♦ โรคไต; สาเหตุและการป้องกันและการรักษาที่เป็นไปได้
ไตมีหน้าที่ควบคุมของเหลวในร่างกายหลายประการ
ไตทำหน้าที่ในการกำจัดสารพิษ ควบคุมความสมดุลของกรด-ด่าง ควบคุมปริมาตรของของเหลวในร่างกายและความเข้มข้นของอิเล็กโทรไลต์ต่างๆ
สารพิษที่ขับออกจากไต ได้แก่ กรดยูริก ครีเอตินีน ไฮโดรเจน โพแทสเซียม แอมโมเนียม เป็นต้น
♦ อาการของโรคไต:
- โรคโลหิตจาง
- โรคไขมันอุดตันในหลอด
- สมาธิลดลง
- อาการบวมน้ำ (ของเหลวสะสมในขา ข้อเท้า ฯลฯ)
- ความเหนื่อยล้า
- ความดันโลหิตสูง
- นอนไม่หลับ
- กล้ามเนื้อเป็นตะคริว
- คลื่นไส้/อาเจียน
- ปอดบวมน้ำ (ของเหลวในปอด)
- หย่อนสมรรถภาพทางเพศ
- ฯลฯ
ระยะของโรค | eGFR* | คำอธิบาย |
---|---|---|
ระยะที่ 1 | >90 | การทำงานของไตปกติ ไตทำงานปกติ |
ระยะที่ 2 | 60 - 89 | ความผิดปกติของไตเล็กน้อย ไตยังทำงานอย่างเพียงพอ |
ระยะที่ 3a | 45 - 59 | ความผิดปกติของไตปานกลาง ไตแสดงอาการผิดปกติ |
ระยะที่ 3b | 30 - 44 | ความผิดปกติของไตในระดับปานกลางถึงรุนแรง ไตแสดงอาการผิดปกติมากขึ้น |
ระยะที่ 4 | 15 - 29 | ความผิดปกติของไตอย่างรุนแรง ไตทำงานเพียงเล็กน้อยเท่านั้น |
ระยะที่ 5 | <15 | ระยะสุดท้ายที่มีความผิดปกติรุนแรงที่สุด ภาวะไตเกือบวายทั้งหมด หรือ ภาวะไตวายทั้งหมด |
* อัตราการทำงานของไต โดยประมาณ
♦ สาเหตุของโรคไตมีมากมาย แต่สาเหตุหลักมาจากปัจจัยด้านอาหาร สารพิษในสิ่งแวดล้อม และสารพิษที่กินเข้าไป:
- ยารักษาโรค: NSAIDs (ยาต้านการอักเสบที่ไม่ใช่สเตียรอยด์) [1][2] สแตติน [3][16] รวมถึง:
อะเซตามิโนเฟน, แอสไพริน, ยาลดอักเสบที่ไม่ใช่สเตียรอยด์, ยากล่อมประสาท / ยาควบคุมอารมณ์ให้คงที่, ยาแก้แพ้, ยาต้านจุลชีพ, ยาต้านไวรัส, ยาเกี่ยวกับหัวใจและหลอดเลือด, เคมีบำบัด, ยาขับปัสสาวะ, เมทแอมเฟตามีน ฯลฯ
ยาทางเภสัชวิทยาทั้งหลาย แทบทั้งหมด ได้พิสูจน์แล้วว่า เพื่อระงับอาการ หรือกดอาการไว้ แต่ผลเสียหรือผลข้างเคียงที่จะเกิดขึ้นคือ ยาหรือสารเหล่านี้มีความเป็นพิษต่ออวัยวะทุกส่วนในระดับต่างๆ
(• สารเหล่านี้ ซึ่งรวมถึงยาแทบทุกชนิดอื่นๆ ได้รับการพิสูจน์แล้วว่าเป็นกลุ่มยาสังเคราะห์ทางเคมีที่เรียกว่า 'ยา Allopathic' สร้างขึ้นบนพื้นฐานของแรงจูงใจในการทำกำไร และเพียงเพื่อแค่ระงับหรือ 'จัดการ' อาการ โดยไม่คำนึงถึงผลข้างเคียงที่จะเกิดขึ้น และการสะสมผลข้างเคียงนั้นเนื่องจากการที่ต้องพึ่งสารระงับอาการมาตลอด ส่งผลให้อวัยวะเกิดความเสียสภาพ จนในที่สุดรุนแรงมากขึ้นจนถึงตายได้ การรักษาดังกล่าวจึงไม่ได้ขึ้นอยู่กับการรักษาที่แท้จริง และไม่ใช่การรักษาบนสาเหตุพื้นฐานที่แท้จริงแต่อย่างใดเลย)[21] Death by Medicine; Dr. Gary Null, PhD - อาหารที่มีโปรตีนสูงจากสัตว์: เนื้อสัตว์ ไก่ ชีส ฯลฯ ที่ทำให้ไตมีกรดยูริกมากเกินไปซึ่งจำเป็นต้องขับออก [5][6][14]
- สารพิษจากสิ่งแวดล้อม: ไกลโฟเสต [4][19], พาราควอต [11], สารกำจัดวัชพืช, ยาฆ่าแมลง, ยาย้อมผม [10]
- ผลิตภัณฑ์อาหารดัดแปลงพันธุกรรม(GMO FOOD):[/b] [4]
- ฟลูออไรด์ในน้ำดื่ม: [20]
- อาหารไขมันสูง [14]
- โทรศัพท์มือถือ Wi-Fi EMR( รังสีแม่เหล็กไฟฟ้า): [12][15]
- โมโนโซเดียมกลูตาเมต, ผงชูรส: [13]
- เกลือ; การบริโภคที่มากเกินไป: [7]
- น้ำตาลหรือโซดารสหวาน/น้ำอัดลม เครื่องดื่มที่มีน้ำตาลเป็นส่วนประกอบทั้งหลาย: [8]
- อาหารสไตล์ตะวันตก: [17][18]
♦ ต่อไปนี้คือแนวทางป้องกันและรักษาโรคไตที่เป็นไปได้ตามที่เห็นในการศึกษาอ้างอิง
- เคอร์คูมิน (ขมิ้น) [d][q][z] ♦ ดูแท็บขมิ้นชันด้วย!
- ขิง [e]
- ชาเขียว [f][n] ♦ ดูแท็บชาเขียวด้วย!
- Honokiol (ลิกแนนที่แยกได้จากเปลือก เมล็ด โคน และใบของแมกโนเลีย ดีลบาตา) [o]
- Kefir (เปปไทด์) [s]
- เห็ดหลินจือ [y]
- เมลาโทนิน (หาได้จากเชอร์รี่, โกจิ, ปลา, ถั่ว) [w] [g]
- ไนอาซิน [h]
- กรดไขมันโอเมก้า-3 [j]
- โอโซนบำบัด [cc]
- น้ำทับทิม [p]
- โปรแอนโธไซยานิดิน (โพลีฟีนอล/แทนนินที่พบในเมล็ดองุ่น แครนเบอร์รี่ บลูเบอร์รี่) [k]
- เควอซิทิน (ฟลาโวนอลจากพืชที่พบในผลไม้ ผัก ใบไม้ เมล็ดพืช ธัญพืช เคเปอร์ หอมแดง คะน้า ฯลฯ) [l][q]
- เรสเวอราทรอล [t] ♦ ดูที่แท็บ 'เบอร์รี่' ด้วย!
