Kidney Function Tests (KFT): Understanding Your Blood Test Series

1. Overview: What this panel reveals and why it is important

The kidney function test is not a single measurement but a coordinated panel that assesses the three primary roles of the kidney: filtration of metabolic waste, regulation of fluid and electrolyte balance, and endocrine functions (erythropoietin production, renin‑angiotensin system, vitamin D activation). Unlike a liver panel that identifies injury patterns, the KFT panel primarily quantifies filtration efficiency (glomerular filtration rate, GFR) and tubular integrity via serum markers and electrolyte composition.

The core of the panel is creatinine—a muscle waste product freely filtered by the glomerulus and not reabsorbed. From creatinine, estimated GFR (eGFR) is calculated, providing a continuous measure of kidney function. Blood urea nitrogen (BUN) adds complementary information about volume status and protein catabolism. The accompanying electrolytes (sodium, potassium, chloride, bicarbonate) reveal the kidney’s ability to maintain internal milieu, and calcium/phosphate reflect mineral metabolism.

No single parameter is interpreted in isolation. The BUN:creatinine ratio distinguishes prerenal states from intrinsic renal disease; the eGFR stages chronic kidney disease; the electrolyte pattern uncovers acid‑base disorders, mineralocorticoid deficiency, or tubular defects. A rise in creatinine must be contextualised—acute or chronic? Steady or rising? Accompanied by oliguria, hypertension, or proteinuria?

The panel also serves as a monitoring tool—for disease progression, nephrotoxic drug effects, and response to interventions (renin‑angiotensin blockade, volume repletion). Serial measurements are infinitely more informative than a single snapshot.

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2. What does it measure

A standard KFT panel (often called renal function panel or basic metabolic panel) typically includes the following. Reference ranges are laboratory‑specific; values below are approximate adult ranges.

Filtration markers:

· Creatinine: 0.6–1.2 mg/dL (male); 0.5–1.1 mg/dL (female). Waste product of muscle creatine metabolism. Not a sensitive marker of early kidney injury—substantial nephron loss occurs before creatinine rises. Affected by muscle mass, diet, age, sex.

· Estimated glomerular filtration rate (eGFR): Calculated from creatinine, age, sex, race (some labs now report race‑free CKD‑EPI equations). >90 mL/min/1.73m² is normal; values <60 for ≥3 months define CKD. Stages kidney disease, not diagnosis.

· Blood urea nitrogen (BUN): 7–20 mg/dL. End‑product of protein metabolism. Elevation reflects decreased GFR, increased protein intake, catabolism, or gastrointestinal bleeding.

· BUN:creatinine ratio: 10:1–20:1. Helps differentiate prerenal (ratio >20:1) from intrinsic renal or postrenal (ratio 10:1–20:1) causes.

Electrolytes and minerals:

· Sodium (Na⁺): 135–145 mEq/L. Reflects water balance, regulated by ADH, thirst, and renal handling.

· Potassium (K⁺): 3.5–5.0 mEq/L. Critical for neuromuscular function; renal excretion is primary route.

· Chloride (Cl⁻): 98–107 mEq/L. Often parallels sodium; helps assess acid‑base status.

· Bicarbonate (HCO₃⁻): 22–29 mEq/L. Serum buffer; low values indicate metabolic acidosis.

· Calcium (Ca²⁺): 8.5–10.2 mg/dL. Total calcium; adjust for albumin if hypoalbuminaemia.

· Phosphorus (PO₄³⁻): 2.5–4.5 mg/dL. Retained in CKD; contributes to secondary hyperparathyroidism.

· Albumin (sometimes included): 3.5–5.0 g/dL. Low in nephrotic syndrome; also a nutritional marker.

Additional tests often ordered with KFT (but not always on standard panel):

· Cystatin C: Alternative filtration marker, less influenced by muscle mass. Increasingly used for confirmatory eGFR calculation.

· Urinalysis: Protein, blood, glucose, specific gravity, microscopy—essential for diagnosing nephritic/nephrotic syndromes, infection, stones.

