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approach to proteinuria and haematuria

in review 5 min read Updated 2026-08-24
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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.

do not miss
  • nephritic syndrome (haematuria + proteinuria + AKI + hypertension) → RPGN workup same day; delay costs nephrons
  • visible haematuria in adults >40 → urological malignancy until proven otherwise (CT urogram + cystoscopy)
  • 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

methodmeasurenotes
urine dipsticksemiquantitative (trace to 4+)detects albumin only; misses light chains, tubular proteins. Affected by urine concentration — always confirm
urine ACR (mg/mmol)albumin-specificpreferred screening and CKD staging (KDIGO). First-morning sample best
urine PCR / UPCR (mg/mmol)total proteindetects non-albumin proteins (light chains, tubular). Use when myeloma or tubulointerstitial disease suspected
24 h urinegold standardrarely needed — spot ACR or UPCR with first-morning void is adequate for most decisions
ACR vs UPCR

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)categoryclinical implication
<3A1 — normalno action
3–30A2 — moderateCKD if persistent ≥3 months; start RAS blockade
>30A3 — severehigh-risk CKD; add SGLT2 inhibitors; nephrology referral
>350 (UPCR)nephrotic-rangesee 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 — young patients (<30 yr); confirm with split collection (first-morning ACR normal, upright sample elevated). Benign; no follow-up needed.

proteinuria workup

flowchart TD
    A["dipstick protein ≥1+\nor ACR ≥3 mg/mmol"] --> B{"exclude transient causes\n(fever, UTI, exercise)"}
    B -->|resolved| C["repeat in 3 months"]
    B -->|persists| D{"quantify:\nACR + UPCR"}
    D -->|"ACR 3–30\n(A2)"| E["CKD staging\nRAS blockade\nannual monitoring"]
    D -->|"ACR >30\n(A3)"| F["nephrology referral\nRAS blockade + SGLT2i\nserologies if glomerular\nsuspicion"]
    D -->|"UPCR >350\n(nephrotic-range)"| G["urgent nephrology\nsee nephrotic syndrome"]
    D -->|"UPCR elevated,\nACR normal"| H["consider overflow\n(SPEP/UPEP, free light chains)\nor 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

featureglomerularurological
RBC morphologydysmorphic, acanthocytes ≥5%isomorphic
castsRBC casts (pathognomonic)absent
clotsabsentmay be present
colourbrown / “cola” / “tea”red / pink
proteinuriaoften presentusually absent
painusually painlessmay have flank/suprapubic pain
RBC casts = glomerulonephritis

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 or non-visible + risk factors (age >40, smoking, occupational exposures) → CT urogram + cystoscopy (CUA guideline)
  • Non-visible, low-risk (age <40, no risk factors, single episode) → repeat urinalysis in 6 months; if persistent, image

Risk factors for urological malignancy: age >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:

patternthinknext step
haematuria + sub-nephrotic proteinuriaIgA nephropathy, thin basement membrane disease, Alport syndrome, lupus nephritisnephrology referral → likely biopsy
haematuria + nephrotic-range proteinuriamembranous with nephritic features, lupus class III–V, MPGNurgent nephrology
haematuria + AKI + hypertensionRPGN — anti-GBM, ANCA vasculitis, lupus, IgA with crescentssame-day nephrology; serologies + biopsy urgently
episodic visible haematuria with URTIsIgA nephropathy (synpharyngitic haematuria)nephrology referral; biopsy if proteinuria or declining eGFR

when to refer to nephrology

  • Persistent proteinuria ACR >30 mg/mmol (A3)
  • Any glomerular haematuria (dysmorphic RBCs, RBC casts, or haematuria + proteinuria)
  • Persistent non-visible haematuria with declining eGFR
  • Acute kidney injury with active sediment
  • Suspected RPGN — same-day referral

when to refer to urology

  • Visible haematuria without glomerular features
  • Non-visible haematuria with risk factors for malignancy (age >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.

related: nephrotic syndrome · acute kidney injury · chronic kidney disease

Key references

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