Retained solute and impaired tubular function cause a large diuresis after decompression
Expansion
After relieving bilateral obstruction, urine output can exceed 200 ml an hour. Causes:
Physiological (appropriate)
- Excretion of retained urea, causing an osmotic diuresis
- Excretion of retained sodium and water accumulated during obstruction
- This component is self-limiting
Pathological
- Tubular damage impairing sodium reabsorption
- Impaired concentrating ability, from a washed-out medullary gradient and downregulated aquaporins
- This component can cause genuine hypovolaemia and electrolyte loss
Management: monitor weight, urine output and electrolytes closely, and replace about half of the urine output with hypotonic fluid rather than matching it litre for litre, which would perpetuate the diuresis. Correct potassium, magnesium and phosphate.
Obstruction also has longer term effects worth remembering: impaired concentrating ability, distal renal tubular acidosis and hyperkalaemia may persist for weeks, and prolonged obstruction causes irreversible fibrosis.