· Urine albumin‑to‑creatinine ratio (UACR): Gold standard for quantifying albuminuria, a marker of glomerular damage and cardiovascular risk.

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3. Other factors connected to this panel

Preanalytical variables:

· Hydration status: Dehydration raises creatinine and BUN (prerenal physiology); over‑hydration lowers them.

· Diet: High cooked meat intake transiently raises creatinine (conversion of creatine to creatinine). Vegetarian/low‑protein diets lower baseline creatinine, leading to higher eGFR for same filtration.

· Muscle mass: Amputation, sarcopenia, neuromuscular disease → lower creatinine production → falsely elevated eGFR.

· Medication interference: Trimethoprim, cimetidine, fenofibrate, some tyrosine kinase inhibitors inhibit tubular creatinine secretion, raising serum creatinine without true GFR decline. This is falsely elevated creatinine.

· Timing: Creatinine peaks ~2 hours post‑exercise; minimal diurnal variation.

· Sample handling: Delayed separation causes glucose consumption and falsely low bicarbonate.

Medications affecting KFT components:

· Elevate creatinine (true nephrotoxicity): Aminoglycosides, IV contrast, amphotericin B, calcineurin inhibitors (tacrolimus, cyclosporine), tenofovir, lithium, NSAIDs (with reduced renal perfusion).

· Elevate creatinine (non‑GFR, secretion inhibition): Trimethoprim, cimetidine, cobicistat, dolutegravir, pyrimethamine.

· Elevate BUN: Corticosteroids (catabolic), tetracyclines (except doxycycline).

· Hypokalaemia: Thiazides, loop diuretics, mineralocorticoids, amphotericin B.

· Hyperkalaemia: ACE inhibitors, ARBs, potassium‑sparing diuretics, NSAIDs, trimethoprim, digoxin (toxicity), heparin, beta‑blockers.

· Hyponatraemia: Thiazides, SSRIs, carbamazepine, oxcarbazepine, desmopressin, cyclophosphamide.

· Metabolic acidosis: Acetazolamide, topiramate, metformin (lactic), salicylates, propofol.

· Hypocalcaemia: Bisphosphonates, cinacalcet, foscarnet, phenytoin, rifampin (vitamin D metabolism).

· Hypercalcaemia: Thiazides, lithium, vitamin D intoxication, calcium‑containing antacids.

Physiological and demographic factors:

· Age: eGFR declines physiologically after ~40 years (≈1 mL/min/1.73m² per year). Elderly have lower muscle mass, so creatinine may be normal despite reduced GFR.

· Sex: Women have lower creatinine and higher eGFR for same filtration (lower muscle mass).

· Race: Historically, race coefficients overestimated eGFR in Black individuals; current guidelines recommend race‑free CKD‑EPI equations.

· Pregnancy: GFR increases 40–50% by second trimester → creatinine falls (normal 0.4–0.6 mg/dL). BUN similarly reduced. Proteinuria thresholds adjusted upward.

· Body habitus: Extreme obesity → higher creatinine production; eGFR equations less accurate.

· Menstrual status: No significant effect.

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4. Disorders related to abnormal values: Pattern recognition

The KFT panel is best interpreted through integrated patterns of creatinine, BUN, electrolytes, and urinalysis. Six dominant clinical scenarios account for >90% of abnormal results.

a. Prerenal azotaemia pattern (Acute kidney injury, pre‑renal)

Laboratory profile:

· Creatinine ↑, BUN ↑

· BUN:creatinine ratio >20:1

· Electrolytes: variable; may see hyperkalaemia, mild metabolic alkalosis if vomiting

· Urinalysis: bland, high specific gravity (>1.020), low fractional excretion of sodium (FeNa <1%)

Differential diagnosis:

· True volume depletion: Haemorrhage, vomiting, diarrhoea, excessive diuresis, burns, third‑spacing (pancreatitis, sepsis)

· Reduced effective circulating volume: Heart failure, cirrhosis, nephrotic syndrome

· Renal artery stenosis (unilateral or bilateral)

· Medications: NSAIDs, ACEi/ARB in setting of renal artery stenosis or volume depletion

Outlier scenarios:

· BUN:creatinine >30:1: Profound prerenal state, or upper GI bleed (blood meal protein load) with normal or mildly reduced GFR.

