Kidney-Safe Nutrition and Medication Use Across Chronic Kidney Disease Stages: Nephrotoxic Drugs, Dietary Risks, and Evidence-Based Strategies for Kidney Protection—A Narrative Review

By Ori Scott, M.Sc. NutritionRegistered Dietitian (Israel)Founder, Healthy Habits Coaching

Abstract

Chronic kidney disease (CKD) alters the handling of medications, electrolytes, minerals, metabolic products, and dietary constituents. Consequently, kidney safety cannot be reduced to lists of “good” and “bad” foods or medications. A clinically meaningful assessment must distinguish direct nephrotoxicity from hemodynamically mediated acute kidney injury, drug accumulation caused by impaired renal clearance, and dietary exposures that become clinically relevant because of disturbances in potassium, phosphorus, sodium, acid-base, fluid, or nitrogen balance.

This narrative review examines medication and nutritional safety across the spectrum of CKD, with particular emphasis on CKD G1–G5 and kidney failure treated with dialysis (G5D). Priority is given to contemporary clinical practice guidelines, systematic reviews, meta-analyses, and other peer-reviewed evidence indexed in PubMed/MEDLINE. Nonsteroidal anti-inflammatory drugs (NSAIDs), selected antimicrobial agents, lithium, proton-pump inhibitors in the context of tubulointerstitial injury, selected antineoplastic agents, herbal preparations, and other potentially nephrotoxic exposures require varying degrees of avoidance, dose modification, or monitoring. Importantly, medications that alter renal hemodynamics but confer long-term kidney protection, including renin-angiotensin system inhibitors and sodium-glucose cotransporter-2 inhibitors, should not be indiscriminately classified as nephrotoxins.

Nutritional management is similarly stage- and context-dependent. Sodium moderation is supported by evidence demonstrating improvements in blood pressure and albuminuria/proteinuria. Protein intake requires individualization according to CKD stage, nutritional status, comorbidity, and dialysis treatment. Contemporary evidence does not support indiscriminate restriction of potassium-rich plant foods in every patient with CKD; potassium management should consider serum potassium, medications, acid-base status, gastrointestinal function, dietary sources, and the bioavailability of potassium-containing additives. Phosphorus management should likewise account for source and bioavailability, with particular attention to highly absorbable inorganic phosphate additives.

The principal clinical implication is that kidney protection requires individualized medication reconciliation and medical nutrition therapy rather than universal food-prohibition lists. Kidney function, albuminuria, biochemical abnormalities, nutritional status, comorbid disease, concomitant therapy, and dialysis status should determine the intensity and nature of intervention.

Keywords: chronic kidney disease; CKD; nephrotoxicity; nephrotoxic drugs; renal nutrition; medical nutrition therapy; medication safety; NSAIDs; potassium; phosphorus; sodium; dietary protein; dietary supplements; acute kidney injury; kidney protection.

1. Introduction

Kidney-safe nutrition is an important part of chronic kidney disease management because CKD affects how the body handles medications, electrolytes, minerals, metabolic products, and dietary constituents. Chronic kidney disease is a heterogeneous clinical condition defined by abnormalities of kidney structure or function that persist for at least three months and have implications for health. Contemporary CKD assessment incorporates both glomerular filtration rate (GFR) and albuminuria because prognosis cannot be adequately characterized by serum creatinine or estimated GFR (eGFR) alone.

The progressive loss of kidney function has consequences extending beyond filtration. The kidney contributes to electrolyte and acid-base homeostasis, mineral metabolism, endocrine regulation, fluid balance, and the elimination of numerous medications and their metabolites. Declining kidney function can therefore alter the clinical consequences of exposures that are well tolerated in individuals with normal kidney function.

The term nephrotoxicity should nevertheless be used precisely. A food containing potassium is not nephrotoxic merely because potassium excretion may become impaired in advanced CKD. Similarly, a renally eliminated medication is not necessarily nephrotoxic because its dose must be reduced when GFR declines. Conversely, certain medications can directly or indirectly produce kidney injury through mechanisms including altered renal perfusion, acute tubular injury, acute interstitial nephritis, crystal nephropathy, thrombotic microangiopathy, or chronic tubulointerstitial damage.

Failure to distinguish these mechanisms can produce two opposite clinical errors: unnecessary avoidance of nutritious foods and beneficial medications, or under-recognition of exposures that genuinely increase the probability of acute kidney injury (AKI) or CKD progression.

