Urinalysis & Urine Microscopy

📋 Key Information Summary

📋

Urinalysis with dipstick and microscopy is the single most cost-effective nephrology investigation available in primary care and emergency medicine in Australia.
Midstream urine (MSU) collection with prompt refrigeration or boric acid preservation is essential to minimise false-positive culture and morphological artefact.
Dipstick haematuria (≥1+ / ≥10 RBC/µL) requires confirmation on microscopy; false positives occur with myoglobinuria, alkaline urine & menstrual contamination.
Dipstick protein (≥1+) should always be quantified using albumin-to-creatinine ratio (ACR) on a spot urine — ACR is MBS-rebated in Australia and replaces 24-hour collections in most settings.
ACR >3.5 mg/mmol (women) or >2.5 mg/mmol (men) on two of three samples over ≥3 months defines persistent albuminuria (KDIGO stage A2–A3).
Red cell casts are pathognomonic for glomerulonephritis — their presence mandates urgent nephrology referral.
White cell casts suggest pyelonephritis or acute interstitial nephritis; WBC casts with eosinophiluria points toward drug-induced interstitial nephritis.
Granular ("muddy brown") casts are the hallmark of acute tubular necrosis (ATN).
Dysmorphic RBCs (acanthocytes) with >5% on phase-contrast microscopy indicate a glomerular source of haematuria; isomorphic RBCs suggest urological causes.
WBC esterase and nitrite on dipstick have high specificity for UTI but limited sensitivity; microscopy and culture remain the gold standard.
Glycosuria in the absence of hyperglycaemia suggests proximal tubular dysfunction (Fanconi syndrome) rather than diabetes.
Aboriginal and Torres Strait Islander peoples experience significantly higher rates of CKD and glomerulonephritis; routine urinalysis should be incorporated into annual health checks under MBS Item 715.

Introduction & Australian Epidemiology

Urinalysis with urine microscopy is an indispensable investigation in nephrology and general practice. It provides rapid, inexpensive, and clinically rich information about renal parenchymal disease, urinary tract infection, systemic disorders, and metabolic derangements. The urine dipstick serves as a sensitive screening tool, while microscopy of a freshly centrifuged specimen provides diagnostic specificity — identifying cellular elements, casts, and crystals that delineate the site and nature of renal pathology.

In Australia, chronic kidney disease (CKD) affects approximately 1 in 10 adults, with over 1.7 million Australians estimated to have indicators of kidney disease (AIHW 2023). Aboriginal and Torres Strait Islander peoples experience end-stage kidney disease at rates 6–8 times higher than non-Indigenous Australians, and glomerulonephritis remains a disproportionately common cause in this population. Dipstick urinalysis is a core component of the MBS Item 715 Aboriginal and Torres Strait Islander health check and is recommended annually for at-risk populations.

The combination of dipstick urinalysis and urine microscopy allows clinicians to distinguish glomerular from non-glomerular haematuria, to identify the nephrotic spectrum (proteinuria), to detect infection, and to recognise tubular injury patterns — often before serum creatinine rises. Red cell casts indicate glomerulonephritis, white cell casts suggest pyelonephritis or interstitial nephritis, and granular ("muddy brown") casts indicate acute tubular necrosis (ATN). Understanding these findings is fundamental to appropriate triage, investigation, and referral in Australian clinical practice.

⚠️

Clinical priority: The presence of red cell casts on urine microscopy is virtually diagnostic of glomerulonephritis and warrants urgent nephrology referral (within 1–2 weeks) to facilitate early renal biopsy and immunosuppressive therapy where appropriate.

Urinalysis & Urine Microscopy clinical infographic — pathophysiology, clinical clues, diagnosis, imaging, and management — Tap or click image to enlarge — Urinalysis & Urine Microscopy: pathophysiology, clinical clues, diagnosis, imaging, and management.

Specimen Collection & Processing

Accurate urinalysis depends on correct specimen collection, handling, and processing. In Australian practice, the midstream urine (MSU) specimen remains the standard for both dipstick and microscopy.

