Acute Phosphate Nephropathy

Acute phosphate nephropathy is acute or subacute kidney injury caused by deposition of calcium phosphate crystals in the renal tubules and interstitium (nephrocalcinosis), typically after oral sodium phosphate bowel preparation.

• It follows large oral phosphate loads (sodium phosphate solutions or tablets) with a phosphate load of up to 45 g in 24 hours that exceeds renal excretory capacity.
• Risk factors: age above 55 years, female sex, chronic kidney disease, hypovolaemia, hypertension, heart failure, ACE inhibitors, angiotensin receptor blockers, diuretics, NSAIDs, and repeated dosing.
• Rare causes: phosphate enemas in renal impairment, intravenous phosphate, tumour lysis, phosphate supplements, vitamin D toxicity.

Asymptomatic in most; discovered when creatinine rises days to months after bowel preparation.

• Mild proteinuria or bland urine, hypertension, rarely oliguria; non-oliguric kidney injury is typical.
• Acute symptoms of hyperphosphataemia: hypocalcaemia (tetany, paraesthesia), nausea, vomiting.
• Differential diagnosis: acute tubular necrosis, acute interstitial nephritis, contrast nephropathy, volume depletion, glomerulonephritis, obstruction, oxalate nephropathy, hypercalcaemic nephropathy.
• Complications: chronic kidney disease (often permanent, with progression to end stage kidney disease in a minority), electrolyte disorders, nephrocalcinosis, anaemia and hypertension.

History of oral sodium phosphate preparation within 1 to 3 months (up to 6 months), usually with a baseline creatinine for comparison.

• Creatinine and eGFR, electrolytes (high phosphate, low calcium, high or normal potassium), parathyroid hormone, urinalysis (usually bland with mild proteinuria), ultrasound (normal or echogenic kidneys; nephrocalcinosis may be visible on CT).
• Renal biopsy shows tubular and interstitial calcium phosphate deposits (basophilic, von Kossa positive) with tubular atrophy and fibrosis; biopsy is needed if the picture is atypical.
• Exclude other causes of kidney injury.

Supportive

• In established cases, give fluids to correct volume depletion (0.9 percent saline 1 L over 4 to 6 hours guided by volume status), stop nephrotoxins (NSAIDs, ACE inhibitors, angiotensin receptor blockers, diuretics), and avoid further phosphate exposure.

Pharmacological

• No specific drug; manage electrolytes: hypocalcaemia (calcium gluconate 10 percent 10 mL IV slowly if symptomatic), hyperphosphataemia (calcium carbonate 500 mg to 1 g with meals; avoid aluminium), hyperkalaemia (calcium gluconate, insulin with glucose, salbutamol).
• Blood pressure control after volume restored.

Procedures: dialysis for refractory hyperkalaemia, acidosis, fluid overload or uraemia.

Prevention:

• Avoid oral sodium phosphate preparations in high risk patients (age above 55 years, kidney disease, dehydration, hypertension, heart failure, and drugs affecting kidney perfusion).
• Use a polyethylene glycol preparation: 4 L split dose (2 L the evening before and 2 L on the morning of the procedure), or 2 L plus a stimulant laxative such as bisacodyl 10 mg.
• Encourage oral fluids before and after bowel preparation; do not repeat within 7 days.

Special groups: elderly and diabetic patients (polyethylene glycol only), pregnancy (polyethylene glycol).

Red flags: oliguria, hyperkalaemia above 6.0 mmol/L, symptomatic hypocalcaemia, creatinine doubling.

Follow-up: creatinine and eGFR at 1 to 2 weeks, 3 months and 6 to 12 months; chronic kidney disease care when function does not recover.