approach to proteinuria and haematuria
Proteinuria and haematuria are urinary markers of kidney disease that may present alone or together. The combination — particularly dysmorphic haematuria with proteinuria — strongly suggests glomerular pathology and warrants urgent nephrology input. Isolated proteinuria drives CKD staging and renoprotection decisions. Isolated haematuria requires distinguishing glomerular from urological causes.
- nephritic syndrome (haematuria + proteinuria + AKI + hypertension) → RPGN workup same day; delay costs nephrons
- visible haematuria in adults ≥35–40 → exclude urological malignancy (cystoscopy + upper-tract imaging)
- nephrotic-range proteinuria (UPCR >350 mg/mmol) with hypoalbuminaemia → thrombotic risk, urgent nephrology — see nephrotic syndrome
- pulmonary-renal syndrome — haemoptysis + haematuria + AKI → anti-GBM or ANCA vasculitis; nephrology and ICU same day
proteinuria
quantification
| method | measure | notes |
|---|---|---|
| urine dipstick | semiquantitative (trace to 4+) | detects albumin only; misses light chains, tubular proteins. Affected by urine concentration — always confirm |
| urine ACR (mg/mmol) | albumin-specific | preferred screening and CKD staging (KDIGO). First-morning sample best |
| urine PCR / UPCR (mg/mmol) | total protein | detects non-albumin proteins (light chains, tubular). Use when myeloma or tubulointerstitial disease suspected |
| 24 h urine | gold standard | rarely needed — spot ACR or UPCR with first-morning void is adequate for most decisions |
ACR is the standard for CKD screening and staging. UPCR is better when non-albumin proteinuria matters — overflow (myeloma light chains) or tubular proteinuria. If dipstick is negative but renal disease is suspected, request UPCR.
classification by severity (KDIGO)
| ACR (mg/mmol) | category | clinical implication |
|---|---|---|
| <3 | A1 — normal | no action |
| 3–30 | A2 — moderate | CKD if persistent ≥3 months; start RAS blockade; consider SGLT2 inhibitors if ACR ≥20 |
| >30 | A3 — severe | high-risk CKD; RAS blockade + SGLT2 inhibitors; nephrology referral |
| UPCR ≥50 (~0.5 g/day) | biopsy threshold | consider renal biopsy, especially if glomerular features (KDIGO 2025 IgAN) |
| UPCR >350 (~3.5 g/day) | nephrotic-range | see nephrotic syndrome |
Confirm persistence — repeat ACR on two of three first-morning samples over 3 months before labelling CKD.
transient / benign causes to exclude first
Fever, exercise, UTI, menstruation, dehydration, heart failure exacerbation. Orthostatic proteinuria in patients <30 yr (first-morning ACR normal, upright elevated) — benign, no follow-up.
If dipstick-positive, exclude transient causes → quantify with ACR + UPCR → manage per severity table above. UPCR elevated with normal ACR → consider overflow proteinuria (SPEP/UPEP, free light chains) or tubular proteinuria.
haematuria
confirm and classify
- Dipstick positive for blood → microscopy to confirm true haematuria (≥3 RBCs per HPF). Dipstick detects haem — false positives with myoglobinuria, haemoglobinuria.
- Visible (macroscopic) vs non-visible (microscopic) — different workup urgency.
glomerular vs non-glomerular
| feature | glomerular | urological |
|---|---|---|
| RBC morphology | dysmorphic, acanthocytes ≥5% | isomorphic |
| casts | RBC casts (pathognomonic) | absent |
| clots | absent | may be present |
| colour | brown / “cola” / “tea” | red / pink |
| proteinuria | often present | usually absent |
| pain | usually painless | may have flank/suprapubic pain |
RBC casts on urine microscopy are pathognomonic for glomerular bleeding and warrant urgent nephrology referral — do not wait for serologies. Acanthocytes ≥5% are also highly specific for glomerular origin.
haematuria workup
Glomerular haematuria (dysmorphic RBCs, RBC casts, or concurrent proteinuria):
- Nephrology referral
- Serologies: ANA, ANCA, anti-GBM, C3/C4, ASO/anti-DNase B, hepatitis B/C, HIV
- SPEP/UPEP, free light chains if >40 yr
- Renal biopsy — guided by clinical context; IgA nephropathy is the most common cause of glomerular haematuria worldwide
Non-glomerular / urological haematuria (isomorphic RBCs, no casts, no significant proteinuria):
- Visible haematuria → cystoscopy + CT urogram (preferred upper-tract imaging for gross bleeding)
- Non-visible + risk factors (age ≥35–40, smoking, occupational exposures) → cystoscopy + renal ultrasound (CUA approach); reserve CT urogram for US-positive or higher-risk patients. Uniform CT for all microhaematuria increases radiation-induced cancers and cost for marginal detection gain
- Non-visible, low-risk (age <35, no risk factors, single episode) → repeat urinalysis in 6 months; if persistent, image
Risk factors for urological malignancy: age ≥35–40, smoking history, occupational carcinogen exposure (aromatic amines — dyes, rubber, plastics), prior pelvic radiation, cyclophosphamide exposure, chronic catheterisation.
combined haematuria and proteinuria
The combination narrows the differential to glomerular disease in most cases:
| pattern | think | next step |
|---|---|---|
| haematuria + sub-nephrotic proteinuria | IgA nephropathy, thin basement membrane disease, Alport syndrome, lupus nephritis | nephrology referral → likely biopsy |
| haematuria + nephrotic-range proteinuria | membranous with nephritic features, lupus class III–V, MPGN | urgent nephrology |
| haematuria + AKI + hypertension | RPGN — anti-GBM, ANCA vasculitis, lupus, IgA with crescents | same-day nephrology; serologies + biopsy urgently |
| episodic visible haematuria with URTIs | IgA nephropathy (synpharyngitic haematuria) | nephrology referral; biopsy if proteinuria or declining eGFR |
referral
Nephrology — persistent ACR >30 (A3), any glomerular haematuria, haematuria + proteinuria, acute kidney injury with active sediment, suspected RPGN (same day).
Urology — visible haematuria without glomerular features, non-visible haematuria with malignancy risk factors (age ≥35–40, smoking), structural abnormality on imaging.
traps
- Dipstick protein misses non-albumin proteins — a negative dipstick does not exclude myeloma-related proteinuria. Request UPCR or free light chains if clinical suspicion exists.
- Attributing haematuria to anticoagulation — anticoagulants do not cause haematuria; they unmask existing pathology. Always investigate.
- Ignoring isolated microscopic haematuria in young patients — if dysmorphic or with proteinuria, this may be early IgA nephropathy or Alport syndrome. Repeat urinalysis and check ACR.
- Overcalling dipstick haematuria — myoglobinuria (rhabdomyolysis) and haemoglobinuria (haemolysis) trigger the dipstick. Microscopy confirms true haematuria.
- Dismissing transient proteinuria without follow-up — repeat at 3 months. Persistent A2+ proteinuria changes CKD staging and management.