Basic Metabolic Panel without Calcium

Sodium is the principal extracellular cation, accounting for most of plasma osmolality and determining extracellular fluid volume. Its concentration is tightly regulated by thirst, antidiuretic hormone, and renal sodium handling. Because water balance profoundly affects measured sodium concentration, dysnatraemia typically reflects disturbances in water homeostasis rather than total body sodium per se.

Hyponatraemia is the most common electrolyte disorder in hospital and ambulatory practice, prompting evaluation of volume status, hormone excess (SIADH, adrenal insufficiency, hypothyroidism), and medication effects. Hypernatraemia signals free water deficit or, less commonly, salt overload. Both extremes carry neurological risk when severe or rapid.

Potassium is the major intracellular cation; only a small fraction resides in extracellular fluid, yet that fraction determines membrane potential in cardiac and skeletal muscle. Renal excretion is tightly regulated by aldosterone, distal sodium delivery, and acid-base status, and transcellular shifts (driven by insulin, pH, and adrenergic tone) can change serum potassium rapidly.

Hypokalaemia predisposes to arrhythmia, muscle weakness, and metabolic alkalosis; common causes include diuretics, gastrointestinal losses, and hyperaldosteronism. Hyperkalaemia is a medical emergency when severe, often driven by renal impairment, potassium-sparing diuretics, ACE inhibitors, or transcellular shifts in acidosis or tissue injury. Pre-analytical pseudohyperkalaemia from haemolysis or delayed separation is a frequent false alarm.

Chloride is the predominant extracellular anion, accompanying sodium in maintaining electroneutrality and osmotic balance. Renal chloride reabsorption parallels sodium to a large degree, though the two can dissociate in metabolic acid-base disorders. Gastric secretion is rich in chloride, so vomiting causes hypochloraemic alkalosis.

Chloride is essential to calculating the anion gap, which helps classify metabolic acidosis. Hypochloraemia accompanies many causes of metabolic alkalosis (vomiting, loop diuretics), while hyperchloraemia can result from normal-anion-gap acidosis (renal tubular acidosis, diarrhoea) or from high chloride intake and fluids.

Total CO₂ represents serum bicarbonate plus dissolved carbon dioxide, with bicarbonate comprising more than 95 per cent in venous samples at physiological pH. Bicarbonate is the principal extracellular buffer, regulated by renal retention and excretion in response to metabolic and respiratory acid-base disturbances.

Low bicarbonate signals metabolic acidosis (renal failure, ketoacidosis, lactic acidosis, renal tubular acidosis) or respiratory alkalosis with renal compensation. High bicarbonate suggests metabolic alkalosis (vomiting, diuretic use, volume contraction) or compensated respiratory acidosis. The anion gap and clinical context are essential to distinguish causes.

Urea is synthesised in the liver from ammonia generated during amino-acid catabolism and is excreted by the kidneys. Its plasma concentration reflects the balance between protein intake, hepatic urea synthesis, and renal clearance. Because urea is freely filtered and variably reabsorbed along the nephron—especially when urine flow is low—BUN is influenced by both GFR and volume status.

Elevated BUN can signal reduced GFR (acute or chronic kidney disease), volume depletion (pre-renal azotaemia), high protein intake, gastrointestinal bleeding, or catabolic states. A disproportionately high BUN relative to creatinine (BUN:creatinine ratio above 20:1) suggests pre-renal azotaemia or gastrointestinal bleeding. Low BUN is less clinically significant but may accompany liver disease, overhydration, or very low protein intake.

Creatinine is a breakdown product of muscle creatine phosphate, released into the circulation at a relatively constant rate proportional to muscle mass and filtered freely at the glomerulus with minimal tubular reabsorption. Its plasma concentration inversely reflects glomerular filtration rate, making it the most widely used endogenous marker of kidney function, though it is insensitive to early GFR decline.

Creatinine is the cornerstone of estimated GFR equations (CKD-EPI, MDRD) used to stage chronic kidney disease and to dose renally cleared drugs. Acute rises signal acute kidney injury; chronic elevation reflects chronic kidney disease. Creatinine is influenced by muscle mass, so lower values are normal in older adults, women, and those with low muscle mass, while bodybuilders and high-meat consumers may have values at the upper reference limit without renal impairment.

Glucose is the primary circulating fuel for most tissues and the sole obligate substrate for the brain under normal conditions. Its concentration is tightly regulated by insulin, glucagon, and counter-regulatory hormones, with the liver and kidney modulating production and uptake. Fasting glucose reflects hepatic glucose output balanced against basal insulin secretion and peripheral glucose disposal.

Fasting glucose is the first-line screening test for diabetes (≥126 mg/dL on two occasions) and pre-diabetes (100–125 mg/dL). Random or non-fasting glucose is less specific but values ≥200 mg/dL with symptoms are diagnostic. Hypoglycaemia (below 70 mg/dL) prompts evaluation for excess insulin, adrenal insufficiency, or glycogen-storage disorders. Glucose is time-sensitive and requires prompt separation to avoid ex vivo glycolysis by blood cells.

The BUN:creatinine ratio is a derived marker that compares two filtration products with differing tubular handling. Because urea reabsorption increases when tubular flow slows (as in volume depletion), while creatinine remains relatively constant, the ratio rises in pre-renal states and falls when urea production is low or tubular flow is high.

A ratio above 20:1 suggests pre-renal azotaemia (volume depletion, heart failure, renal artery stenosis) or increased urea production (gastrointestinal bleeding, high protein intake, catabolic illness). A ratio below 10:1 can be seen with overhydration, liver disease (reduced urea synthesis), or a low-protein diet. Intrinsic renal disease typically preserves the ratio near the reference range, so the ratio helps distinguish pre-renal from intrinsic acute kidney injury.