and referral bias in the veterinary medical database[J]. Preventive Veterinary Medicine, 2010, 94(3/4):264-271.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[7]

蔡旋, 肖长峰, 徐天翼, 等. 高蛋白饲粮对老年猫生产指标及血清生化指标的影响[J]. 中国饲料, 2018(21):27-30.

CAI X

,

XIAO C F

,

XU T Y

, et al. Effect of high protein feed on production performance and serum biochemical indexes of old cats[J]. China Feed, 2018(21):27-30. (in Chinese)

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[8]

刘佳瑞. 苏州地区猫下泌尿道综合征的流行病学调查及典型病例分析[D].硕士学位论文. 南京: 南京农业大学, 2018.

LIU J R

. Epidemiological investigation and analysis of typical cases of cat lower urinary tract syndrome in Suzhou area[D].Master's Thesis. Nanjing: Nanjing Agricultural University, 2018. (in Chinese)

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[9]BARTGES J

,

POLZIN D

. Nephrology and urology of small animals[M]. Oxford:Wiley-Blackwell, 2011.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[10]SPARKES A H

,

CANEY S

,

CHALHOUB S

, et al. ISFM consensus guidelines on the diagnosis and management of feline chronic kidney disease[J]. Journal of Feline Medicine and Surgery, 2016, 18(3):219-239.

Chronic kidney disease (CKD) is one of the most commonly diagnosed diseases in older cats. In most cats, CKD is also a progressive disease and can be accompanied by a wide range of clinical and clinicopathological changes. These ISFM Consensus Guidelines have been developed by an independent panel of clinicians and academics to provide practical advice on the diagnosis and management of this complex disease.Although CKD is a common clinical problem in cats, the manifestations of disease vary between individuals. Thus there is a need for careful and repeat evaluation of cats with CKD and adjustment of therapy according to individual needs. In addition to addressing problems arising from CKD and improving quality of life (QoL) for the patient, therapy may also target slowing the underlying progression of disease and hence prolonging life. While maintaining QoL is of paramount importance in our patients, this can be challenging when multiple therapies are indicated. In some cases it is necessary to prioritise therapy, given an understanding of what is likely to most benefit the individual patient.In preparing these Guidelines, the Panel has carefully reviewed the existing published literature, and has also graded the quality of evidence for different interventions to help to provide practical recommendations on the therapeutic options for feline CKD. This is a field of veterinary medicine that has benefited from some excellent published clinical research and further research findings will undoubtedly modify the recommendations contained in these Guidelines in the future.© The Author(s) 2016.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[11]KRONFELD D S

. Dietary management of renal senescence and failure in dogs[J]. Australian Veterinary Journal, 1994, 71(10):328-331.

The need for dietary management of renal senescence and the beginning of chronic renal failure should be evaluated in all middle-aged dogs. One survey found that 35% were overweight and 10% underweight; another that 25% were mildly azotaemic, with 5% showing slight clinical signs of chronic renal failure. Dogs in prime condition or overweight are candidates for a diet low in energy (for example 3.0-3.3 kcal/g dry matter, DM), but thin dogs need a higher caloric density (such as 4.0-4.5 kcal/g DM). Healthy older dogs need higher dietary protein than the minimum for maintenance (about 20% on a metabolisable energy basis, ME) of young mature dogs. Thin older dogs showing signs of renal insufficiency may benefit from moderate protein and near-minimal phosphorus in the diet. In dogs with chronic renal failure, clinical, haematological and biochemical responses to the combination of low protein (13-16% ME) and low phosphorus (0.4% DM) were positive in one clinical trial but not in three others. Only beneficial responses, such as less proteinuria, less renal impairment and lower mortality, have been reported for diets containing low phosphorus and moderate protein (20-31% ME). Individual dietary goals for energy, protein and phosphorus should be chosen for each middle-aged or older dog; these goals may be met by a single product or mixtures of products.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[12]LAFLAMME D P

,

HANNAH S S

. Discrepancy between use of lean body mass or nitrogen balance to determine protein requirements for adult cats[J]. Journal of Feline Medicine and Surgery, 2013, 15(8):691-697.