Collection Method

Midstream urine (MSU): Clean-catch, midstream specimen after retracting the foreskin or cleansing the vulva. Discard the initial stream to minimise urethral flora contamination.
Catheter specimen: Aspirate from the catheter port (not the drainage bag) using aseptic technique.
Suprapubic aspiration: Gold standard for neonatal specimens; eliminates contamination risk entirely.
First morning specimen: Preferred for ACR quantification and pregnancy screening — most concentrated and most comparable between samples.

Handling & Timing

⚠️

Time-critical: Urine should be examined within 1 hour of collection or refrigerated at 4°C to prevent bacterial multiplication, cast dissolution, and cell lysis. If a delay >2 hours is anticipated, add a boric acid preservative container (available through pathology providers in Australia).

For urine microscopy specifically, the specimen should be fresh, at room temperature, and analysed by an experienced scientist or clinician. Refrigerated specimens may show precipitation of amorphous urates or phosphates, which should not be confused with pathological crystals.

Dipstick Interpretation

The urine dipstick (e.g., Siemens Multistix®, Roche Combur-Test®) provides a rapid semi-quantitative assessment of multiple analytes. Each pad reacts via a specific chemical mechanism, and clinicians must understand both the capabilities and limitations of each test.

pH

Normal urine pH ranges from 4.5–8.0. Persistent alkaluria (pH >7.0) may suggest infection with urease-producing organisms (e.g., Proteus mirabilis) or renal tubular acidosis (RTA) Type 1 (distal). Acidic urine (pH <5.0) is seen with metabolic acidosis, high-protein diets, and uric acid stone formers.

Specific Gravity (SG)

Normal range 1.001–1.035. Low SG (<1.010) may indicate impaired concentrating ability (interstitial nephritis, CKD, diabetes insipidus). High SG (>1.030) suggests dehydration or glycosuria. The dipstick SG is based on ionic concentration and can be falsely elevated by glucose, protein, or intravenous contrast agents.

Protein

Dipstick result	Approximate concentration	Action
Negative	<150 mg/L (<0.15 g/L)	No further action if low risk
Trace	150–300 mg/L	Repeat; quantify with ACR if persistent
1+	300 mg/L (~0.3 g/L)	Quantify with spot ACR (MBS-rebated)
2+	1000 mg/L (~1.0 g/L)	Quantify with ACR; consider nephrotic-range workup
3+	3000 mg/L (~3.0 g/L)	Nephrology referral; quantify urgently
4+	>5000 mg/L (>5.0 g/L)	Urgent nephrology — likely nephrotic syndrome

The dipstick pad is most sensitive to albumin and has poor sensitivity for Bence Jones proteins (light chains), Tamm-Horsfall protein, or beta-2 microglobulin. In suspected myeloma, always request urine protein electrophoresis (UPEP) and serum free light chain assay.

ℹ️

False-positive protein: Highly alkaline urine (pH >8.0), concentrated urine, prolonged immersion of dipstick, or contamination with vaginal discharge.

Blood (Haemoglobin / Myoglobin)

The blood pad detects free haemoglobin and myoglobin via the peroxidase-like activity of the haem moiety. It does NOT detect intact RBCs directly — rather, it detects haem released from lysed red cells.

Dipstick result	Approximate RBC count	Interpretation
Negative	<10 RBC/µL	Normal
Trace / Non-haemolysed	10–25 RBC/µL	Confirm on microscopy
1+ / Small	25–50 RBC/µL	Microscopic haematuria; assess morphology
2+ / Moderate	50–200 RBC/µL	Investigate: glomerular vs non-glomerular
3+ / Large	>200 RBC/µL	Significant haematuria; urgent evaluation
Trace intact / Intact RBCs only	Variable	Few intact RBCs, no free Hb; may be artefactual

⚠️

False-positive blood pad: Myoglobinuria (rhabdomyolysis), alkaline urine (pH >9.0), microbial peroxidases, oxidising cleaning agents on specimen container, menstrual contamination. Always correlate with urine colour and microscopy.

ℹ️

False-negative blood pad: Ascorbic acid (vitamin C) ingestion, high specific gravity, formalin contamination, or large amounts of protein can inhibit the peroxidase reaction.

