• 2 Kidneys lie retroperitoneally at level of T12–L3 vertebrae. Left kidney somewhat more superior than the right. On average 11 cm in length, 6 cm wide and 3 cm thick. Composed of inner cortex, outer medulla, calyces, pelvis and ureter.
  
• Supplied by renal arteries from aorta. 20% of cardiac output so 1 L blood (600 ml plasma) per minute. 20% is filtered into Bowman’s space. GFR 120 ml/min. Drain into renal veins. GFR depends on BP, renal perfusion, afferent and efferent arteriole tone.

Taking referral/answering bleep

• When did it start? Quantity? Clots? Is patient passing urine or in retention? Is patient pyrexial, pain – cystitis/pyelonephritis? Recent catheterisation? Prostate disease?
  
• Pregnant? Known bladder malignancy? On any anticoagulants? 30% of patients with painless haematuria have a malignancy.

Definitions and causes

• Microscopic haematuria: non-visible haematuria. Two or more red cells per high power field in MSU unrelated to exercise, menses or trauma.
  
• Macroscopic haematuria: visible haematuria.
  
• Haematuria: bleeding from glomerulus to urethra. Can be divided into glomerular and non-glomerular. Glomerular haematuria: usually with proteinuria, hypertension and renal dysfunction. Commonest is IgA Nephropathy, Type IV collagen nephropathy, Alport’s disease. Non-glomerular haematuria: stones, tumour, papillary necrosis.
  
• Investigations: FBC, U&E, CRP, urinalysis. Cystoscopy, intravenous urogram, renal USS. β-hCG. PSA and formal microscopy, culture and sensitivities. False positive dipstick for blood may be seen with menstruation or trauma (exercise or recent sex or local lesions – ulcers, warts). Haematuria, red cell casts, proteinuria – consider glomerulonephritis. CRP/echocardiogram/blood cultures if endocarditis considered (rare). Renal biopsy: to diagnose renal glomerular disease.
  
• Red flags: painless macroscopic haematuria, symptomatic microscopic haematuria in absence of UTI. Age >50, abdominal mass on examination, smokers.

Referral guidance for haematuria

• Urology referral: unexplained macroscopic (visible) haematuria at any age, microscopic haematuria (all ages) with hesitancy, dysuria, frequency or urgency and absence of UTI, persisting asymptomatic microscopic haematuria age 40 or older.
  
• Nephrology referral: microscopic haematuria and ↓eGFR, haematuria and HTN >140/90 mmHg, proteinuria (ACR >30 mg/mmol or PCR >50 mg/mmol), macroscopic haematuria and intercurrent infection, usually chest, family history of renal disease or haematuria.

On arrival

• Indications for admission: look for UTI and coagulopathy. Admit if clot retention, cardiovascular instability, uncontrolled pain, sepsis, acute renal failure, coagulopathy, severe co-morbidity, heavy haematuria or social restrictions. Those not needing admission should drink plenty of clear fluids and return for further medical attention if the following occur: clot retention or worsening haematuria despite adequate fluid intake, uncontrolled pain or fever, or inability to cope at home. Repeat observations and review medications and consider stopping anticoagulants depending on their need. ↓BP or ↑HR may suggest sepsis or haemorrhage.
  
• Follow-up by a urological team ideally within the 2 week cancer referral target. Consider bladder and prostate cancer in those males over 40. In those under 40, cystoscopy may not be mandatory if another cause found.
  
• Significant macroscopic (visible) bleeding can cause clot retention resulting in outflow obstruction and often a three-way catheter irrigation system should be used. In bleeding of this severity, reverse all anticoagulation and get urological advice. Ensure check Hb and replace blood. Will need urgent cystoscopy if persists and imaging of whole renal tract.
  
• Microscopic haematuria (not visible but positive dipstick) and protein consider as UTI. Lack of protein in dipstick could suggest tumour or stones.
  
• Microscopic haematuria and proteinuria consider nephrology and a more medical cause, e.g. glomerulonephritis.

