Urinalysis reflects kidney/urinary tract function + metabolic/systemic status. Should precede other invasive renal investigations. 3 parts: physical, chemical, microscopic.
Midstream (routine), clean-catch (culture), catheter (bedridden/obstruction), infant (plastic bag/suprapubic aspiration). Examine within 2hr; else refrigerate or preserve (toluene, conc. HCl, thymol/formaldehyde).
Volume: normal 600-2000mL/24h. Polyuria (>2L) — physiological/diabetes/renal disease/diuretics/DI. Oliguria (<500mL) — fluid restriction, loss, renal disease, transfusion reaction, Addison’s. Anuria (<125mL) — renal ischaemia, tumours, stones.
Colour: normal straw-amber (urochrome). Colourless=dilute; dark brown=oliguria; smoky=haematuria; cola=intravascular haemolysis; yellow-brown=bilirubin; orange-brown=urobilinogen; dark on standing=alkaptonuria; milky=pus/chyle.
Chyluria (lymph in urine — filariasis, lymphatic obstruction). Lipiduria (fat globules — nephrotic syndrome, fractures).
Specific gravity: normal 1.003-1.035 (avg 1.016). ↑ by glycosuria/proteinuria/dehydration; ↓ by ↑fluid intake/DI/end-stage kidney. Isosthenuria (fixed at 1.010) = severe renal damage (CKD), lost concentrating+diluting ability.
Proteinuria = glomerular injury marker. Tests: heat+acetic acid, sulfosalicylic acid (all protein types), Heller’s (nitric acid ring), dipstick (mainly albumin — misses Bence Jones). Esbach’s albuminometer = quantitative 24hr (nephrotic syndrome workup).
Categories: heavy(>4g/day)/moderate(1-4g)/mild(<1g); or renal/prerenal/postrenal.
Glycosuria: normal blood glucose 70-120mg/dL, renal threshold ~180-200mg/dL. Benedict’s test (semiquantitative, NOT glucose-specific, any reducing sugar) vs dipstick (glucose-specific, oxidase/peroxidase). Renal glycosuria = benign, ↓threshold, unrelated to diabetes. Alimentary glycosuria = transient postprandial spillover. Other sugars: fructosuria (Seliwanoff’s), lactosuria (Rubner’s), pentosuria (Bial’s).
Ketonuria: 3 ketone bodies — acetoacetic acid, β-hydroxybutyric acid, acetone. Reflects METABOLIC not renal status (fat used as fuel — DKA or starvation). Tests: Rothera’s (acetoacetic acid+acetone, purple ring), Gerhardt’s/ferric chloride (acetoacetic acid, less sensitive), Hart’s (β-hydroxybutyric acid — what other 2 miss), dipstick.
Causes: DKA; non-diabetic — starvation, vomiting/diarrhoea, von Gierke’s disease, hyperemesis gravidarum, lactic acidosis.
Bilirubin/urobilinogen: bilirubin normally ABSENT (only conjugated can be excreted). Fouchet’s test, dipstick (diazo→azobilirubin).
Urobilinogen tests: Ehrlich’s test, dipstick.
Blood: haematuria (intact RBCs) vs haemoglobinuria (free Hb, intravascular haemolysis) vs myoglobinuria (crush injury). Tests (benzidine, orthotoluidine, dipstick) share principle: haem peroxidase-like activity liberates O2 from H2O2 → colour change. Dysmorphic RBCs = glomerular bleeding.
Sediment = organized (cells, casts, crystals) + unorganized (crystalline/amorphous, pH-dependent).
Cells: RBCs (>2/hpf abnormal; dysmorphic = glomerular). WBCs (>5/hpf = pyuria = UTI; + leukocyte casts = renal origin). Glitter cells (swollen neutrophils, Brownian motion granules — dilute urine, chronic pyelonephritis). Epithelial cells (transitional/squamous; malignant cells in bladder tumours).
Casts: formed ONLY in kidney (Tamm-Horsfall protein, distal/collecting tubules) — always = renal disease. Cylindrical, parallel sides, rounded ends (cylindroids = abortive, tapering). Classified by matrix (hyaline/waxy), cells (RBC/leukocyte/epithelial/mixed), inclusions (granular/fatty), pigments.
Crystals: not normally present. Oxalate/urate/cystine = renal stone history; urate alone = gout. Acidic urine: oxalates/urates/cystine. Alkaline urine: phosphates/carbonate/ammonium urate.
Recurring pattern across glycosuria/ketonuria/bilirubin/blood tests = colour-change reaction from a specific chemistry (reducing sugar reduction, haem peroxidase activity, diazo coupling) — shared design logic, not independent facts. Bilirubin present/absent pattern across 3 jaundice types = one of highest-yield reasoning chains — distinguishes obstructive/hepatocellular/haemolytic jaundice from ONE simple test. Bence Jones thermal solubility = distinctive bedside screening clue for myeloma. Casts formed exclusively in kidney = why their presence localises abnormality to renal parenchyma, unlike crystals/free cells which can arise anywhere along the tract.
Urine analysis (urinalysis) reflects the functional state of the kidneys and urinary tract, and also provides information about metabolic or systemic (non-renal) disorders. It should precede all other invasive/non-invasive investigations for renal function, given how much information a simple, non-invasive test yields. Examination comprises three components: physical, chemical, and microscopic.
Urine should be examined within 2 hours of collection. If delay is unavoidable, preserve by refrigeration (without preservative), or with preservatives such as toluene (thin surface layer), concentrated HCl, or thymol/formaldehyde (the latter preserves cells and casts).
