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Potassium, acidosis and metabolic complications

TL;DR — Hyperkalaemia and metabolic acidosis are both consequences of reduced excretory reserve and barriers to disease-modifying therapy. Novel potassium binders lower potassium and can enable RAS/MRA continuation, but most trials measure biochemical control or medication persistence rather than kidney failure (Agarwal 2019, PMID 31533906) (Natale 2020, PMID 32588430) (Huang 2025, PMID 40542996). Oral alkali raises bicarbonate, yet VALOR-CKD found veverimer did not slow CKD progression (HR 0.99, 95% CI 0.80–1.20), in a trial with a small bicarbonate separation (Tangri 2024, PMID 38261535). Management evidence must separate correction of a laboratory value, symptom or function benefit, and long-term kidney outcome.

Hyperkalaemia as a treatment limiter

Risk reflects GFR, diabetes, diet, acidosis and medications. Stopping protective RAS therapy may lower potassium while sacrificing kidney and cardiovascular benefit.

Patiromer enablement

AMBER showed a 19.5 percentage-point increase in persistence with spironolactone at 12 weeks (Agarwal 2019, PMID 31533906). It did not establish long-term kidney benefit.

Sodium zirconium cyclosilicate

NEUTRALIZE studied potassium and bicarbonate in stage 3–5 CKD; small size and short duration limit clinical-outcome inference (Ash 2024, PMID 38622759).

Binder evidence

Cochrane review found potassium lowering but uncertainty about patient-important outcomes and comparative strategies (Natale 2020, PMID 32588430).

Acidosis

Low bicarbonate associates with progression and muscle effects, but confounding by disease severity is substantial. Sodium load and pill burden accompany bicarbonate treatment.

VALOR-CKD

Veverimer did not improve the kidney composite, and achieved bicarbonate separation was about 1 mEq/L, limiting interpretation of the biological hypothesis (Tangri 2024, PMID 38261535).

Intervention endpoints

Strategy Trial-level effect What remains unknown
Patiromer enablement 86% vs 66% remained on spironolactone; difference 19.5 points (10.0–29.0) Long-term kidney/CV effect (Agarwal 2019, PMID 31533906)
Novel binder meta-analysis RAASi optimization RR 1.38 (1.16–1.65); potassium −0.71 mEq/L Durability and hard outcomes (Huang 2025, PMID 40542996)
Potassium binders overall Biochemical potassium lowering Comparative patient-important evidence limited (Natale 2020, PMID 32588430)
Sodium zirconium cyclosilicate Potassium and bicarbonate feasibility in CKD Small, short NEUTRALIZE study (Ash 2024, PMID 38622759)
Veverimer Kidney composite HR 0.99 (0.80–1.20) Only ~1 mEq/L bicarbonate separation; hypothesis incompletely tested (Tangri 2024, PMID 38261535)
Sodium bicarbonate/citrate Raises bicarbonate Sodium burden, tolerability and kidney-outcome certainty

Alkali therapy: two well-conducted trials pointing opposite ways

A large positive open-label trial. The UBI study randomized 740 patients with CKD stages 3–5 (mean age 67.8 ± 14.9, creatinine clearance 30 ± 12 mL/min, serum bicarbonate 21.5 ± 2.4 mmol/L) to sodium bicarbonate (~1.1 mmol/kg/day) or standard care for 36 months. Creatinine doubling occurred in 62/364 (17.0%) on standard care versus 25/376 (6.6%) on bicarbonate (p < 0.001); dialysis initiation in 45 (12.3%) versus 26 (6.9%) (p = 0.016); and death in 25 (6.8%) versus 12 (3.1%) (p = 0.004), with no significant effect on blood pressure, body weight or hospitalisation (Di Iorio 2019, PMID 31598912). A mortality halving from oral bicarbonate is a very large effect for a cheap intervention, and the trial was open-label with standard care rather than placebo as comparator.

A large negative placebo-controlled trial. VALOR-CKD randomized 1,480 patients with eGFR 20–40 and serum bicarbonate 12–20 mEq/L across 320 sites in 35 countries to veverimer (a hydrochloric acid binder) or placebo, after an active run-in that raised mean bicarbonate from 17.5 ± 1.4 to 23.4 ± 2.0 mEq/L. After randomized withdrawal, the between-group bicarbonate difference was only about 1 mEq/L (22.0 ± 3.0 versus 20.9 ± 3.3 at month 3) and stayed there for 24 months. The composite of ESKD, sustained ≥40% eGFR decline or kidney-failure death occurred in 149/741 versus 148/739 (HR 0.99, 95% CI 0.8–1.2; p = 0.90), with no safety differences (Tangri 2024, PMID 38261535).