This study was undertaken to contrast the minimum protein intake needed to maintain nitrogen balance or lean body mass (LBM) in adult cats using a prospective evaluation of 24 adult, neutered male cats fed one to three different diets. Following a 1-month baseline period during which all cats consumed a 34% protein diet, cats were fed a 20% (LO), 26% (MOD) or 34% (HI) protein diet for 2 months. During the baseline period and following the 2-month feeding period, nitrogen balance was assessed using a 96-h complete collection of urine and feces, and LBM was assessed using dual energy X-ray absorptiometry. Weight loss increased in a linear manner with decreasing protein intake (P <0.01), despite no significant difference in calorie intake. Linear regression of the data indicated that approximately 1.5 g protein/kg (2.1 g/kg(0.75)) body weight is needed to maintain nitrogen balance, while 5.2 g protein/kg (7.8 g/kg(0.75)) body weight is needed to maintain LBM. This study provides evidence that nitrogen balance studies are inadequate for determining optimum protein requirements. Animals, including cats, can adapt to low protein intake and maintain nitrogen balance while depleting LBM. Loss of LBM and an associated reduction in protein turnover can result in compromised immune function and increased morbidity. Current Association of American Feed Control Officials (AAFCO) and National Research Council (NRC) standards for protein adequacy may not provide adequate protein to support LBM. The minimum daily protein requirement for adult cats appears to be at least 5.2 g/kg (7.8 g/kg(0.75)) body weight, well in excess of current AAFCO and NRC recommendations. Further research is needed to determine the effect, if any, of body condition, age and gender on protein requirements.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[13]CIRILLO M

,

LOMBARDI C

,

CHIRICONE D

, et al. Protein intake and kidney function in the middle-age population:contrast between cross-sectional and longitudinal data[J]. Nephrology Dialysis Transplantation, 2014, 29(9):1733-1740.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[14]

郭全付, 毛焕东, 乌新春, 等. 不同蛋白质饮食对慢性肾病患者肾功能的影响[J]. 西部医学, 2015, 27(2):190-192,195.

GUO Q F

,

MAO H D

,

WU X C

, et al. Effects of different protein diet on renal function in patients with chronic kidney disease[J]. Medical Journal of West China, 2015, 27(2):190-192,195. (in Chinese)

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[15]SCHERK M A

,

LAFLAMME D P

. Controversies in veterinary nephrology:renal diets are indicated for cats with international renal interest society chronic kidney disease stages 2 to 4:the con view[J]. The Veterinary Clinics of North America Small Animal Practice, 2016, 46(6):1067-1094.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[16]SCHENCK P

. Home-prepared dog and cat diets[M].2nd ed. Oxford: Wiley-Blackwell, 2010.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[17]

National Research Council. Nutrient requirements of dogs and cats[S]. Washington,D.C.: The National Academies Press, 2006.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[18]BARBER P

. Diagnosis and management of chronic renal failure in the cats[J]. In Practice, 2003, 25(6):306-313.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[19]DOBENECKER B

,

WEBEL A

,

KIENZLE E T

. Effect of high phosphorus intake from different sources on parameters of renal health in cats[J]. Feline Medicine and Surgery, 2018, 20(4):339-343.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[20]ALEXANDER J

,

STOCKMAN J

,

ATWAL J

, et al. Effects of the long-term feeding of diets enriched with inorganic phosphorus on the adult feline kidney and phosphorus metabolism[J]. The British Journal of Nutrition, 2019, 121(3):249-269.

Renal disease has a high incidence in cats, and some evidence implicates dietary P as well. To investigate this further, two studies in healthy adult cats were conducted. Study 1 (36 weeks) included forty-eight cats, stratified to control or test diets providing 1·2 or 4·8 g/1000 kcal (4184 kJ) P (0 or approximately 3·6 g/1000 kcal (4184 kJ) inorganic P, Ca:P 1·2, 0·6). Study 2 (29 weeks) included fifty cats, stratified to control or test diets, providing 1·3 or 3·6 g/1000 kcal (4184 kJ) P (0 or approximately 1·5 g/1000 kcal (4184 kJ) inorganic P, Ca:P 1·2, 0·9). Health markers, glomerular filtration rate (GFR) and mineral balance were measured regularly, with abdominal ultrasound. Study 1 was halted after 4 weeks as the test group GFR reduced by 0·4 (95 % CI 0·3, 0·5) ml/min per kg, and ultrasound revealed changes in renal echogenicity. In study 2, at week 28, no change in mean GFR was observed (P &gt;0·05); however, altered renal echogenicity was detected in 36 % of test cats. In agreement with previous studies, feeding a diet with Ca:P &lt;1·0, a high total and inorganic P inclusion resulted in loss of renal function and changes in echogenicity suggestive of renal pathology. Feeding a diet containing lower total and inorganic P with Ca:P close to 1·0 led to more subtle structural changes in a third of test cats; however, nephrolithiasis occurred in both diet groups, complicating data interpretation. We conclude that the no observed adverse effects level for total dietary P in adult cats is lower than 3·6 g/1000 kcal (4184 kJ), however the effect of inorganic P sources and Ca:P require further investigation.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[21]

