Two Truths and a Lie: Nutrition in CKD
The 2022 NSMC Internship is broken down into four rotations. One rotation is called Podcasting. There are two deliverables for that rotation:
Why Nephrology, a solo essay recorded as a podcast
Two Truths and a Lie, a group project that requires mixing multiple speakers, from multiple continents into a cohesive podcast.
Pod Three divided into two teams to complete the second deliverable, here is one of those teams.
Cast:
Anoushka Krishnan
Cristina Popa
Priya John
Momen Abbasi
References
T. Alp Ikizler,Jerrilynn D. Burrowes,Laura D. Byham-Gray,Daniel Teta,Angela Yee-Moon Wang,Lilian Cuppari KDOQI Clinical Practice Guideline for Nutrition in CKD: 2020 Update September 2020 AJKD/NKF
Rosman J.B., Langer K., Brandl M., Piers-Becht T.P., van der Hem G.K., ter Wee P.M., Donker A.J. Protein-restricted diets in chronic renal failure: A four year follow-up shows limited indications. Kidney Int. Suppl. 1989;27:96–102.
Cianciaruso B., Pota A., Bellizzi V., Di Giuseppe D., Di Micco L., Minutolo R., Pisani A., Sabbatini M., Ravani P. Effect of a low- versus moderate-protein diet on progression of CKD: Follow-up of a randomized controlled trial. Am. J. Kidney Dis. 2009;54:1052–1061.
Locatelli F., Del Vecchio L., Aicardi V. Nutritional Issues with Incremental Dialysis: The Role of Low-Protein Diets. Semin. Dial. 2017;30:246–250.
Lew QJ, Jafar TH, Koh HW, Jin A, Chow KY, Yuan JM, Koh WP. Red Meat Intake and Risk of ESRD. J Am Soc Nephrol. 2017 Jan;28(1):304-312. doi: 10.1681/ASN.2016030248.
S Joshi, . Plant based diets for kidney disease: a guide for clinicians. Am J Kidney Diseases, 2020; 77, 287-296
Goraya N, Simoni J, Jo C, Wesson D.E. Treatment of metabolic acidosis in patients with stage 3 chronic kidney disease with fruits and vegetables or oral bicarbonate reduces urine angiotensinogen and preserves glomerular filtration rate.Kidney Int. 2014; 86: 1031-1038
Goraya N, Simoni J, Jo C, Wesson D.E. A comparison of treating metabolic acidosis in CKD stage 4 hypertensive kidney disease with fruits and vegetables or sodium bicarbonate. Clin J Am Soc Nephrol. 2013; 8: 371-381
Goraya N, Simoni J, Jo C, Wesson D.E. Dietary acid reduction with fruits and vegetables or bicarbonate attenuates kidney injury in patients with a moderately reduced glomerular filtration rate due to hypertensive nephropathy. Kidney Int. 2012; 81: 86-93
Yusuf T, Raji YR, Lasisi TJ, Daniel A, Bamidele OT, Fasunla AJ, Lasisi AO. Predictors of Taste Dysfunction and Its Severity Among Patients With Chronic Kidney Disease. Ear Nose Throat J. 2021 Jul 19:1455613211019708.
Kim TH, Kim YH, Bae NY, Kang SS, Lee JB, Kim SB. Salty taste thresholds and preference in patients with chronic kidney disease according to disease stage: A cross-sectional study. Nutr Diet. 2018 Feb;75(1):59-64
McMahon EJ, Campbell KL, Bauer JD. Taste perception in kidney disease and relationship to dietary sodium intake. Appetite. 2014 Dec;83:236-241.
Márquez-Herrera RM, Núñez-Murillo GK, Ruíz-Gurrola CG, Gómez-García EF, Orozco-González CN, Cortes-Sanabria L, Cueto-Manzano AM, Rojas-Campos E. Clinical Taste Perception Test for Patients With End-Stage Kidney Disease on Dialysis. J Ren Nutr. 2020 Jan;30(1):79-84.
Kusaba T, Mori Y, Masami O, Hiroko N, Adachi T, Sugishita C, Sonomura K, Kimura T, Kishimoto N, Nakagawa H, Okigaki M, Hatta T, Matsubara H. Sodium restriction improves the gustatory threshold for salty taste in patients with chronic kidney disease. Kidney Int. 2009 Sep;76(6):638-43.