This review therefore evaluates kidney-relevant dietary and medication exposures according to mechanism, CKD stage, biochemical context, and quality of supporting evidence.

2. Methods

2.1 Review design

A focused narrative review was undertaken to synthesize clinically relevant evidence concerning nutritional exposures, medications, over-the-counter products, and supplements in adults with CKD.

The principal evidence framework was based on the KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease and the KDOQI Clinical Practice Guideline for Nutrition in CKD: 2020 Update. Peer-reviewed systematic reviews and meta-analyses indexed in PubMed/MEDLINE were preferentially used to evaluate individual nutritional and pharmacologic questions.

Because this is a narrative review rather than a prospectively registered systematic review, the literature synthesis should not be interpreted as an exhaustive identification or quantitative pooling of all eligible studies.

2.2 Literature search

PubMed/MEDLINE was searched using combinations of controlled vocabulary and free-text concepts related to:

• chronic kidney disease;

• renal insufficiency;

• kidney failure;

• acute kidney injury;

• nephrotoxicity;

• chemically induced kidney disease;

• medication safety;

• NSAIDs;

• antimicrobial nephrotoxicity;

• dietary protein;

• sodium;

• potassium;

• phosphorus and phosphate;

• food additives;

• dietary supplements; and

• herbal preparations.

Representative concepts included the MeSH terms Renal Insufficiency, Chronic, Kidney Failure, Chronic, Acute Kidney Injury, and relevant diet-, drug-, and chemically induced disease terminology.

Priority was given to clinical practice guidelines, systematic reviews, meta-analyses, randomized controlled trials where relevant, and high-quality observational studies when randomized evidence was unavailable or inappropriate.

Older sources were retained when they represented foundational evidence or when more recent evidence did not supersede the relevant clinical principle.

2.3 Interpretation of evidence

The evidence was interpreted according to study design, consistency, directness, population, CKD severity, and clinical applicability. Association was not interpreted as proof of causality. In particular, observational associations involving medications such as proton-pump inhibitors were distinguished from evidence establishing direct causal nephrotoxicity.

Recommendations were also separated from evidence of biochemical effects. A statistically significant change in serum potassium, phosphorus, blood pressure, or eGFR does not necessarily establish an improvement in kidney failure, cardiovascular events, mortality, or quality of life.

3. CKD Stage as a Framework for Kidney Safety

CKD is conventionally classified by GFR category:

GFR category	eGFR (mL/min/1.73 m²)	Description
G1	≥90	Normal or high GFR in the presence of other evidence of CKD
G2	60–89	Mildly decreased
G3a	45–59	Mildly to moderately decreased
G3b	30–44	Moderately to severely decreased
G4	15–29	Severely decreased
G5	<15	Kidney failure
G5D	Dialysis	Kidney failure treated with dialysis

This classification is clinically useful but insufficient by itself. Albuminuria, the cause of CKD, age, diabetes, cardiovascular disease, volume status, serum potassium, acid-base status, nutritional status, concomitant medications, and previous AKI materially influence risk.

Consequently, the same eGFR does not imply an identical dietary or medication prescription for every patient.

4. What Constitutes a Kidney-Relevant Exposure?

Four categories should be distinguished.

Direct or clinically established nephrotoxicity describes an exposure capable of causing structural or functional kidney injury. Aminoglycoside-associated tubular toxicity is an example.

Hemodynamically mediated kidney dysfunction occurs when medications alter renal vascular tone or intraglomerular pressure. NSAIDs are an important example, particularly during volume depletion or in susceptible individuals.

Reduced renal elimination occurs when kidney dysfunction increases systemic exposure to a medication or metabolite. The medication itself need not damage the kidney; rather, CKD increases the risk of nonrenal toxicity unless dosing is modified.

CKD-dependent nutritional risk occurs when an otherwise normal nutrient becomes difficult to regulate. Potassium and phosphorus illustrate this distinction. Neither should be described generically as a nephrotoxin.

This mechanistic framework is more clinically defensible than labeling exposures simply “safe” or “unsafe.”

5. Medications and Kidney Safety

5.1 Nonsteroidal Anti-inflammatory Drugs

NSAIDs constitute one of the most important preventable medication-related kidney exposures in CKD.

