Haematuria (Evaluation)

Meet the patient

A 64-year-old man, a 40-pack-year smoker who spent thirty years in a dye plant, notices painless red urine for three days. No dysuria, no colic, no fever, no clots. His dipstick is strongly blood-positive; his GP gave trimethoprim a week ago and the urine is still red. He is on apixaban for atrial fibrillation.[1]

Three exam questions are now live, and you must answer them in order: is this really haematuria, where is it coming from, and what must you never attribute it to? This whole topic is the answer to those three questions.[1]

What haematuria actually is — and why a positive dipstick is not enough

Haematuria is red blood cells in the urine — a sign, never a diagnosis. Two thresholds define it at the bedside. Visible (macroscopic, gross) is urine that is red, pink, brown or cola-coloured to the naked eye. Non-visible (microscopic) is urine of normal colour that shows blood only on dipstick and is confirmed by more than 3 RBCs per high-power field on microscopy of a centrifuged midstream specimen.[6]

Everyone reaches for the dipstick and stops there. That is the classic trap. The dipstick detects haem peroxidase activity, which is present in intact red cells, free haemoglobin and myoglobin alike — so it is positive in true haematuria, haemoglobinuria and myoglobinuria, and cannot tell them apart. A positive dipstick must be confirmed by microscopy before the label 'haematuria' is ever written.[5]

False positives on dipstick: myoglobinuria (rhabdomyolysis — very high CK), haemoglobinuria (intravascular haemolysis — low haptoglobin, raised LDH), concentrated or oxidatively contaminated urine (povidone-iodine, bleach), and beetroot or drugs such as phenazopyridine. False negatives come from dilute urine or ascorbic acid (vitamin C) interfering with the peroxidase reaction — true haematuria can hide behind a negative stick.[6]

Glomerular vs urological — the split that decides everything

The single most important judgement in haematuria is glomerular or urological, because it decides the referral, the imaging and whether anyone biopsies a kidney. The deciding clue is the shape of the red cell under the microscope — dysmorphic with casts (glomerular) versus isomorphic and intact (urological). Run this split on every patient.[1]

[6]

Symptom context sets the urgency, on top of the source split.[1]

• Painless visible haematuria — cancer until proven otherwise; urgent cystoscopy and CT urogram.
• Painful visible haematuria — stone (colic, loin to groin) or infection (dysuria, frequency, fever); cancer must still be excluded once the acute event settles.
• Symptomatic microscopic haematuria — investigate the cause (UTI, stone) and re-check after treatment.
• Asymptomatic microscopic haematuria — risk-stratify by age, sex, smoking and RBC count.[6]

The cardinal trap — painless visible haematuria is cancer until proven otherwise

If you take one sentence from this topic, take this one: painless visible haematuria in an adult is cancer until proven otherwise, and it earns an urgent suspected-cancer referral. It is the single most malignant presentation of red urine, and the cancer yield is the headline number that drives the whole work-up.[1]

[1]

Bladder cancer is the commonest urological malignancy and the commonest diagnosis made on a haematuria work-up. It is three to four times more common in men, peaks over 60, and is tied tightly to tobacco — the single biggest modifiable risk factor, behind about half of cases.[2]

The cancer-risk history you must elicit on every haematuria patient, on autopilot:[2]

The anticoagulant trap — everyone blames the warfarin. Bleeding from any cause is amplified on warfarin, DOACs or antiplatelets, but a therapeutic INR is never an acceptable sole explanation for visible haematuria. Anticoagulants do not cause de novo haematuria — they reveal underlying pathology, often cancer. Investigate in parallel, never instead.[1]

Why the shape of the red cell betrays its origin

Blood appears in the urine because something has broken a barrier meant to hold it back — and the shape of the cell tells you which barrier. Understand the glomerular filtration barrier and you understand the whole topic.[5]

