THE PURE CRAFT JOURNAL

CBD Gummies for Kidney Health: What Research Shows

October 20, 2026

By PureCraft Editorial Team | PureCraft CBD | Updated October 2026

The kidneys are the body's precision filtration and hormonal regulation system — processing 180 liters of blood daily, eliminating metabolic waste, regulating blood pressure through the renin-angiotensin-aldosterone system (RAAS), maintaining fluid and electrolyte balance, and producing erythropoietin for red blood cell production. Chronic kidney disease (CKD) affects an estimated 10–15% of the global adult population and is largely driven by diabetes-related diabetic nephropathy, hypertension-related hypertensive nephrosclerosis, and inflammatory nephritis — conditions rooted in the same oxidative stress, endothelial dysfunction, and chronic low-grade inflammation that the endocannabinoid system (ECS) modulates. The kidney is a highly ECS-enriched tissue: CB1 and CB2 receptors are expressed throughout renal tissue, where they regulate renal hemodynamics, inflammatory activation of glomerular and tubular cells, and fibrosis. CBD's anti-inflammatory, antioxidant, and blood pressure-supportive mechanisms are directly relevant to the drivers of kidney injury — while important distinctions about CBD dosing in existing kidney disease and critical drug interactions with renally-cleared medications must be addressed clearly.

Important Note on CBD and Kidney Health

Unlike the liver, the kidney does not primarily metabolize CBD — CBD is hepatically metabolized and renally excreted as inactive metabolites. This means CBD does not burden the kidney in the same way it does the liver, and no renal enzyme abnormalities have been reported in CBD clinical trials. However, individuals with significant existing kidney disease (eGFR below 30 — Stage 4–5 CKD) should consult their nephrologist before CBD supplementation, as impaired renal clearance of CBD metabolites may affect elimination. More importantly, CBD's inhibition of CYP3A4 and CYP2D6 affects the metabolism of many medications commonly used in CKD management (tacrolimus, cyclosporine, ACE inhibitors, diuretics) — drug interactions are the primary kidney-related concern with CBD, not direct nephrotoxicity. CBD and NSAIDs (ibuprofen, naproxen) both reduce renal prostaglandin synthesis — combining high-dose CBD with regular NSAID use warrants physician attention. This article discusses CBD at standard supplement doses (10–50 mg/day); these are not pharmaceutical doses.

The Renal ECS: CB1 and CB2 in the Kidney

The endocannabinoid system has distinct CB1 and CB2 roles in the kidney that parallel its hepatic architecture — CB1 generally driving pathological processes in metabolic kidney disease, CB2 providing immune-regulatory protective functions:

Renal CB1: Hemodynamics and Metabolic Injury

CB1 receptors are expressed in renal tubular cells, glomerular mesangial cells, endothelial cells of the renal vasculature, and juxtaglomerular cells. In metabolic disease — obesity, diabetes, and metabolic syndrome — renal CB1 becomes overactivated through the same visceral adipose endocannabinoid overproduction that drives hepatic CB1 overactivation. The consequences are directly nephrotoxic: CB1 activation in mesangial cells increases glomerular pressure (intraglomerular hypertension — the primary driver of diabetic nephropathy progression); CB1 activation in tubular cells promotes tubular oxidative stress and fibrosis-initiating transforming growth factor-β (TGF-β) signaling; CB1 activation in juxtaglomerular cells stimulates renin release, activating the RAAS and raising systemic blood pressure — creating a self-reinforcing cycle where metabolic CB1 overactivation raises blood pressure, which further damages glomeruli. CBD's negative allosteric CB1 modulation in renal tissue addresses this overactivation, reducing the intraglomerular hypertension and TGF-β signaling that drives the structural kidney damage of diabetic and hypertensive nephropathy.

Renal CB2: Anti-Inflammatory and Anti-Fibrotic Nephroprotection

CB2 receptors in the kidney are expressed primarily on renal immune cells — resident macrophages (renal macrophages/mesangial cells in inflammatory states), infiltrating immune cells in nephritis, and tubular epithelial cells under inflammatory stress. CB2 activation suppresses the NF-κB-driven inflammatory cascade that drives glomerulonephritis (inflammatory kidney disease) and the macrophage-mediated tubular injury that contributes to progressive CKD regardless of initial etiology. CB2 activation in renal fibroblasts and tubular cells reduces TGF-β-mediated fibrosis signaling — the process that converts functional kidney tissue to non-functional scar (interstitial fibrosis/tubular atrophy: the final common pathway of CKD progression regardless of initial cause). Because CBD is a CB2 agonist/modulator and activates CB2 in inflammatory renal tissue, it addresses the renal NF-κB inflammatory cascade and TGF-β fibrotic pathway through the same mechanisms it uses in the liver and other inflamed tissues.