Inhibition of renal prostaglandin synthesis can reduce prostaglandin-dependent renal blood flow and precipitate a decline in GFR, particularly when renal perfusion is already compromised. NSAIDs are additionally associated with acute interstitial nephritis, sodium retention, hypertension, and other renal syndromes.

A systematic review and meta-analysis of community-based observational studies reported an increased risk of AKI during current NSAID exposure. Among individuals with pre-existing CKD, the pooled odds ratio was 1.63 (95% CI 1.22–2.19).

Absolute risk is not identical among patients. Older age, CKD, hypovolemia, heart failure, concomitant diuretic therapy, and medications affecting the renin-angiotensin system may increase susceptibility.

Chronic unsupervised NSAID use should therefore be discouraged in CKD. This does not imply that no patient with CKD can ever receive an NSAID; risk-benefit assessment, indication, duration, dose, concurrent therapy, and monitoring remain clinically relevant.

5.2 Aminoglycosides

Aminoglycosides, including gentamicin, tobramycin, and amikacin, can accumulate within proximal tubular cells and produce tubular injury. Risk is influenced by cumulative exposure, dosing strategy, underlying kidney function, concurrent nephrotoxins, and clinical illness.

Where aminoglycoside therapy is necessary, kidney function and therapeutic drug concentrations should be monitored according to the specific agent and clinical setting.

5.3 Vancomycin

Vancomycin exposure has been associated with AKI, particularly with greater systemic exposure and in the presence of other risk factors or nephrotoxic agents. Contemporary dosing strategies increasingly use pharmacokinetic monitoring to achieve therapeutic exposure while reducing toxicity.

Vancomycin should not be characterized as universally contraindicated in CKD; serious infections may require its use. Appropriate dosing and monitoring are therefore more accurate concepts than blanket avoidance.

5.4 Proton-Pump Inhibitors

Proton-pump inhibitors (PPIs) have been associated with acute interstitial nephritis and observational associations with AKI and CKD. The strength of evidence differs substantially from that for well-established nephrotoxins, and residual confounding is an important limitation of long-term observational studies.

The clinically appropriate response is therefore not indiscriminate PPI discontinuation. Long-term treatment should have an identifiable indication and should be periodically reassessed.

5.5 Lithium

Lithium has clinically important renal implications. Chronic exposure may impair urinary concentrating capacity and can be associated with chronic tubulointerstitial disease in susceptible individuals. Because lithium is predominantly eliminated by the kidney and has a narrow therapeutic index, changes in kidney function, sodium balance, volume status, and interacting medications can substantially alter lithium concentrations.

Patients receiving lithium require appropriate therapeutic drug and kidney-function monitoring.

5.6 Renin-Angiotensin System Inhibitors Are Not Conventional Nephrotoxins

Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers deserve particular clarification.

These agents reduce intraglomerular pressure and can produce an anticipated initial change in GFR. That physiological response should not be automatically interpreted as toxic kidney injury. In appropriately selected patients, renin-angiotensin system inhibition is an established kidney-protective strategy, particularly in albuminuric CKD.

Serum creatinine and potassium require monitoring after initiation and dose escalation.

5.7 SGLT2 Inhibitors

Sodium-glucose cotransporter-2 inhibitors similarly produce characteristic hemodynamic changes in glomerular filtration but have become central components of kidney-protective therapy in appropriate CKD populations.

Classifying SGLT2 inhibitors as “kidney-toxic” because eGFR may initially decline would therefore misrepresent the evidence.

6. Nutrition and Kidney Safety

6.1 Sodium

Excessive sodium intake is clinically relevant in CKD because of its relationship with blood pressure, extracellular volume, and albuminuria/proteinuria.

A meta-analysis of 11 randomized trials involving 738 participants with CKD stages 1–4 found that moderate dietary sodium restriction reduced clinic and ambulatory blood pressure and reduced proteinuria and albuminuria.

KDIGO recommends sodium intake below approximately 2 g sodium per day for most adults with CKD, while recognizing that individual clinical circumstances may modify this target.

From a food-based perspective, reducing sodium frequently requires attention to processed meats, packaged foods, restaurant meals, instant products, salty snacks, sauces, and other manufactured foods rather than focusing exclusively on discretionary salt.