国家学术委员会下属的国家研究委员会主编. 犬猫营养需要[M]. 丁利敏,夏兆飞,译. 北京: 中国农业大学出版社, 2010.

National Research Council of The National Academies. Nutrient requirements of dogs and cats[M].DING L M,XIA Z F,translated. Beijing: China Agricultural University Press, 2010. (in Chinese)

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[22]CRUZ SCHAEFER G

,

VIDOR S B

,

JEREMIAS J T

, et al. Clinical and nutritional follow-up of cats with chronic kidney disease fed with a renal prescription diet[J]. Acta Scientiae Veterinariae, 2021, 49:1801.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[23]PARKER V J

. Nutritional management for dogs and cats with chronic kidney disease[J]. The Veterinary Clinics of North America:Small Animal Practice, 2021, 51(3):685-710.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[24]ETTINGER S J

,

FELDMAN E C

. Textbook of veterinary internal medicine[M].[S.l.]: Elsevier Science Health Science div, 1983.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[25]

张丁心, 陈利群. 新型磷结合剂在慢性肾脏病高磷血症治疗中的应用研究进展[J]. 中国现代医药杂志, 2021, 23(1):104-108.

ZHANG D X

,

CHEN L Q

. Application of new phosphorus binding agent in the treatment of hyperphosphatemia in chronic kidney disease[J]. Modern Medicine Journal of China, 2021, 23(1):104-108. (in Chinese)

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[26]CHACAR F C

,

KOGIKA M M

,

ZAFALON R V A

, et al. Vitamin D metabolism and its role in mineral and bone disorders in chronic kidney disease in humans,dogs and cats[J]. Metabolites, 2020, 10(12):499.

Some differences regarding Vitamin D metabolism are described in dogs and cats in comparison with humans, which may be explained by an evolutionary drive among these species. Similarly, vitamin D is one of the most important regulators of mineral metabolism in dogs and cats, as well as in humans. Mineral metabolism is intrinsically related to bone metabolism, thus disturbances in vitamin D have been implicated in the development of chronic kidney disease mineral and bone disorders (CKD-MBD) in people, in addition to dogs and cats. Vitamin D deficiency may be associated with Renal Secondary Hyperparathyroidism (RSHPT), which is the most common mineral disorder in later stages of CKD in dogs and cats. Herein, we review the peculiarities of vitamin D metabolism in these species in comparison with humans, and the role of vitamin D disturbances in the development of CKD-MBD among dogs, cats, and people. Comparative studies may offer some evidence to help further research about vitamin D metabolism and bone disorders in CKD.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[27]ISAKOVA T

,

WAHL P

,

VARGAS G S

, et al. Fibroblast growth factor 23 is elevated before parathyroid hormone and phosphate in chronic kidney disease[J]. Kidney International, 2011, 79(12):1370-1378.

Fibroblast growth factor 23 (FGF23) regulates phosphorus metabolism and is a strong predictor of mortality in dialysis patients. FGF23 is thought to be an early biomarker of disordered phosphorus metabolism in the initial stages of chronic kidney disease (CKD). We measured FGF23 in baseline samples from 3879 patients in the Chronic Renal Insufficiency Cohort study, which is a diverse cohort of patients with CKD stage 2-4. Mean serum phosphate and median parathyroid hormone (PTH) levels were in the normal range, but median FGF23 was markedly greater than in healthy populations, and increased significantly with decreasing estimated glomerular filtration rate (eGFR). High levels of FGF23, defined as being above 100 RU/ml, were more common than secondary hyperparathyroidism and hyperphosphatemia in all strata of eGFR. The threshold of eGFR at which the slope of FGF23 increased was significantly higher than the corresponding threshold for PTH based on non-overlapping 95% confidence intervals. Thus, increased FGF23 is a common manifestation of CKD that develops earlier than increased phosphate or PTH. Hence, FGF23 measurements may be a sensitive early biomarker of disordered phosphorus metabolism in patients with CKD and normal serum phosphate levels.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[28]FINCH N C

,

GEDDES R F

,

SYME H M

, et al. Fibroblast growth factor 23 (FGF-23) concentrations in cats with early nonazotemic chronic kidney disease (CKD) and in healthy geriatric cats[J]. Journal of Veterinary Internal Medicine, 2013, 27(2):227-233.

