Comprehensive Metabolic Panel

Glucose is the primary circulating carbohydrate fuel, tightly regulated by insulin, glucagon, and counter-regulatory hormones. Fasting plasma glucose reflects the balance between hepatic glucose output and peripheral uptake; postprandial values rise and fall with insulin secretion and tissue sensitivity.

Fasting glucose screens for diabetes and prediabetes. Persistent elevation signals impaired insulin secretion or resistance; hypoglycaemia prompts evaluation for hyperinsulinism, adrenal insufficiency, or other causes.

Urea is the end product of hepatic ammonia detoxification from amino-acid catabolism. It is filtered freely by the glomerulus and partially reabsorbed in the tubule, so its plasma concentration reflects glomerular filtration, protein intake, and volume status.

BUN is a coarse marker of renal function, elevated in prerenal azotaemia (volume depletion), intrinsic kidney disease, and high protein catabolism. The BUN:creatinine ratio helps distinguish prerenal from renal causes.

Creatinine is the non-enzymatic breakdown product of muscle creatine phosphate, produced at a fairly constant rate and filtered by the glomerulus with minimal tubular secretion or reabsorption, making it a practical endogenous marker of glomerular filtration.

Serum creatinine is the cornerstone of renal function assessment and feeds into estimated GFR equations. Elevations indicate declining filtration; very low values reflect reduced muscle mass or dilution.

eGFR is calculated from serum creatinine, age, sex, and race (using equations such as CKD-EPI 2021), estimating the volume of plasma filtered by the glomeruli per minute and normalised to body surface area. It is a derived rather than measured parameter.

eGFR stages chronic kidney disease (G1–G5) and guides medication dosing, contrast decisions, and referral. Values below 60 mL/min/1.73 m² for more than three months define CKD.

The ratio of BUN to creatinine amplifies changes in urea reabsorption relative to creatinine filtration. Prerenal states (volume depletion, heart failure) increase tubular urea reabsorption and raise the ratio; intrinsic renal injury raises both proportionally.

A ratio above 20:1 suggests prerenal azotaemia, gastrointestinal bleeding, or high protein catabolism; a ratio below 10:1 may reflect low protein intake, liver disease, or overhydration.

Sodium is the principal extracellular cation, governing plasma osmolality and therefore water distribution across compartments. Its concentration is tightly regulated by antidiuretic hormone, the renin–angiotensin–aldosterone axis, and renal tubular handling.

Hyponatraemia reflects excess water relative to sodium (dilutional or true loss); hypernatraemia signals water deficit or excess sodium. Both extremes carry neurological risk, and the rate of change matters as much as the absolute value.

Potassium is the major intracellular cation, essential for membrane potential, neuromuscular excitability, and cardiac repolarisation. Plasma concentration is maintained by renal excretion, aldosterone, insulin, and cellular shifts.

Hypokalaemia increases the risk of arrhythmia and muscle weakness; hyperkalaemia is a medical emergency that can cause life-threatening arrhythmia. Both require prompt correlation with clinical state, ECG, and medications.

Chloride is the principal extracellular anion, moving with sodium to maintain electroneutrality and playing a role in acid–base balance through renal and gastrointestinal handling.

Hyperchloraemia is seen in normal-anion-gap metabolic acidosis and volume resuscitation with saline; hypochloraemia accompanies vomiting, diuretic use, and metabolic alkalosis. Changes in chloride help classify acid–base disorders.

Total CO₂ measured in venous chemistry is predominantly bicarbonate, the principal extracellular buffer. It reflects the metabolic component of acid–base balance and shifts with renal compensation for respiratory disorders.

Low CO₂ signals metabolic acidosis or respiratory alkalosis with renal compensation; high CO₂ indicates metabolic alkalosis or chronic respiratory acidosis. Interpretation requires arterial blood gas or clinical context.

About half of plasma calcium is protein-bound (mainly to albumin), with the remainder ionised and physiologically active. Total calcium thus depends on albumin concentration; ionised calcium is the gold standard when albumin is abnormal.