6.2 Potassium

Potassium illustrates why CKD nutrition should not be based on indiscriminate food prohibition.

Hyperkalemia becomes increasingly relevant as kidney function declines, but serum potassium reflects considerably more than dietary potassium intake. Kidney function, medications, metabolic acidosis, insulin status, gastrointestinal losses, constipation, and cellular potassium distribution can all contribute.

A systematic review evaluating potassium restriction in CKD identified only limited evidence. The available studies suggested that restriction can modestly reduce serum potassium, but the overall evidence base was of low or very low quality for several clinically important outcomes.

Accordingly, the presence of CKD alone does not establish that every potassium-rich fruit, vegetable, legume, or whole food must be restricted.

Particular attention should be given to highly bioavailable potassium additives and potassium chloride-containing salt substitutes when hyperkalemia is present or risk is substantial.

Dietary treatment should therefore be guided by repeated serum potassium measurements, kidney function, medications, acid-base status, dietary pattern, and the source and quantity of potassium consumed.

6.3 Phosphorus

Phosphorus metabolism becomes progressively disturbed in advanced CKD and contributes to the complex pathophysiology of CKD-mineral and bone disorder.

However, phosphorus exposure cannot be adequately assessed by total phosphorus content alone.

Inorganic phosphate additives used in processed foods can contribute a readily absorbable phosphorus load. By contrast, a proportion of phosphorus in plant foods is bound within phytate and has lower gastrointestinal bioavailability.

Contemporary renal nutrition therefore increasingly emphasizes phosphorus source and bioavailability rather than indiscriminately eliminating plant foods solely because tables list them as containing phosphorus.

Foods and beverages containing phosphate additives deserve particular attention when phosphorus reduction is clinically indicated. Ingredient lists containing terms incorporating “phos” can help identify many added phosphates.

Phosphorus management should ultimately be interpreted alongside serum phosphate, calcium, parathyroid hormone, CKD stage, overall protein requirements, and nutritional status.

6.4 Protein

The relationship between dietary protein and CKD is complex.

Protein restriction has been studied as a strategy for reducing nitrogenous waste and potentially slowing progression of nondialysis CKD. A systematic review and meta-analysis of 19 randomized trials involving 2,492 participants reported lower risks of kidney failure and end-stage kidney disease with low-protein interventions, although effects on mortality were not clearly demonstrated.

The clinical application of these findings requires caution. Excessive restriction can compromise nutritional adequacy, particularly in older adults, individuals with poor appetite, inflammatory illness, involuntary weight loss, frailty, or protein-energy wasting.

KDIGO 2024 suggests maintaining approximately 0.8 g protein/kg body weight/day in adults with CKD G3–G5 and advises avoidance of high protein intake (>1.3 g/kg/day) in adults with CKD at risk of progression.

This recommendation should not be transferred directly to patients receiving maintenance dialysis. Dialysis changes protein requirements, and prevention of protein-energy wasting becomes particularly important.

7. Herbal Products and Dietary Supplements

The assumption that a product is kidney-safe because it is “natural” is not scientifically defensible.

Herbal products present several distinct concerns: intrinsic nephrotoxicity, pharmacologically active ingredients, interactions with prescription medications, contamination, adulteration, uncertain dose standardization, and limited evaluation in CKD populations.

Aristolochic acid represents a well-established example of severe herbal-associated nephrotoxicity.

Patients with CKD should therefore be asked specifically about teas, traditional medicines, powders, bodybuilding products, electrolyte preparations, vitamin/mineral supplements, and products marketed for “detoxification” or “kidney cleansing.”

Potassium-containing supplements and potassium-based salt substitutes warrant particular attention in patients susceptible to hyperkalemia.

Supplement review should be incorporated into medication reconciliation rather than treated as a separate lifestyle issue.

