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Diet and nutrition

TL;DR — Nutrition in CKD is a multi-objective problem: preserve nutritional status while managing sodium, protein, potassium, acid load and treatment burden. MDRD did not establish a kidney benefit from intensive protein restriction on its primary GFR endpoint (Klahr 1994, PMID 8114857) (Levey 1999, PMID 10541304), whereas a later meta-analysis of 19 trials (2,492 participants) did find lower risk of kidney failure with a low-protein diet (OR 0.59, 95% CI 0.41–0.85) and of ESRD (OR 0.64, 0.43–0.96), with no effect on all-cause death (OR 1.17, 0.67–2.06) — an unresolved contrast between the single large trial and the pooled smaller ones (Yan 2018, PMID 30403710). KDOQI 2020 provides the major nutrition guideline framework (Ikizler 2020, PMID 32829751). Plant-predominant patterns may reduce acid load and improve fibre quality, but blanket potassium restriction can remove cardiometabolic foods without proving fewer clinical events (Carrero 2020, PMID 32528189) (Clegg 2020, PMID 32775988).

Protein

MDRD randomized 840 patients across two studies (585 with GFR 25–55 to usual [1.3 g/kg/day] versus low [0.58] protein; 255 with GFR 13–24 to low versus very-low [0.28] protein plus keto acids), each crossed with usual versus low blood-pressure targets. Over mean 2.2 years the projected three-year GFR decline did not differ significantly between diet groups; the low-protein group declined faster in the first four months and more slowly thereafter, and study 2 showed only a marginal difference (P=0.07) with no delay in ESRD or death (Klahr 1994, PMID 8114857) (Levey 1999, PMID 10541304). The 2018 meta-analysis of 19 trials reached the opposite headline conclusion (kidney failure OR 0.59, 0.41–0.85; eGFR-decline mean difference −1.85 mL/min/1.73 m²/year, P=0.001) while cautioning that the optimal intake level is unknown and nutritional status must be watched (Yan 2018, PMID 30403710). The discrepancy is a live methodological question, not a settled small effect.

Sodium

Lower sodium can reduce blood pressure and albuminuria and potentiate RAS blockade. The kidney endpoint is inseparable from volume status, intake measurement and adherence.

Potassium

Serum potassium depends on excretion, medications, acidosis and food bioavailability. Plant potassium is not equivalent to additives; restriction should follow phenotype rather than CKD label alone (Sumida 2023, PMID 37610407).

Plant-predominant patterns

Potential advantages include fibre, lower dietary acid and less phosphorus additive exposure; risks include inadequate energy/protein and hyperkalaemia in susceptible patients (Carrero 2020, PMID 32528189).

Ketoanalogues

A meta-analysis of 16 trials (1,344 participants, median follow-up 13 months) found ketoanalogue supplementation of a protein-restricted diet gave significantly higher GFR, lower urea nitrogen and phosphorus, higher calcium and a marginally lower ESKD risk in participants without diabetes, with no difference in all-cause mortality, albumin, mid-arm muscle circumference, lean body mass or subjective global assessment (Chen 2024, PMID 39340710). Trials combine supplements with intensive dietitian support; generalizability and adherence remain central limitations.

Measurement

Diet recalls, urinary biomarkers, serum chemistry and nutritional status answer different questions. Clinical endpoints should include hospitalization and quality of life.

Nutrition questions must stay separate

The distinctions below synthesize the MDRD evidence and KDOQI nutrition framework (Klahr 1994, PMID 8114857; Ikizler 2020, PMID 32829751).

Domain Intended effect Main risk of over-interpretation
Protein restriction Reduce nitrogenous load and hyperfiltration Adherence, energy deficit and malnutrition can overwhelm a small kidney effect
Sodium reduction Lower volume, pressure and albuminuria Intake measurement is noisy; clinical outcomes are rarely primary
Potassium restriction Prevent recurrent hyperkalaemia Removes plant foods and fibre when food source and bioavailability are ignored
Plant-predominant pattern Lower acid load; improve fibre and food quality Evidence is not equivalent to a hard-outcome randomized trial
Very-low-protein + ketoanalogues Reduce solute load while supplying amino-acid precursors Requires specialist support and has limited generalizability