Leucocyte Esterase (WBC)

Leucocyte esterase is an enzyme produced by neutrophils and, to a lesser extent, macrophages. A positive result suggests pyuria (>10 WBC/µL) and may indicate urinary tract infection, interstitial nephritis, or other inflammatory conditions.

Result	Approximate WBC count	Clinical action
Negative	<10 WBC/µL	UTI unlikely (NPV ~95%)
Trace	10–25 WBC/µL	Borderline; send for microscopy + culture if symptomatic
Small (1+)	25–75 WBC/µL	Send MSU for M+C
Moderate (2+)	75–500 WBC/µL	Send MSU; consider empirical antibiotics if symptomatic
Large (3+)	>500 WBC/µL	High likelihood of UTI; treat empirically per eTG

ℹ️

False-negative WBC esterase: Proteinuria (>5 g/L), glycosuria (>30 g/L), high SG, or urine standing >2 hours at room temperature (lysis of WBCs). In symptomatic patients with negative dipstick, always send for microscopy and culture.

Nitrite

Many Gram-negative bacteria (e.g., E. coli, Klebsiella, Proteus) convert urinary nitrate to nitrite. A positive nitrite test has high specificity (~95%) for bacteriuria but poor sensitivity (~45–60%) because:

Gram-positive organisms (Enterococcus, Staphylococcus saprophyticus) do not reduce nitrate.
Urine must remain in the bladder ≥4 hours for sufficient nitrate conversion (first morning specimen preferred).
Low dietary nitrate intake or diuresis reduces substrate availability.

Combined leucocyte esterase + nitrite: If both are positive, the positive predictive value for UTI exceeds 95% in symptomatic patients. If both are negative, UTI is unlikely (NPV >95%) and microscopy/culture may be deferred unless the patient is immunocompromised, pregnant, or has a complicated presentation.

Glucose

The dipstick glucose pad uses glucose oxidase to detect glycosuria. Normally, all filtered glucose is reabsorbed by SGLT2 transporters in the proximal tubule; glycosuria appears when the renal threshold (~10 mmol/L) is exceeded.

Scenario	Interpretation
Glycosuria with hyperglycaemia	Diabetes mellitus — confirm with HbA1c or fasting glucose
Glycosuria with normoglycaemia	Renal glycosuria (benign) or proximal tubular dysfunction (Fanconi syndrome)
SGLT2 inhibitor use	Expected — dapagliflozin (Forxiga®), empagliflozin (Jardiance®) inhibit SGLT2
Glycosuria in pregnancy	Lowered renal threshold in pregnancy; may be physiological but screen for GDM

Ketones

The dipstick detects acetoacetate (and, to a lesser extent, acetone) but does NOT detect beta-hydroxybutyrate, which is the predominant ketone in diabetic ketoacidosis (DKA). Positive ketones on dipstick may be seen in starvation, prolonged fasting, low-carbohydrate diets, DKA (late), and alcoholic ketoacidosis. In established DKA, serum beta-hydroxybutyrate (MBS-rebated) is a superior marker for monitoring.

Bilirubin & Urobilinogen

Conjugated bilirubin in urine (positive dipstick) suggests hepatobiliary disease (obstructive jaundice, hepatitis). Unconjugated bilirubin is not water-soluble and does not appear in urine. Elevated urobilinogen suggests haemolytic anaemia or hepatocellular disease. Absent urobilinogen with positive bilirubin suggests complete biliary obstruction.

Urine Microscopy: Casts, Cells & Crystals

Urine microscopy is the definitive step in urinalysis. A standardised examination of a centrifuged specimen (10–15 mL at 1500–2000 rpm for 5 minutes, resuspend the sediment in 0.5–1 mL of supernatant) under high-power field (×400) provides diagnostic information unavailable from the dipstick alone.

Phase-contrast microscopy is preferred for RBC morphology assessment but may not be available in all Australian laboratories; bright-field microscopy remains acceptable for cast and crystal identification.

