▸ Based on the glucose oxidase reaction and does not cross-react with other sugars

▸ Plasma glucose tubular absorption threshold is 9–10 mmol/L

▸ Glycosuria occurs when the filtered load of glucose exceeds the ability of the proximal tubule to reabsorb it, eg, diabetes mellitus, Cushing's syndrome, etc

▸ The threshold for tubular reabsorption can be altered in isolated tubular dysfunction like renal glycosuria or generalised ones like Fanconi syndrome, cystinosis or Wilson’s disease, where blood glucose is normal

▸ Ketones are products of fat metabolism not normally found in urine

▸ Among the ketones, only acetoacetic acid and acetone that react with nitroprusside are detected by dipsticks

▸ Positive in diabetes mellitus, pregnancy, ketogenic diet

▸ In hypoglycaemia, presence of ketones suggests ketotic hypoglycaemia, if absent, points to fatty acid metabolic abnormalities like medium chain acyl CoA dehydrogenase deficiency

▸ Ketonuria is a physiological response to starvation; many small children get morning ketonuria with normal ‘starvation’ overnight

▸ Ketonuria also occurs with cold exposure and extended periods of exercise

▸ Generally, patients on a typical western diet tend to have slightly lower acidic urinary pH

▸ For accurate measurement of pH, urine sample should be sealed to prevent CO₂ evaporation

▸ Delaying the test >30 min at room temperature makes urine alkaline due to the breakdown of urea

▸ Mundane clinical conditions like diarrhoea and vomiting that result in dehydration are the common causes of acidic urine

▸ Interestingly in conditions like pyloric stenosis with metabolic alkalosis, urine is paradoxically acidic due to the preferential excretion of hydrogen ions to conserve potassium in the blood

▸ Urine pH can help to determine the cause of metabolic acidosis (pH>5 indicates renal tubular acidosis rather than an inborn error of metabolism) and distinguish different types of renal tubular acidosis3

▸ Alkaline urine in patient with urinary tract infection suggests urea splitting organism like Proteus, which can cause magnesium–ammonium phosphate crystals, which form staghorn calculi3

▸ Alkaline urine can also form calcium carbonate and calcium phosphate stones

▸ Acidic urine is associated with uric acid stones

▸ Urine pH is actively monitored in therapeutic alkalisation for conditions like salicylate poisoning and tumour lysis syndrome

▸ SG test is based on the change of pH dye due to binding H⁺ ions, which in turn linearly corresponds to urine osmolality

▸ Hence physiologically SG test reflects hydration status and concentrating ability of the kidney

▸ <1.010 indicates relative hydration

▸ >1.020 indicates relative dehydration

▸ SG is high in urine with significant proteinuria

▸ As SG test is closely related to H⁺ ion concentration it can be falsely elevated at urine pH <6 and falsely lowered by urine pH >7

▸ Poor correlation with pathological urine to estimate urine osmolality4

▸ Increased with glycosuria, proteinuria, syndrome of inappropriate antidiuretic hormone secretion4

▸ Decreased with diuretics, diabetes insipidus, adrenal insufficiency, aldosteronism and impaired tubular function

▸ Low SG in a dehydrated patient indicates impaired concentrating ability, which points towards a renal tubular dysfunction

▸ Bilirubin is not normally detected in the urine

▸ Even a trace of bilirubin in the urine requires further investigations

▸ Bilirubin is destroyed by light and air, hence should be tested promptly or stored properly

▸ Prehepatic cause like haemolysis causes rise of urobilinogen in the urine

▸ Hepatocellular disease like hepatitis results in presence of bilirubin and urobilinogen in urine

▸ Urobilinogen is the product of bacterial action of direct bilirubin in the gut

▸ Urobilinogen can be present in normal urine in small amounts

▸ Presence of bilirubin and absence of urobilinogen points towards an obstructive cause.

▸ Administration of antibiotics may result in decreased level of urobilinogen due to sterilisation of bowel