Protein restriction: what MDRD actually showed

MDRD is cited more often than it is read, and its result is more equivocal than either advocates or critics allow. In Study B (255 patients, baseline GFR 13–24 mL/min/1.73 m², mean follow-up 2.2 years), the very-low-protein diet (0.28 g/kg/day plus keto acid–amino acid supplement) gave only a marginally slower GFR decline than the low-protein diet (0.58 g/kg/day) — p = 0.066. But in correlational analysis pooling both arms and adjusting for baseline progression factors, a 0.2 g/kg/day lower achieved total protein intake was associated with a 1.15 mL/min/year slower GFR decline (p = 0.011), about 29% of the mean decline; after adjusting for achieved intake, prescribed diet had no independent effect (Levey 1996, PMID 8629624). The trial thus provides randomized evidence that is at best borderline and observational evidence within the trial that is stronger — a dissociation caused by imperfect adherence, and one that cannot distinguish protein restriction from whatever else distinguishes adherent patients.

Long-term follow-up complicates it further. Tracking 585 Study A participants (GFR 25–55, randomized to 0.58 versus 1.3 g/kg/day for 2–3 years) through registries to the end of 2000, kidney failure occurred in 327 (56%) and the composite of kidney failure or death in 380 (65%). Adjusted hazard ratios over the whole period were 0.89 (95% CI 0.71–1.12) and 0.88 (0.71–1.08) — but the effect was concentrated in the first six years (0.68, 0.51–0.93 and 0.66, 0.50–0.87) and reversed afterwards (1.27, 0.90–1.80 and 1.29, 0.94–1.78), with interaction p = 0.008 and 0.002 (Levey 2006, PMID 17162142). Dietary data after the trial ended were unavailable, so whether the late reversal reflects lost benefit, nutritional harm accumulating, or the natural history of a cohort whose diet was no longer being managed cannot be determined. A two-to-three-year dietary intervention with a benefit that inverts after six years is not a settled recommendation.

Sodium restriction: the best-evidenced dietary intervention

Meta-analysis of 11 randomized trials in 738 adults with non-dialysis CKD stages 1–4 achieved urinary sodium excretion of 104 mEq/day (95% CI 76–131) on low-sodium versus 179 mEq/day (165–193) on high-sodium — a mean difference of −80 mEq/day (−107 to −53; p < 0.001). That separation produced mean reductions of 4.9 mmHg (95% CI 3.1–6.8) in clinic systolic and 5.9 mmHg (2.3–9.5) in ambulatory systolic blood pressure, 2.3 mmHg (1.2–3.5) and 3.0 mmHg (1.7–4.3) in clinic and ambulatory diastolic pressure, and reductions of 0.39 g/day (0.22–0.55) in proteinuria and 0.05 g/day (0.01–0.09) in albuminuria (Garofalo 2018, PMID 29882800). No trial has tested hard kidney outcomes, and the trials are short.

Dietary pattern beats nutrient counting

Among 2,539 CRIC participants followed a median 7 years for progression and 12 for death (977 progression events, 836 deaths), the highest versus lowest adherence to an overall plant-based diet index carried 26% lower all-cause mortality (HR 0.74, 95% CI 0.62–0.88; p-trend < 0.001) and to a healthy plant-based index 21% lower (HR 0.79, 0.66–0.95; p-trend = 0.03). Each 10-point higher unhealthy plant-based diet score was associated with higher CKD progression (HR 1.14, 1.03–1.25) and mortality (HR 1.11, 1.00–1.23) (Amir 2024, PMID 38103719). "Plant-based" is therefore not a single exposure: refined grains, sugar and processed plant foods score as plant-based and move risk the other way. Diet is self-reported and confounding by overall health behaviour is unresolved.

The potassium-restriction question is genuinely open

The KDIGO Controversies Conference on potassium homeostasis states the position plainly: evidence increasingly shows beneficial associations between plant-based eating patterns and cardiovascular and kidney outcomes, supporting "a paradigm shift from the idea of dietary restriction toward fostering patterns of eating that are associated with better outcomes", while noting the paucity of data on whether dietary modification actually restores abnormal serum potassium to normal (Clase 2020, PMID 31706619).

A 16-person randomized crossover pilot in advanced CKD on RAS inhibition subsequently compared six weeks of a potassium-rich diet (40 mmol/day added through fruit, vegetables and nuts) with the participants' regular diet. Serum potassium met the prespecified non-inferiority criterion (between-period difference 0.03 mmol/L, 95% CI −0.32 to 0.27); two participants developed hyperkalaemia and continued the diet after sodium zirconium cyclosilicate. This establishes short-term feasibility in selected, closely monitored patients, not comparative clinical benefit or population-level safety (Moest 2026, PMID 42636918).

