Basic Metabolic Panel, Plasma

Glucose is the primary circulating monosaccharide and the obligate fuel for brain and red cells. Its concentration is tightly regulated by insulin, glucagon, cortisol, and other counter-regulatory hormones. Plasma glucose reflects the balance between hepatic output, dietary absorption, and peripheral uptake, with higher levels favouring glycation of proteins and oxidative stress.

Glucose is the cornerstone of diabetes screening and management. Fasting values ≥126 mg/dL on two occasions, or random values ≥200 mg/dL with symptoms, establish diabetes. Impaired fasting glucose (100–125 mg/dL) signals prediabetes. Hypoglycaemia (<70 mg/dL) prompts evaluation for insulinoma, adrenal insufficiency, or medication effect.

Sodium is the principal extracellular cation, accounting for most of the osmolality of plasma and extracellular fluid. Its concentration is regulated by the thirst mechanism, antidiuretic hormone, and renal handling. Because water moves freely across cell membranes, plasma sodium reflects total-body water balance relative to sodium content rather than sodium deficiency or excess alone.

Hyponatraemia (<135 mmol/L) is the most common electrolyte disorder, caused by water excess (SIADH, heart failure, cirrhosis, primary polydipsia) or sodium loss (diuretics, adrenal insufficiency, cerebral salt wasting). Hypernatraemia (>145 mmol/L) reflects water deficit or, less often, sodium excess. Both require assessment of volume status and urine osmolality to guide therapy.

Potassium is the dominant intracellular cation, with less than 2% of total-body stores in the extracellular space. The steep transmembrane gradient is maintained by the sodium–potassium ATPase and is critical for membrane potential, cardiac conduction, and neuromuscular excitability. Aldosterone, insulin, and acid–base status modulate renal and transcellular potassium shifts.

Hypokalaemia (<3.5 mmol/L) increases the risk of arrhythmia, especially in patients on digoxin, and is caused by diuretics, gastrointestinal losses, renal tubular disorders, or inadequate intake. Hyperkalaemia (>5.0 mmol/L) is life-threatening when severe, with causes including renal failure, aldosterone deficiency, acidosis, and medication (ACE inhibitors, spironolactone, NSAIDs).

Chloride is the major extracellular anion, accompanying sodium to maintain electrical neutrality and osmotic balance. It moves in and out of cells via exchangers, particularly the bicarbonate–chloride exchanger in red cells and renal tubules, linking chloride to acid–base regulation. Plasma chloride is driven by sodium concentration, water balance, and bicarbonate levels.

Hyperchloraemia often mirrors hypernatraemia or reflects non-anion-gap metabolic acidosis (renal tubular acidosis, diarrhoea, saline infusion). Hypochloraemia accompanies prolonged vomiting (loss of HCl), diuretic use, or metabolic alkalosis. The anion gap (sodium minus the sum of chloride and bicarbonate) is a key derived marker in acid–base assessment.

Total CO₂ measures bicarbonate plus dissolved carbon dioxide and carbonic acid in plasma; at physiological pH bicarbonate accounts for more than 95% of the value, so total CO₂ is effectively a surrogate for serum bicarbonate. Bicarbonate is the principal extracellular buffer, regulated by renal reabsorption and respiratory CO₂ excretion.

Low CO₂ (<22 mmol/L) suggests metabolic acidosis (lactic acidosis, ketoacidosis, renal failure, diarrhoea) or respiratory alkalosis. Elevated CO₂ (>29 mmol/L) indicates metabolic alkalosis (vomiting, diuretics, alkali ingestion) or compensated respiratory acidosis. The anion gap and arterial blood gas refine the diagnosis.

Urea is the end product of amino-acid catabolism, synthesised in the liver from ammonia and excreted by the kidneys. Blood urea nitrogen reflects the balance between protein intake, hepatic synthesis, and glomerular filtration. Because urea is freely filtered and then partially reabsorbed in the proximal tubule (reabsorption increases with lower flow), BUN is sensitive to both renal function and volume status.

Elevated BUN (azotaemia) suggests reduced GFR (acute or chronic kidney disease), prerenal factors (volume depletion, heart failure, high-protein intake, gastrointestinal bleeding), or postrenal obstruction. The BUN:creatinine ratio helps distinguish prerenal (ratio >20) from intrinsic renal causes (ratio 10–15). Low BUN is seen with liver failure or severe malnutrition.

Creatinine is a non-enzymatic breakdown product of creatine phosphate in muscle, released at a relatively constant rate proportional to muscle mass. It is freely filtered at the glomerulus with minimal tubular reabsorption, making it a practical endogenous marker of glomerular filtration rate. Secretion by the proximal tubule causes mild overestimation of GFR, especially at lower filtration rates.

Creatinine is the reference marker for estimating GFR (eGFR equations: CKD-EPI, MDRD). Rising creatinine signals acute kidney injury or worsening chronic kidney disease; the rate of rise helps distinguish prerenal, intrinsic, and postrenal causes. Serial values and the BUN:creatinine ratio add context. Because creatinine depends on muscle mass, very low or high values may be normal in sarcopenic or athletic individuals.

eGFR is calculated from serum creatinine, age, sex, and (in some equations) race using validated formulas such as CKD-EPI 2021. It estimates the volume of plasma filtered by the glomeruli per minute, standardised to body surface area. eGFR declines with age and kidney disease; values below 60 mL/min/1.73 m² for more than three months define chronic kidney disease.

eGFR is the cornerstone of CKD staging (G1–G5) and guides medication dosing, nephrology referral, and cardiovascular risk stratification. Acute changes prompt evaluation for AKI. Because the equation depends on creatinine, it is less accurate in extremes of muscle mass, malnutrition, and acute kidney injury; cystatin C–based eGFR can confirm borderline results.

Calcium circulates in three forms: ionised (physiologically active, ~50%), protein-bound (mainly to albumin, ~40%), and complexed to anions (~10%). Total calcium reflects all three; the ionised fraction is tightly regulated by parathyroid hormone, vitamin D, and calcitonin. Bone is the principal reservoir, with the skeleton serving as a buffer for plasma levels.

Hypercalcaemia (>10.2 mg/dL) is most often due to primary hyperparathyroidism or malignancy; other causes include vitamin D toxicity, granulomatous disease, and immobilisation. Hypocalcaemia (<8.5 mg/dL) suggests hypoparathyroidism, vitamin D deficiency, chronic kidney disease, or hypomagnesaemia. Because albumin binds calcium, total calcium must be corrected for albumin or ionised calcium measured directly when albumin is abnormal.