The normal barrier has three layers — the fenestrated endothelium, the glomerular basement membrane (GBM) with its negatively-charged type-IV collagen network, and the podocyte foot processes with their slit diaphragms (nephrin, podocin). Together they hold back all blood cells and most protein. Damage it — by immune-complex deposition (IgA nephropathy, lupus), inflammation (post-infectious GN), genetic thinning or collagen alteration (thin basement membrane disease, Alport), or podocyte effacement — and red cells squeeze through.[5]

The squeeze is what makes the cell dysmorphic. An RBC forced through rents in the GBM and the slit diaphragm emerges distorted — with blebs, vesicles and the ring-shaped acanthocytes (annular cells with bleb-like protrusions). Acanthocytes over 5 per cent of urinary RBCs strongly suggest a glomerular source. Cells that lodge and aggregate in the tubule, enmeshed in Tamm-Horsfall protein, become red-cell casts — pathognomonic of glomerular bleeding.[5]

Urological bleeding skips the barrier entirely. Blood leaks from capillaries and venules of the renal pelvis, ureter, bladder, prostate or urethra straight into the urinary space, with no mechanical deformation — so the cells look isomorphic (intact, biconcave, uniform). There is no cast formation, because the tubule is upstream of the bleed.[8]

Why the colour is a clue, not a verdict. Bright-red fresh blood implies a lower-tract source with short transit time; brown, tea or cola urine implies older, haemolysed blood — often glomerular, where RBCs lyse in acidic urine — or upper-tract bleeding with longer dwell time. The colour narrows the field, but microscopy remains the pivot.[5]

The named trap — dipstick positive, no red cells

A dipstick that reads positive for blood with no red cells on microscopy is myoglobin or haemoglobin, not haematuria. That dissociation is the single most testable microscopy finding in the topic, and it points straight at rhabdomyolysis or intravascular haemolysis.[5]

The differential of red or brown urine that is NOT haematuria — exclude these before you label it:[1]

• Myoglobin (rhabdomyolysis) — very high CK, muscle pain, a collapse or trauma story.
• Haemoglobin (intravascular haemolysis) — low haptoglobin, raised LDH, fragmented red cells.
• Beetroot (beeturia), rifampicin, phenazopyridine, sulfasalazine — drugs and foods that stain the urine but carry no cells.
• Porphyrins (acute intermittent porphyria), food dyes, anthocyanins.[1]

When the dipstick is positive but the spun sediment is empty, measure creatine kinase and plasma free haemoglobin or haptoglobin — those two tests separate myoglobinuria from haemoglobinuria in a minute.[5]

What you hear and see at the bedside

The history is the single most informative step in haematuria — it localises the site and flags cancer risk before any investigation is ordered. Establish visibility, colour, pain, timing in the stream, clots, associated symptoms and risk factors.[1]

Pain is the cardinal discriminator of urgency. Painless visible haematuria raises the suspicion of malignancy and is the red flag. Painful visible haematuria points to stone (ureteric colic — sudden, severe, loin to groin, nausea and vomiting), infection (dysuria, frequency, urgency, suprapubic pain, fever, sometimes rigors in pyelonephritis), or clot colic (a clot grinding down the ureter and spasming it).[10]

Timing in the stream is the urological triad of site — reproduce it verbatim, it is a guaranteed viva mark.[8]

Ask about clots and clot retention. Clots imply heavier, lower-tract bleeding; vermiform (worm-like) clots suggest upper-tract moulding; clot retention — inability to void with a painful palpable bladder — is a urological emergency.[11]

The associated-symptom cluster that points to the glomerulus: brown or cola urine with oedema, hypertension and oliguria is the nephritic syndrome (IgA nephropathy, post-infectious GN). Ask about a recent sore throat or skin infection — post-streptococcal GN follows by 1 to 3 weeks, whereas IgA nephropathy bleeds synpharyngitically (concurrent with the pharyngitis, no latency). Seek the systemic clues of lupus (rash, arthralgia), vasculitis (sinusitis, haemoptysis) and Alport syndrome (family history of deafness and renal failure).[5]

