Acute kidney injury with oxalate deposition in a patient with a high anion gap metabolic acidosis and a normal osmolal gap.

BACKGROUND: Ethylene glycol ingestion can lead to acute kidney injury from tubular deposition of oxalate crystals.  The diagnosis of ethylene glycol intoxication is based on a history of ingestion, clinical examination, high anion gap metabolic acidosis, high osmolal gap, and a measured serum level of ethylene glycol.  However, depending on the delay in time from ingestion to arrival to a hospital, the osmolal gap may become normal, thereby creating a confusing clinic picture for the treating clinician. CASE: A 71 year-old man with a history of alcohol abuse had been unconscious for an unknown period of time.  Upon hospitalization, he was found to have a high anion gap metabolic acidosis but a normal serum osmolal gap and subsequently developed acute kidney injury.  The serum lactic acid and glucose levels were unremarkable, and there were no ketones in the serum. Urine analysis showed numerous red blood cells and calcium oxalate crystals.  The renal biopsy showed multiple oxalate crystals in the renal tubules demonstrating birefringence under polarized light. Given the history of alcohol abuse, the clinical presentation, the unexplained high anion gap metabolic acidosis, and the biopsy findings, ethylene glycol intoxication was deemed the most likely diagnosis. CONCLUSIONS: In cases of ethylene glycol intoxication, a high serum osmolal gap is supportive of ethylene glycol intoxication, but a normal serum osmolal gap does not exclude the diagnosis, especially when the time of ingestion is unknown. Physicians should be aware of potentially normal serum osmolal gap values in cases of ethylene glycol intoxication.

Serum amyloid A renal amyloidosis in a chronic subcutaneous ("skin popping") heroin user.

BACKGROUND: Systemic AA amyloidosis is a long-term complication of several chronic inflammatory disorders. Organ damage results from the extracellular deposition of proteolytic fragments of the acute-phase reactant serum amyloid A (SAA) as amyloid fibrils. Drug users that inject drug by a subcutaneous route ("skin popping") have a higher chance of developing secondary amyloidosis. The kidneys, liver, and spleen are the main target organs of AA amyloid deposits. More than 90% of patients with renal amyloidosis will present with proteinuria, nephrotic syndrome, or renal function. CASE PRESENTATION: A 37 year-old female presented to the hospital with a one-week history of pain and redness in her right axilla. Her relevant medical history included multiple skin abscesses secondary to "skin popping", heroin abuse for 18 years, and hepatitis C. The physical examination revealed "skin popping" lesions, bilateral costovertebral angle tenderness, and bilateral knee swelling. The laboratory workup was significant for renal insufficiency with a serum creatinine of 5 mg/dL and 14.8 grams of urine protein per 1 gram of urine creatinine. The renal biopsy findings were consistent with a diagnosis of renal amyloidosis due to serum amyloid A deposition and acute tubulointerstitial nephritis. CONCLUSIONS: AA renal amyloidosis among heroin addicts seems to be associated with chronic suppurative skin infection secondary to "skin popping". It is postulated that the chronic immunologic stimulation by one or more exogenous antigens or multiple acute inflammatory episodes is an important factor in the pathogenesis of amyloidosis in these patients. Therefore, AA renal amyloidosis should always be considered in chronic heroin users presenting with proteinuria and renal impairment.