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ULY CLINIC
ULY CLINIC
17 Mei 2025, 12:25:05
Anuria

Anuria is clinically defined as a urine output of less than 100 mL in 24 hours. It is a critical sign often indicating either severe urinary tract obstruction or acute renal failure (ARF) due to various underlying mechanisms. Despite its severity, anuria is relatively rare, as the kidneys typically maintain a minimum urine output of approximately 75 mL daily even in the setting of renal failure.
Pathophysiology and Major Causes
Anuria results from either a failure of urine formation by the kidneys or an obstruction preventing urine excretion. The main categories include:
Pre-renal causes: Severe hypoperfusion leading to acute tubular necrosis (ATN).
Renal causes: Acute tubular necrosis, cortical necrosis, acute glomerulonephritis, vasculitis, hemolytic-uremic syndrome.
Post-renal causes: Urinary tract obstruction at any level, including bladder outlet obstruction, ureteral blockage, or bilateral ureteral obstruction.
Medical causes of Anuria – Summary table 1
Condition / Cause | Typical Urine Pattern | Key Associated Findings |
Acute tubular necrosis | Oliguria → may progress to anuria (before polyuric phase) | Hyperkalaemia (weakness, arrhythmias); uraemia (anorexia, nausea, twitching, seizures, Kussmaul respirations); signs of heart failure (oedema, JVD, crackles, dyspnoea) |
Bilateral cortical necrosis | Abrupt change from oliguria to complete anuria | Gross haematuria, flank pain, fever |
Acute glomerulonephritis | Anuria or severe oliguria | Mild fever, malaise, flank pain, gross haematuria, facial/general oedema, hypertension, headache, pulmonary congestion (crackles, dyspnoea) |
Haemolytic–uraemic syndrome | Early anuria (1–10 days) | Vomiting, diarrhoea, abdominal pain, purpura, melena, fever, hypertension, hepatomegaly, oedema, pallor, URTI signs |
Bilateral renal artery occlusion | Sudden anuria or profound oliguria | Severe continuous upper-abdominal & flank pain, nausea, vomiting, ↓ bowel sounds, fever ≤ 38.9 °C, diastolic hypertension |
Bilateral renal vein occlusion | Occasionally anuria | Acute low-back pain, fever, flank tenderness, haematuria; pulmonary emboli: sudden dyspnoea, pleuritic pain, tachypnoea, crackles |
Severe urinary-tract obstruction | Acute/total anuria (may alternate with dribbling) | Suprapubic fullness, burning or painful voiding, overflow incontinence, flank pain, N/V, fever, chills, cloudy-foul urine |
Systemic vasculitis | Occasionally anuria | Malaise, myalgia, polyarthralgia, fever, hypertension, haematuria, proteinuria, pallor, possible skin lesions (urticaria, purpura) |
Contrast-induced nephropathy | Oliguria → rarely anuria | Recent radiographic contrast exposure; rising creatinine, similar uraemic symptoms |
Drug-induced nephrotoxicity | Oliguria / anuria | Aminoglycosides, heavy metals, anaesthetics, solvents, adrenergics/anticholinergics (retention); symptoms mirror ATN |
Other nephrotoxins (e.g., ethyl alcohol) | Oliguria / anuria | Variable; depends on agent and degree of tubular injury |
Clinical Presentation
Patients with anuria may present with:
Complete absence or severe reduction in urine output.
Symptoms of urinary tract obstruction: lower abdominal or flank pain, bladder distention, burning micturition, overflow incontinence.
Signs of systemic illness or renal failure: edema, hypertension, uremic symptoms (nausea, vomiting, confusion), electrolyte imbalances.
In acute renal failure cases, anuria may be accompanied by:
Hyperkalemia symptoms: muscle weakness, arrhythmias.
Uremia manifestations: anorexia, pruritus, lethargy, seizures.
Signs of volume overload and heart failure: edema, jugular venous distension, crackles on lung auscultation.
Initial assessment and history
A comprehensive history should focus on:
Voiding patterns and recent changes.
Fluid intake and last urine output timing.
Past medical history: kidney disease, urinary tract infections, prostate issues, stones, congenital abnormalities.
Medication history: nephrotoxic drugs or agents that affect bladder function.
Surgical history involving the abdomen, urinary tract, or kidneys.
Physical examination should include:
Vital signs monitoring.
Abdominal inspection and palpation for bladder distension or masses.
Flank examination and percussion over the costovertebral angles.
Auscultation for renal artery bruits.
Neurological examination if neurogenic bladder is suspected.
Diagnostic approach
Bladder catheterization: Attempt immediate catheterization to relieve obstruction and quantify urine output.
Urine volume >75 mL suggests lower urinary tract obstruction.
Urine volume <75 mL may indicate renal parenchymal disease or higher urinary tract obstruction.
Laboratory tests: Serum electrolytes, renal function tests (BUN, creatinine), urinalysis, and markers of infection or hemolysis.
Imaging: Ultrasonography is the first-line to detect obstruction or kidney abnormalities.
If obstruction suspected but unclear, consider cystoscopy, retrograde pyelography, and renal scanning.
Additional renal function studies may be warranted if no obstruction is identified.
Emergency interventions
Relieve obstruction promptly via catheterization or surgical intervention if catheter insertion is not possible.
Initiate fluid management with daily fluid allowance restricted to 600 mL above previous day’s urine output to avoid fluid overload.
Restrict dietary potassium and sodium; provide balanced nutrition with controlled protein intake.
Monitor vital signs, fluid balance, and daily weights closely.
Prepare for nephrostomy or ureterostomy if surgical drainage is needed.
Treat underlying causes such as infection, vasculitis, or thrombotic events accordingly.
Special populations
Neonates: Anuria is absence of urine for 24 hours; may be primary (renal agenesis/dysplasia) or secondary (renal ischemia, thrombosis).
Elderly: Anuria may develop gradually due to underlying pathology, and immobility can reduce ability to void despite urine production.
Prognosis and Follow-up
Anuria is a medical emergency requiring rapid diagnosis and intervention to prevent life-threatening complications such as uremia, electrolyte disturbances, and volume overload. Early identification and treatment of underlying causes can improve outcomes. Long-term follow-up is essential for monitoring renal function recovery and preventing recurrence.
References