01Purpose and principlesWhat the assessment is for and the core concepts behind it.
Urinalysis is a low-cost physiological biopsy, but only when collection and interpretation are disciplined. Reagent pads screen chemical properties; microscopy identifies cells, casts, organisms and crystals; culture establishes bacterial growth; ACR or PCR quantifies protein. None substitutes for the others.
Casts form in renal tubules and therefore help localise disease above the lower urinary tract. Red-cell casts are strongly concerning for glomerulonephritis, while renal tubular epithelial cells and coarse granular casts can support acute tubular injury. Absence of an active sediment does not exclude biopsy-proven disease, particularly after delay or dilute urine.
The clinical question determines action. Asymptomatic bacteriuria, sterile pyuria, non-visible haematuria and nephritic urine have different pathways. Treat the patient and source, not every colour change or isolated dipstick pad.
Key points
- A fresh midstream clean-catch sample with documented timing and symptoms is the starting point. Catheter, menstruation, vigorous exercise, antiseptic contamination and delayed analysis can change results.
- Dipstick 'blood' detects haem pigment, not intact red cells. Haematuria, haemoglobinuria and myoglobinuria can all be positive; microscopy and the clinical setting separate them.
- Nitrite supports nitrate-reducing bacteria but is insensitive with frequent voiding, low dietary nitrate or organisms that do not reduce nitrate. A negative result never excludes UTI or pyelonephritis.
- Leucocyte esterase reflects white cells and can occur with infection, stones, interstitial nephritis, tuberculosis or contamination. Culture and symptoms determine whether antibiotics are appropriate.
- Dipstick protein mainly detects albumin and is affected by concentration and pH. NICE recommends quantitative urine ACR for initial detection of clinically important proteinuria.
- Glucose on dipstick can reflect hyperglycaemia or reduced proximal tubular reabsorption, including SGLT2 inhibitor effect. Check blood glucose and medicines before diagnosing diabetes.
- Ketones indicate fat metabolism and can accompany diabetic ketoacidosis, starvation, vomiting or pregnancy. In SGLT2-treated patients, clinically important ketoacidosis can occur with less marked hyperglycaemia.
- Dysmorphic red cells and red-cell casts support glomerular bleeding; white-cell casts suggest renal parenchymal inflammation; granular 'muddy brown' casts support tubular injury but sediment sensitivity is imperfect.
- Crystals depend on urine pH, concentration, medicines and storage. Their presence does not prove a stone, while stone disease can occur without diagnostic crystalluria.
- Interpret the whole pattern: blood plus albumin and impaired function differs from isolated nitrite, and a bland dipstick does not exclude obstruction or early interstitial disease.
02Indications, selection and cautionsWhen it is useful, when urgency changes and important limitations.
Protein with dysmorphic erythrocytes or red-cell casts, hypertension, oedema and impaired function favours glomerular inflammation. Systemic rash, haemoptysis or rapidly rising creatinine increases urgency.
Renal tubular epithelial cells and pigmented granular casts in an ischaemic, septic or toxic context support acute tubular injury. Creatinine trajectory and urine output remain necessary for severity.
Dysuria, frequency or fever with pyuria, bacteriuria and sometimes nitrite supports infection. Flank pain, rigors, pregnancy, male sex, immunosuppression or obstruction changes complexity and escalation.
White cells without routine bacterial growth can reflect prior antibiotics, stones, interstitial nephritis, sexually transmitted infection, renal tuberculosis or contamination. Repeat and target tests rather than extending empirical antibiotics blindly.
Strong dipstick blood with few or no erythrocytes suggests myoglobin or free haemoglobin. Muscle pain, high CK or haemolysis tests identify a systemic pigment source that can itself cause AKI.
Many squamous epithelial cells, mixed flora and discordant symptoms suggest poor collection. Repeat a correctly obtained sample unless the patient is too unwell for diagnostic delay.
03Method and interpretationA systematic approach to the test and its findings.
Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.
- 01
Fresh reagent-strip urinalysisFirst step - Why
- Screen blood, leucocytes, nitrite, protein, glucose, ketones, pH and concentration at the bedside or laboratory.
- Interpretation and limitations
- Record exact grade rather than 'positive'. Check expiry, timing and discolouring medicines; correlate every pad with symptoms, ACR, microscopy or blood testing as appropriate.
- 02
Urine albumin-to-creatinine ratio - Why
- Quantify albuminuria sensitively and classify chronic kidney risk.
- Interpretation and limitations
- Use an early-morning confirmation for ACR 3 to 70 mg/mmol in stable adults under NICE/UKKA guidance; values above 70 generally do not require confirmation before action, but acute illness can transiently raise albumin.
- 03
Urine microscopy - Why
- Identify erythrocyte morphology, leucocytes, epithelial cells, casts, organisms and crystals.
- Interpretation and limitations
- Request and examine promptly when glomerulonephritis, tubular injury or crystals are suspected. Technique and delay affect yield; a negative sediment is not an absolute exclusion test.
- 04
Midstream urine culture and sensitivities - Why
- Confirm clinically relevant bacteriuria and direct antimicrobial choice.
- Interpretation and limitations
- Collect before antibiotics where safe and report pregnancy, catheter and symptoms. Mixed growth often indicates contamination, while lower counts may still matter in a strongly symptomatic patient.
- 05
Serum creatinine, potassium, bicarbonate and FBC - Why
- Determine renal impact and systemic severity of the urine abnormality.