Casts

Urinary casts are cylindrical structures formed within the renal tubular lumen from Tamm-Horsfall mucoprotein (uromodulin). They reflect the conditions of the tubular microenvironment at the time of their formation. All casts have a characteristic parallel-sided, rounded-end morphology.

Cast type	Appearance	Clinical significance
Hyaline casts	Transparent, low refractive index; visible only under reduced light	Normal finding (<2/LPF); increased with exercise, dehydration, CKD. Non-specific.
RBC casts	Reddish-brown; contain entrapped RBCs within the cast matrix	Pathognomonic of glomerulonephritis (IgA nephropathy, lupus nephritis, ANCA vasculitis, anti-GBM disease). Urgent nephrology referral.
WBC casts	Granular, contain intact or degenerating neutrophils	Pyelonephritis, acute interstitial nephritis (drug-induced), lupus nephritis. Distinguish from WBC clumps (non-cast).
Granular casts	Coarse or fine granules; "muddy brown" appearance in ATN	Hallmark of acute tubular necrosis (ATN). Also seen in CKD, GN. Coarse > fine = more severe tubular injury.
Muddy brown casts	Dark brown, coarsely granular; contain tubular epithelial cell debris	Highly specific for ischaemic or nephrotoxic ATN (contrast nephropathy, aminoglycosides, rhabdomyolysis).
Waxy casts	Highly refractile, sharp broken edges, homogeneous	Chronic kidney disease, advanced tubular atrophy. Indicates longstanding renal parenchymal disease.
Fatty casts	Contain refractile lipid droplets (Maltese cross under polarised light)	Nephrotic syndrome (lipiduria). Seen with oval fat bodies.
TEC casts	Contain tubular epithelial cells	Acute tubular necrosis, toxic nephropathy (e.g., ethylene glycol), interstitial nephritis.
Pigmented casts	Brown (myoglobin) or red-brown (haemoglobin)	Rhabdomyolysis (myoglobin), haemolysis (haemoglobin).

🚨

Red cell casts = glomerulonephritis until proven otherwise. Their identification, even in small numbers (≥1 cast), should prompt immediate nephrology referral. Obtain serum complement (C3, C4), ANA, ANCA (MPO & PR3), anti-GBM antibodies, serum and urine protein electrophoresis, hepatitis B/C serology, and HIV serology.

Cells

Cell type	Findings	Significance
Red blood cells	>2 RBC/HPF is abnormal (>2000/mL)	Haematuria — assess morphology (see below)
Dysmorphic RBCs	Irregular membrane: acanthocytes (ring forms with blebs), fragmented RBCs	Glomerular origin — passage through damaged GBM causes distortion
Isomorphic RBCs	Uniform, round, biconcave — normal morphology	Non-glomerular source: urothelial, calculi, tumour, BPH
White blood cells	>5 WBC/HPF is abnormal (pyuria)	UTI, interstitial nephritis, prostatitis, TB, interstitial cystitis
Eosinophils	Hansel's stain or Wright's stain >1% of urinary WBCs	Drug-induced interstitial nephritis (PPIs, NSAIDs, antibiotics), cholesterol atheroemboli
Tubular epithelial cells (TECs)	Large, round, single nucleus; may be vacuolated	ATN, toxic nephropathy, rejection (transplant). >5/HPF is significant.
Squamous cells	Large, flat, irregular; with nucleus	Contamination from external genitalia. If abundant, repeat MSU collection.
Oval fat bodies	TECs containing lipid droplets; Maltese cross under polarised light	Nephrotic syndrome (lipiduria)

Bacteria & Yeasts

Bacteria visible on unspun urine microscopy suggest >10⁵ CFU/mL. However, bacteria should always be confirmed by culture (MBS-rebated midstream urine culture with antimicrobial susceptibility). Yeast forms (oval budding cells, pseudohyphae) suggest Candida species — particularly in catheterised patients, diabetics, and immunocompromised hosts.