Fibroblast growth factor (FGF-23) has an important role in phosphate regulation. Its clinical relevance in cats with CKD has not been explored previously.The study objectives were (1) to determine whether FGF-23 concentrations are increased in nonazotemic cats, cats which developed azotemia within 12 months of screening compared with cats that remained non-azotemic, and (2) to evaluate the relationships between FGF-23 and PTH and FGF-23 and glomerular filtration rate (GFR).Sixty-two healthy client-owned geriatric cats, 14 of which developed azotemia during the 12-month follow-up period.Healthy nonazotemic cats were recruited prospectively into the study and followed for 12 months. At the study end-point, cats were categorized into 3 groups according to plasma creatinine concentration. PTH, FGF-23, and additional biochemical variables were evaluated at baseline and after 12 months. GFR was measured by a corrected slope-intercept iohexol clearance method.FGF-23 concentrations at baseline were found to be significantly increased in cats that developed azotemia (P = .001) compared with cats that did not develop azotemia. A significant positive relationship was identified between FGF-23 and PTH, whereas the relationship between FGF-23 and GFR was negative.FGF-23 concentrations predicted development of azotemia in geriatric cats. Positive relationships between FGF-23 and PTH suggest an association between FGF-23 and renal secondary hyperparathyroidism.Copyright © 2013 by the American College of Veterinary Internal Medicine.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[29]PARKER V J

,

HARJES L M

,

DEMBEK K

, et al. Association of vitamin D metabolites with parathyroid hormone,fibroblast growth factor-23,calcium,and phosphorus in dogs with various stages of chronic kidney disease[J]. Journal of Veterinary Internal Medicine, 2017, 31(3):791-798.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[30]SALUSKY I B

. Are new vitamin D analogues in renal bone disease superior to calcitriol?[J]. Pediatric Nephrology, 2005, 20(3):393-398.

Progression of chronic kidney disease is associated with an early reduction in serum calcitriol levels; thus, therapy with calcitriol should be initiated early in the course of chronic kidney disease to prevent the development of secondary hyperparathyroidism. Initial studies demonstrated a potential role of calcitriol in the prevention of growth retardation in children with chronic kidney disease prior to dialysis. But the optimal parathyroid hormone (PTH) levels that will maximize growth response during calcitriol treatment remain to be defined. Therapy with calcitriol has been shown to control the biochemical and skeletal manifestations of secondary hyperparathyroidism, but patients developed hypercalcemia, hyperphosphatemia and adynamic osteodystrophy. Thus, new vitamin D analogues with a lower hypercalcemic response have been developed. Although comparative studies are lacking, current evidence indicates that these new active vitamin D sterols (19-nor-paracalcitol and doxercalciferol) adequately control secondary hyperparathyroidism with minimal changes in serum calcium and phosphorus levels during treatment with calcium-containing binders. The long-term effect of such therapies on the skeleton and the process of vascular calcifications remain to be evaluated.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[31]KOVESDY C P

,

AHMADZADEH S

,

ANDERSON J E

, et al. Association of activated vitamin D treatment and mortality in chronic kidney disease[J]. Archives of Internal Medicine, 2008, 168(4):397-403.

