Bone marrow oxalosis: An unusual cause of cytopenia in end-stage renal disease; report of two cases

Systemic oxalosis can be either primary or secondary hyperoxaluria. Oxalosis is a phenomenon in which calcium oxalate crystals deposit in various visceral organs leading to bone marrow (BM) failure and recurrent renal stones. We describe two rare cases of BM oxalosis. Hyperoxaluria is strongly associated with nephrolithiasis and nephrocalcinosis. Both the patients presented with recurrent renal stones and a variable degree of BM failure. BM oxalosis should be considered as a possible diagnosis in patients in recurrent nephrolithiasis and cytopenia.

Pulmonary Oxalosis Caused by Aspergillus Niger Infection / 결핵

The Aspergillus species produces metabolic products that play a significant role in the destructive processes in the lung. We experie nced a case of chronic necrotizing pulmonary aspergillosis caused by an Aspergillus niger infection, which contained numerous calcium oxalate crystals in the necrotic lung tissue. A 46-year-old man, who had a history of pulmonary tuberculosis, presented with high fever, intermittent hemoptysis and pulmonary infiltrations with a cavity indicated by the chest radiograph. Despite being treated with several antibiotics and anti-tuberculosis regimens, the high fever continued. The sputum cultures yielded A. niger repeatedly, and intravenous amphotericin B was then introduced. The pathological specimen obtained by a transbron chial lung biopsy revealed numerous calcium oxalate crystals in a background of acute inflam matory exudates with no identification of the organism. Intravenous amphotericin B was con tinued at a total dose of 1600 mg, and at that time he was afebrile, although the intermittent hemoptysis continued. On the 63rd hospital day, a massive hemoptysis (about 800 mL) developed, which could not be controlled despite embolizing the left bronchial artery. He died of respiratory failure the next day. It is believed that the oxalic acid produced by A. niger was the main cause of the patient's pulmonary injury and the ensuing massive hemoptysis.

A Case of Acute Renal Failure by Oxalate Poisoning / 대한신장학회잡지

We experienced a case of acute renal failure by oxalate poisoning in a 44-year-old Korean woman. She presented with hematemesis and epigastric pain after drinking of oxalate in a suicidal attempt. After admission, acute renal failure was developed and the patient was treated with hemodialysis. On renal biopsy, there were numerous calcium oxalate crystals which appeared clearly in Hematoxylin-eosin stained sections and were refractile under polarized light microscope. We report a case of acute renal failure by oxalate poisoning with review of the literature.

Primary Oxalosis: A case report

Primary oxalosis is a rare genetic disorder caused by a deficiency of the peroxisomal enzyme alanine-glyoxylate aminotransferase(type I) and D-glyceric dehydrogenase(type II). It is characterized by the triad of radiopaque urolithiasis, nephrocalcinosis, and latered renal function. We report a case of primary oxalosis in a 10-year-old Korean girl. She presented with chronic renal failure at 9 years of age. Ultrasonographic examination revealed bilateral, multiple renal and ureteral stones. Removed stones were chemically analysed to be composed of calcium oxalate. She underwent renal transplantation after prolonged period of dialysis. Removed kidneys were firm and gritty. Cut sections showed numerous tiny yellow sandy stones and a large staghorn stone. Specimen X-ray also exhibited disseminated fine granular and often coalescent radiopaque materials throughout the cortex and medulla. Microscopically numerous varying-sized crystals were noted in the kidney in globular or rhomboid appearance. The crystals were semitranslucent and doubly refractile under the polarized light. Diffuse interstitial fibrosis and chronic inflammation as well as glomerular obsolescence were also noted. The oxalate deposit was diffuse and marked, and was thought to be intimately related to the parenchymal damage and fibrosis.