The two results are less contradictory than they look, and the reconciliation is the finding. VALOR-CKD achieved a separation of roughly 1 mEq/L — the trial tested a drug, and the drug barely separated the arms on the biomarker it was supposed to move, because placebo-arm bicarbonate also rose after the run-in. UBI achieved and maintained a therapeutic bicarbonate dose but without blinding. So the field currently has no adequately powered, blinded trial in which serum bicarbonate was substantially and durably separated between arms — which means the question "does correcting acidosis slow CKD?" is unanswered rather than answered negatively.

Diet as the alkali. Randomizing 108 macroalbuminuric non-diabetic CKD patients with metabolic acidosis to base-producing fruit and vegetables (enough to halve dietary acid), oral sodium bicarbonate 0.3 mEq/kg/day, or usual care for five years, plasma total CO2 rose in both active arms without differing between them, and five-year eGFR decline was smaller in both (bicarbonate −12.3, 95% CI −12.9 to −11.7; fruit and vegetables −10.0, −10.6 to −9.4) than usual care (−18.8, −19.5 to −18.2; p < 0.01), with no difference between the active arms. Fruit and vegetables additionally produced lower systolic blood pressure, lower LDL and Lp(a) and higher serum vitamin K1 (Goraya 2019, PMID 30995657). Sample size is small and allocation was to a dietary behaviour, but this is the only comparison showing that the route of alkali delivery changes cardiovascular risk indicators.

Potassium binders: potassium control is not the outcome

Enabling RAAS inhibition. DIAMOND screened 1,642 patients with HFrEF and current or prior RAASi-related hyperkalaemia, enrolled 1,195 in a patiromer run-in with RAASi optimisation, achieved target doses in 878 (84.6%), and randomized 439 to continue patiromer and 439 to placebo. The adjusted mean potassium change was +0.03 versus +0.13 mmol/L (difference −0.10 mmol/L, 95% CI −0.13 to 0.07; p < 0.001) over median 27 weeks. Patiromer reduced hyperkalaemia above 5.5 mmol/L (HR 0.63, 0.45–0.87; p = 0.006), reduced MRA dose reduction (HR 0.62, 0.45–0.87; p = 0.006) and lowered total hyperkalaemia events (77.7 versus 118.2 per 100 person-years; HR 0.66, 0.53–0.81; p < 0.001), with hierarchical win ratios favouring patiromer for hyperkalaemia-related morbidity (1.53; p < 0.001) and total RAASi use (1.25; p = 0.048) (Butler 2022, PMID 35900838).

Note what DIAMOND does and does not show. It shows a binder keeps people on guideline-dose RAASi and MRA. It does not show that doing so improves cardiovascular or kidney outcomes, because the trial was not powered for them and the design — randomized withdrawal after a run-in — selects for tolerance.

Testing an actual outcome. DIALIZE-Outcomes randomized 2,690 thrice-weekly haemodialysis patients with predialysis potassium ≥5.5 mmol/L to sodium zirconium cyclosilicate titrated to normokalaemia or placebo. The primary composite of sudden cardiac death, stroke, or arrhythmia-related hospitalisation, intervention or emergency visit occurred in 119 (8.8%) versus 119 (8.9%) — HR 0.98, 95% CI 0.76–1.26 — with no effect on individual outcomes, despite decisively better potassium control (normokalaemia at 12 months 74.0% versus 47.0%; OR 3.36, 2.64–4.26). The trial was terminated early with only ~33% of planned events and high study-drug discontinuation, which limits generalisability; hypokalaemia occurred in 3.0% versus 1.4% (Fishbane 2025, PMID 40618849).

The Cochrane review of potassium binders in CKD frames the same gap: the newer resins have better gastrointestinal tolerability than polystyrene sulfonates, but evidence on clinically relevant endpoints such as cardiac complications and death remains limited (Natale 2020, PMID 32588430).