This creates a direct conflict inside dietary advice for CKD. The foods that carry the mortality benefit in CRIC (Amir 2024, PMID 38103719) and the blood-pressure and lipid benefits in the acidosis literature (see potassium, acidosis and metabolic complications) are the same foods that low-potassium counselling removes. The conflict has not been resolved by any trial randomizing potassium liberalisation against restriction with clinical endpoints, and the availability of potassium binders has changed the terms of the argument without settling it.

Intervention Effect size Evidence quality
Protein restriction (prescribed) Kidney failure HR 0.89 (0.71–1.12) overall; 0.68 (0.51–0.93) first 6 years, 1.27 (0.90–1.80) after (Levey 2006, PMID 17162142) RCT with long registry follow-up; time-interaction unexplained
Protein intake (achieved) 0.2 g/kg/day lower intake ↔ 1.15 mL/min/yr slower GFR decline (Levey 1996, PMID 8629624) Within-trial correlation, not randomized contrast
Sodium restriction −80 mEq/day → SBP −4.9 mmHg, proteinuria −0.39 g/day (Garofalo 2018, PMID 29882800) 11 RCTs, 738 patients; no hard endpoints
Healthy plant-based pattern Mortality HR 0.74 (0.62–0.88) highest vs lowest adherence (Amir 2024, PMID 38103719) Prospective cohort; self-reported diet
Potassium liberalisation Serum potassium difference 0.03 mmol/L (−0.32 to 0.27); 2/16 required sodium zirconium cyclosilicate (Moest 2026, PMID 42636918) Six-week crossover pilot; feasibility and biochemical safety only

Hydration: a strong observational signal, a null trial

Higher water intake is associated with better kidney function in observational data, and the association has driven widespread advice. CKD WIT randomized 631 adults with stage 3 CKD (eGFR 30–60 with micro- or macroalbuminuria, 24-hour urine volume under 3.0 L; mean age 65.0, 63.4% men, mean eGFR 43, median urine albumin 123 mg/day) at nine Ontario centres to coaching to drink more water or to maintain usual intake. Coaching worked: the mean change in 24-hour urine volume was 0.6 L/day higher in the hydration group (95% CI 0.5–0.7; p < 0.001). Kidney function did not follow: eGFR change over 12 months was −2.2 mL/min/1.73 m² with hydration and −1.9 without, an adjusted between-group difference of −0.3 (95% CI −1.8 to 1.2; p = 0.74) (Clark 2018, PMID 29801012).

This belongs beside the urate trials on the pathophysiology page as a second demonstration that a robust epidemiological association plus a plausible mechanism plus successful target engagement can still yield no effect.

Ultra-processed food: consistent across incidence and progression

Incidence. Among 14,679 middle-aged ARIC participants without CKD at baseline and followed a median 24 years, there were 4,859 incident CKD events. The incidence rate was 16.5 per 1,000 person-years (95% CI 15.6–17.4) in the highest quartile of ultra-processed food consumption and 14.7 (13.9–15.5) in the lowest; after adjustment for lifestyle, demographic and behavioural confounders the highest quartile carried 24% higher risk (HR 1.24, 95% CI 1.15–1.35), with an approximately linear dose–response (Du 2022, PMID 35679994).

Progression. In CRIC, with 1,047 CKD progression events over median 7 years and 1,104 deaths over median 14 years, the highest versus lowest tertile of ultra-processed food intake (NOVA classification) carried higher risk of progression (HR 1.22, 95% CI 1.04–1.42; p-trend 0.01) and mortality (HR 1.21, 1.04–1.40; p-trend 0.004). The progression association was concentrated in participants with baseline eGFR ≥60 (HR 2.61, 95% CI 1.32–5.18) and absent below 60 (p-interaction 0.003) (Sullivan 2023, PMID 37028638).

The eGFR interaction is a useful corrective to the assumption that dietary advice should intensify as CKD advances: the measurable association with progression exists where kidney function is still preserved. Both studies rest on self-reported diet, and processing category correlates with income, food environment and health behaviour in ways adjustment cannot fully separate.