Treatment of secondary hyperparathyroidism (SHPT) with activated vitamin D analogues is associated with better survival in patients receiving dialysis. It is unclear whether such a benefit is present in patients with predialysis chronic kidney disease (CKD).We examined the association of oral calcitriol treatment with mortality and the incidence of dialysis in 520 male US veterans (mean [SD] age, 69.8 [10.3] years; 23.5% black) with CKD stages 3 to 5 and not yet receiving dialysis (mean [SD] estimated glomerular filtration rate, 30.8 [11.3]). Associations were examined by the Kaplan-Meier method and in Poisson regression models with adjustment for age, race, comorbidities, smoking, blood pressure, body mass index, use of phosphate binders, estimated glomerular filtration rate, proteinuria, white blood cell count, percentage of lymphocytes, and levels of parathyroid hormone, calcium, phosphorus, albumin, bicarbonate, and hemoglobin.Two hundred fifty-eight of 520 subjects received treatment with calcitriol, 0.25 to 0.5 microg/d, for a median duration of 2.1 years (range, 0.06-6.0 years). The incidence rate ratios for mortality and combined death and dialysis initiation were significantly lower in treated vs untreated patients (P <.001 for both in the fully adjusted models). Treatment with calcitriol was associated with a trend toward a lower incidence of dialysis. These results were consistent across different subgroups.Treatment with the activated vitamin D analogue calcitriol appears to be associated with significantly greater survival in patients with CKD not yet receiving dialysis. Randomized clinical trials are required to verify the causality of these associations and to examine whether similar associations are seen with different activated vitamin D analogues.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[32]PALMER S C

,

MCGREGOR D O

,

MACASKILL P

, et al. Meta-analysis:vitamin D compounds in chronic kidney disease[J]. Annals of Internal Medicine, 2007, 147(12):840-853.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[33]CUNNINGHAM J

. New vitamin D analogues for osteodystrophy in chronic kidney disease[J]. Pediatric Nephrology, 2004, 19(7):705-708.

Vitamin D therapy for patients with chronic kidney disease has until recently comprised alfacalcidol or calcitriol, both of which effectively attenuate secondary hyperparathyroidism and the target organ consequences thereof. Unfortunately, both these agents also have significant calcaemic and phosphataemic actions leading to frequent episodes of hypercalcaemia, hyperphosphataemia and an increase in the CaxP product. It is likely that these in turn have adverse effects on cardiovascular and survival outcomes by promoting soft tissue and vascular calcification. These drawbacks have fuelled a search for vitamin D compounds with a wider therapeutic window. Experimentally, some of these have exhibited remarkable dissociation between their ability to suppress parathyroid hormone (PTH) and concomitant calcaemic actions. In the case of 22-oxacalcitriol, the calcaemic potency relative to parathyroid suppression is 100th of that of calcitriol. 22-oxacalcitriol, with paricalcitol and doxercalciferol, are now widely used. Clinical studies of these agents, while confirming efficacy that is at least as good as alfacalcidol/calcitriol, have not consistently shown benefit in head to head comparison. Experience with these agents in the paediatric arena is very limited. One placebo-controlled study has now been completed in children-paricalcitol appeared effective and well tolerated. Calcimimetics, which simultaneously lower PTH, calcium and the CaxP product are about to enter the clinical arena-early studies in adults look promising, although they will need careful evaluation in children. These two therapies are likely to be additive and will probably complement one another effectively.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[34]LEVIN A

,

LI Y C

. Vitamin D and its analogues:do they protect against cardiovascular disease in patients with kidney disease?[J]. Kidney International, 2005, 68(5):1973-1981.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[35]ZHENG Z F

,

SHI H L

,

JIA J Y

, et al. Vitamin D supplementation and mortality risk in chronic kidney disease:a Meta-analysis of 20 observational studies[J]. BMC Nephrology, 2013, 14:199.

Vitamin D insufficiency correlates with mortality risk among patients with chronic kidney disease (CKD). The survival benefits of active vitamin D treatment have been assessed in patients with CKD not requiring dialysis and in patients with end stage renal disease (ESRD) requiring dialysis.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[36]BHAN I

,

THADHANI R

. Vitamin D therapy for chronic kidney disease[J]. Seminars in Nephrology, 2009, 29(1):85-93.

Vitamin D has played a central role in the nephrologist's armamentarium, with active vitamin D analogues enjoying broad use for treatment of secondary hyperparathyroidism. Increasing data are now coming to light about the broader biological actions of vitamin D, including wide-ranging effects in several endocrine pathways, cardiovascular disease, infectious disease, and even the progression of chronic kidney disease (CKD). As additional agents are emerging to help with control of metabolic bone disease, these nontraditional pathways of vitamin D action will become increasingly important to consider when formulating a treatment plan. Although the only approved use for vitamin D analogues in CKD is the treatment of secondary hyperparathyroidism, well-conducted clinical trials may soon broaden the scope of this therapy. This article reviews the role of vitamin D therapy in CKD and looks to the answers that future research may bring.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[37]WU C C

,

LIAO M T

,

HSIAO P J

, et al. Antiproteinuria effect of calcitriol in patients with chronic kidney disease and vitamin D deficiency:a randomized controlled study[J]. Journal of Renal Nutrition, 2020, 30(3):200-207.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[38]KETTELER M

,

BLOCK G A

,

EVENEPOEL P

, et al. Executive summary of the 2017 KDIGO chronic kidney disease-mineral and bone disorder (CKD-MBD) guideline update:what's changed and why it matters[J]. Kidney International, 2017, 92(1):26-36.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[39]SPIEGEL D M

,

BRADY K

. Calcium balance in normal individuals and in patients with chronic kidney disease on low- and high-calcium diets[J]. Kidney International, 2012, 81(11):1116-1122.