· Prerenal physiology with FeNa >2%: If patient on diuretics, or underlying CKD (cannot conserve sodium).

· Rapidly rising creatinine with normal BUN:creatinine ratio: Consider not prerenal; move to intrinsic causes.

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b. Intrinsic renal parenchymal disease pattern

Intrinsic renal disease encompasses glomerular, tubular, interstitial, and vascular pathologies. The pattern varies by primary site of injury.

i. Acute glomerulonephritis / nephritic syndrome:

· Creatinine ↑ (variable acuity)

· BUN:creatinine ratio normal or elevated (if oliguric)

· Urinalysis: Dysmorphic RBCs, RBC casts, proteinuria (subnephrotic or nephrotic)

· Electrolytes: often normal early; hyperkalaemia if oliguric

· Associated: hypertension, oedema

ii. Nephrotic syndrome:

· Creatinine normal or mildly ↑

· Urinalysis: Heavy proteinuria (UACR >300 mg/g, often >3000), oval fat bodies, no RBC casts

· Albumin ↓, total protein ↓

· Electrolytes: normal unless CKD develops; oedema due to sodium retention

iii. Acute tubular necrosis (ATN):

· Creatinine ↑ over days

· BUN:creatinine ratio <20:1 (often 10–15:1)

· Urinalysis: Muddy brown granular casts, renal tubular epithelial cells

· FeNa >2% (unless contrast‑induced or early sepsis)

· Causes: ischaemia (prolonged prerenal), nephrotoxins (aminoglycosides, IV contrast, myoglobin, cisplatin)

iv. Acute interstitial nephritis (AIN):

· Creatinine ↑ (often subacute onset, days to weeks)

· Urinalysis: White blood cells, WBC casts, eosinophiluria (not sensitive), haematuria

· Systemic features: fever, rash, arthralgias (drug‑induced)

· Causes: NSAIDs, penicillins, cephalosporins, sulfa, proton pump inhibitors, allopurinol

Outlier scenarios:

· Rapidly rising creatinine with normal urine output (non‑oliguric AKI): Common with aminoglycosides, contrast nephropathy.

· Creatinine rise with only mild proteinuria and bland urine: Consider vascular causes (atheroemboli, renal artery thrombosis), or myeloma cast nephropathy (urine dipstick protein may be only light chains).

· Nephrotic syndrome with acute creatinine rise: Consider superimposed ATN, renal vein thrombosis, or rapidly progressive glomerulonephritis.

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c. Postrenal (obstructive) pattern

Laboratory profile:

· Creatinine ↑, BUN ↑

· BUN:creatinine ratio often normal or elevated (if prolonged obstruction causes pre‑renal component)

· Urinalysis: May be normal, haematuria, or pyuria

· Imaging: Hydronephrosis on ultrasound

Differential diagnosis:

· Ureteric obstruction: Stones, tumour, retroperitoneal fibrosis, iatrogenic (ligation)

· Bladder outlet: Benign prostatic hyperplasia, prostate cancer, urethral stricture, neurogenic bladder

Outlier scenarios:

· Creatinine normal despite unilateral obstruction: If contralateral kidney normal, creatinine remains normal.

· Post‑renal AKI with low BUN:creatinine ratio: If patient is malnourished or has liver disease (low urea production).

· Anuria (<100 mL/day): Complete obstruction (also bilateral cortical necrosis, severe ATN).

