Kidney

How much blood the kidneys filter per minute -- but as an ESTIMATE, not a direct measurement. It takes a creatinine value and runs it through an equation (CKD-EPI) along with age and sex. The word doing the heavy lifting is estimated: a narrative review of kidney-function equations lays out plainly that these are estimating equations, each with assumptions and error, not a direct read of filtration. (cite: Kidney function estimation equations: a narrative review, 2025, PMC12031902)

Typical range: Conventional: roughly ≥90 mL/min/1.73m² is often labeled "normal," with 60-89 common and usually read alongside other markers; below 60 sustained is where clinical concern rises. No separate functional-medicine "optimal" number applies -- the more useful reading is the trend across several tests, not one value against a cutoff, because eGFR has real biological day-to-day variation even in healthy people. (cite: Biological variation and reference change value of eGFR, systematic review and meta-analysis, 2022, PMC9583397)

Food first: There is no food or supplement that "raises eGFR" in a healthy person. The evidence-based approach is protecting the blood vessels the filter is made of -- steady blood sugar, healthy blood pressure, less added sugar -- plus adequate (not forced-extreme) hydration. Adequate rather than excessive protein is the goal: a controlled feeding trial in healthy adults found a higher-protein pattern did not harm kidney function over the study, but anyone with existing kidney disease needs individualized protein guidance. (cite: Effect of a High-Protein Diet on Kidney Function in Healthy Adults, OmniHeart Trial, 2013, PMC3602135)

When to see someone: Because creatinine comes from muscle, eGFR carries a muscle-mass bias -- a very muscular person can read falsely low, and a low-muscle, older or frail person can get a "reassuring" number that overstates true function. One reading is a snapshot, not a verdict; a value sitting just inside or just outside a cutoff means far less than the direction over several tests. Never self-diagnose kidney disease from a single eGFR.

A waste product the muscles produce at a fairly steady rate that the kidney clears, so the amount left in the blood is a rough readout of how well filtration is running. It is the usual input for eGFR. (cite: Endogenous markers of kidney function and renal drug clearance processes of filtration, secretion, and reabsorption, 2023, PMC9910221)

Typical range: Conventional: roughly 0.7-1.3 mg/dL (men), 0.6-1.1 mg/dL (women), lab- and assay-dependent and heavily influenced by muscle mass. No functional-medicine "optimal" range applies separately -- creatinine is interpreted through eGFR and alongside cystatin C, not as a standalone wellness target.

Food first: There is nothing to deliberately move here nutritionally in a healthy person. The honest read is to interpret creatinine through eGFR and cystatin C, and to protect the vascular filter (blood sugar, blood pressure, hydration) rather than target the number itself.

When to see someone: The muscle-mass and recent-meat/creatine effects mean a single creatinine value can mislead in either direction. It is read alongside eGFR and, where the estimate is in doubt, cystatin C -- never used alone to conclude anything about kidney health.

A small protein made by nearly every cell in the body at a steady rate and cleared by the kidney; crucially, its blood level is barely affected by muscle mass, diet, or sex the way creatinine is, which makes a cystatin C-based eGFR a valuable cross-check exactly where creatinine misleads -- the very muscular, the very frail, the elderly. When a creatinine eGFR and a cystatin C eGFR disagree, that disagreement is itself information a clinician can use. (cite: Kidney function estimation equations: a narrative review, 2025, PMC12031902)

Typical range: Conventional: roughly 0.6-1.0 mg/L (assay-dependent); the cystatin C eGFR is read on the same scale as creatinine eGFR (≥90 often "normal," below 60 sustained a concern). No separate functional-medicine "optimal" range applies.

Food first: Nothing to move nutritionally. Its role is diagnostic cross-check; the useful action is asking a clinician to add it when the creatinine eGFR is in doubt (heavily muscled or low-muscle bodies).

When to see someone: Cystatin C can be nudged by thyroid dysfunction, high-dose steroids, and marked inflammation independent of true filtration, so it is interpreted by a clinician alongside creatinine rather than trusted in isolation. It is a cross-check, not a self-managed wellness number.