Decision and interpretation matrix

Dimension Question Guardrail
Diagnostic axis Cause + G category + A category Avoid treating eGFR as the diagnosis
Time axis Chronicity and trajectory Separate acute change from persistent disease
Risk axis Kidney failure + cardiovascular events + death Show competing events
Treatment axis Eligibility, absolute benefit, harm, burden Do not rank drugs by relative effect alone
Measurement axis Assay, equation, repeatability State what was actually measured
Equity axis Testing, referral, access, affordability Audit downstream care, not labels only
Patient axis Symptoms, function, life participation Include outcomes patients prioritize
Evidence axis RCT, cohort, model, guideline Do not collapse designs

Evidence ledger

This ledger makes the page’s evidentiary mix inspectable. It does not imply that every source answers every question.

PMID Record used Role and boundary
8114857 The effects of dietary protein restriction and blood-pressure control on the progression of chronic renal disease: MDRD. (Klahr 1994, PMID 8114857) Intervention study; eligibility, comparator, endpoint and follow-up bound inference.
10541304 Dietary protein restriction and the progression of chronic renal disease: what have all of the results of the MDRD study shown? (Levey 1999, PMID 10541304) Observational or conceptual evidence; association is not treatment effect.
30403710 Effect of diet protein restriction on progression of chronic kidney disease: systematic review and meta-analysis. (Yan 2018, PMID 30403710) Synthesis; heterogeneity and included-study definitions constrain transport.
32829751 KDOQI Clinical Practice Guideline for Nutrition in CKD: 2020 Update. (Ikizler 2020, PMID 32829751) Guideline or commentary; recommendation evidence depends on its review.
32528189 Plant-based diets to manage the risks and complications of chronic kidney disease. (Carrero 2020, PMID 32528189) Observational or conceptual evidence; association is not treatment effect.
32775988 Impact of Dietary Potassium Restrictions in CKD on Clinical Outcomes: Benefits of a Plant-Based Diet. (Clegg 2020, PMID 32775988) Observational or conceptual evidence; association is not treatment effect.
37610407 New Insights Into Dietary Approaches to Potassium Management in Chronic Kidney Disease. (Sumida 2023, PMID 37610407) Observational or conceptual evidence; association is not treatment effect.
39340710 Ketoanalogue supplementation combined with protein-restricted diets in advanced chronic kidney disease: systematic review and meta-analysis. (Chen 2024, PMID 39340710) Synthesis; heterogeneity and included-study definitions constrain transport.
38490803 KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. (KDIGO CKD Work Group 2024, PMID 38490803) Guideline or commentary; recommendation evidence depends on its review.
38519239 Executive summary of the KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease: known knowns and known unknowns. (Levin 2024, PMID 38519239) Guideline or commentary; recommendation evidence depends on its review.
32061315 Global, regional, and national burden of chronic kidney disease, 1990-2017. (GBD CKD Collaboration 2020, PMID 32061315) Modelled projection; the estimate follows from the model inputs and assumptions, not from observed randomized follow-up.
22038337 A population-based approach for the definition of chronic kidney disease: CKD Prognosis Consortium. (Cirillo 2012, PMID 22038337) Synthesis; heterogeneity and included-study definitions constrain transport.
23243116 Cohort profile: the chronic kidney disease prognosis consortium. (Matsushita 2013, PMID 23243116) Observational or conceptual evidence; association is not treatment effect.
37787795 Estimated GFR, Albuminuria, and Adverse Outcomes: individual-participant data meta-analysis. (CKD Prognosis Consortium 2023, PMID 37787795) Synthesis; heterogeneity and included-study definitions constrain transport.
30348535 Relationship of Estimated GFR and Albuminuria to Concurrent Laboratory Abnormalities. (Inker 2019, PMID 30348535) Synthesis; heterogeneity and included-study definitions constrain transport.
34554658 New Creatinine- and Cystatin C-Based Equations to Estimate GFR without Race. (Inker 2021, PMID 34554658) Observational or conceptual evidence; association is not treatment effect.
33652433 The 2020 Updated KDOQI Clinical Practice Guidelines for Nutrition in Chronic Kidney Disease. (Ikizler 2021, PMID 33652433) Guideline or commentary; recommendation evidence depends on its review.
32737016 ISRNM commentary on the KDOQI Clinical Practice Guideline for Nutrition in CKD. (Kistler 2021, PMID 32737016) Guideline or commentary; recommendation evidence depends on its review.
36594428 Protein restriction for diabetic kidney disease. (Jiang 2023, PMID 36594428) Synthesis; heterogeneity and included-study definitions constrain transport.
38261535 VALOR-CKD trial of veverimer in CKD with metabolic acidosis. (Tangri 2024, PMID 38261535) Intervention study; eligibility, comparator, endpoint and follow-up bound inference.
38457574 Sodium citrate versus sodium bicarbonate for metabolic acidosis in CKD. (Sorohan 2024, PMID 38457574) Intervention study; eligibility, comparator, endpoint and follow-up bound inference.
31533906 Patiromer to enable spironolactone in resistant hypertension and CKD: AMBER. (Agarwal 2019, PMID 31533906) Intervention study; eligibility, comparator, endpoint and follow-up bound inference.
40542996 Novel potassium binders, hyperkalemia and RAAS inhibitor optimization: meta-analysis. (Huang 2025, PMID 40542996) Synthesis; heterogeneity and included-study definitions constrain transport.
38622759 Sodium zirconium cyclosilicate in CKD, hyperkalemia, and metabolic acidosis: NEUTRALIZE. (Ash 2024, PMID 38622759) Intervention study; eligibility, comparator, endpoint and follow-up bound inference.
32588430 Potassium binders for chronic hyperkalaemia in people with CKD. (Natale 2020, PMID 32588430) Synthesis; heterogeneity and included-study definitions constrain transport.