8. Professional CKD Safety Table

Table 1. Kidney-relevant foods, nutrients, medications, supplements, and exposures across CKD categories

Exposure	Principal mechanism/concern	G1–G2	G3a	G3b	G4	G5 nondialysis	G5D	Practical interpretation
Chronic oral NSAID use	Reduced prostaglandin-dependent renal perfusion; AKI; AIN; sodium retention	Caution	Avoid unnecessary chronic use	Avoid when possible	Generally avoid unless specifically justified	Generally avoid	Individual medical assessment	Risk rises with CKD, age, volume depletion and interacting therapy
Aminoglycosides	Proximal tubular toxicity	Monitor when required	Dose/monitor	Dose/monitor closely	Specialist dosing/monitoring	Specialist dosing	Dialysis-specific dosing	Use may be necessary for serious infection
Vancomycin	AKI risk; exposure-dependent toxicity	Monitor	Renal dosing/monitoring	Renal dosing/monitoring	Intensive dosing/monitoring	Intensive dosing/monitoring	Dialysis-specific dosing	Not automatically contraindicated
Lithium	Renal elimination; concentrating defect; chronic tubulointerstitial injury	Monitor	Increased monitoring	Increased monitoring	Specialist assessment	Usually highly problematic	Specialist management	Narrow therapeutic index
PPI therapy	AIN; observational AKI/CKD associations	Use for valid indication	Reassess chronic indication	Reassess	Reassess	Reassess	Reassess	Evidence does not justify indiscriminate discontinuation
ACE inhibitor/ARB	Alters intraglomerular pressure; hyperkalemia possible	Indication-dependent	Often kidney protective when indicated	Often kidney protective	Often kidney protective with monitoring	Individualize	Individualize	Not a conventional nephrotoxin
SGLT2 inhibitor	Initial hemodynamic eGFR change; long-term kidney protection	Indication-dependent	Kidney protective when indicated	Kidney protective when indicated	Eligibility depends on agent/indication/eGFR	Individualize	Generally not initiated as dialysis therapy	Do not confuse initial eGFR dip with nephrotoxicity
Excess sodium	BP, volume expansion, albuminuria	Limit excess	Limit excess	Limit excess	Limit excess	Individualize closely	Individualize with fluid status	Processed foods are major sources
Potassium-rich whole foods	Hyperkalemia only in susceptible settings; food matrix matters	Usually no routine restriction	Laboratory-guided	Laboratory-guided	Frequently requires closer assessment	Individualized	Dialysis-specific	Do not universally ban fruits/vegetables
Potassium additives/KCl salt substitutes	Highly available potassium load	Usually acceptable unless risk exists	Caution with hyperkalemia	Greater caution	Often important	Often important	Individualized	Check ingredient labels
Phosphate additives	Highly absorbable inorganic phosphorus	Limit unnecessary exposure	Limit unnecessary exposure	Increased relevance	Important	Important	Important	Often a more appropriate first target than plant foods
Whole grains/legumes/nuts	Potassium/phosphorus present; plant phosphorus partly phytate-bound	Generally compatible	Individualize	Individualize	Laboratory-guided	Laboratory-guided	Dialysis-specific	Avoid blanket prohibition
Protein	Excess may increase metabolic burden; inadequate intake risks wasting	Avoid extremes	~0.8 g/kg/d generally appropriate	~0.8 g/kg/d generally appropriate	Individualize carefully	Individualize carefully	Requirements generally higher	Nutritional status modifies prescription
Herbal “kidney detox” products	Unknown efficacy; possible nephrotoxins, interactions, contamination	Avoid unsupported products	Avoid	Avoid	Avoid	Avoid	Avoid	No established role for “kidney cleansing”
Potassium supplements	Hyperkalemia	Indication-dependent	Monitor	Caution	High caution	High caution	Dialysis-specific	Use only for a defined indication
High-dose/complex supplements	Accumulation, contamination, interactions	Review	Review	Review	Close review	Close review	Close review	Include supplements in medication reconciliation
Dehydration/volume depletion	Reduced renal perfusion; AKI risk	Avoid	Increasing importance	High relevance	High relevance	High relevance	Fluid strategy differs	Particularly important during vomiting/diarrhea/fever

Interpretive note: The table is a clinical framework, not a prescribing or food-prohibition algorithm. CKD category alone does not determine medication safety or dietary restriction. Albuminuria, serum potassium, phosphorus, bicarbonate, blood pressure, volume status, comorbidities, nutritional status, concomitant medications, and dialysis modality must also be considered.

9. Why Universal “Renal Food Lists” Are Problematic

Traditional educational materials frequently classify foods according to potassium or phosphorus concentration and then translate those values into extensive lists of prohibited foods.

This approach has important limitations.

First, biochemical risk is patient-specific. A person with CKD G3 and persistently normal serum potassium does not necessarily require the same potassium prescription as a patient with recurrent hyperkalemia.