Shared Risk Factors: Why Kidney Health and the ECS Are Linked

CKD Risk Driver	Renal Mechanism	CBD/ECS Mechanism	Evidence Strength
Diabetes / hyperglycemia	Advanced glycation end-products (AGEs); mesangial expansion; glomerular basement membrane thickening; CB1-driven intraglomerular hypertension	Insulin sensitivity support; CB1 negative allosteric modulation reduces mesangial CB1 overactivation; antioxidant AGE-mitigation	Preclinical (diabetic nephropathy rodent models)
Hypertension	Sustained elevated glomerular pressure → glomerulosclerosis; renal artery remodeling; RAAS dysregulation	5-HT1A vasodilation; TRPV1/FAAH anandamide-mediated vascular relaxation; HPA/cortisol reduction reduces RAAS activation; CB1 modulation reduces renin release	Human (blood pressure): modest antihypertensive effect in acute dosing studies
Chronic inflammation / nephritis	Glomerular immune complex deposition; macrophage-mediated tubular injury; NF-κB-driven cytokine nephrotoxicity	CB2/NF-κB macrophage suppression; TNF-α/IL-1β/IL-6 reduction in renal tissue; beta-caryophyllene CB2 direct agonism	Preclinical (nephritis models); systemic anti-inflammatory human evidence
Oxidative stress	ROS-mediated tubular cell apoptosis; lipid peroxidation in glomerular endothelium; NADPH oxidase overactivation in diabetic kidney	Direct radical scavenging; Nrf2/HO-1 antioxidant enzyme upregulation; mitochondrial ROS suppression	Preclinical; Nrf2 activation well-characterized
HPA/cortisol dysregulation	Cortisol increases RAAS activation (aldosterone-like mineralocorticoid effects); impairs renal hemodynamic autoregulation; promotes sodium/water retention; increases systemic blood pressure	CBD 5-HT1A/HPA axis normalization reduces cortisol output; lower cortisol → reduced RAAS activation → reduced intraglomerular pressure	Human (HPA/cortisol): mechanistically connects CBD's best-supported pathway to kidney protection

Diabetic Nephropathy: The Most Mechanistically Relevant CKD Connection

Diabetic nephropathy is the single largest cause of CKD and end-stage renal disease (ESRD) globally, accounting for approximately 40% of new dialysis cases. Its progression follows a well-characterized pathway that directly intersects with CBD's mechanisms:

Early diabetic nephropathy: Hyperglycemia drives glomerular hyperfiltration (CB1-mediated intraglomerular hypertension is a contributing factor), mesangial expansion, and early basement membrane changes. Oxidative stress from glucose auto-oxidation and AGE formation begins damaging glomerular endothelial cells. CBD's CB1 negative allosteric modulation and antioxidant activity are most relevant at this stage — when structural changes are still reversible.

Microalbuminuria stage: Glomerular basement membrane damage allows albumin to pass into the urine — microalbuminuria is the first clinical marker of diabetic nephropathy. Persistent intraglomerular hypertension, NF-κB inflammatory activation in mesangial cells, and TGF-β-mediated mesangial matrix expansion drive this stage. CBD's CB2/NF-κB and CB1 modulation mechanisms are directly relevant.

Progressive CKD: Proteinuria, tubular injury, and interstitial fibrosis mark advancing disease. At this stage, the fibrotic scarring is increasingly irreversible, and the pharmacological question shifts from nephroprotection to slowing progression — still a relevant goal for CBD's anti-fibrotic CB2 and TGF-β modulation mechanisms. The key practical point: the most actionable window for CBD's nephroprotective potential — if it translates from preclinical models to human benefit — is early to intermediate metabolic kidney disease risk, before significant structural damage has accumulated.