Urea is a nitrogen waste product from protein breakdown that the kidney clears, so BUN rises when filtration falls -- but it also moves with hydration, protein intake, GI bleeding, and other factors, which is why it is read alongside creatinine rather than on its own. The BUN:creatinine ratio helps separate causes: a high ratio often points to dehydration or low blood flow rather than intrinsic kidney damage. (cite: Endogenous markers of kidney function and renal drug clearance, 2023, PMC9910221)

Typical range: Conventional: BUN roughly 7-20 mg/dL; BUN:creatinine ratio roughly 10:1 to 20:1 (lab-dependent). No functional-medicine "optimal" range applies -- this pair is interpreted together and in context, not as standalone wellness targets.

Food first: Nothing to deliberately target. Adequate hydration and adequate (not excessive) protein keep BUN in a sensible, interpretable place; a high-protein pattern did not harm kidney function in healthy adults in the OmniHeart trial, while anyone with existing kidney disease needs individualized protein guidance. (cite: Effect of a High-Protein Diet on Kidney Function in Healthy Adults, OmniHeart Trial, 2013, PMC3602135)

When to see someone: A high BUN or high BUN:creatinine ratio can reflect dehydration, a high-protein meal, GI bleeding, or reduced blood flow -- not necessarily kidney damage -- so it is never interpreted alone. A rising trend across tests matters more than one value.

Whether the filter is leaking. Albumin is a blood protein a healthy filter holds back; when small amounts start showing up in urine, that is one of the earliest signals the filtering surface is under strain -- and it can appear while eGFR still reads perfectly normal. The reason it matters beyond the kidney is mechanistic: the filtering surface is lined by a delicate gel-like layer on the blood-vessel wall called the glycocalyx, and albumin leak is understood as a marker of glycocalyx and endothelial dysfunction -- damage to the blood-vessel lining itself, not only the kidney. (cite: The glycocalyx -- linking albuminuria with renal and cardiovascular disease, 2015, PMID 26460356)

Typical range: Conventional: roughly <30 mg/g is the usual "normal" cutoff; 30-300 mg/g and >300 mg/g are the moderately- and severely-increased bands used clinically. No separate functional-medicine "optimal" number -- lower is better, and the change over time is what a clinician tracks.

Food first: The evidence-based moves are vascular, not a targeted nutrient: steady blood sugar and blood pressure, less added sugar, adequate hydration, and a better potassium-to-sodium balance from whole foods IF there is no diagnosed kidney disease (see the potassium reversal below).

When to see someone: ACR can be transiently elevated by exercise, fever, infection, or menstruation, so a single positive is repeated before it means anything. A normal eGFR with a rising ACR is exactly the early strain the single eGFR number misses -- this is a clinician conversation, tracked as a trend, not a self-diagnosis.

A broader dipstick-and-microscopy look at the urine -- protein, blood, glucose, and cells -- that can flag filter leak (protein), infection or stones (blood, cells), or spilled glucose (a blood-sugar signal). It is a wider, cheaper screen that points toward which more specific test (like ACR) to run next.

Typical range: Conventional: normal is essentially negative-to-trace protein, no glucose, no significant blood or cells (results are qualitative/semi-quantitative and lab-dependent). No functional-medicine "optimal" range applies -- this is a screen, read in context.

Food first: Nothing to target directly. Where protein shows up, the vascular levers behind ACR apply; where glucose shows up, blood-sugar control is the lever; adequate hydration supports the system generally. (cite: Hydration and Chronic Kidney Disease Progression, 2016, PMID 27161565)

When to see someone: Urinalysis findings are non-specific and easily thrown off by hydration, recent exercise, contamination, or a transient infection, so any abnormal result is confirmed and interpreted by a clinician rather than acted on from the strip alone.

The end product of breaking down purines, cleared largely by the kidney. It is not a filtration marker the way creatinine is, but it sits at the junction of metabolism, blood vessels, and the kidney: when it runs high, elevated uric acid is tied to endothelial dysfunction -- the same blood-vessel-lining trouble that shows up as albumin leak -- through mechanisms that reduce nitric oxide and raise vascular stress. (cite: Hyperuricemia and Endothelial Function: From Molecular Background to Clinical Perspectives, 2018, doi 10.1016/j.atherosclerosis.2018.10.007)

Typical range: Conventional: roughly 3.4-7.0 mg/dL (men), 2.4-6.0 mg/dL (women), lab-dependent. No formal functional-medicine "optimal" range is well validated; lower-within-range is generally viewed as more favorable for vascular and kidney load, but that is a mechanistic read, not a validated target.

