Renal biopsy case Niels Marcussen Odense University Hospital Denmark

Case history 77-year-old male was in January 2010 operated for colon adenocarcinoma. For many years he has been treated for hypertension with beta-blockers, diuretics and alfa-blockers. In April 2010 he underwent colonoscopy which did not show any signs of recurrent disease. Prior to the colonoscopy, he was orally given sodium phosphate (OSP) bowel purgative.

Case history II Two weeks later he was again admitted to hospital due to intestinal bleeding. At the time of admission his s-creatinine was 700  mol/l and after rehydration 450  mol/l. Proteinuria 1.1 g/d. No hyperphosphatemia or hypercalcemia. A renal biopsy was done in May 2010.

Immunofluorescense (normal) and Electron microscopy

Acute Phosphate Nephropathy (APhN) Described in 2003 by S. Desmeules et al. (N Engl J M 349:1006, 2003) Two weeks after ingesting phosphosoda a 71-year-old woman presented with malaise and elevated s- creatinine. Analysis of the renal biopsy by X-ray dispersion spectrum: Desmeules et al. 2003

Pathogenesis of APhN Massive phosphate intake Diarrhea-induced hypovolemia Decreased proximal tubular reabsorption of phosphate, especially following second dose of OSP Hypovolemia leads to salt and water reabsorption in the tubules Marked increase in Ca-Ph product in the distal tubular lumen Markowitz and Perazella KI 76: , 2009

Risk factors for APhN Advanced age Female gender Lower body weight Chronic renal disease Hypertension ACE-inhibitors, Angiotensin-receptor blockers, diuretics

Case II 77-years-old woman with known hypertension, treated with Ca-antagonist and diuretics was admitted with increased s- creatinine (224  mol/l). 3 months prior to admission her s- creatinine was 54  mol/l. The patient had 2 months prior to admission received OSP. Urine stix was negative for blood, 1+ for protein og 2+ for leucocytes. No hypercalcemia or hyperphosphatemia. Ultrasound normal. Renal biopsy was performed.

Clinical outcome Markowitz et al and 2009: 21 patients – 4 progressed to end-stage renal failure. – 16 declined in s-creatinine to a mean of about 210  mol/l – 4 reached a creatinine of less then 176  mol/l No one returned to baseline.

APhN, pathological changes Acute changes (up to 3 weeks): – Acute tubular degenerative changes – Interstitial edema – Abundant tubular calcium phosphate deposits Chronic changes (after 3 weeks): – Tubular atrophy – Interstitial fibrosis – Abundant tubular calcium phosphate deposits

Acute phosphate nephropathy Diagnostic criteria: – AKI – Recent exposure to OSP bowel purgatives – Renal biopsy with characteristic findings – No hypercalcemia – No other known significant renal injury Markowitz & Perazella- Kidney Int 76:1027, 2009