- รูบาร์บ(โกฐน้ำเต้า) [bb]
- งา, น้ำมันงา (ลิกนิน) [m][r]
- อาหารมังสวิรัติ/อาหารจากพืช [v]
- วิตามินดี [aa] ♦ ดูแท็บ 'วิตามินดี' ด้วย!
- สังกะสี [a][c]
♦ การเลือกรับประทานอาหารที่ดีต่อสุขภาพ เป็นด่างและมีโภชนาการที่สมดุลมากขึ้น โดยพิจารณาจาก:
ผัก | ปริมาณ PRAL | กรดยูริก มก./100 กรัม | |
---|---|---|---|
ผักโขม | -14.0 | 61 | ![]() |
แครอท | -5.7 | 2.5 | ![]() |
ฟักทอง | -5.6 | 66.3 | ![]() |
คื่นฉ่าย | -5.2 | ![]() |
|
แตงกวา | -5.0 | 11.1 | ![]() |
กะหล่ำปลีจีน ผักกวางตุ้ง | -5.0 | 8.2 | ![]() ![]() |
หัวไชเท้าตะวันออก | -4.89 | ![]() |
|
หัวไชเท้า | -3.7 | ![]() |
|
บรอกโคลี | -3.6 | 81.8 | ![]() |
แป้ง/คาร์โบไฮเดรต | ปริมาณ PRAL | กรดยูริก มก./100 กรัม | |
มันเทศ | -8.15 | 20.1 | ![]() |
มันฝรั่ง | -6.08 | 7.5 | ![]() |
ขนมปังโฮลวีต | -3.55 | ![]() |
|
สปาเก็ตตี้/พาสต้า | 2.22 | ![]() |
|
ข้าวกล้อง | 2.3 | 43.7 | ![]() |
ข้าวโอ๊ต | 2.8 | ![]() |
|
ข้าวฟ่าง | 2.93 | ![]() |
|
โปรตีน | ปริมาณ PRAL | กรดยูริก มก./100 กรัม | |
โปรตีนจากผักที่มีพื้นผิว แห้ง | -10.58 | ![]() |
|
ถั่ว | -9.6 | ![]() |
|
นมถั่วเหลือง | -1.6 | 25.8 | ![]() |
เต้าหู้ | 2.25 | 23.3 | ![]() |
ถั่วเลนทิล | 3.5 | ![]() |
|
เทมเป้ | 5.7 | ![]() |
|
ไขมันและน้ำมัน | ปริมาณ PRAL | กรดยูริก มก./100 กรัม | |
อะโวคาโด/น้ำมันอะโวคาโด [ζ] | -8.2 | ![]() |
|
ถั่ว (เฮเซลนัท) | -4.1 | ![]() |
|
ถั่วลิสง | -2.9 | ![]() |
|
งา | -0.17 | ![]() |
|
น้ำมันงา | 0.3 | ![]() |
|
น้ำมันรำข้าว | 0 | ![]() |
|
เครื่องดืม | ปริมาณ PRAL | ||
น้ำแครอท | -4.8 | ![]() |
|
น้ำผักรวม | -3.6 | ![]() |
|
ชาเขียว | -1.2 | ![]() |
|
น้ำ | 0 | ![]() |
|
ของว่าง/ของหวาน/ผลไม้ | ปริมาณ PRAL | ||
ลูกเกด | -21 | ![]() |
|
อินทผลัม | -11.9 | ![]() |
|
อะโวคาโด | -8.2 | ![]() | |
กล้วย | -6.9 | ![]() |
|
กีวีฟรุต | -4.1 | ![]() |
|
เฮเซลนัท | -2.8 | ![]() |
|
สับปะรด | -2.7 | ![]() |
[ζ] อะโวคาโด/น้ำมันประกอบด้วย:
ไขมันทั้งหมด: 14g/100g
* ไขมันไม่อิ่มตัวเชิงซ้อน: 1.8g/100g (Omega-6)
* ไขมันไม่อิ่มตัวเชิงเดี่ยว: 9.8g/100g (โอเมก้า-3)
(* ไขมันเหล่านี้ช่วยลดคอเลสเตอรอลชนิดไม่ดีได้ [LDL])
อาหารที่เป็น สีเขียว ถือว่ามีประโยชน์ต่อสุขภาพโดยรวมมากกว่า แม้ว่าจะแสดงค่า GI ที่สูงกว่าอาหารที่มี สีแดงก็ตาม
ถ้าหมอไม่ได้สั่งให้คุณเข้มงวดในการรับประทานอาหารที่มีน้ำตาลในเลือดต่ำ และคุณไม่ได้รับการวินิจฉัยว่าเป็นโรคเบาหวาน ทางที่ดีควรเลือกอาหารประเภท สีเขียว และทานสิ่งเหล่านี้ร่วมกับถั่ว หรือผลิตภัณฑ์จากถั่ว และอาหาร GI ต่ำอื่นๆ สำหรับอาหาร GI ต่ำที่ดีต่อสุขภาพโดยรวม
♦ Glycemic Index (ดัชนีน้ำตาล; GI), และ Glycemic Load (ปริมาณน้ำตาล; GL)
อาหาร | GI | ขนาดเสิร์ฟ | GL | คะแนน PRAL | |
---|---|---|---|---|---|
เบคอน | 0 | 0 | 16.56 | ![]() |
|
ตับวัว | 0 | 0 | 22.73 | ![]() |
|
เนื้อโคขุน | 0 | 0 | 12.5 | ![]() |
|
ชีส | 0 | 0 | 34.0 | ![]() |
|
อกไก่ | 0 | 0 | 16.5 | ![]() |
|
ตับไก่ | 0 | 0 | 20.49 | ![]() |
|
ปีกไก่ | 0 | 0 | 13.93 | ![]() |
|
ปลา; ปลาคาร์พ | 0 | 0 | 11.75 | ![]() |
|
ปลาแมคเคอเรล | 0 | 0 | 7.28 | ![]() |
|
ปลาหมึกยักษ์ | 0 | 0 | 8.69 | ![]() |
|
หอยนางรม | 0 | 0 | 1.88 | ![]() |
|
เนื้อหมู | 0 | 0 | 7.9 | ![]() |
|
ปลาแปรรูป; ลูกชิ้นปลา | 0 | 0 | 7.72 | ![]() |
|
เรนโบว์ปลาเทราต์ | 0 | 0 | 10.8 | ![]() |
|
แซลมอน | 0 | 0 | 11.5 | ![]() |
|
แซลมอน; กระป๋อง | 0 | 0 | 14.0 | ![]() |
|
ไส้กรอกแฟรงก์เฟิร์ตเตอร์ | 0 | 0 | 10.6 | ![]() |
|
สาหร่าย | 0 | 0 | -4.8 | ![]() |
|
แกะ เนื้อแกะ | 0 | 0 | 11.58 | ![]() |
|
กุ้ง | 0 | 0 | 12.56 | ![]() |
|
ปลาหมึก, ปลาหมึกหอก | 0 | 0 | 9.37 | ![]() |
|
โปรตีนจากผักที่มีพื้นผิว แห้ง | 0 | 0 | -10.58 | ![]() |
|
ทูน่ากระป๋อง | 0 | 0 | 10.09 | ![]() |
|
ไวน์ | 0 | 0 | - | ![]() |
|
อะโวคาโด/น้ำมันอะโวคาโด | 10 | 200 กรัม | 0.2 | -8.2 | ![]() |
กะหล่ำปลีจีน ผักกวางตุ้ง | 12 | 200 กรัม | 2.5 | -5.0 | ![]() ![]() |
ถั่วลิสง | 13 | 25 กรัม | 0.26 | 6.2 | ![]() |
ถั่ว | 14-45 | 50 กรัม | 0.26 | -9.6 | ![]() |
หน่อไม้ฝรั่ง | 15 | 200 กรัม | 0.6 | -2.2 | ![]() |
หน่อไม้ | 15 | 50 กรัม | 0.075 | -8.0 | ![]() |
บรอกโคลี | 15 | 100 กรัม | 0.45 | -3.6 | ![]() |
กะหล่ำปลี | 15 | 200 กรัม | 1.2 | -4.3 | ![]() |
กะหล่ำดอก | 15 | 50 กรัม | 0.5 | -1.3 | ![]() |
แตงกวา | 15 | 200 กรัม | 0.6 | -5.0 | ![]() |
เห็ดหอมสด | 15 | 100 กรัม | 0.15 | -1.4 | ![]() |
หัวหอม | 15 | 50 กรัม | 0.375 | -2.0 | ![]() |