Question Trial Answer Limit
Does oral alkali slow CKD? UBI, n=740 (PMID 31598912) Creatinine doubling 6.6% vs 17.0%; death 3.1% vs 6.8% Open-label vs standard care
Does an acid binder slow CKD? VALOR-CKD, n=1,480 (PMID 38261535) HR 0.99 (0.8–1.2) Only ~1 mEq/L bicarbonate separation achieved
Does the alkali source matter? Goraya, n=108 (PMID 30995657) Equal eGFR effect; better BP, LDL, Lp(a), vitamin K1 with fruit/vegetables Small; behavioural allocation
Does a binder keep people on RAASi/MRA? DIAMOND, n=878 randomized (PMID 35900838) Yes: hyperkalaemia HR 0.63; MRA dose reduction HR 0.62 Not powered for clinical outcomes
Does controlling potassium reduce arrhythmic events? DIALIZE-Outcomes, n=2,690 (PMID 40618849) No: HR 0.98 (0.76–1.26) despite OR 3.36 for normokalaemia Stopped early at ~33% of planned events

The cost of stopping: hyperkalaemia-driven RAASi discontinuation

The potassium binder trials above test whether a drug lets people stay on RAAS inhibitors. The observational literature quantifies what happens when they do not. In population-based cohorts of adults with CKD and a de novo episode of RAASi-related hyperkalaemia (serum potassium ≥5.5 mmol/L) — 7,200 in Manitoba and 71,290 in Ontario, with mean potassium 5.8 and 5.7 mEq/L and mean eGFR 41 mL/min/1.73 m² in both — discontinuation of the RAAS inhibitor was associated with higher all-cause mortality (Manitoba HR 1.32, 95% CI 1.22–1.41; Ontario HR 1.47, 1.41–1.52), higher cardiovascular mortality (1.28, 1.13–1.44 and 1.32, 1.25–1.39) and higher risk of dialysis initiation (1.65, 1.41–1.85 and 1.11, 1.08–1.16), with a negative control outcome (cataract surgery) included to probe residual confounding (Leon 2022, PMID 35085685).

Consistency across two independent provincial cohorts and the inclusion of a negative control strengthen the inference, but the design cannot exclude that discontinuation marks deteriorating health rather than causing it. Read alongside DIAMOND — which shows a binder can keep people on target-dose RAASi and MRA but was not powered for outcomes (Butler 2022, PMID 35900838) — the two literatures bracket the question from opposite sides without closing it: the observational data show the association between stopping and harm, the randomized data show the drug prevents stopping, and no trial links the two.

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
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.
32588430 Potassium binders for chronic hyperkalaemia in people with CKD. (Natale 2020, PMID 32588430) Synthesis; heterogeneity and included-study definitions constrain transport.
40542996 Novel potassium binders, hyperkalemia and RAAS inhibitor optimization: meta-analysis. (Huang 2025, PMID 40542996) 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.
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.
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.
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.
32829751 KDOQI Clinical Practice Guideline for Nutrition in CKD: 2020 Update. (Ikizler 2020, PMID 32829751) Guideline or commentary; recommendation evidence depends on its review.
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.
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.
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.
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.
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.
41493296 Hyperkalaemia with empagliflozin, finerenone or both: CONFIDENCE secondary analysis. (Agarwal 2026, PMID 41493296) Intervention study; eligibility, comparator, endpoint and follow-up bound inference.

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

  • Does binder-enabled continuation of RAS or MRA therapy preserve the kidney and cardiovascular benefit that continuation exists to protect? AMBER measured 12-week persistence and the meta-analysis measured RAASi optimization, not outcomes (Agarwal 2019, PMID 31533906) (Huang 2025, PMID 40542996). → OQ-6
  • Was the alkali hypothesis tested or merely under-delivered? VALOR-CKD achieved only about 1 mEq/L of bicarbonate separation and returned HR 0.99 (0.80–1.20) (Tangri 2024, PMID 38261535).
  • What bicarbonate separation, sustained for how long, would constitute an adequate test — and can it be achieved without a prohibitive sodium and pill burden?

  • Does SGLT2-inhibitor or combination therapy alter hyperkalaemia risk enough to change monitoring? Adding empagliflozin to finerenone did not reduce hyperkalaemia over 180 days (Agarwal 2026, PMID 41493296).

  • Does correcting metabolic acidosis slow CKD? No adequately powered blinded trial has achieved a substantial durable bicarbonate separation: UBI was open-label against standard care (PMID 31598912) and VALOR-CKD separated the arms by only about 1 mEq/L (PMID 38261535). The question is unanswered, not answered negatively.

  • Does the source of alkali matter independently of the bicarbonate achieved? Fruit and vegetables matched bicarbonate to the same eGFR effect while improving blood pressure, LDL, Lp(a) and vitamin K1 in a 108-patient trial (Goraya 2019, PMID 30995657).
  • Does keeping patients on RAASi and MRA via a potassium binder improve outcomes? DIAMOND establishes the enabling effect but was not powered for cardiovascular or kidney endpoints (Butler 2022, PMID 35900838).