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d. Chronic kidney disease (CKD) pattern

Laboratory profile:

· eGFR <60 mL/min/1.73m² for ≥3 months

· Creatinine ↑ (but may be normal in early CKD)

· Progressive rise in creatinine over months to years

· Electrolytes: normokalaemic until advanced; later hyperkalaemia, metabolic acidosis (low HCO₃⁻), hyperphosphataemia, hypocalcaemia (or normal Ca with low vitamin D)

· Albuminuria (UACR ≥30 mg/g) confirms glomerular damage

· Renal ultrasound: small echogenic kidneys (except in diabetic nephropathy, amyloidosis, polycystic kidney disease)

Differential diagnosis:

· Diabetic nephropathy (most common)

· Hypertensive nephrosclerosis

· Chronic glomerulonephritis (IgA nephropathy, FSGS, membranous)

· Polycystic kidney disease

· Chronic tubulointerstitial nephritis (reflux nephropathy, analgesic nephropathy, lead)

· Unknown aetiology (CKD of uncertain cause)

Outlier scenarios:

· eGFR <30 with normal creatinine: Very low muscle mass (elderly, amputee, vegetarian). Confirm with cystatin C or measured GFR.

· CKD with normal‑sized kidneys: Diabetic nephropathy, HIV nephropathy, amyloidosis, acute on chronic.

· CKD with disproportionately high haemoglobin: Not expected; suspect polycythaemia, smoking, or renal artery stenosis.

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e. Isolated electrolyte abnormalities

i. Hyponatraemia (Na <135):

· Assess volume status (hypovolaemic, euvolaemic, hypervolaemic)

· Hypovolaemic: GI/skin losses, diuretics

· Euvolaemic: SIADH (medications, lung disease, CNS disorders), hypothyroidism, adrenal insufficiency, polydipsia

· Hypervolaemic: Heart failure, cirrhosis, CKD

ii. Hyperkalaemia (K >5.0):

· Pseudohyperkalaemia: haemolysis, thrombocytosis, leucocytosis

· Decreased excretion: CKD, ACEi/ARB, potassium‑sparing diuretics, type 4 renal tubular acidosis (hyporeninaemic hypoaldosteronism – diabetes, obstructive uropathy)

· Cellular shift: acidosis, tumour lysis, rhabdomyolysis, digoxin toxicity

· High intake: rare with normal renal function

iii. Metabolic acidosis (low HCO₃⁻):

· With normal anion gap: Diarrhoea, renal tubular acidosis (RTA), ureterosigmoidostomy, acetazolamide

· With elevated anion gap: CKD (uraemic acidosis), ketoacidosis, lactic acidosis, toxins

iv. Hypocalcaemia (Ca <8.5):

· CKD (low 1,25‑vitamin D, hyperphosphataemia)

· Hypoparathyroidism, vitamin D deficiency, pancreatitis, chelation (citrate)

v. Hyperphosphataemia (PO₄ >4.5):

· CKD (decreased excretion), hypoparathyroidism, tumour lysis, rhabdomyolysis

Outlier scenarios:

· Hyperkalaemia with normal eGFR and no medications: Suspect type 4 RTA (hyporeninaemic hypoaldosteronism) – check aldosterone/renin.

· Hypokalaemia with metabolic acidosis: Diarrhoea, RTA (type 1 or 2).

· Hypokalaemia with metabolic alkalosis: Vomiting, diuretics, mineralocorticoid excess.

· Hypercalcaemia with renal impairment: Primary hyperparathyroidism, malignancy, sarcoidosis, myeloma.

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f. Discrepancy between creatinine and eGFR

Scenario: eGFR low but creatinine normal

· Common in elderly, low muscle mass, vegetarians, amputees.

· Not true kidney disease; confirm with cystatin C.

Scenario: eGFR normal but creatinine elevated

· High muscle mass (bodybuilders, certain ethnicities), cooked meat intake, or drug interference (trimethoprim).

· Repeat after withholding interfering drugs/standardising diet.

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5. Best way to address aberrant levels: A holistic approach

Critical principle: The KFT panel reflects kidney function, not kidney disease. An abnormal creatinine is not a prescription for dialysis; it is a call to identify the cause (acute vs chronic, prerenal vs renal vs postrenal) and reversible factors. Empiric therapies without diagnosis are potentially harmful (e.g., volume expansion in heart failure, ACEi in renal artery stenosis).

a. Diagnostic algorithm, not therapeutic trial

Step 1: Confirm the abnormality

· Repeat KFT if mild, isolated, or suspected artefact (non‑fasting, exercise, drug interference).