เต้าหู้ | 15 | 100 กรัม | 0.3 | 2.25 | ![]() |
ถั่วดำ | 17-31 | 50 กรัม | 0.05 | -13.6 | ![]() |
มะเขือ | 20 | 100 กรัม | 0.6 | -3.4 | ![]() |
ถั่ว | 9-70 | 50 กรัม | 0-0.08 | -8.4 | ![]() |
มะขามดิบ | 23 | 35 กรัม | 6 | -11 | ![]() |
มะเขือเทศ | 23 | 100 กรัม | 0.875 | -4.1 | ![]() |
ดาร์กช็อกโกแลต | 25 | 50 กรัม | 5.75 | - | ![]() |
สตรอเบอร์รี่ | 25 | 200 กรัม | 2.5 | 6.8 | ![]() |
ขนมปังโฮลวีต | 28-67 | 156 กรัม | 4 | 3.5 | ![]() |
กระเทียม | 30 | 20 กรัม | 1.68 | -2.6 | ![]() |
ถั่ว | 30 | 50 กรัม | 6.17 | - | ![]() |
นมถั่วเหลือง | 30 | 200 กรัม | 1.8 | -1.6 | ![]() |
นมวัว | 31 | 1 ถ้วย | 2.7 | - | ![]() |
พาสลีย์ | 32 | 100 กรัม | 0.97 | -11.13 | ![]() |
แอปเปิ้ล | 35 | 125 กรัม | 4.8 | - | ![]() |
แครอท | 35 | 200 กรัม | 3.5 | -5.7 | ![]() |
มะเดื่อ; สด | 35 | 50 กรัม | 2.3 | -4.88 | ![]() |
งา | 35 | 10 กรัม | 0.35 | 0.3 | ![]() |
มะเดื่อ; แห้ง | 40 | 30 กรัม | 6.6 | -4.88 | ![]() |
ข้าวโอ้ต | 40 | 50 กรัม | 11.25 | - | ![]() |
ลำไย; สด | 45 | 125 กรัม | 8.46 | - | ![]() |
สัปปะรด | 45 | 125 กรัม | 6.8 | -2.21 | ![]() |
สปาเก็ตตี้ / พาสต้า | 46 | 1 ถ้วย | 20 | - | ![]() |
กล้วย | 48 | 100 กรัม | 9.6 | -6.9 | ![]() |
ทุเรียน | 49 | 50 กรัม | 5.5 | - | ![]() |
หอย หอยแมลงภู่ หอยเชล | 50 | 50 กรัม | 1.85 | 11.1 | ![]() |
มะม่วง | 50 | 200 กรัม | 12 | -3.01 | ![]() |
มันเทศ | 50 | 150 กรัม | 17.25 | -8.15 | ![]() |
ข้าวกล้อง | 51-78 | 30 กรัม | 11.32 | 2.3 | ![]() |
มะละกอ | 55 | 200 กรัม | 7.7 | -4.03 | ![]() |
ข้าวบาสมาติ; สีขาว | 57 - 80 | 30 กรัม | 13.92 | 1.7 | ![]() |
น้ำผึ้ง | 60 | 10 กรัม | 4.5 | - | ![]() |
ไอศกรีม | 60 | 100 กรัม | 12.64 | 28.7 | ![]() |
ขนมปังข้าวสาลี; สีขาว | 60 | 40 กรัม | 3.8 | -3.55 | ![]() |
ฟักทอง | 64 | 150 กรัม | 4.8 | - | ![]() |
ข้าวโพด | 65 | 150 กรัม | 15.5 | * | ![]() |
ลูกเกด | 65 | 25 กรัม | 11 | -21 | ![]() |
ข้าว; ข้าวหอมมะลิขาว | 68-116 | 100 กรัม | 58.4 | - | ![]() |
มันฝรั่ง | 70 | 200 กรัม | 21 | -6.08 | ![]() |
เบียร์ | 90 | ½ ลิตร | 13.5 | - | ![]() |
ข้าวเหนียว | 92-98 | 100 กรัม | 19.41 | - | ![]() |
น้ำตาลทราย | 98 | 5 กรัม | 3.4 | - | ![]() |
อินทผลัม | 100 | 12.5 กรัม | 8.125 | -11.9 | ![]() |
น้ำตาล; สีขาว | 100 | 5 กรัม | 4.8 | - | ![]() |
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♦ อ้างอิง
- [1] Acute renal failure after treatment with non-steroidal anti-inflammatory drugs.
Non-steroidal anti-inflammatory drugs (NSAIDs) are known to have adverse effects on kidney function. Situations with a stimulated renin-angiotensin system such as volume depletion or pre-existing chronic renal failure predispose to acute renal failure (ARF) via inhibition of prostaglandin synthesis by NSAIDs. To date, NSAIDs are frequently used as antipyretic drugs even in situations predisposing to ARF. Within 20 months, seven children presenting with diarrhoea and/or vomiting and fever were treated with therapeutic doses (11.5-32 mg/kg per day) of ibuprofen for 1 to 3 days before developing ARF.
CONCLUSION:
non-steroidal anti-inflammatory drugs are potentially dangerous in situations with even moderate volume depletion.
Eur J Pediatr. 2004 Mar;163(3):148-50. Epub 2004 Jan 24. PMID: 14745553
- [2] Severe acute kidney injury associated with non-steroidal antiinflammatory drugs in cirrhosis: a case-control study.
BACKGROUND AND AIM: Non-steroidal anti-inflammatory drugs (NSAIDs) may cause impairment of kidney function in patients with cirrhosis. Investigational studies demonstrated reversibility of kidney dysfunction after drug withdrawal, but information based on clinical practice is lacking. Study aim was to investigate the characteristics and outcome of Acute Kidney Injury (AKI) developing in patients with cirrhosis treated with NSAIDs.
CONCLUSIONS:
Patients with cirrhosis treated with NSAIDs may develop severe AKI which may be irreversible and associated with poor short-term outcome.
J Hepatol. 2015 Apr 11. Epub 2015 Apr 11. PMID: 25872166
- [3] Unintended effects of statins in men and women in England and Wales: population based cohort study using the QResearch database.