Second, food source and bioavailability matter. Phosphorus from inorganic additives is not nutritionally equivalent to phytate-bound phosphorus in plant foods.

Third, extensive restriction of fruits, vegetables, legumes, whole grains, nuts, and other nutrient-dense foods can reduce dietary variety and potentially compromise fiber and micronutrient intake.

Recent evaluation of online dietary advice for hyperkalemia has demonstrated substantial inconsistency, including simultaneous recommendations and restrictions involving closely related foods. This reinforces the limitations of isolated food-list approaches.

The preferred strategy is therefore individualized medical nutrition therapy based on biochemical abnormalities, dietary assessment, medication review, CKD stage, and overall nutritional adequacy.

10. Practical Framework for Kidney Protection

Kidney protection should begin with identification of the cause and severity of CKD rather than dietary restriction alone.

Assessment should include eGFR and albuminuria, particularly urine albumin-to-creatinine ratio where appropriate. Blood pressure, diabetes, cardiovascular risk, previous AKI, volume status, serum potassium, bicarbonate, and relevant parameters of mineral metabolism should be considered according to disease stage.

Medication reconciliation should include prescription medications, OTC analgesics, vitamins, minerals, herbal preparations, sports supplements, electrolyte powders, and salt substitutes.

Avoidance of unsupervised chronic NSAID exposure is among the most practical medication-safety interventions.

At the same time, evidence-based kidney-protective pharmacotherapy should not be withheld merely because a medication produces predictable changes in renal hemodynamics. Renin-angiotensin system inhibitors and SGLT2 inhibitors are prominent examples.

Nutrition intervention should prioritize dietary quality and identified biochemical abnormalities rather than impose maximum restriction at the time of CKD diagnosis.

As CKD advances, collaboration among nephrology, primary care, pharmacy, and renal nutrition professionals becomes increasingly important because the margins between deficiency, adequate intake, and excessive exposure may narrow.

11. Evidence Limitations and Research Gaps

Several limitations affect the evidence base.

Nutritional trials in CKD frequently involve relatively small populations, heterogeneous CKD etiologies and stages, short follow-up periods, and substantial challenges in accurately measuring dietary exposure.

The evidence supporting dietary potassium restriction is particularly limited compared with the frequency with which broad potassium restrictions have historically been prescribed.

Phosphorus research is complicated by incomplete food-composition data and variation in the bioavailability of organic and inorganic phosphorus.

Medication-associated kidney outcomes present different methodological challenges. Randomized trials designed specifically to establish nephrotoxicity are frequently unavailable or unethical, leaving observational pharmacovigilance and cohort data as important evidence sources. Confounding by indication and comorbidity must therefore be considered.

There is also insufficient evidence to translate many nutritional observations into precise CKD-stage-specific food thresholds.

Future research should prioritize clinically important outcomes rather than biochemical endpoints alone and should evaluate dietary patterns, food additives, plant-based dietary strategies, medication-nutrient interactions, and patient-centered approaches that minimize unnecessary restriction.

12. Discussion

The central finding of this review is that kidney safety cannot be adequately communicated through a binary classification of foods and medications as “safe” or “toxic.”

True nephrotoxicity represents only one component of risk. CKD also alters pharmacokinetics, renal hemodynamics, electrolyte excretion, mineral metabolism, acid-base physiology, and nutritional requirements.

NSAIDs provide a clinically important example of an exposure with well-supported renal risk, particularly in susceptible patients. Aminoglycosides, lithium, and selected other medications require similarly deliberate management.

By contrast, renin-angiotensin system inhibitors and SGLT2 inhibitors illustrate the danger of equating an early change in GFR with nephrotoxicity. Both medication classes can provide kidney protection in appropriately selected populations.

The same principle applies to nutrition.

Potassium-rich foods should not automatically be characterized as dangerous merely because advanced CKD can impair potassium excretion. Phosphorus-containing plant foods should not be considered equivalent to highly absorbable inorganic phosphate additives. Protein restriction should not be pursued without considering the competing risk of inadequate intake and protein-energy wasting.

The practical objective is therefore not maximum dietary restriction. It is appropriate exposure for the individual patient's physiology and clinical circumstances.

This distinction becomes increasingly important as CKD progresses because therapeutic complexity increases while nutritional vulnerability may simultaneously worsen.