- Interpretation and limitations
- A rising creatinine, hyperkalaemia or acidosis with active sediment lowers the threshold for urgent renal referral. Leucocytosis or anaemia can guide infection, haemolysis and chronicity assessment.
- 06
Creatine kinase and haemolysis screen - Why
- Investigate dipstick haem with absent urinary erythrocytes.
- Interpretation and limitations
- Marked CK supports rhabdomyolysis; anaemia, bilirubin, LDH, haptoglobin and blood film support intravascular haemolysis. Both require cause-directed systemic management.
04Clinical next stepsHow the result changes management or prompts escalation.
01Active nephritic urineEscalate possible glomerulonephritisFirst stepEscalationBlood and protein with impaired function, hypertension, casts or systemic inflammatory features.+
- 1Repeat a clean sample, quantify ACR/PCR, obtain urgent renal biochemistry, FBC and blood pressure, and review baseline and urine output.
- 2Discuss promptly with nephrology; send targeted complements, ANCA, ANA, anti-GBM, infection and paraprotein testing as advised rather than delaying referral for a complete panel.
- 3If pulmonary haemorrhage, oliguria, severe hypertension, hyperkalaemia or rapid deterioration is present, admit for emergency renal assessment and possible biopsy/treatment.
02Possible UTICulture and classify complexityUrinary symptoms, fever or systemic illness with leucocytes, nitrite or bacteriuria.+
- 1Assess sepsis, pregnancy, flank pain, retention, stones, catheter, male anatomy and immunosuppression; obtain culture before treatment when this does not delay sepsis antibiotics.
- 2Choose antimicrobial and duration from the current local/NICE pathway, prior cultures, allergy, renal function and resistance risk rather than dipstick alone.
- 3Arrange imaging or urology review for suspected infected obstruction, recurrence, atypical organism or failure to improve; do not keep repeating empirical courses without source review.
03Unexpected dipstickVerify before labelling diseaseAsymptomatic blood, protein, glucose, leucocytes or pigment found incidentally.+
- 1Exclude transient collection factors such as menstruation, exercise, fever and contamination, then repeat under correct conditions at the guideline interval.
- 2Quantify albumin with ACR, culture when infection is plausible, examine microscopy for persistent blood and check glucose or CK for the relevant chemical signal.
- 3Route persistent haematuria through age-appropriate urology criteria and renal haematuria through ACR, eGFR and nephrology criteria; these routes may need to run together.
05Procedure and medicine safetyRelevant preparation, treatment and contraindications.
Empirical antimicrobial for urinary infection
Select agent, dose and duration from current local and NICE guidance using site, severity, culture history, allergy, pregnancy and renal function.Do not treat an isolated dipstick or most asymptomatic bacteriuria. Obstruction needs drainage, and several antibiotics require renal adjustment or can worsen potassium and kidney function.
SGLT2 inhibitor awareness
Continue or pause only according to an individualised clinical sick-day and peri-procedure plan; timing varies by medicine, illness severity and procedure.Glycosuria is pharmacological and does not prove uncontrolled diabetes. Nausea, abdominal pain, tachypnoea or ketones during illness requires urgent blood ketone and acid-base assessment.
06Risks, monitoring and follow-upComplications, safety checks and further assessment.
- Repeat urinalysis after transient triggers settle and confirm persistent albuminuria quantitatively rather than following dipstick intensity as a surrogate.
- For nephritic findings, trend creatinine, potassium, bicarbonate, urine output, blood pressure and ACR/PCR while nephrology determines biopsy and immunosuppression urgency.
- For treated infection, review culture and narrow or change antibiotics, documenting renal-dose adjustments and clinical response rather than ordering routine test-of-cure for everyone.
- Persistent non-visible haematuria needs blood pressure, eGFR and ACR surveillance even after negative urological investigation because renal disease can evolve.
- When pigment nephropathy is possible, follow CK or haemolysis markers, potassium, calcium, phosphate, fluid balance and renal function through the acute pathway.
07Special situationsVariants, exceptions and circumstances that change the usual approach.
Blood pad detects chemistry
The reagent reacts to haem peroxidase activity. Microscopy distinguishes intact urinary red cells from myoglobin or haemoglobin and prevents three different diseases sharing one label.
Casts carry an address
Because casts form in tubules, cells embedded within them localise inflammation or bleeding to the kidney rather than bladder or urethra.
Albumin needs quantification
A concentrated urine can look strongly protein-positive and dilute urine weakly positive. ACR corrects partly for concentration and detects lower albumin amounts more sensitively.
Nitrite is a rule-in clue
Adequate bladder dwell time and a nitrate-reducing organism are required. Frequent voiding or enterococci can produce symptomatic infection with negative nitrite.
A bland sediment can still be serious
Obstruction, vascular disease and some interstitial or early glomerular processes may produce few cells. Always integrate urine findings with creatinine, output and imaging.
08Common pitfallsFrequent interpretation and management errors.
- 01
Calling dipstick blood haematuria without confirming whether urinary erythrocytes are present.
- 02
Excluding infection because nitrite is negative in a symptomatic or septic patient.
- 03
Treating leucocyte esterase alone with repeated antibiotics despite sterile cultures.
- 04
Using dipstick protein instead of ACR to detect and classify lower-level albuminuria.
- 05
Waiting for every immunology result before discussing rapidly progressive nephritic findings with nephrology.
- 06
Assuming crystals prove a stone or that absent crystals exclude stone disease.