What can and cannot be concluded

  • Risk associations do not by themselves establish that changing the marker changes risk.
  • A relative effect must be paired with baseline risk, follow-up and the exact endpoint.
  • Albuminuria, acute eGFR change, chronic eGFR slope and kidney failure are not interchangeable.
  • Subgroup consistency is not evidence that every subgroup had adequate power.
  • Guideline recommendations combine evidence with values, feasibility, cost and service capacity.
  • Older adults require competing-mortality and treatment-burden framing.
  • Dialysis and transplantation comparisons are vulnerable to eligibility and immortal-time bias.
  • Modelled lifetime benefit is not a randomized observed benefit.
  • A biochemical response without a patient-important outcome remains a surrogate result.
  • This page is research synthesis, not individualized medical advice.

Research-design checklist

  • Define CKD cause, G category, A category and chronicity at baseline.
  • Report the creatinine or cystatin C equation and laboratory calibration.
  • Prespecify acute and chronic eGFR slopes when haemodynamic effects are expected.
  • Keep sustained GFR decline, kidney failure and replacement therapy separable.
  • Report absolute event risks, follow-up and confidence intervals with relative effects.
  • Treat death as a competing event where it can preclude kidney failure.
  • Measure hyperkalaemia, acute kidney injury and treatment discontinuation consistently.
  • Include symptoms, function, life participation and treatment burden.
  • Describe background RAS, SGLT2, MRA and GLP-1 therapy explicitly.
  • Prespecify albuminuria and cause strata without over-reading underpowered interactions.
  • Record screening, prescribing, persistence and monitoring as separate implementation steps.
  • Report representation, access and affordability variables needed for equity analysis.

Open questions

  • Why do MDRD and the pooled smaller trials disagree about protein restriction? MDRD found no significant effect on its primary GFR endpoint while a 19-trial meta-analysis found kidney failure OR 0.59 (0.41–0.85); adherence, follow-up length and trial size are candidate explanations (Klahr 1994, PMID 8114857) (Yan 2018, PMID 30403710). → OQ-15
  • Can a plant-predominant pattern lower acid load without causing clinically important hyperkalaemia? Potassium bioavailability differs by food source, but no hard-outcome diet trial has tested the trade-off (Carrero 2020, PMID 32528189) (Sumida 2023, PMID 37610407). → OQ-16
  • Do ketoanalogue trials generalise beyond intensive dietitian support, and does the GFR advantage translate into ESKD delay in people with diabetes? The signal was confined to participants without diabetes (Chen 2024, PMID 39340710).

  • Which nutritional-status measure should gate a protein-restriction decision, given that albumin, lean mass and global assessment did not move in the ketoanalogue trials (Chen 2024, PMID 39340710)?

  • Why did the protein-restriction benefit in MDRD invert after six years (HR 0.68 then 1.27; interaction p=0.008), and is the late signal harm or loss of dietary management data (Levey 2006, PMID 17162142)?