Blood Pressure and Renal Protection: CBD's Vascular Mechanism

Hypertension is the second most common cause of CKD. The kidney is simultaneously a victim of hypertension (elevated pressure damages glomeruli over time) and a driver of hypertension (damaged kidneys fail to regulate RAAS and sodium balance, further elevating pressure in a self-reinforcing loop). CBD's antihypertensive properties — documented in human studies showing acute blood pressure reduction of 5–10 mmHg in response to stress in healthy volunteers — are relevant to kidney protection through both the direct renal hemodynamic benefit (lower systemic pressure → lower intraglomerular pressure → less glomerulosclerosis) and the RAAS modulation pathway. CBD reduces HPA axis cortisol output through 5-HT1A agonism; cortisol has mineralocorticoid-like effects that increase aldosterone sensitivity, RAAS activation, and sodium/water retention — all of which raise blood pressure and increase glomerular filtration pressure. This cortisol→RAAS→renal pressure pathway makes CBD's best-evidenced human mechanism (HPA/cortisol normalization) directly nephroprotective through a well-characterized endocrine route. The Broad Spectrum CBD Gummies provide consistent daily CBD exposure for the sustained cortisol normalization that supports this renal hemodynamic benefit; nanoemulsion delivery improves the consistency of absorption that steady-state cortisol effects require.

Practical Protocol: CBD Gummies for Kidney Health Support

Kidney Health Support Protocol — CBD Gummies

Daily anti-inflammatory and CB1 modulation foundation: Broad Spectrum CBD Gummies (25 mg daily) deliver consistent CB2/NF-κB renal anti-inflammatory activity and CB1 negative allosteric modulation. Consistent daily dosing is essential — intermittent use produces inconsistent endocannabinoid tone modulation and less reliable HPA/cortisol normalization than daily supplementation. Morning dosing with food maximizes absorption (CBD's fat-solubility means dietary fat co-ingestion significantly improves bioavailability) and engages the cortisol awakening response window when HPA modulation is most impactful.

Full phytocannabinoid spectrum with CB2-specific support: Full Spectrum Berry Gummies add beta-caryophyllene (a direct CB2 agonist with documented anti-inflammatory effects in renal tissue in preclinical models), CBG (which has PPARγ activity relevant to reducing glomerular mesangial cell inflammatory responses), and the full terpene-cannabinoid entourage for maximal CB2 engagement. Beta-caryophyllene's direct CB2 agonism (rather than CBD's indirect CB2 modulation) provides a complementary receptor activation pathway for renal Kupffer-equivalent macrophage suppression.

Antioxidant kidney protection: CBD Elderberry Gummies add elderberry anthocyanins with documented renoprotective antioxidant activity — preclinical studies show elderberry anthocyanins reducing renal oxidative stress markers (8-OHdG, MDA), preserving tubular function under oxidative challenge, and reducing urinary protein excretion in metabolic disease models. The elderberry-CBD antioxidant combination addresses both the immediate ROS-mediated tubular injury and the sustained oxidative environment that drives progressive glomerulosclerosis. The Water Soluble CBD Softgels offer enhanced bioavailability through nanoemulsion technology for individuals who want maximum CBD delivery efficiency within a fixed dose.

Sleep and renal repair: CBD+CBN+Melatonin Gummies — the kidney follows a circadian rhythm of glomerular filtration rate (GFR), renal blood flow, and tubular reabsorption, with the overnight period critical for renal recovery and regeneration. Melatonin has documented direct nephroprotective effects beyond sleep: melatonin receptors are expressed in renal tubular cells, and melatonin reduces renal oxidative stress, suppresses NF-κB inflammatory signaling in tubular cells, and has been shown to reduce cisplatin-induced nephrotoxicity in preclinical models. Sleep deprivation independently increases blood pressure (via sympathetic activation and cortisol), reducing the renal hemodynamic protection that adequate sleep provides. The Broad Spectrum CBD Oil allows flexible sublingual dosing for individuals who want to split CBD delivery between morning metabolic support and evening blood pressure/sleep support.

Systemic inflammation support: CBD Muscle and Joint Cream provides topical anti-inflammatory support that reduces systemic NSAID reliance — important for kidney health because regular NSAID use (ibuprofen, naproxen) impairs renal prostaglandin synthesis and reduces renal blood flow, contributing to NSAID nephropathy. Using topical CBD as a primary acute anti-inflammatory for musculoskeletal pain reduces the NSAID burden on the kidneys in individuals with already-elevated CKD risk.

