Hyperphosphatemia, a Cause of High Anion Gap Metabolic Acidosis: Report of a Case and Review of the Literature.

BACKGROUND Hyperphosphatemia is a common problem in patients with kidney failure. It is usually mild and rarely severe enough to cause metabolic acidosis on its own. Besides kidney failure, use of phosphate containing enemas, rhabdomyolysis, and tumor lysis syndrome are common causes of severe hyperphosphatemia. CASE REPORT A 74-year-old man with a history of diabetes mellitus type II, arterial hypertension, and end stage renal disease, who was on hemodialysis and who had undergone hemicolectomy for ischemic bowel disease, and had not eaten for several days, developed severe metabolic acidosis, with an anion gap (AG) of 31 meq/L, -uncorrected for serum albumin. At that time he had a high level of beta-hydroxybutyrate and severe hyperphosphatemia (16.5 mg/dL). Metabolic acidosis and hyperphosphatemia were corrected with hemodialysis, confirming the role of hyperphosphatemia in the development of high AG metabolic acidosis. CONCLUSIONS Although our patient had many reasons to develop high AG metabolic acidosis, hyperphosphatemia played a significant role in his acidosis. Severe hyperphosphatemia is rarely mentioned as a cause of high AG acidosis. It should be added to the long list of causes of this metabolic disorder. Physiological basis of acid base changes are discussed.

Recurrent Syncope and Cardiac Arrest in a Patient with Systemic Light Chain Amyloidosis Treated with Bortezomib.

About 10-15% of patients with multiple myeloma develop light chain (AL) amyloidosis. AL amyloidosis is a systemic disease that may involve multiple organs, often including the heart. It may present clinically with bradyarrhythmia and syncope. The proteasome inhibitor bortezomib has been used with clinical efficacy in treating patients with AL amyloidosis but also implicated as a possible cause of cardiomyocyte injury. We report a case of a 48-year-old man with AL amyloidosis and increased frequency of syncope and cardiac arrest after starting bortezomib. The biologic and clinical plausibility of a heightened risk for cardiac arrest in patients with cardiac AL amyloidosis and history of syncope being treated with bortezomib is a possibility that is not well documented in the medical literature and warrants further investigation.

Rare and unusual clinicopathologic presentation of renal AL amyloidosis.

Rarely, renal light chain (AL) amyloidosis may present without significant proteinuria owing to glomerular sparing and amyloid deposition confined to the vasculature and tubulointerstitium.