Bedside and examination. Check blood pressure (hypertension points to a glomerular process), temperature (infection) and postural measurements (anaemia from heavy bleeding). Palpate for a palpable bladder (clot retention), a renal mass (renal-cell carcinoma, polycystic kidneys) and loin tenderness (pyelonephritis, stone). Digital rectal exam in men: smooth enlarged prostate (BPH), nodular hard prostate (cancer), tender boggy prostate (prostatitis). Exclude a local penile, urethral or vaginal source that could contaminate the sample.[8]

Glomerular causes — the nephrology arm

The glomerular arm is the young adult's story: IgA nephropathy, thin basement membrane disease, post-infectious GN and Alport syndrome between them cover most of the questions. Recognise the pattern and the referral writes itself.[5]

IgA nephropathy — the mechanism behind the synpharyngitic bleed. Galactose-deficient IgA1 (Gd-IgA1) is recognised by autoantibodies, forming immune complexes that deposit in the mesangium; mesangial proliferation and complement activation damage the barrier. Mucosal IgA produced during a respiratory infection deposits in the mesangium simultaneously — which is why the bleed and the sore throat arrive together.[5]

Thin basement membrane vs Alport — the discriminator that earns the mark. Both are type-IV collagen diseases (COL4A3 or COL4A4 in thin basement membrane; COL4A5 in X-linked Alport). Thin basement membrane thins the GBM but keeps it structurally intact and benign. Alport splits the GBM progressively and brings deafness, lenticonus and renal failure. The hearing test, the eye exam and the family history settle it.[5]

Post-streptococcal GN — the complement story. Nephritogenic group A streptococci (throat or skin) drive subepithelial immune-complex deposition — the classic 'lumpy-bumpy' membrane — with low C3 that recovers in 6 to 8 weeks. If C3 stays low beyond 8 weeks, think lupus nephritis or membranoproliferative GN.[5]

ANCA vasculitis and anti-GBM are the glomerular emergencies. Pauci-immune or linear IgG deposition along the GBM produces crescentic GN with severe haematuria, proteinuria and a rapidly falling eGFR. Anti-GBM disease may coexist with pulmonary haemorrhage (Goodpasture syndrome). Send ANCA and anti-GBM today and arrange an urgent biopsy — delay causes irreversible scarring.[5]

Urological causes — the cancer arm

The urological arm is the older patient's story, and cancer leads it. Isomorphic red cells, no casts, little or no proteinuria — the work-up is CT urogram plus cystoscopy, full stop.[8]

Bladder cancer — the mechanism of the painless bleed. Urothelial carcinoma grows as a papillary, friable mass that bleeds on its surface; high-grade lesions and carcinoma in situ bleed more diffusely. The bleeding is painless because the tumour has not invaded the muscle. Squamous-cell carcinoma follows schistosomiasis — chronic egg deposition and squamous metaplasia.[7]

Renal-cell carcinoma — the disappearing triad. Flank pain, haematuria and a palpable mass was once the textbook presentation; today most RCCs are found incidentally on imaging. RCC bleeds when tumour invades the collecting system or necrotic tumour erodes a vessel.[4]

Nephrolithiasis — the size-versus-bleed mismatch. Stones cause haematuria by mechanical abrasion of the urothelium, but the bleeding does not track stone size — a tiny migrating stone can produce visible haematuria. The trap: up to 20 per cent of ureteric stones show no haematuria on dipstick, so its absence does not exclude a stone.[11]

BPH — the terminal-bleed story. Androgen-driven stromal and glandular hyperplasia with neovascularisation produces fragile prostatic veins; the bladder neck compresses the prostate at the end of voiding, which is why the bleed classically lands in the terminal stream. Acute retention with catheterisation can precipitate heavy bleeding.[8]