Brennan F, Stevenson J, Brown M. The Pathophysiology and Management of Taste Changes in Chronic Kidney Disease: A Review. J Ren Nutr. 2020 Sep;30(5):368-379.
Rodriguez-Benot A, Martin-Malo A, Alvarez-Lara MA, Rodriguez M, Aljama P. Mild hyperphosphatemia and mortality in hemodialysis patients. Am J Kidney Dis. 2005;46(1):68-77.
Kalantar-Zadeh K, Kuwae N, Regidor DL, et al. Survival predictability of time-varying indicators of bone disease in maintenance hemodialysis patients. Kidney Int. 2006;70(4):771-780.
Wald R, Walsh MW. In Search of the Optimal Target for Phosphate Control: Episode 1. J Am Soc Nephrol. 2021;32(3):526-528.
Edmonston DL, Isakova T, Dember LM, et al. Design and Rationale of HiLo: A Pragmatic, Randomized Trial of Phosphate Management for Patients Receiving Maintenance Hemodialysis. Am J Kidney Dis. 2021;77(6):920-930.e1.
SCRIPT
Anoushka: Hello and welcome to our next episode of two truths and a lie, an NSMC podcast. Let us go over the ground rules first. One at a time, each member of our education panel will make a statement, and another panel member will give their take on whether they think it is a truth or a lie. Our presenter then will educate us all on whether the statement is correct or incorrect. And why. So let us warm up our lie detectors for today. Let's meet our players firstly. I am your host, Dr. Anoushka Krishnan nephrologist from Perth, Australia. Our other panelists for today are Dr Cristina Popa, Dr Priya John, and Dr. Momen Abbasi. Could each of you please introduce yourselves.
Priya: Hey everyone. This is Dr Priya John. I'm a consultant nephrologist from Hyderabad, India. Hello everyone.
Momen: Hello everyone! This is Dr Momen. I'm a nephrology fellow in Hadassah medical center in Jerusalem.
Cristina: Hi there. My name is Cristina Popa. An early career nephrologist.
Anoushka: Great. So let us start. Priya will present her statement first and Momen will give us his thoughts.
Priya: Thank you Anoushka. So here comes the largely debatable part about diet in chronic kidney disease, the protein restriction part. Is it recommended or not? 2020 KDOQI Guidelines recommend low-protein of 0.5-0.6 gram per kg/ideal body weight in chronic kidney disease, stage three to five in metabolically stable diabetic and non diabetic patients for reducing the risk of progression to end-stage renal disease, death, and improving the quality of life.
Momen: Okay. I think that was the recommendation in the past. But I heard that a plant-based diet can slow the progression of CKD. So I will allow myself to think that it is a lie. But I would love to hear more about it from you, Priya.
Priya: Thanks Momen. Yeah. This statement is false. So before we get into the statement per se, I would like to define what ‘metabolically stable’ here means.“Metabolically stable” indicates absence of any active inflammatory or infectious diseases; no hospitalization within two weeks; absence of poorly controlled diabetes and consumptive diseases such as cancer; absence of antibiotics or immunosuppressive medications; and absence of significant short-term loss of body weight.
Before we discuss the protein requirement in CKD, let's see what is LPD, VLPD, High protein diet. The recommended level for VLPD is 0.28-0.43 g/kg ideal body weight) /day(with additional keto acid/amino acid analogs to meet protein requirements (0.55-0.60 g/kg per day).
LPD is low protein diet providing 0.55 to 0.60 g dietary protein/kg ideal body weight/day
HPD is >1.2gm/kg ideal body weight /per day.