· Check urinalysis and urine microscopy – the single most informative next test.

· If acute kidney injury (AKI), assess haemodynamics (BP, volume status, urine output).

Step 2: Distinguish acute vs chronic

· Compare with prior creatinine/eGFR.

· Renal ultrasound: small kidneys = chronic; normal/large size = acute or certain chronic diseases (diabetes, amyloidosis, PCKD, HIV).

Step 3: Identify the dominant pattern

· Prerenal, intrinsic renal (glomerular/tubular/interstitial/vascular), postrenal, CKD, isolated electrolyte, or creatinine‑eGFR discordance.

Step 4: Narrow the differential

· Prerenal: Assess volume status, cardiac function, FeNa, renal Doppler for stenosis.

· Glomerular: ANA, ANCA, anti‑GBM, complements, cryoglobulins, hepatitis B/C, HIV, SPEP/UPEP (if >40 years).

· Tubulointerstitial: Drug history, eosinophil count, eosinophiluria, urine culture.

· Postrenal: Ultrasound, post‑void residual, CT if stone suspected.

· CKD: Quantify albuminuria, renal ultrasound, treat complications (anaemia, acidosis, bone disease).

Step 5: Treat the underlying cause

· Prerenal: Volume repletion (IV fluids if hypovolaemic); discontinue NSAIDs, ACEi/ARB temporarily; treat heart failure/cirrhosis.

· Obstruction: Relieve obstruction (catheter, nephrostomy, stenting, stone removal).

· Drug‑induced AIN: Discontinue offending drug; consider corticosteroids if severe/refractory.

· Glomerulonephritis: Immunosuppression (corticosteroids, cyclophosphamide, rituximab) per specific diagnosis.

· CKD: Control blood pressure (<130/80), ACEi/ARB for albuminuria, SGLT2 inhibitors (proven reno‑protection), glycaemic control, dietary management, prepare for renal replacement therapy if eGFR <20.

Step 6: Manage complications (CKD)

· Anaemia: Iron supplementation (oral/IV), erythropoiesis‑stimulating agents (ESA) when Hb <10.

· Metabolic acidosis: Oral sodium bicarbonate if HCO₃ <22.

· Hyperkalaemia: Dietary potassium restriction, loop diuretics, potassium binders (patiromer, sodium zirconium cyclosilicate).

· Mineral bone disorder: Vitamin D supplementation, phosphate binders (calcium‑based, sevelamer, lanthanum).

· Cardiovascular risk: Statin (if indicated by age or risk), antiplatelet therapy for secondary prevention.

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b. Role of supplements and holistic medicine – supportive only

Nutritional supplements in CKD (adjunctive, evidence‑based):

· Active vitamin D (calcitriol, paricalcitol): For CKD stages 4–5 with secondary hyperparathyroidism and low serum calcium. Prescription only; not a supplement.

· Vitamin D3 (lichen‑derived cholecalciferol): For vitamin D deficiency (25‑OH‑D <30 ng/mL). Improves bone health, may slow CKD progression. Use vegan D3.

· Iron: Oral ferrous bisglycinate (better tolerated) or IV iron for iron deficiency anaemia. Avoid iron overload (check ferritin, TSAT).

· B‑complex vitamins: Water‑soluble vitamins may be depleted in dialysis; routine supplementation not proven beneficial in non‑dialysis CKD.

· Sodium bicarbonate: For metabolic acidosis; not a supplement but a prescription. Some advocate dietary alkali (citrate‑rich fruits/vegetables) to reduce acid load.

Herbs and Phytochemicals from Indian subcontinent (adjunctive, not primary):

· Punarnava (Boerhavia diffusa): Traditional diuretic; no robust evidence for renal protection. Use with caution – may interact with diuretics.

· Varuna (Crataeva nurvala): Traditional use for urinary stones; limited evidence for stone prevention.

