Renal biopsy case

Niels MarcussenOdense 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 76:1027-34, 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. 2005 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/lNo 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