What is the diagnosis from this renal biopsy?
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One of the earliest clinical descriptions was in a letter to the New England Journal of Medicine by Dr. Simon Desmeules and co-workers published in 2003. Markowitz has described the pathology - I recommend his paper in JASN. In 2009, I published a case discussion of this topic in Kidney International. The FDA has issued a warning about acute phosphate nephropathy: ""Acute phosphate nephropathy is a form of acute kidney injury that is associated with deposits of calcium-phosphate crystals in the renal tubules that may result in permanent renal function impairment. Acute phosphate nephropathy is a rare, serious adverse event ..."
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Answer from Image Quiz
September 14, 2011: The answer is Acute Phosphate Nephropathy.
Explanation The stain that was used is the von Kossa stain (von Kossa J (1901) Ueber die im Organismus kunstlich erzeugbaren Verkalkungen. Beit Path Anat 29:163). The silver nitrate in the staining solution (silver ion is positive charge) binds with the anionic ionic (negative charge) portion of the salt. The silver ions react with phosphate or carbonate not calcium, by binding the positive silver ion with the negative phosphate or carbonate portion. The resulting silver salt (silver phosphate), will be seen as black.
A 72 year-old female with a history of hypertension had an episode of hematochezia, and underwent outpatient colonoscopy. Internal hemorrhoids were cauterized, and two polyps removed. She had no further bleeding. Two weeks later she developed progressive weakness and presented to the emergency department. Medications included lisinopril 20 mg per day and occasional ibuprofen for joint pain. Physical exam was unrevealing with a normal blood pressure. Laboratory data showed on urine dipstick 1+ protein, but was otherwise negative. The urine sediment on microscopy was bland. Serum creatinine was 3.5 mg/dL (1.0 mg/dL three months previously), BUN 65 mg/dL, K 5.2 mEq/L, calcium 8.5 mg/dL, phosphorus 7.5 mg/dL and albumin 3.8 g/dL.
Renal biopsy performed, examined using a special stain -- shown above.
The picture shows what? What stain was used?
Explanation The stain that was used is the von Kossa stain (von Kossa J (1901) Ueber die im Organismus kunstlich erzeugbaren Verkalkungen. Beit Path Anat 29:163). The silver nitrate in the staining solution (silver ion is positive charge) binds with the anionic ionic (negative charge) portion of the salt. The silver ions react with phosphate or carbonate not calcium, by binding the positive silver ion with the negative phosphate or carbonate portion. The resulting silver salt (silver phosphate), will be seen as black.
One of the earliest clinical descriptions was in a letter to the New England Journal of Medicine by Dr. Simon Desmeules and co-workers published in 2003. Markowitz has described the pathology - I recommend his paper in JASN. In 2009, I published a case discussion of this topic in Kidney International. The FDA has issued a warning about acute phosphate nephropathy: ""Acute phosphate nephropathy is a form of acute kidney injury that is associated with deposits of calcium-phosphate crystals in the renal tubules that may result in permanent renal function impairment. Acute phosphate nephropathy is a rare, serious adverse event ..."
Key Features:
- Characterized by acute and subsequent chronic renal failure following exposure to oral sodium phosphate (OSP) bowel purgatives.
- Renal biopsy findings include acute and chronic tubular injury with prominent tubular and interstitial calcium phosphate deposits.
- The acute tubular degenerative changes involve all tubular segments from proximal to distal to collecting duct and included epithelial simplification, luminal ectasia, loss of proximal tubular brush border, enlarged reparative nuclei with prominent nucleoli, shedding of cellular fragments into the tubular lumina, and dropout of tubular epithelial cells.
- The tubular injury is accompanied by interstitial edema.
- The presence of bundant calcium phosphate deposits in distal tubules and collecting ducts
- The calcifications are located within the cytoplasm of tubular epithelial cells, within tubular lumina, and less prominently within the interstitium.
- Risk factors include older age, female gender, hypertension, chronic kidney disease (CKD), and treatment with angiotensin converting enzyme inhibitors, angiotensin receptor blockers, and diuretics.