Crystals

Crystal type	pH preference	Appearance	Significance
Calcium oxalate	Any pH	Envelope (dihydrate) or dumbbell/biconcave (monohydrate)	Normal in small numbers. Large quantities: ethylene glycol poisoning, hyperoxaluria, Crohn's disease, jejunoileal bypass.
Uric acid	Acidic (<5.5)	Rhomboid, rosette, or barrel-shaped; yellow-brown	Often benign (concentrated acidic urine). Associated with gout, tumour lysis syndrome. Precursor to uric acid stones.
Struvite (triple phosphate)	Alkaline (>7.0)	"Coffin-lid" rectangular prisms	Urease-producing bacteria (Proteus); associated with staghorn calculi.
Calcium phosphate	Alkaline (>6.5)	Needle-shaped or rosette; colourless	Seen in alkaline urine; may be associated with RTA Type 2 or hyperparathyroidism.
Cystine	Acidic	Flat hexagonal plates with well-defined edges	Pathognomonic of cystinuria (autosomal recessive). Confirm with urine cystine quantification.
Amorphous urates	Acidic	Granular, yellow-brown; dissolve on warming	Non-pathological; artefact of refrigeration.
Amorphous phosphates	Alkaline	Granular, colourless; dissolve with acetic acid	Non-pathological; artefact of refrigeration.
Drug crystals	Variable	Variable morphology (e.g., aciclovir — fine needles; sulfonamides — characteristic shapes; indinavir — star-burst)	Obstructive AKI possible with aciclovir, sulfonamides, methotrexate.

ℹ️

Amorphous crystals (urates and phosphates) form during refrigeration and are clinically insignificant. Always examine urine at room temperature. Persistent cystine crystals in a non-refrigerated specimen are diagnostic of cystinuria.

Proteinuria: Quantification

Persistent proteinuria is both a marker and a driver of progressive kidney disease. Quantification is essential after a positive dipstick to stratify risk, guide investigation, and monitor treatment response.

Quantification Methods

Method	Specimen	Normal values	MBS item	Advantages
Albumin-to-Creatinine Ratio (ACR)	Random spot urine (first morning preferred)	<2.5 mg/mmol (♂) <3.5 mg/mmol (♀)	MBS 69414	Single sample; corrects for concentration; most sensitive for early albuminuria (diabetic nephropathy, hypertensive nephrosclerosis)
Protein-to-Creatinine Ratio (PCR)	Random spot urine	<15 mg/mmol	MBS 69414	Correlates well with 24-hr total protein; includes all proteins (not just albumin); useful when glomerular protein loss is the primary concern
24-hour urine protein	Timed 24-hour collection	<150 mg/24hr	MBS 69410 (quantitative urine protein)	Traditional gold standard; cumbersome, error-prone collection; now largely replaced by ACR/PCR in Australia
Urine dipstick protein	Random urine	Negative (<150 mg/L)	N/A (point-of-care)	Screening only; must be quantified if positive

KDIGO Classification of Albuminuria

A1 — Normal to mildly increased

ACR <3 mg/mmol

No clinically significant albuminuria. Routine monitoring in low-risk patients; annual ACR in diabetics and hypertensives.

Setting: Primary care — annual review

A2 — Moderately increased (formerly "microalbuminuria")

ACR 3–30 mg/mmol

Early marker of diabetic nephropathy, hypertensive nephrosclerosis, or glomerular disease. Confirm on 2 of 3 samples over ≥3 months. Initiate ACEi/ARB therapy; optimise BP & glycaemic control.

Setting: GP with nephrology review if haematuria or declining eGFR

A3 — Severely increased (formerly "macroalbuminuria")

ACR >30 mg/mmol

Overt nephropathy. High risk of CKD progression, cardiovascular events, and ESKD. Nephrology referral indicated. Maximise RAAS blockade; consider SGLT2 inhibitor (dapagliflozin Forxiga® — PBS Authority for CKD with albuminuria).

Setting: Nephrology — specialist review

ACR vs PCR: When to Use Which?

ACR is the preferred first-line test in Australia for screening and monitoring of CKD (KDIGO, RACGP, Kidney Health Australia). It is more sensitive for detecting early nephropathy because albumin is the first protein to leak through a damaged glomerular barrier.