· Gokshura (Tribulus terrestris): Used for urinary disorders; no proven benefit in CKD. May increase potassium.

· Amla (Emblica officinalis): Antioxidant; some preclinical data on nephroprotection. Human data insufficient.

· Curcumin: Anti‑inflammatory; may reduce proteinuria in some studies. Requires bioavailable formulation.

· Never use in undiagnosed AKI, severe CKD, or without medical supervision.

Critical warning:

· Avoid all herbal products containing undisclosed NSAIDs or corticosteroids (common in adulterated proprietary formulations).

· Do not use potassium‑sparing herbs (e.g., dandelion root, horsetail, nettle) with ACEi/ARB – risk of severe hyperkalaemia.

· Star fruit (carambola): Neurotoxin and nephrotoxin in CKD; contraindicated.

· Avoid high‑dose vitamin C (>500 mg/day) in CKD – risk of oxalate nephropathy.

· Avoid high‑dose vitamin D without monitoring – risk of hypercalcaemia, vascular calcification.

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c. Dietary and lifestyle approach (plant‑forward, ecologically sustainable)

Core principles for kidney health:

· Plant‑dominant low‑protein diet: For non‑dialysis CKD (stages 3–5), moderate protein restriction (0.6–0.8 g/kg ideal body weight/day) from plant sources reduces uraemic toxin generation, acid load, phosphorus burden, and may slow CKD progression. Plant protein also provides fibre, lowers blood pressure, and improves metabolic profile.

· Sodium restriction: <2 g/day (5 g salt). Reduces BP, proteinuria, and fluid overload.

· Potassium management: Not all CKD patients require potassium restriction; depends on serum K⁺, use of RAAS inhibitors, and residual diuresis. Plant‑based diets are naturally potassium‑rich, but cooking methods (leaching) can reduce potassium content if needed.

· Phosphorus management: Restrict inorganic phosphate additives (ultra‑processed foods, colas, processed meats). Organic phosphate in plant foods has lower bioavailability (phytate not digested by humans) – plant‑based diets advantageous.

· Adequate calcium: Dietary calcium (leafy greens, fortified plant milks, tofu) preferred; calcium‑based phosphate binders if indicated.

· Maintain healthy weight, regular physical activity.

· Avoid tobacco, alcohol, NSAIDs (over‑the‑counter).

Plant‑based protein sources (ecologically responsible):

· Legumes (lentils, chickpeas, beans), tofu, tempeh, edamame, mycoprotein, quinoa, hemp seeds.

· For patients requiring low potassium/phosphorus: refined plant proteins (tofu after leaching, mycoprotein) may be used.

· No requirement for animal protein for adequate nutrition in CKD.

Specific dietary considerations by CKD stage:

· CKD 1–2 (normal GFR, albuminuria): DASH‑style or Mediterranean diet; sodium restriction; emphasis on fruits, vegetables, whole grains.

· CKD 3–4 (moderate–severe): Plant‑dominant low‑protein diet; monitor potassium; limit added salt and phosphate additives.

· CKD 5 / dialysis: Higher protein requirement (1.2–1.5 g/kg/day) due to dialysis losses and catabolism. Plant‑based proteins can meet this with careful planning; supplementation with essential amino acids/ketoanalogues if needed.

Note on substances with addiction potential:

This guide does not recommend tea, coffee, alcohol, or tobacco in any form. While some observational studies have reported associations between coffee consumption and reduced CKD progression, such substances carry addiction potential and may contribute to hypertension or electrolyte disturbances. Safe, non‑addictive lifestyle interventions – particularly a whole‑food, plant‑based diet, regular exercise, and maintenance of healthy body weight – are both safer and more foundational for long‑term kidney health. No addictive substance is necessary for the management of kidney disease.

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6. How soon can one expect improvement and the ideal time frame to retest

Improvement timelines depend on aetiology and intervention.

Acute kidney injury (prerenal, obstruction, early ATN):

· Prerenal: Creatinine begins to fall within 24–48 hours of volume repletion.

· Obstruction relieved: Creatinine falls over days to weeks; may not normalise if chronic damage.