  • Does sodium restriction change kidney or cardiovascular outcomes, or only blood pressure and proteinuria? No trial has tested hard endpoints despite a 4.9 mmHg systolic effect from an 80 mEq/day reduction (Garofalo 2018, PMID 29882800).
  • Should potassium restriction be abandoned in favour of dietary patterns? The foods carrying the mortality benefit in CRIC (Amir 2024, PMID 38103719) are the ones low-potassium counselling removes, and no trial has randomized liberalisation against restriction with clinical endpoints (Clase 2020, PMID 31706619).

  • Is "plant-based" a coherent exposure when the unhealthy version of the same index predicts higher CKD progression (HR 1.14, 1.03–1.25) (Amir 2024, PMID 38103719)?

  • Why did a 0.6 L/day increase in urine volume — successful target engagement — produce no eGFR difference at 12 months in stage 3 CKD (Clark 2018, PMID 29801012), when observational hydration associations are consistent?

  • Why is ultra-processed food intake associated with CKD progression at eGFR ≥60 (HR 2.61, 1.32–5.18) but not below 60 (p-interaction 0.003) (Sullivan 2023, PMID 37028638) — biology, reverse causation, or dietary change after diagnosis?
  • Can the ultra-processed food association be separated from income and food environment in any observational design (Du 2022, PMID 35679994)?

References

  1. Klahr et al. The effects of dietary protein restriction and blood-pressure control on the progression of chronic renal disease: MDRD. N Engl J Med. 1994;330(13):877-884. PMID 8114857
  2. Levey et al. Dietary protein restriction and the progression of chronic renal disease: what have all of the results of the MDRD study shown? J Am Soc Nephrol. 1999;10(11):2426-2439. PMID 10541304
  3. Yan et al. Effect of diet protein restriction on progression of chronic kidney disease: systematic review and meta-analysis. PLoS One. 2018;13(11):e0206134. PMID 30403710
  4. Ikizler et al. KDOQI Clinical Practice Guideline for Nutrition in CKD: 2020 Update. Am J Kidney Dis. 2020;76(3 Suppl 1):S1-S107. PMID 32829751
  5. Carrero et al. Plant-based diets to manage the risks and complications of chronic kidney disease. Nat Rev Nephrol. 2020;16(9):525-542. PMID 32528189
  6. Clegg et al. Impact of Dietary Potassium Restrictions in CKD on Clinical Outcomes: Benefits of a Plant-Based Diet. Kidney Med. 2020;2(4):476-487. PMID 32775988
  7. Sumida et al. New Insights Into Dietary Approaches to Potassium Management in Chronic Kidney Disease. J Ren Nutr. 2023;33(6S):S6-S12. PMID 37610407
  8. Chen et al. Ketoanalogue supplementation combined with protein-restricted diets in advanced chronic kidney disease: systematic review and meta-analysis. J Nephrol. 2024;37(8):2113-2125. PMID 39340710
  9. KDIGO CKD Work Group et al. KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney Int. 2024;105(4S):S117-S314. PMID 38490803
  10. Levin et al. Executive summary of the KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease: known knowns and known unknowns. Kidney Int. 2024;105(4):684-701. PMID 38519239
  11. GBD CKD Collaboration et al. Global, regional, and national burden of chronic kidney disease, 1990-2017. Lancet. 2020;395(10225):709-733. PMID 32061315
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  13. Matsushita et al. Cohort profile: the chronic kidney disease prognosis consortium. Int J Epidemiol. 2013;42(6):1660-1668. PMID 23243116
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  16. Inker et al. New Creatinine- and Cystatin C-Based Equations to Estimate GFR without Race. N Engl J Med. 2021;385(19):1737-1749. PMID 34554658
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  18. Kistler et al. ISRNM commentary on the KDOQI Clinical Practice Guideline for Nutrition in CKD. J Ren Nutr. 2021;31(2):116-120.e1. PMID 32737016
  19. Jiang et al. Protein restriction for diabetic kidney disease. Cochrane Database Syst Rev. 2023;1(1):CD014906. PMID 36594428
  20. Tangri et al. VALOR-CKD trial of veverimer in CKD with metabolic acidosis. J Am Soc Nephrol. 2024;35(3):311-320. PMID 38261535
  21. Sorohan et al. Sodium citrate versus sodium bicarbonate for metabolic acidosis in CKD. Medicine (Baltimore). 2024;103(10):e37475. PMID 38457574
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  25. Natale et al. Potassium binders for chronic hyperkalaemia in people with CKD. Cochrane Database Syst Rev. 2020;6(6):CD013165. PMID 32588430
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