MAIN OUTCOME MEASURE:
First recorded occurrence of cardiovascular disease, moderate or serious myopathic events, moderate or serious liver dysfunction, acute renal failure, venous thromboembolism, Parkinson's disease, dementia, rheumatoid arthritis, cataract, osteoporotic fracture, gastric cancer, oesophageal cancer, colon cancer, lung cancer, melanoma, renal cancer, breast cancer, or prostate cancer.
CONCLUSIONS:
Claims of unintended benefits of statins, except for oesophageal cancer, remain unsubstantiated, although potential adverse effects at population level were confirmed and quantified.
BMJ. 2010;340:c2197. Epub 2010 May 20. PMID: 20488911
- [4] Genetically engineered crops, glyphosate and the deterioration of health in the United States of America
A huge increase in the incidence and prevalence of chronic diseases has been reported in the United States (US) over the last 20 years.
Similar increases have been seen globally.
The herbicide glyphosate was introduced in 1974 and its use is accelerating with the advent of herbicide-tolerant genetically engineered (GE) crops.
Evidence is mounting that glyphosate interferes with many metabolic processes in plants and animals and glyphosate residues have been detected in both. Glyphosate disrupts the endocrine system and the balance of gut bacteria, it damages DNA and is a driver of mutations that lead to cancer.
Conclusions
These data show very strong and highly significant correlations between the increasing use of glyphosate, GE crop growth and the increase in a multitude of diseases.
Many of the graphs show sudden increases in the rates of diseases in the mid-1990s that coincide with the commercial production of GE crops.
The large increase in glyphosate use in the US is mostly due to the increase in glyphosate-resistant GE crops.
Journal of Organic Systems, 9(2), 2014
- [5] Dietary acid load: A novel nutritional target in chronic kidney disease?
Nonvolatile acid is produced from the metabolism of organic sulfur in dietary protein, and the production of organic anions (anion is a negatively charged ion) during the combustion of neutral foods.
Organic anion salts that are found primarily in plant foods are directly absorbed in the gastrointestinal tract and yield bicarbonate.
The difference between endogenously produced nonvolatile acid and absorbed alkali precursors yields the dietary acid load, technically known as the net endogenous acid production, and must be excreted by the kidney to maintain acid-base (alkaline) balance.
Although typically around 1 mEq/kg/day, dietary acid load is lower with greater intake of fruits and vegetables.
In the setting of chronic kidney disease, a high dietary acid load invokes adaptive mechanisms to increase acid excretion despite reduced nephron number, such as increased per nephron ammoniagenesis and augmented distal acid excretion mediated by the renin-angiotensin system and endothelin-1.
These adaptations may promote renal injury.
Additionally, high dietary acid loads produce low-grade, subclinical acidosis that may result in bone and muscle loss.
Early studies suggest that lowering the dietary acid load can improve subclinical acidosis, preserve bone and muscle, and slow decline of glomerular filtration rate in animal models and humans. Studies focusing on hard clinical outcomes are needed.
Adv Chronic Kidney Dis. 2013 Mar; 20(2): 141–149. doi: 10.1053/j.ackd.2012.11.001
- [6]
♦ ต่อไปนี้เป็นการเลือกอาหารตามหลักการ 'ปริมาณกรดในไตที่อาจเกิดขึ้น' (PRAL)
• ตัวเลขติดลบ หมายถึง อาหารที่เป็นเบส/ด่าง ตัวเลขบวก อาหารที่เป็นกรดการขึ้นรูปอัลคาไลน์ ค่าPRAL การเกิดกรด ค่าPRAL ผักโขม -11.8 โกโก้นม 114 ผักคะน้า -8.0 ชีส 20.0 ถั่ว -7.4 ปลาคอด 19.8 กล้วย -6.9 ไข่แดง 18.1 แครอท; raw -5.7 ไก่ 16.5 ผักชีฝรั่ง -5.0 ปลาซาร์ดีนในน้ำมัน 15.9 ผักกาดหอม -4.3 เห็ด -4.2 หอยแมลงภู่ 15.2 มะเขือเทศ -4.1 เนื้อหมู 14.7 บร็อคโคลี -3.6 แซลมอน 14.0 แตงกวา -2.4 กุ้ง 13.2 หน่อไม้ฝรั่ง -2.2 เนื้อวัว 12.5 มะเขือ -2.0 ไข่ทั้งตัว 9.0 หัวหอม -2.0 ข้าวโพด Tortilla 4.8 กะหล่ำ -1.3 นมที่ไม่ได้แยกไขมันออก 0.2 ชาเขียว -0.3
- [7] Volume Overload and Adverse Outcomes in Chronic Kidney Disease: Clinical Observational and Animal Studies.
In rats subjected to unilateral nephrectomy and a high-salt diet, the extracellular water significantly increased.
This fluid retention was associated with an increase in blood pressure, proteinuria, renal inflammation with macrophage infiltration and tumor necrosis factor-a overexpression, glomerular sclerosis, and cardiac fibrosis.
These findings suggest that patients with CKD might be particularly susceptible to the detrimental effects of salt-induced fluid retention and provide evidence to support salt restriction and volume control in CKD.
Conclusions:
Volume overload exhibits a strong association with CKD progression and CVD morbidity or mortality in patients with stage 3 to 5 CKD.
In animal models of CKD, salt-induced fluid retention results in renal and cardiovascular damage, which is ameliorated by diuretics.
Szu-Chun Hung, MD; Yi-Shin Lai, MS; Ko-Lin Kuo, MD, PhD; Der-Cherng Tarng, MD, PhD
- [8] Associations of sugar and artificially sweetened soda with albuminuria and kidney function decline in women.
Sugar-sweetened soda is reported to be associated with increased risk for diabetes and albuminuria, but there are currently limited data on how sugar or artificially sweetened soda may be related to kidney function decline.
RESULTS:
Consumption of ≥2 servings per day of artificially sweetened (diet) soda was independently associated with eGFR (Glomerular filtration rate) decline ≥30% (OR 2.02, 95% CI 1.36 to 3.01) and ≥3 ml/min per 1.73 m(2) per year (OR 2.20, 95% CI 1.36 to 3.55). No increased risk for eGFR decline was observed for<2 servings per day of diet soda. No associations were noted between diet soda and MA or sugar soda and MA or eGFR decline.
CONCLUSIONS:
Consumption of≥2 servings per day of artificially sweetened soda is associated with a 2-fold increased odds for kidney function decline in women.
Clin J Am Soc Nephrol. 2010 Sep 30. Epub 2010 Sep 30. PMID: 20884773
- [9] Sugary soda consumption and albuminuria: results from the National Health and Nutrition Examination Survey, 1999-2004.
End-stage renal disease rates rose following widespread introduction of high fructose corn syrup in the American diet, supporting speculation that fructose harms the kidney.
Sugar-sweetened soda is a primary source of fructose.
RESULTS:
Weighted albuminuria prevalence was 11%, and 17% consumed 2+ sugary soft drinks/day.
The confounder-adjusted odds ratio for sugary soda was 1.40 (95% confidence interval: 1.13, 1.74).
CONCLUSIONS:
Findings suggest that sugary soda consumption may be associated with kidney damage
PLoS One. 2008;3(10):e3431. Epub 2008 Oct 17. PMID: 18927611
- [10] The association between prolonged occupational exposure to paraphenylenediamine (hair-dye) and renal impairment.
INTRODUCTION:
Paraphenylenediamine (PPD) is widely used in hair dyes and cosmetic skin application.