Haemorrhagic cystitis — name the four triggers. Bacterial infection (E. coli), radiation (a late effect, months to years after pelvic radiotherapy), cyclophosphamide (the acrolein metabolite — prevented by mesna), and viral (BK virus, adenovirus in transplant patients). Refractory cases climb an escalation ladder of intravesical alum, formalin, hyperbaric oxygen and internal iliac embolisation.[7]

Investigations — confirm, exclude transient, then branch by microscopy

The strategy is two-branched, but the first two steps are common to every patient: confirm true haematuria and exclude transient causes, then branch by the microscopy pattern and the cancer-risk profile.[3]

Step 1 — confirm and exclude transient causes, in every patient.[10]

• Repeat urinalysis and microscopy on a clean-catch midstream specimen (menstruating women: repeat mid-cycle). A single positive dipstick that is microscopy-negative is not haematuria.
• Exclude infection — urine culture; treat the UTI and re-check urinalysis 4 to 6 weeks after, because transient post-infective haematuria resolves and persistent haematuria does not.
• Exclude transient causes — heavy exercise (re-check after 48 hours of rest), trauma (catheterisation, contact sport), menstruation.
• Document the visibility, the timing in the stream, the clots and the cancer-risk history.[10]

Step 2 — first-line bloods, in all. Urea and electrolytes with eGFR; UACR (urine albumin-to-creatinine ratio) or PCR; FBC (anaemia from bleeding, eosinophilia); coagulation (PT/INR, APTT); CRP or ESR; and a blood pressure.[5]

Step 3 — branch by the microscopy pattern.[6]

Branch A — glomerular pattern (dysmorphic RBCs, casts, proteinuria) goes to nephrology. Send UACR and eGFR; complement C3 and C4 (low C3 with normal C4 in post-infectious GN; both low in lupus and MPGN); ANA and anti-dsDNA (lupus); ANCA, anti-MPO and anti-PR3 (ANCA vasculitis); anti-GBM (Goodpasture); hepatitis B, hepatitis C and HIV serology; serum IgA (raised in 30 to 50 per cent of IgA nephropathy); ASO and anti-DNase B (post-streptococcal). Reserve renal biopsy for nephritic syndrome, nephrotic-range proteinuria, rapidly progressive GN, declining eGFR, or diagnostic uncertainty — it gives the definitive diagnosis and prognosis.[5]

Branch B — urological pattern (isomorphic RBCs) or any visible haematuria goes to urology. CT urogram for the upper tract, cystoscopy for the bladder, urine cytology if high risk.[4]

Imaging the two tracts — CT urogram for the upper, cystoscopy for the bladder

Haematuria imaging is built around two non-negotiable questions: what is in the upper tract, and what is in the bladder. CT urogram answers the first, cystoscopy answers the second, and visible haematuria gets both.[4]

CT urogram — the investigation of choice for the upper tract. Three phases: unenhanced (calcified stones), nephrographic (renal parenchymal masses), and excretory or delayed (upper-tract urothelial tumours as filling defects in the enhanced collecting system). It is the single most comprehensive upper-tract study, but it carries radiation and a contrast-nephropathy risk — check the eGFR first, hydrate, and use low-osmolar contrast with caution in CKD.[4]

Cystoscopy — the gold standard for the lower tract, and the only test that can see, biopsy and resect a bladder lesion. It is mandatory for any visible haematuria and for microscopic haematuria in intermediate- or high-risk patients. Flexible cystoscopy is a well-tolerated outpatient procedure; a systematic review found sensitivity 87 to 100 per cent and specificity 64 to 100 per cent for bladder cancer in adults presenting with haematuria.[7]

Urine cytology — high specificity, variable sensitivity. It is highly sensitive for high-grade tumours and carcinoma in situ but misses low-grade lesions, so it is an adjunct in high-risk patients and for upper-tract surveillance. Negative cytology does not exclude cancer.[7]

When CT is off the table — ultrasound and MR urogram. Renal and bladder ultrasound is a reasonable first line in pregnancy, in young low-risk patients, and where CT is contraindicated (contrast allergy, CKD) — but it is less sensitive for upper-tract urothelial lesions and small renal masses. MR urogram is the cross-sectional option when radiation or iodinated contrast is contraindicated (pregnancy, severe allergy), provided gadolinium is acceptable.[4]