  • Why did decisively better potassium control produce no reduction in arrhythmic events on dialysis (Fishbane 2025, PMID 40618849) — is predialysis hyperkalaemia a marker rather than a cause, or was the trial simply underpowered after early termination?

  • Does hyperkalaemia-driven RAASi discontinuation cause the excess mortality and dialysis initiation associated with it (HRs 1.32–1.47 and 1.11–1.65 across two provincial cohorts) (Leon 2022, PMID 35085685), or does discontinuation mark deteriorating health? The evidence that binders prevent discontinuation (Butler 2022, PMID 35900838) and the evidence that discontinuation is associated with harm have never been joined in a single trial.

References

  1. Agarwal et al. Patiromer to enable spironolactone in resistant hypertension and CKD: AMBER. Lancet. 2019;394(10208):1540-1550. PMID 31533906
  2. Natale et al. Potassium binders for chronic hyperkalaemia in people with CKD. Cochrane Database Syst Rev. 2020;6(6):CD013165. PMID 32588430
  3. Huang et al. Novel potassium binders, hyperkalemia and RAAS inhibitor optimization: meta-analysis. Drugs. 2025;85(8):1013-1031. PMID 40542996
  4. Tangri et al. VALOR-CKD trial of veverimer in CKD with metabolic acidosis. J Am Soc Nephrol. 2024;35(3):311-320. PMID 38261535
  5. Ash et al. Sodium zirconium cyclosilicate in CKD, hyperkalemia, and metabolic acidosis: NEUTRALIZE. Kidney360. 2024;5(6):812-820. PMID 38622759
  6. 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
  7. 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
  8. GBD CKD Collaboration et al. Global, regional, and national burden of chronic kidney disease, 1990-2017. Lancet. 2020;395(10225):709-733. PMID 32061315
  9. Cirillo et al. A population-based approach for the definition of chronic kidney disease: CKD Prognosis Consortium. J Nephrol. 2012;25(1):7-12. PMID 22038337
  10. Matsushita et al. Cohort profile: the chronic kidney disease prognosis consortium. Int J Epidemiol. 2013;42(6):1660-1668. PMID 23243116
  11. CKD Prognosis Consortium et al. Estimated GFR, Albuminuria, and Adverse Outcomes: individual-participant data meta-analysis. JAMA. 2023;330(13):1266-1277. PMID 37787795
  12. Inker et al. Relationship of Estimated GFR and Albuminuria to Concurrent Laboratory Abnormalities. Am J Kidney Dis. 2019;73(2):206-217. PMID 30348535
  13. 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
  14. 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
  15. 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
  16. 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
  17. Ikizler et al. The 2020 Updated KDOQI Clinical Practice Guidelines for Nutrition in Chronic Kidney Disease. Blood Purif. 2021;50(4-5):667-671. PMID 33652433
  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. 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
  21. 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
  22. 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
  23. 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
  24. 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
  25. Sorohan et al. Sodium citrate versus sodium bicarbonate for metabolic acidosis in CKD. Medicine (Baltimore). 2024;103(10):e37475. PMID 38457574
  26. Agarwal R, et al. Risk of Hyperkalemia With Empagliflozin, Finerenone, or Both: Secondary Analysis of the CONFIDENCE Randomized Trial. J Am Coll Cardiol. 2026;87(7):772-784. PMID 41493296
  27. Di Iorio BR, et al. Treatment of metabolic acidosis with sodium bicarbonate delays progression of chronic kidney disease: the UBI Study. J Nephrol. 2019;32(6):989-1001. PMID 31598912
  28. Goraya N, et al. Fruit and Vegetable Treatment of Chronic Kidney Disease-Related Metabolic Acidosis Reduces Cardiovascular Risk Better than Sodium Bicarbonate. Am J Nephrol. 2019;49(6):438-448. PMID 30995657
  29. Butler J, et al. Patiromer for the management of hyperkalemia in heart failure with reduced ejection fraction: the DIAMOND trial. Eur Heart J. 2022;43(41):4362-4373. PMID 35900838
  30. Fishbane S, et al. The randomized DIALIZE-Outcomes trial evaluated sodium zirconium cyclosilicate in hemodialysis. Kidney Int. 2025;108(4):686-694. PMID 40618849
  31. Leon SJ, et al. Hyperkalemia-Related Discontinuation of Renin-Angiotensin-Aldosterone System Inhibitors and Clinical Outcomes in CKD: A Population-Based Cohort Study. Am J Kidney Dis. 2022;80(2):164-173.e1. PMID 35085685