PCR is useful when total protein loss needs assessment — for example, in suspected nephrotic syndrome (PCR >500 mg/mmol, equivalent to >3.5 g/day) or when non-albumin proteins (e.g., light chains in myeloma) may be contributing. In practice, a PCR >100 mg/mmol roughly corresponds to >1 g/day of proteinuria.

⚠️

Pitfall — single positive ACR: Transient proteinuria may result from exercise, fever, UTI, heart failure, or menstruation. Always confirm persistent albuminuria with ≥2 abnormal samples over ≥3 months before labelling as CKD, except in diabetic patients with established retinopathy (a single ACR >3 mg/mmol is sufficient).

Causes of Non-Glomerular Proteinuria

Tubular: Low-molecular-weight proteins (beta-2 microglobulin, alpha-1 microglobulin) — ATN, interstitial nephritis, Fanconi syndrome. PCR usually <100 mg/mmol.
Overflow: Excess circulating proteins filtered beyond tubular reabsorption capacity — myeloma (Bence Jones / free light chains), rhabdomyolysis (myoglobin), haemolysis (haemoglobin).
Post-renal: Tamm-Horsfall protein, inflammatory exudate from lower urinary tract — UTI, prostatitis, malignancy.

Haematuria: Glomerular vs Non-Glomerular

Haematuria — the presence of blood in the urine — is a common finding in primary care and emergency medicine. Distinguishing glomerular from non-glomerular haematuria is the critical initial diagnostic step, as it determines the subsequent investigation pathway and urgency of referral.

Definitions

Microscopic haematuria: ≥3 RBC/HPF on centrifuged specimen (or ≥10 RBC/µL on automated urinalysis); dipstick 1+ to 2+. Patient appears to have clear urine.
Macroscopic (frank) haematuria: Visible blood in urine — from cola-coloured to frankly red. Always pathological and warrants investigation.
Persistent microscopic haematuria: Haematuria on ≥2 of 3 specimens over ≥3 months, in the absence of transient causes.

Distinguishing Glomerular from Non-Glomerular Haematuria

Feature	Glomerular	Non-Glomerular
Urine colour	Cola / smoky / brown	Pink / red / frankly bloody
RBC morphology	Dysmorphic (>5% acanthocytes on phase-contrast)	Isomorphic (uniform, biconcave)
RBC casts	Present (pathognomonic)	Absent
Proteinuria	Often significant (ACR >30 mg/mmol or PCR >100 mg/mmol)	Minimal or absent (<1+ on dipstick)
Associated symptoms	Oedema, hypertension, oliguria	Dysuria, frequency, flank pain, clots
Clinical context	Young adult, recent URTI, rash (Henoch-Schönlein), joint pain (SLE), sinusitis (GPA)	Age >40, smoker, occupational exposures, BPH, recent catheterisation
Common aetiologies	IgA nephropathy, lupus nephritis, Alport syndrome, anti-GBM, ANCA vasculitis	UTI, urolithiasis, urothelial carcinoma, BPH, exercise-induced, trauma
Investigation pathway	Nephrology referral → serology → renal biopsy	Urology referral → imaging (US, CT KUB) → cystoscopy

Investigation Algorithm

Confirm haematuria

Repeat dipstick + microscopy on fresh MSU. Rule out: menstruation, UTI, exercise, trauma, catheterisation, sexual activity. Treat UTI first, then repeat after 2–4 weeks.

Assess RBC morphology

Phase-contrast microscopy (if available): >5% dysmorphic RBCs / acanthocytes → glomerular pathway. Isomorphic RBCs → non-glomerular / urological pathway.

Check for red cell casts & proteinuria

Red cell casts → urgent nephrology referral. ACR >30 mg/mmol with haematuria → nephrology referral. No casts, minimal protein → urological workup.

Urological pathway (age >40, risk factors)

Renal tract ultrasound (MBS 55023) → CT urography (if US normal) → flexible cystoscopy (MBS 36816). Smokers, age >40, occupational dye/rubber exposure: high risk for urothelial carcinoma.

