Synopsis
Use dipstick, quantitative protein testing, culture and urine sediment together to localise renal and urinary disease while recognising contamination, false results and time-critical nephritic patterns.
- 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.
Key red flags
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.
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.
Investigation priorities
Screen blood, leucocytes, nitrite, protein, glucose, ketones, pH and concentration at the bedside or laboratory.
Management branches
Blood and protein with impaired function, hypertension, casts or systemic inflammatory features.
- Repeat a clean sample, quantify ACR/PCR, obtain urgent renal biochemistry, FBC and blood pressure, and review baseline and urine output.
- Discuss promptly with nephrology; send targeted complements, ANCA, ANA, anti-GBM, infection and paraprotein testing as advised rather than delaying referral for a complete panel.
- If pulmonary haemorrhage, oliguria, severe hypertension, hyperkalaemia or rapid deterioration is present, admit for emergency renal assessment and possible biopsy/treatment.