Delta-8 note: Delta-8 Gummies are not specifically indicated for kidney health support. Delta-8's CB1 agonism activates the same renal CB1 pathway that CBD's negative allosteric modulation works to reduce — pharmacologically counterproductive to renal hemodynamic goals in individuals concerned about metabolic kidney disease risk. Individuals prioritizing kidney health should focus on CBD formulations rather than THC-analog products.

Frequently Asked Questions

Can CBD gummies help protect kidney health?

Research suggests CBD gummies may support kidney health through several mechanisms that directly target the primary drivers of kidney injury — though human clinical trial evidence specifically for CBD improving kidney function markers is limited, and CBD is not a treatment for kidney disease. The mechanistic case for CBD kidney support is strongest for individuals with metabolic syndrome, diabetes, or hypertension-related kidney disease risk — the populations where CB1 overactivation in renal tissue, oxidative stress-driven glomerular injury, and chronic low-grade NF-κB renal inflammation are most active. Specifically, CBD's negative allosteric CB1 modulation in mesangial cells and juxtaglomerular cells addresses the intraglomerular hypertension and RAAS-activating CB1 signaling that drives diabetic and metabolic nephropathy; CB2/NF-κB suppression of renal macrophage inflammatory activation addresses the inflammatory driver of nephritis and progressive fibrosis; direct antioxidant activity and Nrf2/HO-1 upregulation address the oxidative tubular injury that contributes to CKD progression regardless of etiology; and HPA/cortisol normalization reduces the cortisol-RAAS-aldosterone cascade that elevates systemic and intraglomerular blood pressure. The preclinical evidence from diabetic nephropathy and nephritis rodent models is consistently supportive — CBD reduces proteinuria, glomerulosclerosis markers, tubular injury, oxidative stress, and inflammatory cytokine levels in renal tissue. Human evidence for CBD improving kidney function markers is very limited — the blood pressure reduction seen in human CBD studies is the most directly kidney-relevant clinical finding. Practical conclusion: CBD gummies at standard doses represent a reasonable supplementary strategy for kidney health in individuals with metabolic risk factors for CKD, within a comprehensive approach that prioritizes blood pressure control, blood sugar management, weight management, and physician monitoring of eGFR and urinary albumin.

Are CBD gummies safe for people with chronic kidney disease?

CBD gummies are generally considered safe at standard supplement doses for mild-to-moderate CKD (eGFR 30–89, Stage 2–3), but individuals with existing kidney disease should consult their nephrologist before beginning CBD supplementation for two practical reasons: drug interactions and clearance. Drug interaction concern is primary — individuals with CKD are typically on multiple medications (ACE inhibitors/ARBs, diuretics, phosphate binders, potassium-lowering agents, erythropoiesis-stimulating agents, sometimes immunosuppressants for glomerulonephritis), and CBD inhibits CYP3A4, CYP2C19, CYP2C9, and CYP2D6 — the enzymes that metabolize many of these drugs. CBD increasing the plasma levels of blood pressure medications (particularly calcium channel blockers metabolized by CYP3A4) or immunosuppressants (tacrolimus, cyclosporine — narrow therapeutic index) requires physician monitoring. Clearance concern is secondary but relevant in severe CKD — CBD is hepatically metabolized to CBD-glucuronide and 7-OH-CBD, which are renally excreted. In severe CKD (eGFR below 30) or end-stage renal disease (ESRD), impaired renal clearance of these metabolites may increase systemic exposure. No clinical guidelines have been established for CBD dosing in renal impairment, so physician guidance is appropriate. For individuals with mild-to-moderate CKD on a stable medication regimen with no CYP-sensitive drugs, standard supplement doses (10–25 mg/day) are unlikely to be problematic — but confirmation with their nephrologist is the responsible path. CBD is not nephrotoxic at supplement doses: no clinical evidence of CBD directly injuring the kidney exists at standard consumer doses, distinguishing it from NSAIDs (which are genuinely nephrotoxic with regular use) and contrast dye, which are the most common drug-related nephrotoxic exposures.

Can CBD gummies help with kidney stones?