RESULTS:
The study included seventy-two females with a mean age of 40 +/- 8 years and a median duration of exposure to PPD of 6 years.
Renal impairment, proteinuria and hematuria were observed in 14%, 26.4% and 41.1% of hair dressers, respectively.
Hypertension, skin changes and bronchospasm were found in 19.4%, 38.9% and 22% of participants, respectively.
CONCLUSION:
In this group of hairdressers with regular exposure to PPD, we observed high prevalence of renal impairment, proteinuria and hematuria.
These findings were significantly associated with the use of pure forms of PPD and longer duration of exposure.
Arab J Nephrol Transplant. 2011 Jan;4(1):21-5. PMID: 21469591
- [11] Pesticide use and risk of end-stage renal disease among licensed pesticide applicators in the Agricultural Health Study.
RESULTS:
Positive exposure-response trends were observed for the herbicides alachlor, atrazine, metolachlor, paraquat, and pendimethalin, and the insecticide permethrin.
More than one medical visit due to pesticide use (HR=2.13; 95% CI 1.17 to 3.89) and hospitalisation due to pesticide use (HR=3.05; 95% CI 1.67 to 5.58) were significantly associated with ESRD (end-stage renal disease).
CONCLUSIONS:
Our findings support an association between ESRD and chronic exposure to specific pesticides, and suggest pesticide exposures resulting in medical visits may increase the risk of ESRD.
Occup Environ Med. 2015 Jul 15. Epub 2015 Jul 15. PMID: 26177651
- [12] Effects of intensive cell phone (Philips Genic 900) use on the rat kidney tissue.
RESULTS:
Light microscopic examination of the kidney tissues obtained from the first group of rats (Group 1 was exposed to a cell phone in speech mode for 8 hours/day for 20 days) revealed glomerular damage, dilatation of Bowman's capsule, formation of large spaces between the tubules, tubular damage, perivascular edema, and inflammatory cell infiltration.
The mean severity score was 4.64± 1.7 in group 1, 4.50 ± 0.8 in group 2, and 0 in group 3 (not exposed to cell phone EMR, electro magnetic radiation).
(Rating: AIS 1 – Minor; AIS 2 – Moderate; AIS 3 – Serious; AIS 4 – Severe; AIS 5 – Critical; AIS 6 – Maximal (untreatable))
While there was no significant difference between group 1 and group 2 (P>.05), the mean severity scores of groups 1 and 2 were significantly higher than that of the control group (P = .001 for each).
CONCLUSION:
Considering the damage in rat kidney tissue caused by EMR-emitting cell phones, high-risk individuals should take protective measures.
Urol J. 2013 ;10(2):886-91. PMID: 23801472
- [13] Proteomic Analysis of Kidney in Rats Chronically Exposed to Monosodium Glutamate.
Chronic monosodium glutamate (MSG) intake causes kidney dysfunction and renal oxidative stress in the animal model.
RESULTS:
The differential image analysis showed 157 changed spots, of which 71 spots were higher and 86 spots were lower in the MSG-treated group compared with those in the control group.
Eight statistically significant and differentially expressed proteins were identified:
glutathione S-transferase class-pi, heat shock cognate 71 kDa, phosphoserine phosphatase, phosphoglycerate kinase, cytosolic glycerol-3-phosphate dehydrogenase, 2-amino-3-carboxymuconate-6-semialdehyde decarboxylase,α-ketoglutarate dehydrogenase and succinyl-CoA ligase.
PLoS One. 2014 ;9(12):e116233. Epub 2014 Dec 31. PMID: 25551610
- [14][n] Green Tea Polyphenols Ameliorate the Early Renal Damage Induced by a High-Fat Diet via Ketogenesis/SIRT3 Pathway.
Several reports in the literature have suggested the renoprotective effects of ketone bodies and green tea polyphenols (GTPs).
RESULTS:
The increased renal oxidative stress and the loss of renal function induced by the HFD (High-Fat Diet) were ameliorated by GTPs (green tea polyphenols).
Renal ketogenesis and SIRT3 expression and activity levels, which were reduced by the HFD, were restored by GTPs.
CONCLUSION:
The ketogenesis/SIRT3 pathway mediates the renoprotection of GTPs against the oxidative stress induced by an HFD (High-Fat Diet).
Oxid Med Cell Longev. 2017 ;2017:9032792. Epub 2017 Jul 26. PMID: 28814987
- [15] Wi-Fi (2.45 GHz)- and mobile phone (900 and 1800 MHz)-induced risks on oxidative stress and elements in kidney and testis of rats during pregnancy and the development of offspring.
In conclusion, Wi-Fi- and mobile phone-induced EMR (electro magnetic radiation) caused oxidative damage by increasing the extent of lipid peroxidation and the iron level,while decreasing total antioxidant status, copper, and GSH values.
Wi-Fi- and mobile phone-induced EMR may cause precocious puberty and oxidative kidney and testis injury in growing rats.
Biol Trace Elem Res. 2013 Dec ;156(1-3):221-9. Epub 2013 Oct 8. PMID: 24101576
- [16] HMG-CoA reductase inhibitors induce apoptosis in mouse proximal tubular cells in primary culture.
DNA ladder pattern of 200 kDa typical of apoptosis (cell death) and significant increase in DNA fragmentation were seen after 24 hours of treatment with lovastatin (used to lower ‘bad’ cholesterol and fats/LDL, triglycerides), a HMG-CoA reductase inhibitor.
Kidney Int. 1997 Oct ;52(4):962-72. PMID: 9328935
- [17] The Western-style diet: a major risk factor for impaired kidney function and chronic kidney disease
Abstract
The Western-style diet is characterized by its highly processed and refined foods and high contents of sugars, salt, and fat and protein from red meat.
It has been recognized as the major contributor to metabolic disturbances and the development of obesity-related diseases including type 2 diabetes, hypertension, and cardiovascular disease.
Also, the Western-style diet has been associated with an increased incidence of chronic kidney disease (CKD).
A combination of dietary factors contributes to the impairment of renal vascularization, steatosis and inflammation, hypertension, and impaired renal hormonal regulation.
PMID: 21880837 DOI: 10.1152/ajprenal.00068.2011
- [18] Diet and Chronic Kidney Disease
Kidney disease affects almost 15% of the US population, and prevalence is anticipated to grow as the population ages and the obesity epidemic continues due to Western dietary practices.
The densely caloric Western diet, characterized by high animal protein and low fruit and vegetable content, has fueled the growth of chronic diseases, including chronic kidney disease.
The results from the previously mentioned meta-analysis along with those of other previous studies suggest that many patients will benefit from salt reduction, especially older individuals and those with obesity and/or low GFR (glomerular filtration rate).
In summary, dietary factors are important for determining the workload of each individual nephron.
In the setting of CKD (Chronic Kidney Disease) and reduced working nephron number, each individual nephron is already at risk for hemodynamic injury. High intake of animal protein and egg yolks combined with low intake of fruits and vegetables is extremely conducive for nephron injury, and mechanisms of injury are not duplicative.
S379, https://doi.org/10.1093/advances/nmz011
- [19] Glyphosate's Synergistic Toxicity in Combination with Other Factors as a Cause of Chronic Kidney Disease of Unknown Origin.
Chronic kidney disease of unknown etiology (CKDu) is a global epidemic.
Sri Lanka has experienced a doubling of the disease every 4 or 5 years since it was first identified in the North Central province in the mid-1990s.