Imaging findings worth carrying on the ward round:[8]

Risk-stratifying asymptomatic microscopic haematuria

Visible or symptomatic haematuria bypasses risk stratification — those patients get cystoscopy and CT urogram regardless. The risk bands apply only to asymptomatic microscopic haematuria, and they decide how hard you push the work-up.[6]

AUA/SUFU 2020 — the American risk bands, reproduced verbatim:[6]

NICE NG12 — the UK suspected-cancer pathway, lower threshold than AUA/SUFU:[1]

• Visible haematuria at any age — 2-week-wait suspected-cancer referral.
• Age 45 and over with unexplained non-visible haematuria — 2-week-wait referral.
• Age 60 and over with unexplained non-visible haematuria and either dysuria or a raised white cell count — 2-week-wait referral.[1]

Confirm persistent before you commit. AUA/SUFU recommends confirming microscopic haematuria on two of three properly collected midstream specimens before invasive work-up, to weed out transient false positives. After a negative work-up, low-risk patients have annual urinalysis; any new visible bleeding or symptom triggers urgent re-evaluation, and smoking cessation is the single biggest thing the patient can do.[4]

Management — clot retention first, then the cause

Most haematuria is painless and not acutely life-threatening — but visible haematuria with clots and retention is a urological emergency. Resuscitate first, then run the cause-specific pathway.[1]

Clot retention — the resuscitation bundle:[10]

• Airway and breathing — oxygen if hypoxic; assess for associated sepsis (pyelonephritis).
• Circulation — IV access, fluid resuscitation for hypovolaemia, group-and-save and crossmatch; transfuse for significant anaemia or haemodynamic instability; correct coagulopathy (reverse warfarin with vitamin K or PCC per INR, hold the DOAC, platelets if thrombocytopenic).
• Clot retention — pass a large three-way Foley catheter and begin continuous bladder irrigation with normal saline; if hand irrigation cannot clear the clots, cystoscopic clot evacuation under anaesthesia with diathermy or laser to bleeding lesions.
• Exclude upper-tract obstruction — rising creatinine or hydronephrosis on ultrasound; JJ stent or nephrostomy if clots or tumour obstruct the upper tract.[10]

The urology escalation ladder for refractory bleeding — climb it stepwise when catheter and irrigation fail:[5]

1. Bedside — three-way catheter, continuous bladder irrigation, manual clot evacuation, correct coagulopathy, transfuse.
2. Cystoscopy — clot evacuation, diathermy or laser fulguration, resection of bladder tumour (TURBT), alum bladder wash.
3. Intravesical therapy — 1 per cent alum (astringent), 1 to 4 per cent formalin under anaesthesia (permanent mucosal fixation, reflux risk), silver nitrate, prostaglandin E1 or tranexamic acid.
4. Radiological or surgical — bilateral internal iliac artery embolisation (or selective superior vesical) for refractory arterial bleeding; nephrostomy or JJ stent for upper-tract obstruction; cystectomy with urinary diversion as last resort for life-threatening radiation cystitis.
5. Adjuvant — hyperbaric oxygen for radiation-induced haemorrhagic cystitis; sodium pentosan polysulfate for interstitial cystitis.[4]

Painless visible haematuria — the cancer pathway. Urgent cystoscopy and CT urogram within the 2-week suspected-cancer window. Do not delay for UTI treatment if cancer is the leading concern — investigate in parallel.[1]

Glomerular haematuria — treat the cause, with an ACE inhibitor or ARB as the backbone.[9]

Urological haematuria — treat the cause, surgery-led.[8]