Every day, approximately 250 g of protein is catabolized, leading to protein catabolic products, which are normally cleared by the kidneys and excreted in urine. When kidney function declines, there will be an accumulation of P-cresylsulphate, indoxyl-sulphate, trimethyl aminoxide, fibroblast-growth factor 23 which will progressively impair organ function.The rationale for reducing dietary protein intake in CKD is that a lower protein load reduces hyperfiltration and lowers the production of uremic toxins,
The evidence of LPD comes from RCT’s conducted in early 80’s by Rosman et al who randomized 248 patients to a LPD (0.4-0.6 g/kg/d) who concluded that LPD was only helpful in patients with primary glomerulonephritis. In early 90”s Locatelli et al enrolled 456 adult patients who were randomized to either a LPD (0.6 g/kg body weight daily; n = 226) or a "normal" controlled-protein diet (NPD) (1.0 g/kg daily; n = 230) and were stratified into three groups by baseline plasma creatinine concentrations and this study did not find any benefit of renal survival.
Cianciaruso et al in 2009 randomized 423 patients with CKD stages 4 and 5 to either LPD, 0.55 g/kg/d, or NPD 0.80 g/kg/d. After a median follow-up of 32 months, the LPD had no effect on any of the outcomes, protein-caloric malnutrition, dialysis, death, or the composite outcome of dialysis and death.
Accordingly, several meta-analyses indicate that VLPDs supplemented with keto acids delay the initiation of maintenance dialysis and significantly reduce urea production, along with having potentially beneficial effects on insulin resistance and oxidative stress.
For those with diabetes, protein intakes of 0.6-0.8 g/kg per day are recommended.
In HD and PD, there exists no randomized controlled trials for protein intake and outcomes. Based on observational studies, the recommended protein intake is 1.0-1.2 g/kg per day when in a stable metabolic state and with adequate energy intake. With diabetes, higher protein intake may be required to achieve glycemic control.
It may not be the quantity of protein always but rather the quality of protein. Not all proteins produce the same amount of acid that needs to be neutralized, animal protein, and specifically red meat tends to be higher in methionine and cysteine, both of which generate sulfuric acid in their catabolism. Lew et al. used the Singapore Chinese Health Study to look at total protein and the types of protein in over 63,000 people and examined the risk of ESKD with 15.5 years of follow up. Though total protein was related to the risk of ESKD it was not dose related. However, there was a strong dose-dependent relationship to red meat intake and increased risk of ESKD. This wasn’t seen with other protein sources (poultry, fish, eggs, or dairy products).
There is insufficient evidence to recommend a particular protein type (plant vs. animal) in terms of the effects on CKD progression or nutritional status.
However, several observational studies have suggested that plant proteins may have more reno-protective effects than animal proteins. A diet rich in protein from plant sources may slow the progression of CKD , decrease proteinuria, lower the level of uremic toxins ,phosphorus intake, and the endogenous production of acid .
And now that we have too many good drugs like RAS inhibitors and SGLT2 i why sacrifice some of the good things like food in life for which adherence is thin and not long lasting.
Anoushka: Thank you, Priya. That was very insightful indeed. Well our next presenter is going to be Dr Momen who will now present his statement. And Cristina will then tell us what she thinks about it.
Momen: Okay. Here is my statement. The recommendation to lower serum phosphate, aggressively, toward the normal range in order to improve clinical outcome is based on expert opinion and observational studies only. What do you think, Cristina?
Cristina: We already know that phosphate levels associates with so many adverse outcomes. But we don't really know what is associative, or maybe just the causative information. Maybe the statement is true.
Momen: That's right, Cristina. It is true, you know, hyperphosphatemia is a common complication of advanced kidney disease. And till now, epidemiological studies and experimental data suggested that there is an association between elevated serum phosphate and increased mortality. And based on this data, the nephrology community adopted opinion based guidelines that recommended lowering serum phosphate concentration for the normal range in ESKD patients undergoing maintenance dialysis. Achievement of this goal entails three elements for patients: restriction of dietary phosphate, and adherence to dialysis, and as well as a treatment with phosphate binders. Till now there are no RCTs that have shown that any phosphate binder demonstrated a beneficial effect on hard clinical outcomes and there are no completed randomized, controlled trials that have tested whether lowering serum phosphate levels improves clinical outcomes. Current guidelines are predicated on the assumption that the tight phosphate control will improve outcomes. But the association between high serum phosphate and poor outcomes does not prove causality, moreover, a dietary restriction of phosphate may compromise dietary enjoyment and binders each have important risks. This is a major uncertainty that affects our daily clinical practice. And hopefully there are two large ongoing trials right now, the PHOSPHATE trial and the HiLo trial. And we hope that they will shed more light on this question.