Food first: Lower added sugar and sugar-sweetened beverages (the fructose-uric-acid chain), keep hydration adequate, and moderate very high purine loads if uric acid runs high. These pull on the vascular drivers that also protect the filter.

When to see someone: A single high uric acid value is not a diagnosis; it is a canary connecting what you drink, blood-vessel health, and kidney load. Managing symptomatic gout or markedly elevated uric acid is a clinical decision, not a food-only project.

This marker sits in Transform -- the cofactors enzymes need to turn fuel into usable energy.

A major intracellular electrolyte the kidney sets the level of; potassium and sodium pull in opposite directions on the blood-pressure dial, and most modern diets are heavy on sodium and light on potassium. In a healthy body, potassium-rich whole foods (vegetables, fruit, legumes, tubers) are broadly beneficial, and the potassium-to-sodium balance matters for blood pressure and vascular health. (cite: NIH potassium professional fact sheet, Office of Dietary Supplements)

Typical range: Conventional: roughly 3.5-5.0 mmol/L (lab-dependent). This is a tightly regulated safe band -- both low and high potassium are clinically meaningful -- so there is no "push it higher" wellness target; the goal is staying in range, and in diagnosed kidney disease the safe band is set individually by a clinician.

Food first: For someone WITHOUT diagnosed kidney disease: favour whole-food potassium (vegetables, fruit, legumes, tubers) and a better potassium-to-sodium balance to support blood pressure. (cite: NIH potassium professional fact sheet, Office of Dietary Supplements)

When to see someone: **THIS IS THE CRITICAL REVERSAL ON THIS PAGE. In DIAGNOSED kidney disease the potassium advice flips completely.** When filtration is significantly reduced, the kidney can no longer clear potassium efficiently, and blood potassium can climb to genuinely dangerous levels (hyperkalemia carries real cardiac risk) -- so the potassium-rich foods that help a healthy person can become a serious hazard. The NIH potassium fact sheet is explicit that people with impaired kidney function need individualized guidance rather than general "eat more potassium" advice. If you have diagnosed kidney disease, potassium is a clinician conversation, not a blog or wellness instruction -- your safe range is set by your labs and your nephrology team, and general "eat more potassium" advice does not apply to you. Both halves of that are true, and leaving out the second half would be the failure. (cite: NIH potassium professional fact sheet, Office of Dietary Supplements)

The major extracellular electrolyte the kidney balances to hold water and blood volume; serum sodium is tightly regulated and reflects water balance as much as sodium intake, while dietary sodium's main relevance is its opposing pull against potassium on blood pressure.

Typical range: Conventional: roughly 135-145 mmol/L (lab-dependent). This is a tight regulated band -- abnormal serum sodium is usually a water-balance issue, not a dietary-salt readout -- so there is no wellness "optimal" to target; dietary sodium is managed for blood pressure, not to move the serum number.

Food first: Reduce excess added/processed sodium and improve the potassium-to-sodium ratio with whole foods (again, only where there is no diagnosed kidney disease altering the potassium side). Adequate hydration keeps water balance -- and therefore serum sodium -- stable.

When to see someone: An abnormal serum sodium (high or low) is a water-balance problem that needs clinical evaluation, not a dietary-salt adjustment. People with heart, liver, or kidney disease often have specific sodium and fluid targets set by their clinician that override general advice.

An extracellular electrolyte that moves largely with sodium and participates in acid-base balance; on a metabolic panel it is mostly used alongside sodium and bicarbonate to assess fluid status and acid-base state (for example, in calculating the anion gap), rather than as a standalone marker.

Typical range: Conventional: roughly 98-107 mmol/L (lab-dependent). No functional-medicine "optimal" range applies -- chloride is interpreted as part of the electrolyte/acid-base picture, not on its own.

Food first: Nothing to deliberately target. Chloride follows sodium and hydration; managing those (and any underlying acid-base issue with a clinician) is what moves it, not a specific nutrient.

When to see someone: An isolated abnormal chloride is rarely acted on alone -- it is read within the electrolyte and acid-base panel, and abnormalities are evaluated for their cause (fluid loss, acid-base disturbance) rather than corrected directly.

The blood's main buffer and the readout of acid-base balance -- one of the kidney's core jobs is holding the body's acid-base state in a narrow safe range, and serum bicarbonate (sometimes reported as CO2 or total CO2) reflects how that balance is running. A low bicarbonate can signal metabolic acidosis, which in the kidney context is watched because chronic low-grade acid load may add strain over time.