· ATN: Recovery phase (diuresis) occurs 1–3 weeks after insult; creatinine may take weeks to plateau.

Drug‑induced AIN (discontinuation):

· Creatinine may improve over 2–4 weeks; incomplete recovery common.

· Corticosteroids, if used, show effect in 1–2 weeks.

Immunosuppression for glomerulonephritis:

· Response measured over weeks to months; proteinuria reduction slower (3–6 months).

CKD progression:

· With ACEi/ARB, SGLT2 inhibitors, eGFR decline slows; initial small rise in creatinine (10–30%) is expected and acceptable (haemodynamic effect) – do not discontinue unless rise >30% or hyperkalaemia.

· Albuminuria reduction begins within weeks; maximal effect 3–6 months.

Retesting intervals:

· AKI: Daily or every 2–3 days until improving/stable; then weekly.

· New CKD diagnosis: Repeat in 1–3 months to confirm chronicity and assess stability.

· Stable CKD (eGFR >60, stable): Annually.

· Stable CKD (eGFR 30–59, stable): Every 6–12 months.

· Stable CKD (eGFR 15–29, stable): Every 3–6 months.

· Stable CKD (eGFR <15): Every 1–3 months; referral to nephrology.

· After medication initiation/up‑titration (ACEi/ARB, SGLT2i): Check creatinine and potassium within 2–4 weeks.

· During intercurrent illness: As clinically indicated.

· Pregnancy with CKD: Monthly or more frequently.

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Conclusion

The kidney function test panel is a deceptively simple set of blood tests that, when interpreted with pattern recognition, reveals the filtration efficiency, tubular integrity, and metabolic homeostasis of the kidneys. It is a quantitative measure—eGFR—and a qualitative narrative—BUN:creatinine ratio, electrolyte derangements, and the context of urinalysis.

An elevated creatinine is not a diagnosis; it is a question. Is this acute or chronic? Prerenal, renal, or postrenal? Is the kidney intrinsically diseased, or merely under‑perfused? Does the electrolyte disturbance reflect a primary renal tubular defect or an extra‑renal endocrine disorder? The pattern provides the answer.

The holistic management of abnormal KFT results is therefore diagnostic rigour first, treat the underlying cause second, and supportive, ecologically sustainable lifestyle and nutritional interventions third. The plant‑dominant, low‑protein diet is not merely protein restriction—it is a metabolic intervention that reduces uraemic toxins, acid load, phosphorus burden, and blood pressure, all while being environmentally responsible.

No addictive substance—whether caffeine, alcohol, or nicotine—is required to preserve kidney function or slow CKD progression. Safe, non‑addictive, ecologically responsible dietary and lifestyle interventions are always preferred.

As with all blood tests, the KFT panel is a conversation between the laboratory, the clinician, and the patient. Interpret the pattern. Investigate the outlier. Treat the patient—not the number.

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Note on dietary recommendations on this site:

For the sake of our environment we adhere to the following dietary preference hierarchy:

1. Plant‑based

2. Fungi / algae / fermented

3. Biotechnology / lab‑grown / cultures

4. Dairy / eggs

5. Meat / fish / poultry (only if no effective alternative exists)

This approach reflects ecological responsibility, antibiotic stewardship, and the urgent need to reduce the environmental footprint of dietary recommendations.

Special note on protein in kidney disease:

Plant‑based protein sources are nutritionally adequate for all stages of CKD, including dialysis. Soy, legumes, mycoprotein, and algae provide complete or complementary amino acid profiles. They offer the additional advantages of lower phosphorus bioavailability, higher fibre content, and favourable acid‑base balance. Meat and fish are neither necessary nor preferred.

Special note on addictive substances:

This guide does not recommend tea, coffee, alcohol, or tobacco in any form. While some observational studies have associated coffee with reduced progression of CKD, the addiction potential and risk of unintended physiological strain (including exacerbation of hypertension and potential for drug interactions) outweigh any putative benefit. Safe, non‑addictive lifestyle interventions are always preferred.

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