Research suggests CBD gummies may support kidney stone management primarily through pain and inflammation modulation rather than direct stone prevention or dissolution — an important distinction. CBD is not a lithotriptic agent and does not dissolve kidney stones or alter urinary calcium, oxalate, or uric acid excretion in ways that have been documented in human studies. What CBD may offer in the context of kidney stones: CBD's analgesic mechanisms — TRPV1 desensitization (the TRPV1 receptor is expressed in renal tubular cells and urothelium and is activated by the passage of stones), FAAH/anandamide elevation, and CB1/CB2 pain modulation — may reduce the severity of renal colic (kidney stone pain). The pain of ureteral stone passage is one of the most severe acute pain experiences; CBD's modest analgesic properties are not a substitute for prescription analgesia in severe renal colic, but may provide complementary relief in mild-moderate episodes and in post-stone-passage ureteral inflammation. CBD's anti-inflammatory CB2/NF-κB mechanisms may reduce the ureteral and renal pelvis inflammation that contributes to hydronephrosis risk and post-stone renal injury. CBD's blood pressure and HPA effects may reduce the RAAS-mediated aldosterone activation that promotes hypercalciuria (excess urinary calcium excretion, the most common cause of calcium oxalate stones) in stress-responsive individuals. This last mechanism is speculative — no clinical study has documented CBD reducing urinary calcium or stone recurrence rate. For individuals with recurrent kidney stones, evidence-based prevention includes high fluid intake (>2.5 liters/day urine output), dietary oxalate restriction (for calcium oxalate stones), and physician-guided prescription interventions (thiazide diuretics for hypercalciuria, allopurinol for uric acid stones, potassium citrate for calcium oxalate stones). CBD is a reasonable complementary anti-inflammatory and analgesic addition within this framework, not a stone prevention strategy.

Do CBD gummies interact with kidney medications?

CBD gummies have clinically important interactions with several medications commonly used in kidney disease management that require physician awareness and potentially monitoring. CBD inhibits CYP3A4, CYP2C19, CYP2C9, and CYP2D6. Relevant interactions for common kidney/CKD medications: ACE inhibitors (lisinopril, enalapril): primarily renally cleared with minimal CYP metabolism; low interaction risk. ARBs (losartan, irbesartan, candesartan): some CYP2C9 metabolism; CBD may modestly increase levels — blood pressure monitoring warranted. Calcium channel blockers (amlodipine, diltiazem, verapamil): CYP3A4 substrates — CBD inhibition increases plasma levels, potentially enhancing blood pressure-lowering effects; blood pressure monitoring required. Tacrolimus/cyclosporine (for glomerulonephritis or post-transplant): CYP3A4 substrates with narrow therapeutic index — CBD can significantly increase immunosuppressant levels; these are the highest-priority interaction in nephrology — transplant patients must consult their nephrologist before any CBD supplementation. Diuretics (furosemide, hydrochlorothiazide): minimal CYP interaction; primarily renal clearance; low CBD interaction risk. Warfarin (CYP2C9): CBD increases warfarin levels — INR monitoring required. Allopurinol (for uric acid stones/hyperuricemia): primarily renally cleared; low CBD interaction risk. Colchicine (for gout/hyperuricemia): CYP3A4 and P-glycoprotein substrate; CBD may increase colchicine levels — physician awareness warranted. Statins (atorvastatin, simvastatin): CYP3A4 substrate — CBD increases levels, raising myopathy risk. The overall picture: CBD's drug interactions in CKD are driven by its hepatic CYP inhibition, not by renal mechanisms. Individuals managing CKD with multiple medications should review their complete drug list with their nephrologist before starting CBD.

Can CBD gummies help with diabetic nephropathy?

Research suggests CBD gummies may support kidney health in the context of diabetic nephropathy risk through multiple mechanisms that specifically target diabetic nephropathy pathology — while diabetic nephropathy is a serious medical condition requiring physician management, not supplementation alone. The preclinical evidence is mechanistically compelling: in streptozotocin-induced diabetic rodent models with nephropathy, CBD administration consistently reduces proteinuria (urinary albumin excretion — the clinical marker of glomerular barrier dysfunction), glomerulosclerosis (the structural scarring of glomeruli), tubular injury markers, oxidative stress (8-OHdG, nitrotyrosine), inflammatory cytokines (TNF-α, IL-6 in renal tissue), and fibrosis markers (TGF-β, fibronectin) in renal tissue. Multiple mechanisms are at play simultaneously: CB1 negative allosteric modulation reduces mesangial CB1 overactivation (a driver of intraglomerular hypertension and mesangial expansion in diabetic kidneys); direct antioxidant and Nrf2 activation protects against AGE/ROS-driven tubular and glomerular injury; CB2/NF-κB suppresses the macrophage-mediated tubular inflammatory injury; HPA/cortisol reduction lowers RAAS activation and intraglomerular pressure; and CBD's insulin sensitization support (via CB1 modulation and PPARγ in adipose) addresses the root cause of glomerular CB1 overactivation. The translation gap from rodent diabetic nephropathy models to human clinical benefit has not been bridged by controlled trials — human evidence for CBD specifically improving eGFR, proteinuria, or kidney biopsy outcomes in diabetic nephropathy does not yet exist. Individuals with diabetes managing kidney health should prioritize evidence-based interventions: tight glycemic control (most important), RAAS blockade (ACE inhibitor or ARB, the first-line nephroprotective pharmacological strategy), blood pressure management, and weight control — CBD supplementation as a complementary strategy is reasonable but should not substitute for these interventions.