Volume — a healthy adult excretes 600–2000 mL/24h (infants: 300–600 mL/day).
Colour — normal urine is straw to amber (urochrome pigment, excretion proportional to metabolic rate).
| Colour | Condition |
|---|---|
| Colourless | Dilute urine (polyuria) |
| Dark brown | Oliguria |
| Smoky (red/red-brown) | RBCs (haematuria) |
| Cola-coloured | Intravascular haemolysis |
| Yellow-brown | Bilirubin |
| Orange-brown | Urobilin/urobilinogen |
| Dark on standing | Alkaptonuria (homogentisic acid) |
| Milky | Pus or chyle (chyluria) |
Chyluria — a rare condition where urine contains lymph, from obstruction/rupture of lymphatics into the renal pelvis, ureters, bladder, or urethra; causes include filariasis, abdominal lymphadenopathy, tumours.
Lipiduria — fat globules (triglycerides, cholesterol) in urine, seen in nephrotic syndrome and bone fractures.
Specific gravity — reflects the kidney’s concentrating power; normal range 1.003–1.035 (average 1.016). Measured by urinometer, refractometer, or dipstick (urinometer/refractometer are more accurate). Increased by glycosuria, proteinuria, dehydration; decreased by excessive fluid intake, diabetes insipidus, end-stage kidney disease. Isosthenuria — a fixed specific gravity of 1.010 — indicates severe renal damage (chronic renal failure) with loss of both concentrating and diluting ability.
Detectable urinary protein, indicating glomerular injury. Tests: heat-and-acetic-acid test, sulfosalicylic acid test (detects all protein types — albumin, globulin, glycoproteins, Bence Jones proteins), Heller’s test (nitric acid ring test), and the dipstick method (based on the “protein error of pH indicators” — detects mainly albumin, so may miss Bence Jones protein). Esbach’s albuminometer gives quantitative 24-hour protein estimation, needed for suspected nephrotic syndrome (>3.5 g/24h) or orthostatic proteinuria.
Categories: heavy (>4 g/day), moderate (1–4 g/day), mild (<1 g/day); or structurally as renal (glomerular/tubular), prerenal, and postrenal.
Normal blood glucose is 70–120 mg/dL (rising to 120–160 mg/dL postprandially); glucose is normally fully filtered and reabsorbed at the proximal tubule. Exceeding the renal threshold (usually >180–200 mg/dL) causes glycosuria, as in diabetes mellitus.
Ketone bodies — acetoacetic acid, β-hydroxybutyric acid, acetone — reflect metabolic, not renal, status; they accumulate when fat is used as an energy source due to a carbohydrate metabolism defect (diabetic ketoacidosis) or during starvation. Tests: Rothera’s test (purple ring with sodium nitroprusside, detects acetoacetic acid/acetone), Gerhardt’s (ferric chloride) test (detects acetoacetic acid specifically, less sensitive), Hart’s test (detects β-hydroxybutyric acid, which the other two miss), and dipstick (detects acetoacetic acid).
Causes: diabetic ketoacidosis; non-diabetic — starvation, prolonged vomiting/diarrhoea, glycogen storage disease (von Gierke’s), hyperemesis of pregnancy, lactic acidosis (shock, renal/liver failure, drugs).
Bilirubin is normally absent from urine (only conjugated bilirubin, if present, appears — unconjugated bilirubin is not water-soluble and cannot be excreted renally). Tests: Fouchet’s test (ferric chloride oxidises bilirubin to green biliverdin), dipstick (diazo reaction, forms azobilirubin).
Urobilinogen tests: Ehrlich’s test (pink-to-cherry-red aldehyde complex), dipstick.
Distinguishes haematuria (intact RBCs — renal stones, RCC, glomerular disease), haemoglobinuria (free haemoglobin — intravascular haemolysis), and myoglobinuria (crush injury, strenuous exercise). Tests (benzidine, orthotoluidine, dipstick) share a common principle: the peroxidase-like activity of haem liberates oxygen from hydrogen peroxide, producing a colour change. Glomerular bleeding classically produces dysmorphic (distorted-shape) red cells, distinguishing it from lower urinary tract bleeding.
Urinary sediment/deposit is divided into organized (cells, casts, crystals, other formed elements) and unorganized (crystalline/amorphous material, varying with urine pH) deposits.
Formed only in the kidney — always indicative of renal disease. Formed by solidification of Tamm-Horsfall protein, secreted by the distal convoluted and collecting tubules, forming a fibrillar meshwork that traps cells, cell fragments, or granular material. Cylindrical with parallel sides and rounded ends (cylindroids are abortive casts — one tapering end, non-parallel sides). Classified by matrix (hyaline, waxy), trapped cells (RBC, leukocyte, epithelial, mixed casts), inclusions (granular, fatty), or pigments (haemoglobin, myoglobin, bilirubin).
Not normally present. Oxalate, urate, and cystine crystals occur with a history of renal stones; urate crystals alone occur in gout. Oxalates/urates/cystine favour acidic urine; phosphates, calcium carbonate, and ammonium urates favour alkaline urine.
Urine examination is a laboratory reference topic (physical/chemical/microscopic test panels, each test’s principle and interpretation) rather than a disease mechanism — a rendered diagram would only redraw the reference tables already in notes.md.
Draw the bilirubin/urobilinogen pattern across the three jaundice types by hand as a quick 3x2 grid (Obstructive / Hepatocellular / Haemolytic × Bilirubin / Urobilinogen present-absent-increased) — this is the single highest-yield reasoning chain in the topic and is best learned by active recall of the grid rather than a process diagram.
Personal revision notes, mnemonics and reminders.