Typical range: Conventional: roughly 22-29 mmol/L (lab-dependent). No formal functional-medicine "optimal" range is well validated; staying comfortably within the normal band is the goal, and low-normal or low bicarbonate in someone with reduced kidney function is a clinician's call.

Food first: A whole-food, produce-forward pattern with adequate but not excessive protein supports a gentler net acid load. In diagnosed kidney disease this overlaps the potassium reversal -- produce is potassium-rich -- so the base-load approach there is set by a clinician, not self-managed.

When to see someone: An abnormal bicarbonate is an acid-base finding that needs clinical interpretation (it can reflect breathing, kidney, or metabolic causes). Do not chase a low bicarbonate with baking-soda or alkali self-dosing, especially with any kidney or heart condition -- that is a prescribed therapy with real sodium and electrolyte consequences, managed by a clinician.

This marker sits in Transform -- the cofactors enzymes need to turn fuel into usable energy.

A mineral whose blood level the kidney helps regulate (alongside the parathyroid glands, vitamin D, and bone); serum calcium is tightly controlled, and in the kidney context it matters because reduced kidney function disturbs the calcium-phosphate-vitamin D axis, which is why calcium, phosphate, and related markers are watched together in kidney care.

Typical range: Conventional: roughly 8.5-10.2 mg/dL total calcium (lab-dependent); often interpreted alongside albumin (which binds calcium) or as ionized calcium. No functional-medicine "optimal" range applies -- serum calcium is a tightly regulated number, not a wellness target to raise.

Food first: Aim for adequate dietary calcium (dairy, leafy greens, fortified foods) and adequate vitamin D status for bone and mineral balance -- adequacy, not excess. Serum calcium itself is not a number to target; it is regulated automatically in a healthy person.

When to see someone: An abnormal serum calcium (high or low) needs clinical work-up, not a supplement adjustment -- causes include parathyroid, vitamin D, and kidney issues. In reduced kidney function, calcium and vitamin D are prescribed and monitored carefully because the disturbed calcium-phosphate axis makes both over- and under-correction harmful; this is clinician territory, not self-supplementation.

A mineral the kidney clears and regulates as part of the calcium-phosphate-vitamin D axis and bone metabolism. In healthy kidneys phosphate is well controlled; as filtration falls, the kidney clears phosphate less well and it can rise, which is why phosphate is one of the more important markers to watch in reduced kidney function.

Typical range: Conventional: roughly 2.5-4.5 mg/dL (lab-dependent). No functional-medicine "optimal" range applies -- staying in the normal band is the goal, and a rising phosphate in reduced kidney function is a clinical concern managed by a clinician.

Food first: Favour whole foods over heavily processed foods and colas that carry inorganic phosphate additives; this reduces the readily-absorbed phosphate load. In diagnosed kidney disease, phosphate intake is specifically managed (often restricted, sometimes with prescribed binders) by a clinician.

When to see someone: A high phosphate is a meaningful finding in reduced kidney function and is managed clinically (diet, and sometimes phosphate binders) -- not a self-managed food tweak. Do not use phosphate-containing supplements or laxatives for "kidney support"; excess phosphate is the problem in the kidney context, not the fix.

This marker sits in Transform -- the cofactors enzymes need to turn fuel into usable energy.

A mineral involved in hundreds of enzymatic reactions, cleared and regulated in part by the kidney; serum magnesium reflects under 1% of total body magnesium (an imperfect status marker), and in the kidney context magnesium matters both as a nutrient many diets fall short on and because magnesium clearance itself depends on kidney function.

Typical range: Conventional: roughly 1.7-2.2 mg/dL serum (lab-dependent); some practitioners argue RBC magnesium is more informative, though it is not a routine kidney-panel test. No consensus functional-medicine "optimal" serum target applies.

Food first: Leafy greens, nuts, seeds, legumes, whole grains; magnesium glycinate or citrate are generally better absorbed/tolerated than oxide. In a healthy person, correcting a confirmed shortfall is the evidence-based approach rather than empiric high dosing.

When to see someone: High-dose magnesium supplements cause diarrhea before serious harm in people with normal kidney function, but anyone with reduced kidney function (low eGFR) needs medical guidance before supplementing, since magnesium is renally cleared and can accumulate to dangerous levels. This is the second mineral (with potassium) whose supplementation advice reverses in diagnosed kidney disease.