Nephrological pathway (younger, dysmorphic RBCs, proteinuria)

Serology: C3, C4, ANA, ANCA (MPO/PR3), anti-GBM, ASOT, anti-DNase B, hepatitis B/C, HIV. Renal biopsy if abnormal serology, declining eGFR, or nephrotic-range proteinuria.

Urgent Referral Criteria (Nephrology)

🚨

Macroscopic haematuria with red cell casts
Microscopic haematuria + proteinuria ACR >30 mg/mmol
Rapidly declining eGFR (>25% fall in 3 months, or >15 mL/min/year decline)
Suspected vasculitis: haematuria + constitutional symptoms + purpura / sinusitis / mononeuritis multiplex
Anti-GBM disease: haemoptysis + haematuria (Goodpasture syndrome)
Nephrotic syndrome: oedema + albuminuria ACR >220 mg/mmol + hypoalbuminaemia

Special Populations

🤰 Pregnancy

Asymptomatic bacteriuria: Screen at first antenatal visit (MSU culture). Prevalence 2–7% in Australia. Treat to prevent pyelonephritis and preterm labour. Nitrofurantoin (Macrobid®) 100 mg PO BD × 5 days is first trimester-safe; avoid at term (neonatal haemolytic anaemia). Cephalexin (Keflex®) 500 mg PO TDS is an alternative. ✔ PBS General Benefit

Proteinuria: ACR remains the preferred quantification method. Physiological proteinuria increases in pregnancy; ACR >30 mg/mmol in the context of hypertension suggests pre-eclampsia. 24-hour collection may still be used in some obstetric units.

Haematuria: Always exclude UTI. Persistent haematuria post-partum warrants urological workup. Glomerular haematuria (e.g., lupus nephritis) may flare during pregnancy.

👶 Paediatrics

Collection: Clean-catch (midstream) in toilet-trained children; adhesive bag specimens in infants (high contamination rate — >50%). Suprapubic aspiration remains the gold standard for infants <2 years if accurate specimen is essential.

Haematuria: IgA nephropathy is the most common cause of persistent glomerular haematuria in children in Australia. Post-streptococcal GN (PSGN) presents 1–3 weeks after streptococcal pharyngitis or impetigo. Alport syndrome screening if family history of deafness + haematuria.

Proteinuria: Orthostatic (postural) proteinuria is the most common cause in adolescents — benign. Confirm with split collection: first morning (supine) vs evening (upright) specimen. Nephrotic syndrome in children: minimal change disease is most common; ACR >220 mg/mmol, hypoalbuminaemia <25 g/L, oedema.

Crystalluria: Neonatal uric acid crystals ("brick dust" nappy staining) are normal. Cystine crystals at any age → cystinuria screening.

👴 Elderly

Asymptomatic bacteriuria (ASB): Prevalence 15–50% in aged-care residents in Australia. Routine screening and treatment of ASB is NOT recommended (unless pregnant or pre-urological procedure) — antimicrobial treatment does not reduce mortality and promotes AMR.

Haematuria: Higher pre-test probability for urothelial carcinoma in patients >60 years; early cystoscopy referral is warranted.

Proteinuria: Age-related eGFR decline + nephrosclerosis from long-standing hypertension is common. ACR monitoring remains appropriate; interpret in context of age-adjusted eGFR.

🫘 Renal Impairment

Low GFR with bland sediment: Chronic tubulointerstitial disease, hypertensive nephrosclerosis, or diabetic nephropathy. Few cells, few casts, waxy casts may be seen.

Active sediment: Dysmorphic RBCs + RBC casts + proteinuria in a patient with declining eGFR → active GN → biopsy likely needed.

🛡️ Immunocompromised

UTI interpretation: Lower threshold for MSU culture; leucocyte esterase may be falsely negative due to impaired neutrophil function. CMV, BK virus (transplant), and fungal UTIs should be considered.

Drug-induced interstitial nephritis: PPIs, trimethoprim, aciclovir, immune checkpoint inhibitors (nivolumab, pembrolizumab) — urine eosinophils + WBC casts + AKI. Hansel's stain recommended.