Acute prostatitis with haematuria — the dose, and the trap. Ciprofloxacin 500 mg PO twice daily for 4 weeks (or trimethoprim 200 mg PO twice daily for 4 weeks); IV ceftriaxone 1 g daily or co-amoxiclav for severe infection. Add tamsulosin 0.4 mg PO daily for bladder-outlet symptoms, and avoid vigorous DRE or prostate massage in acute bacterial prostatitis — it can seed bacteraemia.[8]

Special-population traps

Pregnancy. Common causes are UTI and stones; ultrasound is the first-line imaging to avoid radiation, and MR urogram (without gadolinium) is the safest cross-sectional option if ultrasound is non-diagnostic. Use pregnancy-safe antibiotics (cephalexin, amoxicillin; nitrofurantoin with term caution). Physiological hydronephrosis of pregnancy can mimic obstruction — fever, persistent pain or infection is what demands intervention.[10]

Children. Commonest causes are post-infectious GN, IgA nephropathy, Henoch-Schönlein purpura (IgA vasculitis), hypercalciuria and structural anomalies; refer to paediatric nephrology or urology. Cystoscopy and CT are rarely indicated in isolated microscopic haematuria unless there is visible bleeding, significant trauma or a suspicious mass.[9]

The anticoagulated patient. Bleeding is amplified, but cancer must still be excluded — investigate in parallel with reversing the anticoagulant where indicated. A therapeutic INR is never an acceptable sole explanation. Coordinate with haematology for peri-procedural bridging (DOAC hold 24 to 48 hours; warfarin hold 5 days with bridging LMWH if high thrombotic risk).[1]

The immunocompromised or transplant patient. Broaden the differential to BK polyomavirus nephropathy, adenovirus, cytomegalovirus, opportunistic infection (fungal, mycobacterial) and post-transplant lymphoproliferative disorder. Immunosuppression may mask fever; keep a low threshold for biopsy and targeted PCR (BK viral load, adenovirus PCR). Post-transplant haematuria may mean ureteric stricture, BK nephropathy, T-cell rejection, transplant renal-cell carcinoma or viral cystitis.[9]

Sickle cell disease or trait. Renal papillary necrosis causes haematuria through ischaemic injury of the medulla; manage with hydration and analgesia, and avoid NSAIDs where possible. Papillary necrosis also appears in diabetes, analgesic nephropathy and tuberculosis.[9]

Loin pain haematuria syndrome — the diagnosis of exclusion. Recurrent flank pain with microscopic haematuria in young women, only after stones, tumour, obstruction and glomerular disease are all excluded. Managed with analgesia, hydration and an ACE inhibitor; the long-term renal prognosis is favourable.[5]

What you miss — and the traps that cause it

The complications of inadequate investigation are the real exam answers.[5]

• Missed early malignancy — the principal and most dangerous failure; a delayed bladder or renal cancer diagnosis worsens survival.
• Progressive CKD from untreated glomerular disease (IgA nephropathy with heavy proteinuria, vasculitis).
• Obstructive uropathy and AKI from clot retention or papillary or tumour obstruction of the upper tract.[5]

Classic diagnostic errors — each one is an exam question:[8]

• Attributing visible haematuria to UTI, BPH or anticoagulation without CT urogram and cystoscopy — the cardinal pitfall.
• Treating a glomerular disease as urological — the IgA nephropathy patient sent for cystoscopy instead of nephrology and biopsy.
• Missing schistosomiasis in an endemic-region patient with terminal-stream haematuria.
• Not repeating a transient (exercise, UTI, menstruation) haematuria before labelling it pathological.
• Forgetting cytology in high-risk patients with carcinoma in situ, which may be invisible on imaging and even on white-light cystoscopy.
• Accepting a therapeutic INR as the cause of painless visible haematuria without a cancer work-up.
• Missing urinary TB in a patient with sterile pyuria and haematuria from an endemic region.[8]

Prognosis and disposition

Prognosis tracks the underlying cause — early cancer caught through a haematuria work-up is often localised and treatable; glomerular disease spans benign to progressive; transient causes resolve fully.[1]