• Taking referral/answering bleep/attending: (attend quickly if low BP, hypoxic, ↑temp, ↑HR, ↑EWS).
  
• Resuscitate if needed: ABC. Oxygen, check BP, HR, temperature. If low BP then get IV access, check bloods and manage as for shock. Cardiac monitor if AKI and hyperkalaemia. Ensure accurate fluid balance chart. Omit antihypertensive on drug chart. Correct any volume loss. If biochemical evidence of AKI then suspend nephrotoxic medications and ensure all drugs have been assessed for correct dose in AKI. In most cases simply increasing oral or IV fluids is sufficient. A cautious fluid challenge of 250–500 ml over 30 min and then repeated should cause some response.
  
• Measure urine output: determine exact urine output and assess patient’s hydration status. Quantify input oral and IV and losses in the past few days. Weight changes are useful: 1 kg = 1 L.
  
• Reduced urine output: oliguria: <500 ml/day urine output (which is about 20 ml/h). Oliguria is usually pre-renal but may be renal. If pre-renal and patient is dry then give fluids, e.g. 500 ml IV NS over 1 h and review. If the patient has poor intake and is not in heart failure then further fluids needed to improve urine output. Oliguria might suggest hypoperfusion and sepsis or other causes of shock. Attend quickly if low BP, ↑temp, ↑HR, ↑EWS (could be subacute obstruction so consider bladder scan and catheter). If low BP assess as for ↓BP. If renal cause suspected ask about new drugs or IV contrast for an X-ray or angiogram that could precipitate or cause AKI. Is there rhabdomyolysis or severe infection? Check bloods and lactate and possible venous blood gases if AKI. Seek help.
  
• No urine: anuric think obstruction first. Has patient any suprapubic pain or is catheter blocked or is it acute retention? Reasonable to ask staff to flush or change the catheter if one is in place. Bladder scan will tell you if bladder full or empty and then catheterise. If obstruction still considered, then a renal USS is usually diagnostic. The question is at what level: is it urethra, prostate, bladder, ureters, renal? Those with post-renal causes need to be discussed with urology for surgical or radiologically placed drainage before definitive management.
  
• Differential: recording error – fluid balance underestimates urine output. Pre-renal failure – oliguria and recent ↓BP. Cardiogenic, haemorrhagic shock, sepsis, obstructive shock. Excessive antihypertensives. Renal – ischaemic, nephrotoxic drugs, nephritis. Post-renal – obstruction at renal pelvis, ureters, bladder, urethra. Stones, tumour, prostate.

• About: AKI has replaced the term ‘acute renal failure’ to emphasis potential reversibility. AKI is a sudden rapid reduction in GFR and there may be oliguria and anuria. Mortality varies from 10 to 80% depending on population studied. About half have sepsis or hypovolaemia and others have obstruction, nephrotoxic drugs and parenchymal renal diseases. Increased length of stay, mortality and expense. Prevalence of AKI is about 5% in hospital patients. A minority need a nephrologist. Most managed by generalists. Only 1% need dialysis.
  
• Aetiology: reduced renal function: impaired control of water and electrolytes. Impaired excretion of drugs and other metabolites. Impaired acid–base control – need to excrete acid load. Impaired BP control, impaired EPO synthesis, impaired vitamin D hydroxylation.
  
• Note: if you suspect vasculitis, e.g. systemically unwell, rash, fever, ↑CRP, pulmonary haemorrhage, send ANCA/anti-GBM and seek nephrology help immediately.

Risk factors for AKI and poor outcome: age >75, CKD (eGFR <60 ml/min/1.73 m2) cardiac failure, liver disease, DM. Peripheral vascular disease, nephrotoxic medication, hypovolaemia, sepsis.

Related posts:

– Gastroenterology emergencies – Endocrine and diabetic emergencies – Hepatobiliary emergencies – Dermatological emergencies – Emergency drugs (use with BNF) – Ophthalmological emergencies

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