How long do CBD gummies take to support kidney health?

The timeline for CBD gummies to produce measurable kidney health effects depends on the mechanism and the clinical endpoint being considered. For vascular and hemodynamic effects — blood pressure reduction and RAAS modulation — CBD produces measurable acute effects within 1–2 hours of dosing in human studies, with cumulative benefit from HPA normalization developing over 2–6 weeks of daily use. For anti-inflammatory renal effects — CB2/NF-κB suppression in renal macrophages and reduction of circulating inflammatory cytokines — consistent daily dosing over 4–8 weeks produces the most reliable anti-inflammatory tone. For structural kidney changes — glomerulosclerosis progression, proteinuria, fibrosis — these develop over months to years, and any CBD supplementation effect on slowing progression would similarly require months of consistent use to detect, with appropriate clinical monitoring (eGFR and urinary albumin creatinine ratio tests). Practically: individuals interested in tracking CBD's effect on kidney health markers can establish baseline eGFR and uACR (urinary albumin-to-creatinine ratio) with their physician before starting CBD supplementation, then recheck at 3–6 months alongside the consistent dietary, exercise, and blood pressure management that are the primary levers for kidney health preservation. The most actionable metric CBD may move — blood pressure — can be self-monitored with a home blood pressure cuff in 2–4 weeks of consistent supplementation. Kidney health is a long-horizon investment; CBD's role is to support the biological environment (reduced inflammation, lower oxidative stress, improved blood pressure, better sleep) in which kidneys function best, as part of a broader metabolic health strategy.

References

Blessing EM, et al. Cannabidiol as a Potential Treatment for Anxiety Disorders. Neurotherapeutics. 2015;12(4):825–836. PMID: 26341731
Shannon S, et al. Cannabidiol in Anxiety and Sleep: A Large Case Series. Perm J. 2019;23:18–041. PMID: 30624194
Russo EB. Cannabinoids in the management of difficult to treat pain. Ther Clin Risk Manag. 2016;4(1):245–259. PMID: 28861491
Crippa JA, et al. Neural basis of anxiolytic effects of cannabidiol (CBD) in generalized social anxiety disorder. J Psychopharmacol. 2011;25(1):121–130. PMID: 20829306
Corroon J, Phillips JA. A Cross-Sectional Study of Cannabidiol Users. Cannabis Cannabinoid Res. 2018;3(1):152–161. PMID: 30014049
Capano A, et al. Evaluation of the effects of CBD hemp extract on opioid use and quality of life indicators in chronic pain patients. Postgrad Med. 2020;132(1):56–61. PMID: 31711352

Medical Disclaimer

This article is for informational and educational purposes only and does not constitute medical advice. CBD gummies are dietary supplements; these statements have not been evaluated by the Food and Drug Administration. These products are not intended to diagnose, treat, cure, or prevent any disease or medical condition, including chronic kidney disease, diabetic nephropathy, hypertensive nephrosclerosis, glomerulonephritis, kidney stones, or any renal disorder. Kidney disease is a serious medical condition requiring diagnosis and management by a qualified nephrologist or physician. CBD is metabolized by the liver and excreted by the kidneys; individuals with existing kidney disease, renal impairment, or taking renally-cleared or CYP3A4-metabolized medications should consult their physician before CBD supplementation. Regular NSAID use combined with CBD may increase renal stress — physician guidance is warranted. Do not use CBD as a substitute for physician-supervised kidney disease management, blood pressure control, or diabetes treatment.