• Urological malignancy caught early — localised bladder cancer has a 5-year survival over 80 to 90 per cent, falling dramatically once muscle-invasive or metastatic. Early cystoscopy and CT urogram save lives.
• IgA nephropathy — 20 to 40 per cent progress to ESRD over 20 to 25 years, predicted by proteinuria, hypertension, eGFR at diagnosis and biopsy lesions (the MEST-C score).
• Thin basement membrane disease is benign with normal life expectancy; post-infectious GN in children usually resolves completely; Alport syndrome progresses to ESRD, timing by genotype.
• Transient causes (infection, exercise, menstruation, catheter trauma) resolve fully once the trigger is removed.[9]

Disposition:[6]

• Painful visible haematuria with clot retention — admit for catheter and irrigation; urgent urology.
• Painless visible haematuria — urgent suspected-cancer referral (within 2 weeks per NICE NG12) for cystoscopy and CT urogram.
• Glomerular-pattern haematuria with nephritic syndrome or declining eGFR — urgent nephrology referral; consider biopsy.
• Low-risk asymptomatic microhaematuria with a negative work-up — repeat urinalysis annually; shared decision on further imaging.[6]

Ward-round test

Stem 1 — the smoker with red urine. A 64-year-old 40-pack-year smoker on apixaban for atrial fibrillation has three days of painless visible haematuria. What is the single most important sentence in his management, and what must you never attribute the bleed to?[1]

Stem 1 — painless visible haematuria (answer)

Painless visible haematuria in an adult is cancer until proven otherwise — urgent cystoscopy and CT urogram within the NICE NG12 2-week-wait. Never attribute it to the apixaban alone: anticoagulants do not cause de novo haematuria, they reveal underlying pathology, often cancer. Investigate the cancer in parallel with any necessary coagulation correction. Confirm true haematuria by microscopy, secure IV access, check FBC, coagulation and eGFR, and refer.[1]

Stem 2 — the dipstick trap. A 28-year-old collapses after a marathon with cola-coloured urine; the dipstick is strongly blood-positive but microscopy shows no red cells. What is the diagnosis, what confirms it biochemically, and what is the fluid target?[5]

Stem 2 — rhabdomyolysis (answer)

Rhabdomyolysis with pigment nephropathy. The dissociation — dipstick positive for blood, no red cells on microscopy — is myoglobin. Send a creatine kinase (expect thousands), lactate dehydrogenase and haptoglobin to separate myoglobinuria from haemoglobinuria. Treat with aggressive isotonic saline to a urine output of 200 to 300 mL/h until CK falls, and manage hyperkalaemia and compartment syndrome. The same dissociation in an older patient with jaundice would be haemoglobinuria from intravascular haemolysis — low haptoglobin, raised LDH.[5]

Stem 3 — the glomerular pattern. A 22-year-old presents with smoky brown urine, periorbital oedema and blood pressure 160/95, two weeks after a streptococcal sore throat. Microscopy shows dysmorphic RBCs and red-cell casts; C3 is low. Name the diagnosis, the timeline and the complement recovery.[5]

Stem 3 — post-streptococcal glomerulonephritis (answer)

Post-streptococcal glomerulonephritis. The 1 to 3 week latency after a streptococcal throat (or impetigo) infection, the nephritic syndrome (oedema, hypertension, oliguria, cola urine), dysmorphic RBCs and red-cell casts, and a low C3 fit perfectly. ASO and anti-DNase B are raised. Management is supportive — control blood pressure and fluid overload (fluid restriction, furosemide 20 to 40 mg PO daily), treat the infection with penicillin, and dialyse only for severe AKI, hyperkalaemia or overload. C3 normalises in 6 to 8 weeks; if it stays low beyond that, think lupus nephritis or membranoproliferative GN.[5]

Stem 4 — the risk band. A 55-year-old female ex-smoker (20 pack-years) has 18 RBC/HPF on two of three midstream specimens, no symptoms, normal blood pressure and renal function. Which AUA/SUFU risk band, and what work-up?[6]