Calcium balance in chronic kidney disease is poorly understood as calcium deficiency is a stimulus for secondary hyperparathyroidism and consequent bone loss while calcium excess promotes extraosseous calcifications. To help resolve this, we evaluated calcium balance in normal individuals and in patients with chronic kidney disease (CKD) on daily diets containing 800 and 2000 mg elemental calcium. Both normal individuals and patients with late stage 3 and stage 4 CKD were in slightly negative to neutral calcium balance on the 800-mg calcium diet. Normal individuals were in modest positive calcium balance on the 2000-mg diet, while patients with CKD on the same diet were in marked positive calcium balance at least over the 9 days of study; and significantly greater than the normal individuals. Increased calcium intake significantly decreased 1,25-dihydroxy-vitamin D and intact parathyroid hormone levels but did not alter the serum calcium concentration. Thus, our findings have important implications for both preventing calcium deficiency and loading in individuals with late stage 3 and stage 4 CKD.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[40]HOW K L

,

HAZEWINKEL H A

,

MOL J A

. Dietary vitamin D dependence of cat and dog due to inadequate cutaneous synthesis of vitamin D[J]. General and Comparative Endocrinology, 1994, 96(1):12-18.

As in herbivores and omnivores, the biosynthesis of vitamin D3 in the skin exposed to ultraviolet (uv) light is generally expected to also occur in the dog and the cat. The purpose of this in vitro study was to measure the concentrations of vitamin D3 and its precursor 7-dehydrocholesterol (7DHC) in dog and cat skin before and after a quantitatively and qualitatively standardized exposure to uv light. The results are compared to those obtained by the same method in the skin of the rat. The efficiency of extracting 7DHC and vitamin D3 from skin was 72 +/- 8% and 67 +/- 3%, respectively. In dog and cat skin the concentrations of nonesterified 7DHC were below the detection limit of the HPLC system. Therefore, skin extracts were saponified and total 7DHC and vitamin D3 concentrations were measured by normal-phase HPLC. Before irradiation with uv-B light the total concentrations of 7DHC were 1858 +/- 183, 1958 +/- 204, and 17,620 +/- 2345 ng/cm2 skin (mean +/- SEM; n = 5) for the dog, the cat, and the rat, respectively. The corresponding concentrations of vitamin D3 were 211 +/- 44, 193 +/- 18, and 161 +/- 32 ng/cm2 skin for the dog, the cat, and the rat, respectively. Irradiation of standard solutions of 7DHC with 0.15 J uv-B light/min resulted in a time-dependent decrease in 7DHC and a concomitant increase in previtamin D3.(ABSTRACT TRUNCATED AT 250 WORDS)

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[41]MORRIS J G

. Ineffective vitamin D synthesis in cats is reversed by an inhibitor of 7-dehydrocholestrol-Δ7-reductase1,2[J]. The Journal of Nutrition, 1999, 129(4):903-908.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[42]CORBEE R J

,

VAANDRAGER A B

,

KIK M J

, et al. Cutaneous vitamin D synthesis in carnivorous species[J]. Veterinary Medicine Research, 2015, 2(4):1031.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[43]MORRIS J G

. Cats discriminate between cholecalciferol and ergocalciferol[J]. Journal of Animal Physiology and Animal Nutrition, 2002, 86(7/8):229-238.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[44]NGUYEN P

,

REYNOLDS B

,

ZENTEK J

, et al. Sodium in feline nutrition[J]. Journal of Animal Physiology and Animal Nutrition, 2017, 101(3):403-420.