The disease primarily affects people in agricultural regions who are missing the commonly known risk factors for CKD.
Here, we argue that glyphosate in particular is working synergistically with most of the other factors to increase toxic effects.
We propose, further, that glyphosate causes insidious harm through its action as an amino acid analogue of glycine, and that this interferes with natural protective mechanisms against other exposures.
Glyphosate's synergistic health effects in combination with exposure to other pollutants, in particular paraquat, and physical labor in the ubiquitous high temperatures of lowland tropical regions, could result in renal damage consistent with CKDu in Sri Lanka.
Int J Environ Res Public Health. 2019 Jul 31 ;16(15). Epub 2019 Jul 31. PMID: 31370256
- [20] Fluoride in drinking water and diet: the causative factor of chronic kidney diseases in the North Central Province of Sri Lanka.
A significant number of people in the North Central Province of Sri Lanka suffer from chronic kidney diseases (CKD), and the author revisits existing literature related to CKD to find its causative factor.
There is a direct connection between high fluoride levels in drinking water and kidney disease, and there are unhealthy levels of fluoride in the groundwater in Sri Lanka's CKD-affected areas.
Based on the following observations, the author believes with confidence that excess fluoride in drinking water and in the locally grown food in the affected areas are the culprits of CKD in Sri Lanka.
Environ Health Prev Med. 2015 Jul ;20(4):237-42. Epub 2015 Apr 28. PMID: 25916575
- [21] Death by Medicine
Something is wrong when regulatory agencies pretend that vitamins are dangerous, yet ignore published statistics showing that government-sanctioned medicine is the real hazard.
This fully referenced report shows the number of people having in-hospital, adverse reactions to prescribed drugs to be 2.2 million per year.
The number of unnecessary antibiotics prescribed annually for viral infections is 20 million per year.
The number of unnecessary medical and surgical procedures performed annually is 7.5 million per year.
The number of people exposed to unnecessary hospitalization annually is 8.9 million per year.
♦ The most stunning statistic, however, is that the total number of deaths caused by conventional medicine is an astounding 783,936 per year.
It is now evident that the American medical system is the leading cause of death and injury in the US.
(By contrast, the number of deaths attributable to heart disease in 2001 was 699,697, while the number of deaths attributable to cancer was 553,251.5)
By Gary Null, PhD; Carolyn Dean MD, ND; Martin Feldman, MD; Debora Rasio, MD; and Dorothy Smith, PhD
♦ Probable prophylactics and treatments for kidney disease.
- [a]Effects of zinc supplementation on serum zinc and C-reactive protein concentrations in hemodialysis patients.
RESULTS: After supplementation, subjects in the zinc-supplemented group showed significant increases in serum zinc concentrations
A progressive decrease in serum C-reactive protein concentrations was observed in the zinc-supplemented group from the beginning (13.5+/-3.8mg/L SEM) to the end (10.5+/-3.5mg/L SEM) of the study, but this event was not significant. CONCLUSION: Zinc supplementation intake may cause an increase in serum zinc concentrations, leading to a decrease of inflammation in hemodialysis patients.
J Ren Nutr. 2009 Jun 19. PMID: 19541504
- [/b] Effects of monthly dose and regular dosing of intravenous active vitamin D use on mortality among patients undergoing hemodialysis.
Adjusted all-cause mortality risk was reduced 7-17% among patients receiving vitamin D each month of the 3-month interval, with the highest reduction among patients with shorter dialysis duration.
Pharmacotherapy. 2009 Feb;29(2):154-64. PMID: 19170585
- [c] The effects of zinc supplementation on serum zinc concentration and protein catabolic rate in hemodialysis patients.
A significant positive correlation (r = +0.61) was shown between PCR and serum zinc concentrations at the end of the study. Reported dietary protein intake did not change with zinc supplementation. CONCLUSION: Low serum zinc concentrations are reversible with zinc supplementation. Improvement in serum zinc concentration increases the PCR of HD patients.
J Ren Nutr. 2000 Jul;10(3):148-53. PMID: 10921536
- [d] Curcumin ameliorates renal failure in 5/6 nephrectomized rats: role of inflammation.
Studies in mesangial cells were carried out to further establish that the anti-inflammatory effect of curcumin in vivo was mediated essentially by antagonizing TNF-alpha. Curcumin dose dependently antagonized the TNF-alpha-mediated decrease in PPARgamma and blocked transactivation of NF-kappaB and repression of PPARgamma, indicating that the anti-inflamatory property of curcumin may be responsible for alleviating CRF in Nx animals.
Am J Physiol Renal Physiol. 2009 May;296(5):F1146-57. Epub 2009 Feb 18. PMID: 19225048
- [e] Evaluation of the efficacy of ginger, Arabic gum, and Boswellia in acute and chronic renal failure.
Ginger and AG showed renoprotective effects in both models of renal failure. These protective effects may be attributed at least in part to their anti-inflammatory properties as evident by attenuating serum C-reactive protein levels and antioxidant effects as evident by attenuating lipid peroxidation marker, malondialdehyde levels, and increasing renal superoxide dismutase activity. Ginger was more potent than AG in both models of renal failure.
Ren Fail. 2012 ;34(1):73-82. Epub 2011 Oct 21. PMID: 22017619
- [f] Effectiveness of green tea tannin on rats with chronic renal failure.
There were increases in blood urea nitrogen, serum creatinine, and urinary protein, and a decrease in creatinine clearance in the nephrectomized control rats, whereas better results for these parameters were obtained in rats given green tea tannin after nephrectomy, demonstrating a suppressed progression of the renal failure.
Green tea tannin, however, was found to lighten the kidney under such oxidative stress. Mesangial proliferation and glomerular sclerotic lesions, which were conspicuous in the rats that were not given green tea tannin after nephrectomy, were also relieved.
Biosci Biotechnol Biochem. 1996 Jun;60(6):1000-5. PMID: 8695898
- [g] Melatonin ameliorates oxidative stress, inflammation, proteinuria, and progression of renal damage in rats with renal mass reduction.
Melatonin, the major product of the pineal gland, has potent_antioxidant and anti-inflammatory properties, and its production is impaired in chronic renal failure.
Deterioration of renal function (plasma creatinine and proteinuria) and structure (glomerulosclerosis and tubulointerstitial damage) resulting from renal ablation were ameliorated significantly with melatonin treatment.
In conclusion, melatonin administration improves the course of chronic renal failure in rats with renal mass reduction.
Zhonghua Zhong Liu Za Zhi. 2005 Nov;27(11):667-71. PMID: 18077597
- [h] Niacin ameliorates oxidative stress, inflammation, proteinuria, and hypertension in rats with chronic renal failure.
Niacin is known to improve lipid metabolism and exert antioxidant/anti-inflammatory actions.
Although niacin lowered serum creatinine and raised creatinine clearance, the differences did not reach statistical significance.
Thus niacin supplementation helps to attenuate histological injury and mitigate upregulation of oxidative and inflammatory systems in the remnant kidney.
Am J Physiol Renal Physiol. 2009 Jul;297(1):F106-13. Epub 2009 May 6. PMID: 19420110
- [j] Omega-3 fatty acid supplementation attenuates oxidative stress, inflammation, and tubulointerstitial fibrosis in the remnant kidney.
Thus long-term O-3FA (Omega-3 fatty acid) supplementation can reduce or reverse up-regulation of pro-oxidant, pro- inflammatory and pro-fibrotic pathways and attenuate tubulo-interstitial fibrosis in the remnant kidney. Key words: chronic kidney disease, NAD(P)H oxidase, Smad, TGF-beta.