13. Conclusion

Kidney protection in CKD requires integration of medication safety, medical nutrition therapy, biochemical monitoring, and treatment of the underlying drivers of kidney and cardiovascular risk.

Chronic unsupervised NSAID exposure is an important preventable medication-related risk. Other potentially nephrotoxic agents should be used according to indication, kidney function, exposure, alternatives, and appropriate monitoring rather than through indiscriminate prohibition.

Renally eliminated medications require dose assessment as kidney function declines, but reduced renal clearance should not be confused with nephrotoxicity.

Nutritionally, excessive sodium intake deserves attention throughout much of the CKD spectrum. Protein intake should be individualized, with avoidance of high intake in patients at risk of CKD progression and protection against inadequate intake and protein-energy wasting. Potassium restriction should be driven primarily by hyperkalemia risk and clinical context rather than CKD diagnosis alone. Phosphorus management should consider source and bioavailability, particularly the contribution of inorganic phosphate additives.

The most defensible contemporary approach is therefore an individualized one: identify the kidney disease, establish its severity and albuminuria category, review medications and supplements, evaluate biochemical abnormalities and nutritional status, and intervene specifically where risk has been demonstrated.

Educational and Medical Disclaimer

This narrative review is intended solely for educational and scientific purposes. It does not constitute individualized medical advice, diagnosis, prescribing guidance, or treatment.

Information concerning medications is provided to describe evidence and general principles of kidney safety. No medication should be initiated, discontinued, withheld, substituted, or dose-adjusted solely on the basis of this review.

Dietary requirements in CKD vary according to GFR, albuminuria, serum potassium, phosphorus and bicarbonate concentrations, blood pressure, fluid status, diabetes, cardiovascular disease, nutritional status, concurrent medications, dialysis modality, and other individual clinical characteristics.

Patients with CKD should receive individualized medical and nutritional assessment from appropriately qualified healthcare professionals. Acute symptoms, suspected AKI, severe electrolyte abnormalities, oliguria/anuria, significant dehydration, or other acute clinical deterioration require prompt medical assessment.

Author

Ori Scott, M.Sc. NutritionRegistered Dietitian (Israel)Founder, Healthy Habits Coaching

Conflicts of Interest

The author declares no conflicts of interest relevant to this work.

Funding

No external funding was received for the preparation of this review.

Core References

1. Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney International. 2024.

2. Ikizler TA, Burrowes JD, Byham-Gray LD, et al. KDOQI Clinical Practice Guideline for Nutrition in CKD: 2020 Update. American Journal of Kidney Diseases. 2020;76(3 Suppl 1)–S107.

3. Zhang X, Donnan PT, Bell S, Guthrie B. Non-steroidal anti-inflammatory drug induced acute kidney injury in the community dwelling general population and people with chronic kidney disease: systematic review and meta-analysis. BMC Nephrology. 2017;18:256. PMID: 28764659.

4. Garofalo C, Borrelli S, Provenzano M, et al. Dietary salt restriction in chronic kidney disease: a meta-analysis of randomized clinical trials. Nutrients. 2018;10(6):732. PMID: 29882800.

5. Morris A, Krishnan N, Kimani PK, Lycett D. Effect of dietary potassium restriction on serum potassium, disease progression, and mortality in chronic kidney disease: a systematic review and meta-analysis. Journal of Renal Nutrition. 2020;30(4):276–285. Corrected publication indexed under PMID: 34980365.

6. Kelly JT, Rossi M, Johnson DW, Campbell KL. Dietary potassium intake and risk of chronic kidney disease progression in predialysis patients with chronic kidney disease: a systematic review. Advances in Nutrition. 2020. PMID: 32191264.

7. Yan B, Su X, Xu B, Qiao X, Wang L. Effect of diet protein restriction on progression of chronic kidney disease: a systematic review and meta-analysis. PLoS One. 2018;13(11). PMID: 30403710.

8. Gutiérrez OM. Sodium- and phosphorus-based food additives: persistent but surmountable hurdles in the management of nutrition in chronic kidney disease. Advances in Chronic Kidney Disease. 2013;20(2):150–156. PMID: 23439374.

9. St-Jules DE, Fouque D. Revising dietary phosphorus advice in chronic kidney disease G3–5D. Journal of Renal Nutrition. 2020. PMID: 32586712.