High sodium levels in cat food have been controversial for a long time. Nonetheless, high sodium levels are used to enhance water intake and urine volume, with the main objective of reducing the risk of urolithiasis. This article is a review of current evidence of the putative risks and benefits of high dietary sodium levels. Its secondary aim is to report a possible safe upper limit (SUL) for sodium intake. The first part of the manuscript is dedicated to sodium physiology, with a focus on the mechanisms of sodium homeostasis. In this respect, there is only few information regarding possible interactions with other minerals. Next, the authors address how sodium intake affects sodium balance; knowledge of these effects is critical to establish recommendations for sodium feed content. The authors then review the consequences of changes in sodium intake on feline health, including urolithiasis, blood pressure changes, cardiovascular alterations and kidney disease. According to recent, long-term studies, there is no evidence of any deleterious effect of dietary sodium levels as high as 740 mg/MJ metabolizable energy, which can therefore be considered the SUL based on current knowledge.Journal of Animal Physiology and Animal Nutrition © 2016 Blackwell Verlag GmbH.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[45]HUGHES K L

,

SLATER M R

,

GELLER S

, et al. Diet and lifestyle variables as risk factors for chronic renal failure in pet cats[J]. Preventive Veterinary Medicine, 2002, 55(1):1-15.

A case-control study examining diet and lifestyle variables to generate hypotheses of potential risk factors for chronic renal failure in pet cats was conducted in five private practices in Texas, USA and at the Texas A&M University Veterinary Medical Teaching Hospital. A telephone questionnaire was used to gather information from owners of 38 cats newly diagnosed with CRF between December 1994 and 1995 and from owners of 56 control cats. Factor analysis was used to determine whether composite variables should be constructed to summarize the nutritional predictors adequately. The composite variables and other lifestyle variables were analyzed with logistic-regression. Three final exploratory models were developed: ad libitum feeding with fiber; ad libitum with Factor-2 (a composite variable composed of fiber, magnesium, protein, sodium and ash); and fiber alone. Ad libitum feeding and increased ash intake were associated with increased odds of CRF; increased dietary fiber, magnesium, protein and sodium were associated with decreased odds of CRF.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[46]MITANI S

,

YABUKI A

,

TANIGUCHI K

, et al. Association between the intrarenal renin-angiotensin system and renal injury in chronic kidney disease of dogs and Cats[J]. The Journal of Veterinary Medical Science, 2013, 75(2):127-133.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[47]ABDELHAMID A S

,

BROWN T J

,

BRAINARD J S

, et al. Omegafatty acids for the primary and secondary prevention of cardiovascular disease[J]. Cohrane Database of Systematic Reviews, 2018, 7(7):CD003177.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[48]RASIC-MILUTINOVIC Z

,

PERUNICIC G

,

PLJESA S

, et al. Effects of N-3 PUFAs supplementation on insulin resistance and inflammatory biomarkers in hemodialysis patients[J]. Renal Failure, 2007, 29(3):321-329.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[49]BARCELLI U

,

POLLAK V E

. Is there a role for polyunsaturated fatty acids in the prevention of renal disease and renal failure?[J]. Nephron, 1985, 41(3):209-212.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[50]VALLE FLORES J A

,

FARIÑO CORTÉZ J E

,

MAYNER TRESOL G A

, et al. Oral supplementation with omega-3 fatty acids and inflammation markers in patients with chronic kidney disease in hemodialysis[J]. Applied Physiology Nutrition, and Metabolism, 2020, 45(8):805-811.

Chronic kidney disease (CKD) is an increasingly common public health problem that increases the risk of death because of cardiovascular complications by 2–3 times compared with the general population. This research concerns a prospective, randomized, double-blind study in patients with CKD undergoing hemodialysis. The participants were assigned to 1 of 2 groups: the study group (group A; 46 patients) received 4 capsules (2.4 g) of omega-3 fatty acids daily during the 12-week intervention, while patients in the control group (group B; 47 patients) received 4 capsules of paraffin oil. The patients’ general characteristics, nutritional indicators, renal disease markers and inflammatory markers (C-reactive protein, interleukin (IL)-6, IL-10, and tumour necrosis factor alpha (TNF-α)) were evaluated. No differences were found between the general characteristics of the patients (P &lt; 0.05), and no differences were shown in the nutritional indicators and markers of kidney disease (P &lt; 0.05). Patients in group A showed significant decreases in levels of C-reactive protein, IL-6, TNF-α, and the IL-10/IL-6 ratio after 12 weeks of supplementation (P &lt; 0.05). Patients in group B did not show any significant changes in concentrations of inflammatory markers during the intervention (P &lt; 0.05). In conclusion, oral supplementation with omega-3 fatty acids produces a significant decrease in the concentrations of inflammation markers in patients with chronic kidney disease on hemodialysis.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[51]DONADIO J V

,

GRANDE J P

. The role of fish oil/omega-3 fatty acids in the treatment of IgA nephropathy[J]. Seminars in Nephrology, 2004, 24(3):225-243.