Hypercalcaemia raises suspicion for primary hyperparathyroidism, malignancy, or vitamin D toxicity; hypocalcaemia suggests hypoparathyroidism, vitamin D deficiency, or hypoalbuminaemia. Corrected calcium or ionised calcium clarifies when albumin is low.

Total protein reflects the combined concentration of albumin (the dominant hepatic export protein) and globulins (immunoglobulins, acute-phase proteins, carrier proteins). It is affected by hydration, synthesis, catabolism, and loss.

Elevated total protein may indicate dehydration, chronic inflammation, or monoclonal gammopathy; low values suggest malnutrition, liver disease, protein-losing enteropathy or nephropathy. Albumin and the albumin:globulin ratio add specificity.

Albumin is synthesised exclusively by the liver and maintains plasma oncotic pressure, transports lipophilic substances, and serves as a negative acute-phase reactant. Its half-life is approximately three weeks, so changes are gradual.

Hypoalbuminaemia signals chronic liver disease, malnutrition, inflammation, or protein loss (nephrotic syndrome, enteropathy). It affects calcium interpretation and is a prognostic marker in chronic illness.

Globulins comprise immunoglobulins, acute-phase proteins (such as C-reactive protein and haptoglobin), complement, and transport proteins. The calculated globulin is a rough aggregate; serum protein electrophoresis resolves individual fractions.

Elevated globulin suggests chronic inflammation, infection, or monoclonal or polyclonal gammopathy; low globulin may reflect immunodeficiency. The albumin:globulin ratio inverts in chronic liver disease and some inflammatory states.

The A:G ratio is a simple index of the relative proportions of albumin and globulin. It falls when albumin is low or globulin is high, and rises when albumin is disproportionately preserved or globulin is reduced.

A low ratio (<1.0) is seen in cirrhosis, nephrotic syndrome, and gammopathies; a high ratio may reflect immunodeficiency. It is a screening flag rather than a specific diagnosis.

AST is a mitochondrial and cytosolic enzyme found in liver, heart, skeletal muscle, kidney, and red cells. Hepatocellular injury releases cytosolic AST; more severe injury releases mitochondrial AST, and AST from other tissues can elevate with muscle or haemolytic injury.

AST is a marker of hepatocellular damage but less liver-specific than ALT. The AST:ALT ratio helps distinguish causes — below one in steatotic liver disease, above two in alcohol-related injury. Very high AST (>1000 U/L) suggests acute viral, ischaemic, or toxic hepatitis.

ALT is a cytosolic hepatocyte enzyme catalysing amino-group transfer from alanine to alpha-ketoglutarate. Its concentration is highest in liver, with minimal amounts in other tissues, making it the most liver-specific routine aminotransferase.

ALT is the first-line marker of hepatocellular injury. An isolated ALT elevation points strongly to the liver, and the pattern with AST, ALP, and bilirubin classifies hepatocellular versus cholestatic injury. Persistent mild elevation is a common trigger for metabolic dysfunction-associated steatotic liver disease evaluation.

Alkaline phosphatase is a family of isoenzymes expressed in liver (biliary epithelium), bone (osteoblasts), intestine, and placenta. Hepatic and bone isoforms account for most circulating ALP in adults; fractionation or correlation with GGT and bone markers localises the source.

Elevated ALP signals cholestasis (with elevated GGT and bilirubin) or increased bone turnover (fracture healing, Paget disease, bone metastases). An isolated ALP elevation in the absence of liver enzyme abnormalities often reflects bone or, in children and adolescents, physiological bone growth.

Bilirubin is the breakdown product of haem, mainly from senescent red cells. Unconjugated (indirect) bilirubin is transported to the liver bound to albumin, conjugated by UDP-glucuronosyltransferase, and excreted in bile. Total bilirubin is the sum of conjugated and unconjugated fractions.

Elevated total bilirubin causes jaundice when above approximately 2–3 mg/dL. Unconjugated hyperbilirubinaemia suggests haemolysis or Gilbert syndrome; conjugated hyperbilirubinaemia indicates cholestasis or hepatocellular dysfunction. Fractionation clarifies the cause.