Anoushka: Thank you Momen. That was very interesting. Cristina will now present her statement which I will ponder upon, and this will be followed by our final statement by me and Priya will share her opinion on this.
Cristina: Thank you. My statement for today's CKD patients have a higher taste detection threshold for salt.
Anoushka: I think this may be true Cristina, although I must admit, I haven't really looked into the literature into this. I think I did see some interesting studies looking at this in the normal or the general population itself? I do often tell my patients to flavor their foods with herbs, spices, lemon and garlic rather than putting more salt in it. So I'm looking forward to what you have to say.
Cristina: Nice suggestions for your patients. Did you know approximately one third of the CKD patients have a taste dysfunction? Longer CKD duration and advanced CKD stages are associated more with taste dysfunction. Of all 4 kinds of tastes, the salty one is affected the most in CKD patients. A cross-sectional study including more than 400 non-dialysis patients with stage 3-5 CKD and 70 control showed a higher salt concentration is needed for the CKD cohort to detect salt, than in non-CKD. Few small cross-sectional studies revealed decreased salt perception in both hemodialysis and peritoneal dialysis patients compared to non-CKD. Physiologically salty taste occurs through sodium channels on the membranes of the taste bud. A salty taste is perceived only when it is above the background concentration of salivary NaCl to which the taste receptors are adapted. In CKD, a higher salt concentration can inhibit type 1 cells in the buds responsible for salty taste. Other mentionable causes for lower perception of salt can be zinc deficiency, uremic toxins, and higher levels of phosphorus
What do you think?
Anoushka: Well. I think that makes sense, that was great. Thank you, Cristina. And finally, this is my statement. Fruits and vegetable intake of up to two to four cups per day is the equivalent of the administration of sodium bicarbonate dosed at 0.3mmol/kg/day in stage three or four Chronic kidney disease.
Priya: So I'm one of those hard core believers of the DASH diet. So I think it would do the same magic in chronic kidney disease and I look forward to hearing from you.
Anoushka: Okay. So metabolic acidosis, as we all know, is a common complication of advanced chronic kidney disease and this adversely affects bone mineral content and can lead to skeletal muscle catabolism as well as kidney function decline. Western diets that are rich in animal based foods usually contain a high dietary acid load. Conversely, plant-based foods are rich in natural alkali, such as citrate and malate, which can then be converted to bicarbonate. Previous randomized, controlled trials have shown that administration of oral alkali in the form of sodium bicarbonate results in slower eGFR decline.
Alkali therapy can, however, also be provided via diet. In a series of trials, Goraya et al, demonstrated the benefits of fruit and vegetable consumption for metabolic acidosis in those with CKD. In an RCT of 108 patients with CKD stage 3 of 3 years duration, administration of two to four cups of fruits and vegetables per day was, in fact, comparable to oral sodium bicarbonate dosed at 0.3meQ/kg/day in increasing serum bicarbonate levels for the treatment of metabolic acidosis. Gfr decline was attenuated in those receiving alkali therapy: either oral sodium bicarbonate, or fruits and vegetables, compared with those not receiving alkali therapy. No difference in GFR decline was noted between the two groups receiving alkali therapy suggesting that fruits and vegetables may be equivalent to sodium bicarbonate for this purpose.
Further the groups receiving fruits and vegetables benefited from a mean 3.7 kilogram decrease in weight and a mean 7.4mmHg decrease in systolic blood pressure after three years compared with the sodium bicarbonate group. Similar findings were also noted in an RCT of 71 participants with CKD stage 4 that lasted for a year, Additionally compared to high potassium high, acidic meat rich diets, plant-based foods may promote distribution of a greater proportion of dietary potassium intracellularly and excretion of potassium in stools by increasing fecal bulk in the way of dietary fibre. So you may have two in one advantage with this.
In short, I often advise my patients to ‘eat more like a hippy and not like a truckie’.
So that's a wrap from our side. That was a very exciting session. And we certainly learned a lot about myths and facts on diet and CKD. And hopefully you did, too. Thank you so much for listening in.