Stem 4 — intermediate-risk AMH (answer)

Intermediate risk — age 40 to 59 (women), 11 to 25 RBC/HPF, and 10 to 30 pack-years each place her here. Work-up is cystoscopy and renal ultrasound, escalating to CT urogram if the ultrasound is non-diagnostic or symptoms develop. Confirm on two of three specimens first (already done). After a negative work-up she has annual urinalysis and smoking cessation advice; any new visible bleeding or symptom triggers urgent re-evaluation. NICE NG12 in the UK would 2-week-wait her because she is 45 and over with unexplained non-visible haematuria — the UK threshold sits lower than AUA/SUFU by design.[6]

Rapid viva checklist

1. Definition — visible vs non-visible (more than 3 RBC/HPF on microscopy, not dipstick)
2. The glomerular-vs-urological split and its microscopy discriminator
3. Painless visible haematuria is cancer until proven otherwise
4. The dipstick-positive-no-RBCs trap (myoglobin or haemoglobin)
5. AUA/SUFU risk bands and NICE NG12 thresholds
6. CT urogram for the upper tract; cystoscopy for the bladder
7. Glomerular causes — IgA, thin BM, post-strep, Alport — and their discriminators
8. Clot retention bundle and the urology escalation ladder
9. Special populations — pregnancy, children, anticoagulated, transplant
10. Three exam traps (blaming the anticoagulant; UTI-as-discharge diagnosis; missing CIS on cytology)[1]

Coverage self-check

If you cannot answer any ward-round stem from this page alone, re-read the matching section. The page is built to be self-sufficient for final-prof, NEET-PG, INICET, USMLE and PLAB questions on Haematuria (Evaluation).[1]

References

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2. [2]Griffiths TR Current perspectives in bladder cancer management Int J Clin Pract, 2013.PMID 23137019
3. [3]Linder BJ, Bass EJ, Mostafid H, Boorjian SA. Guideline of guidelines: asymptomatic microscopic haematuria BJU Int, 2018.PMID 28921833
4. [4]Taylor JI, Souter LH, Barocas DA, et al. Diagnostic Imaging in the Evaluation of Asymptomatic Microhematuria: Systematic Review and Meta-analysis J Urol, 2023.PMID 36883858
5. [5]Saha MK, Massicotte-Azarniouch D, Reynolds ML, et al. Glomerular Hematuria and the Utility of Urine Microscopy: A Review Am J Kidney Dis, 2022.PMID 35777984
6. [6]Barocas DA, Boorjian SA, Alvarez RD, et al. Microhematuria: AUA/SUFU Guideline J Urol, 2020.PMID 32698717
7. [7]Devlies W, de Jong JJ, Hofmann F, et al. The Diagnostic Accuracy of Cystoscopy for Detecting Bladder Cancer in Adults Presenting with Haematuria: A Systematic Review from the European Association of Urology Guidelines Office Eur Urol Focus, 2024.PMID 37633791
8. [8]Sandhu JS, Bixler BR, Dahm P, et al. Management of Lower Urinary Tract Symptoms Attributed to Benign Prostatic Hyperplasia (BPH): AUA Guideline Amendment 2023 J Urol, 2024.PMID 37706750
9. [9]Rovin BH, Adler SG, Barratt J, et al. KDIGO 2021 Clinical Practice Guideline for the Management of Glomerular Diseases Kidney Int, 2021.PMID 34556256
10. [10]Gupta K, Hooton TM, Naber KG, et al. International clinical practice guidelines for the treatment of acute uncomplicated cystitis and pyelonephritis in women: A 2010 update by the Infectious Diseases Society of America and the European Society for Microbiology and Infectious Diseases Clin Infect Dis, 2011.PMID 21292654
11. [11]Skolarikos A, Geraghty R, Somani B, et al. European Association of Urology Guidelines on the Diagnosis and Treatment of Urolithiasis Eur Urol, 2025.PMID 40268592