The renal biopsy showed tubular injury and interstitial fibrosis with tubular and interstitial non-polarizable calcifications. Renal tubular / interstitial calcifications are most commonly either calcium phosphate or calcium oxalate. A key differential point is that calcium oxalate crystals, as often seen in other cases [image 8, image 9, image 10] are polarizable whereas calcium phosphate is not. "Nephrocalcinosis" applies specifically to the damage caused by calcium phosphate and can occur as a result of numerous hypercalcemic states, such as hyperparathyroidism, vitamin D intoxication, milk-alkali syndrome, or hypercalcemia of malignancy (Markowitz 2007). Thus, both a thorough clinical history and clinical correlation are needed to confirm the etiology of the nephrocalcinosis.
As is the case with many patients undergoing renal biopsies, the history and medication list can be complicated, with numerous potential sources of renal injury that need to be evaluated individually. Remicade (Infliximab / anti-TNF-alpha monoclonal antibody) has been reported to be associated with a variety of proliferative / immune complex / necrotizing / crescentic glomerular disorders, but in this biopsy there was no evidence of such glomerular injury. What glomerular injury was observed (focal partial global glomerular collapse and podocyte injury) in the absence of significant proteinuria suggested the possibility of subacute glomerular injury, possibly ischemic. The underlying chronic vascular disease with 25% glomerular obsolescence was unlikely to account for the acute renal failure. The most likely relevant piece of history in this patient is the colonoscopy requiring bowel preparation with oral sodium phosphate solution (OSPS).
OSPS is the most widespread agent for colonoscopy bowel cleansing in the United States because it does not require large volumes of fluid ingestion and thus is more tolerable for the patient. However, several reports of renal failure following oral sodium phosphate bowel preparation have now been published (Desmeules et al., 2003; Markowitz et al., 2004; Markowitz et al., 2005; Gonlusen et al., 2006). The pathogenesis of renal tubular injury after OSPS ingestion appears to be the result of intestinal absorption and renal excretion of the sodium phosphate, during which some of the phosphate interacts with calcium and forms crystals within the tubular lumen. It has been calculated that up to 4 liters of water would have to be co-ingested to prevent such crystal formation (Patel et al., 2007), thereby eliminating one of the chief advantages to OSPS use.
Herein we have reported an additional case of renal failure following OSPS administration for colonoscopy. Although the overall rate of renal complications with OSPS is unknown, it is likely low given that this phenomenon has only recently been described. Still, it is important for clinicians and renal pathologists to be aware of this, and serves as an example of the importance of obtaining a thorough clinical history, including all prescription and non-prescription medications and substance use.
Contributed by Craig Horbinski, MD, PhD and Sheldon Bastacky, MD