Significant reduction of renal mass initiates a series of hemodynamic and non-hemodynamic events which lead to proteinuria, glomerulosclerosis, tubulo-interstitial injury and end-stage renal failure.
Lipid mediators derived from fatty acids participate in regulation of renal hemodynamic and non-hemodynamic processes that influence progression of renal disease.
Composition of cellular fatty acids and hence related signaling responses are influenced by their dietary contents.
Consumption of omega-3 fatty acids (O-3FA) has proven effective in mitigating atherosclerosis.
Am J Physiol Renal Physiol. 2009 Aug 5. PMID: 19656915
- [k] Ameliorative effects of proanthocyanidin on renal ischemia/reperfusion injury.
RESULTS:
PA (proanthocyanidin) significantly reduced the I/R-induced increases in S(Cr), BUN, and AST.
In addition, PA markedly reduced elevated oxidative stress product, restored decreased antioxidant enzymes, and attenuated histological alterations.
Moreover, PA attenuated the tissue NO(x), levels indicating reduced NO production.
CONCLUSIONS:
The pretreatment of rats with PA reduced the renal dysfunction and morphological changes, ameliorated cellular injury, and restored renal antioxidant enzymes caused by renal I/R.
Ren Fail. 2008;30(9):931-8. PMID: 18925534
- [l] Role of quercetin on hepatic urea production in acute renal failure.
The value of urea production in the liver was determined by measuring of liver arginase activity, the terminal enzyme of urea cycle.
Arginase activity was increased (p < 0.01) as well as urea level (p < 0.001) 48 h after glycerol administration.
Pretreatment by quercetin suppressed the arginase activity in the liver (p < 0.05) and plasma levels of urea (p < 0.01).
So, we have concluded that quercetin may be beneficial in glycerol induced ARF (Acute renal failure).
Ren Fail. 2003 Mar;25(2):149-55. PMID: 12739822
- [m] Sesame lignans suppress age-related disorders of the kidney in mice.
Sesamin is a functional ingredient in sesame (Sesamum indicum) seeds and has many physiological effects.
RESULTS:
Renal lipofuscin deposition was increased in the O-C (regular diet) group compared to that in the Y-C (young mice) group and its deposition with aging was significantly decreased in both O-SE (diet containing sesame lignans) and O-SE+VE (diet containing sesame lignans and α-tocopherol) groups.
CONCLUSIONS:
Sesame lignans might be useful to suppress age-related kidney disorders, and these effects could be enhanced with VE (α-tocopherol).
Eur Rev Med Pharmacol Sci. 2020 May ;24(9):5140-5147. PMID: 32432778
- [o] Honokiol alleviates sepsis-induced acute kidney injury in mice by targeting the miR-218-5p/heme oxygenase-1 signaling pathway.
Honokiol is a low-molecular-weight natural product and has been reported to exhibit anti-inflammatory activity.
The results revealed that honokiol significantly increased the survival rate in mice undergoing a CLP operation.
Inflammatory cytokines, such as TNF-α, IL-6 and IL-1β, were significantly inhibited in honokiol-treated septic mice compared with the CLP group.
In addition, honokiol showed the ability to reverse CLP-induced AKI in septic mice. Furthermore, heme oxygenase-1 (HO-1) expression levels were significantly up-regulated and miR-218-5p wasmarkedly down-regulated in honokiol-treated septic mice as compared to CLP-operated mice.
Cell Mol Biol Lett. 2019 ;24:15. Epub 2019 Feb 22. PMID: 30833971
- [p] Pomegranate Juice Diminishes The Mitochondria-Dependent Cell Death And NF-kB Signaling Pathway Induced By Copper Oxide Nanoparticles On Liver And Kidneys Of Rats.
Pomegranate (L) has been used since ancient times in the traditional medicine of several cultures, particularly in the Middle East.
It is an essential commercial crop full of bioactive compounds with several medical applications.
Pomegranate is very popular for its biological effects exerted by phenolic compounds via free radical scavenging abilities.
It has revealed high antioxidant and anti-inflammatory activities and is beneficial for the amelioration of liver and kidney diseases.
Conclusion:
PJ was proved to be a potential hepato-renal protective agent against liver and kidney damage induced by CuO-NPs via its antioxidant, anti-inflammatory, and anti-apoptotic effects.
Int J Nanomedicine. 2019 ;14:8905-8922. Epub 2019 Nov 15. PMID: 31814719
- [q] Effect of bioflavonoids quercetin and curcumin on ischemic renal injury: a new class of renoprotective agents.
Bioflavonoids are agents with potential immunosuppressive and renoprotective properties. We studied the effects of quercetin and curcumin, two bioflavonoids, on ischemia-reperfusion in the rat.
RESULTS:
Pretreatment with quercetin or curcumin resulted in preservation of histological integrity, with a decrease in tubular damage and interstitial inflammation.
Pretreatment with quercetin or curcumin strongly attenuated this expression.
CONCLUSION:
Quercetin and curcumin reduce ischemia-reperfusion injury and its inflammatory sequelae.
The bioflavonoids hold promise as agents that can reduce immune and nonimmune renal injury, the key risk factors in chronic graft loss.
Transplantation. 1998 Jul 27;66(2):147-52. PMID: 9701255
- [r] Sesame Oil Attenuates Renal Oxidative Stress Induced by a High Fat Diet.
The antioxidative effects of the bioactive compounds enriched sesame oil (e.g. lignans and tocopherols) are well established.
These results suggest that sesame oil could ameliorate HFD (high fat diet)-induced renal damage by suppressing oxidative stress and inflammation.
Prev Nutr Food Sci. 2019 Jun ;24(2):114-120. Epub 2019 Jun 30. PMID: 31328114
- [s] Anti-Inflammatory, Antioxidant, and Antifibrotic Effects of Kefir Peptides on Salt-Induced Renal Vascular Damage and Dysfunction in Aged Stroke-Prone Spontaneously Hypertensive Rats.
A previous study showed that kefir products have anti-inflammatory and anti-hypertensive activities and immunological modulation functions.
...Furthermore, KP treatment significantly increased the renal superoxide dismutase (SOD) activity and the glomerular filtration rate (GFR), which exerted potent protection against salt-induced chronic kidney disease in SHRSP rats.
The results of this study suggest that KPs (Kefir Peptides) ameliorate salt-induced renal damage, tubular atrophy, and glomerular dysfunction through anti-inflammatory, antioxidative stress, and antifibrotic activities, and might be a promising protective agent against high salt-induced renovascular-related diseases.
Antioxidants (Basel). 2020 Aug 26 ;9(9). Epub 2020 Aug 26. PMID: 32858955
- [t] Health Benefits of Resveratrol in Kidney Disease: Evidence from In Vitro and In Vivo Studies.
Different diseases and disorders that affect the kidneys include, but are not limited to, glomerulonephritis, diabetic nephropathy, polycystic kidney disease, kidney stones, renal fibrosis, sepsis, and renal cell carcinoma. Kidney disease tends to develop over many years, making it difficult to identify until much later when kidney function is severely impaired and undergoing kidney failure.
Epidemiological studies have suggested that a diet rich in fruits and vegetables is associated with health benefits including protection against kidney disease and renal cancer.