Beneficial effects of omega-3 polyunsaturated fatty acids (n-3 PUFA) have been reported in recent epidemiologic studies and randomized clinical trials in a variety of cardiovascular and autoimmune diseases. Fish and marine oils are the most abundant and convenient sources of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), the two major n-3 fatty acids that serve as substrates for cyclooxygenase and lipoxygenase pathways leading to less potent inflammatory mediators than those produced through the n-6 PUFA substrate, arachidonic acid. N-3 PUFA can also suppress inflammatory and/or immunologic responses through eicosanoid-independent mechanisms. Although the pathophysiology of IgA nephropathy is incompletely understood, it is likely that n-3 PUFA prevents renal disease progression by interfering with a number of effector pathways triggered by mesangial immune-complex deposition. In addition, potential targets of n-3 PUFA relevant to renal disease progression could be similar to those involved in preventing the development and progression of cardiovascular disease by lowering blood pressure, reducing serum lipid levels, decreasing vascular resistance, or preventing thrombosis. In IgA nephropathy, efficacy of n-3 PUFA contained in fish oil supplements has been tested with varying results. The largest randomized clinical trial performed by our collaborative group provided strong evidence that treatment for 2 years with a daily dose of 1.8 g of EPA and 1.2 g of DHA slowed the progression of renal disease in high-risk patients. These benefits persisted after 6.4 years of follow up. With safety, composition, and dosing convenience in mind, we can recommend two products that are available as pharmaceutical-grade fish-oil concentrates, Omacor (Pronova Biocare, Oslo, Norway) and Coromega (European Reference Botanical Laboratories, Carlsbad, CA).

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[52]

李乐毅. 犬、猫营养素的研究进展[J]. 现代畜牧兽医, 2021(9):80-83.

LI L Y

. Research progress on nutrients for dogs and cats[J]. Modern Journal of Animal Husbandry and Veterinary Medicine, 2021(9):80-83. (in Chinese)

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[53]PLANTINGA E A

,

BEYNEN A C

. Comparative analysis of commercial renal diets for cats,with emphasis on their fatty acid composition[J]. Tijdschrift voor Diergeneeskunde, 2004, 129:656-662.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[54]PLANTINGA E A

,

EVERTS H

,

KASTELEIN A M C

, et al. Retrospective study of the survival of Cats with acquired chronic renal insufficiency offered different commercial diets[J]. Veterinary Record, 2005, 157(7):185-187.

A retrospective study was carried out on the efficacy of seven commercial diets designed to be fed to cats with chronic renal failure. The median survival time of 175 cats that received conventional diets was seven months, whereas the median survival time of 146 cats given one of the seven diets was 16 months. The cats on the most effective of the diets had a median survival time of 23 months and those on the least effective diet had a median survival time of 12 months. The composition of the seven diets was comparable, except that the most effective diet had a particularly high content of eicosapentaenoic acid.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[55]CHEW D J

. Chronic kidney disease (CKD) in dogs&cats-staging and management strategies[C]// 2015 Virginia Veterinary Conference. Virginia: Virginia Veterinary Medical Association, 2015.

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}[56]

何振欢, 肖建华. 犬、猫慢性肾病研究进展[J]. 黑龙江畜牧兽医, 2021(13):41-45.

HE Z H

,

XIAO J H

. Progress of chronic kidney disease in dogs and cats[J]. Heilongjiang Animal Science and Veterinary Medicine, 2021(13):41-45. (in Chinese)

{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}{{custom_ref.label}}{{custom_citation.content}}https://doi.org/{{custom_citation.doi}}https://www.ncbi.nlm.nih.gov/pubmed/{{custom_citation.pmid}}{{custom_citation.url}}本文引用 [{{custom_ref.citedCount}}]摘要{{custom_citation.annotation}}

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网址: 猫饮食的营养结构管理与慢性肾病的关系研究进展 https://m.mcbbbk.com/newsview359457.html

所属分类:萌宠日常
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