Resveratrol, a polyphenol found in grapes and berries, has been reported to have antioxidant, anti-inflammatory, antidiabetic, hepatoprotective, neuroprotective, and anti-cancer properties.
Nutrients. 2019 Jul 17 ;11(7). Epub 2019 Jul 17. PMID: 31319485
- [v] Plant-based diets for prevention and management of chronic kidney disease.
Plant-based diets have been used with growing popularity for the treatment of a wide range of lifestyle-related diseases, including diabetes, hypertension, and obesity. With the reinvigoration of the conservative and dietary management of chronic kidney disease (CKD) and the use of low protein diets for secondary prevention of CKD to delay or prevent dialysis therapy, there is an increasing interest in the potential role of plant-based diets for these patients.
SUMMARY:
Plant-based diets should be recommended for both primary and secondary prevention of CKD.
Concerns of hyperkalemia and protein inadequacy related to plant-based diets may be outdated and unsupported by the current body of literature.
Healthcare providers in general medicine and nephrology can consider plant-based diets as an important tool for prevention and management of CKD.
Curr Opin Nephrol Hypertens. 2019 Nov 12. Epub 2019 Nov 12. PMID: 31725014
- [w] Melatonin and renal protection: novel perspectives from animal experiments and human studies (review).
Chronic kidney disease (CKD) is a serious public health problem.
Current therapies are designed to slow down progression of the disease and avoid the necessity of dialysis or kidney transplantation.
CKD is characterized by chronic inflammation and progressive cell death resulting in fibrotic rebuilding of renal tissue.
Melatonin, the primary product of the pineal gland, has been shown to have pluripotent protective effects in many organs and tissues.
It exerts anti-hypertensive, anti-inflammatory, anti-apoptotic, and antiremodelling actions.
A principal mechanism of these numerous melatonin benefits resides in its extraordinary high efficacy as an antioxidant and scavenger protecting cells both extracellularly and in all subcellular structures.
In humans, melatonin's chronobiological action attenuates sleep disturbances in hemodialyzed patients suffering from a relative melatonin deficiency.
Moreover, melatonin reduces the oxidative burden and improves iron metabolism in hemodialyzed patients.
In conclusion, the pleiotropic physiological actions of melatonin induce beneficial effects at numerous pathophysiological levels related to CKD both under experimental and clinical conditions.
Curr Pharm Des. 2015 ;21(7):936-49. PMID: 25269563
- [y] Preventive and Therapeutic Effect of Ganoderma (Lingzhi) on Renal Diseases and Clinical Applications.
The mechanisms of kidney diseases, such as acute kidney injury (AKI) and chronic kidney disease (CKD), have been intensively studied.
Nonetheless, the morbidity and mortality of AKI and CKD increased in recent years.
Recently, natural products have been increasingly recognized as an alternative source for treating renal diseases on account of the conventional experience and the multi-target characteristics.
Ganoderma lucidum (G. lucidum, Lingzhi) has been used for centuries as nutraceuticals and alternative medicine to improve health and to treat numerous diseases.
Benefiting from various biological activities, such as anti-oxidation, anti-inflammation, anti-tumor growth and metastasis, etc., G. lucidum has been proved to exhibit significant role in preventing and treating various kidney diseases.
In this chapter, we review certain researches and provide comprehensive insights into the reno-protective effects of G. lucidum.
Adv Exp Med Biol. 2019 ;1182:243-262. PMID: 31777022
- [z] Curcumin and chronic kidney disease (CKD): major mode of action through stimulating endogenous intestinal alkaline phosphatase.
Curcumin, an active ingredient in the traditional herbal remedy and dietary spice turmeric (Curcuma longa), has significant anti-inflammatory properties.
Chronic kidney disease (CKD), an inflammatory disease, can lead to end stage renal disease resulting in dialysis and transplant.
Furthermore, it is frequently associated with other inflammatory disease such as diabetes and cardiovascular disorders.
Recent studies have shown that increased intestinal permeability results in the leakage of pro-inflammatory molecules (cytokines and lipopolysaccharides) from gut into the circulation in diseases such as CKD, diabetes and atherosclerosis.
This change in intestinal permeability is due to decreased expression of tight junction proteins and intestinal alkaline phosphatase (IAP).
Curcumin increases the expression of IAP and tight junction proteins and corrects gut permeability.
This action reduces the levels of circulatory inflammatory biomolecules.
This effect of curcumin on intestine can explain why, despite poor bioavailability, curcumin has potential anti-inflammatory effects in vivo and beneficial effects on CKD.
Molecules. 2014 ;19(12):20139-56. Epub 2014 Dec 2. PMID: 25474287
- [aa] 25-vitamin D reduces inflammation in uremic environment.
Chronic kidney disease (CKD) is characterized by loss of renal function and a consequent increase of serum uremic toxins, which contribute to inflammation status. Deficiency of 25-vitamin D, often found in patients with CKD, has been included as an inflammatory factor since it might modulate the immune system.
Supplementation of 25-vitamin D was able to reduce the expression of TRL4, cathelicidin, and MCP-1 in the uremic environment.
This in vitro study showed that the uremic pool activates inflammatory response in monocytes, which was reversed by 25-vitamin D supplementation; this finding suggests that 25-vitamin D has an anti-inflammatory role in the uremic environment.
Sci Rep. 2020 Jan 10 ;10(1):128. Epub 2020 Jan 10. PMID: 31924826
- [bb] Rhubarb Protect Against Tubulointerstitial Fibrosis by Inhibiting TGF-β/Smad Pathway and Improving Abnormal Metabolome in Chronic Kidney Disease.
Tubulointerstitial fibrosis is the final common pathway for all kidney diseases leading to chronic kidney disease (CKD).
We found rhubarb extracts suppressed TGF-β/Smad3-mediated renal fibrosis by reducing the TGF-β1, transforming growth factor-β receptor I (TGF-β RI), transforming growth factor-β receptor II (TGF-β RII), Smad2, p-Smad2, Smad3, p-Smad3, and Smad4, meanwhile increased Smad7.
In addition, rhubarb extracts mitigated renal injury and dysfunction, and either fully or partially reversed the abnormalities of tissue metabolites.
Thus, rebalancing the disorder of TGF-β/Smad signaling and metabolic dysfunction by treatment with rhubarb extracts may represent as an effective therapy for CKD associated with fibrosis.
Front Pharmacol. 2018 ;9:1029. Epub 2018 Sep 13. PMID: 30271345
- [cc] The NLRP3 inflammasome is a potential target of ozone therapy aiming to ease chronic renal inflammation in chronic kidney disease.
Ozone therapy is an effective medical treatment for various diseases.
A previous study has demonstrated its reno-protective effect in chronic kidney disease (CKD), but the mechanism involved is not completely known.
The results showed that ozone therapy at a low concentration improved renal function and ameliorated renal morphological injury in 5/6 nephrectomized rats.
The expression of NLRP3, ASC, and caspase-1-p10 in the kidney of these rats was simultaneously lowered by ozone therapy.
Moreover, renal inflammation caused by IL-1β was significantly alleviated by ozone therapy.
The Pearson correlation analysis indicated that the protein level of IL-1β was positively correlated with renal injury scores.
Taken together, these results indicated that ozone therapy might reduce sterile renal inflammation and slow down CKD progression through the modulation of the NLRP3 inflammasome in 5/6 nephrectomized rats.
Int Immunopharmacol. 2017 Feb ;43:203-209. Epub 2016 Dec 27. PMID: 28038382
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