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An 80-year-old man presented to the emergency department after a fall at home. Serum studies demonstrated an anion and osmolal gap. Examination of the urine sediment showed calcium oxalate monohydrate crystals, suggestive of ethylene glycol toxicity.

A 59-year-old man with diabetes mellitus Type II, arterial hypertension and depressive disorder was hospitalized due to unexplained severe inebriation followed by sedation. Regular medications consisted of metformin 1500 mg, enalapril 20 mg and paroxetine 20 mg. Blood tests showed a creatinine of 0.9 mg/dL (79 μmol/L), glucose 110 mg/dL (6.1 mmol/L) and potassium 6.4 mmol/L. Blood gas test showed a pronounced metabolic acidosis, with pH 7.04, bicarbonate 3 mmol/L, PCO2 10 mmHg, lactic acid 4.8 mmol/L, Na 145 mmol/L, chloride 105.4 mmol/L and anion gap 43 mmol/L. Cerebrospinal fluid analysis and cerebral computerized tomography scan were normal. The patient’s condition, including cognitive status, was rapidly deteriorating, requiring orotracheal intubation. Anuria developed in the following few hours, requiring the referral to our hospital. Laboratory data confirmed the high anion gap metabolic acidosis and showed a serum creatinine of 3.8 mg/dL (336 μmol/L). Renal replacement therapy was soon initiated with continuous venovenous haemodiafiltration; after 21 h acid–base status was normalized, but anuria persisted requiring intermittent haemodialysis. Examination of urine sediment (Figure 1) showed both needle-shaped and dumbbell-shaped calcium oxalate monohydrate crystals; these crystals are considered a clue to ethylene glycol poisoning since oxalate derives from the metabolism of ethylene glycol [1, 2]. Furthermore, renal damage most likely results from a crystal-induced injury to proximal tubule cells [3]. Fig. 1. Urine sediment showing both needle-shaped and dumbbell-shaped (upper right side) calcium oxalate dihydrate crystals. The coma lasted 2 weeks; upon regaining consciousness the patient admitted to having ingested automobile anti-freeze (containing ethylene glycol) in a suicide attempt. Progressive recovery of renal function occurred 4 weeks after admission; renal replacement therapy was interrupted 2 weeks later. A prompt examination of urine sediment, often forgotten in the current ‘high-tech’ medicine, would have suggested the correct diagnosis and allowed administration of fomepizole or ethanol to prevent brain and renal damage.

Ureterocele calculi are developed in cavities with urinary retention but far from the upper renal cavities. The structural features of three ureterocele calcium oxalate stones were observed by scanning electron microscope coupled with X ray microanalysis. The urinary parameters of the three patients were also determined. The stone A consisted of loose structure of large calcium oxalate dihydrate crystals and small spheres of hydroxyapatite. The interior contains disorganized plate-like calcium oxalate monohydrate crystals. The stone B was formed by a compact outer layer of calcium oxalate monohydrate columnar crystals. The structure of stone interior was similar to the stone A. The stone C was formed by concentric layers composed of either calcium oxalate monohydrate columnar crystals or hydroxyapatite. The core consisted of agglomerated calcium oxalate monohydrate crystals, hydroxyapatite and organic matter. From the urinary biochemical data it was deduced that two ureterocele patients (who formed A and B stones) were hypercalciuric (calcium > 300 mg/24 h), being 6.5 the urinary pH value of the patient that formed the A stone, and 7.0 the urinary pH of the patient that formed the C stone. The rest of urinary parameters for the three patients were normal. Thus, one of the requisite conditions for unattached stone development is the existence of a place inside the urinary tract where the solid particles that act as calculus initiator of the stone can be retained enough time to exert this action.

This 73-year-old man presented with a self-inflicted stab wound, plasma ethanol level of 27 mg per deciliter, and a pH of 6.91. Analysis of the urine showed calcium oxalate monohydrate crystals. Free crystals were extensive.

Crystal-induced membranolysis of human red blood cells has been quantltated for calcium oxalate monohydrate and calcium oxalate dihydrate crystals. Calcium oxalate monohydrate crystals are significantly more membranolytic than calcium oxalate dihydrate crystals at constant surface area. If the crystal morphology of calcium oxalate monohydrate is altered by grinding, the lytic potential at constant surface area is markedly reduced. However, altered calcium oxalate dihydrate crystals are as lytic as natural calcium oxalate dihydrate crystals at constant surface area. Differences in the calcium oxalate monohydrate and dihydrate crystal structures, specifically the structural characteristics of the disordered water channel in calcium oxalate dihydrate, can explain these different membranolytic characteristics.

Studies of calcium oxalate crystals in urine suggest similarities to crystal growth in calcium oxalate renal calculi. Previous reports indicate that urinary crystals in patients in whom stones form are larger than those in normal subjects. We report herein a study on crystal size by structure and habit (shape) based on direct microscopic measurement of crystals in the urine of 27 normal subjects and in 6 of 22 patients in whom stones form. The mean size of all crystals in normal subjects is 12.0 plus or minus 7.8 µm. Calcium oxalate monohydrate crystals are significantly smaller than calcium oxalate dihydrate (p less than 0.01). In 22 patients with stones there was no correlation between crystalluria and severity or duration of disease. The mean crystal size in 6 patients did not support the conclusion that patients in whom stones form excrete larger crystals than normal subjects.

Previous studies have shown that magnesium deficiency accelerates renal tubular calcium oxalate monohydrate deposition in rats on chronic hyperoxaluric, lithogenic protocols. The present study was conducted to investigate the effect of magnesium deficiency on intratubular calcium oxalate formation in rats from the 1st day of administration of a hyperoxaluric agent. The objectives were to delineate early ultrastructural features of the formation, mechanisms of retention, and development of renal tubular crystal deposits and to characterize the crystalluria in rats on the hyperoxaluric/hypomagnesuric protocol. Intratubular calcium oxalate monohydrate deposits were found in magnesium deficient rats after only 24 hours of ad libitum administration of 1 per cent ethylene glycol drinking water. Animals on regular food diet did not display renal tubular deposition after 11 days of ethylene glycol administration. Strand- and sheet-like organic material emanating from the luminal wall of the tubules was adherent to the crystals, thereby serving to immobilize them within the tubule. Calcium oxalate monohydrate crystals predominated in the urines of hyperoxaluric/hypomagnesuric animals with intratubular deposits while dihydrate crystals were the primary constituent of urines from rats administered ethylene glycol alone (no intratubular deposition). The results support the supposition that under certain conditions magnesium deficiency is a significant risk factor for intrarenal calcium oxalate deposition and stone formation. Furthermore the identification of calcium oxalate monohydrate crystalluria may be an important indicator of the propensity toward intranephronic calcium oxalate formation and urolithiasis.

Rat renal inner papillary collecting tubule cells (RPCT) have been isolated and maintained in primary culture. The cells have been found to be of only one type and they have maintained the characteristics of RPCT cells. The RPCT cells in culture appear as a monolayer with intermittent clumps of rounded cells. When small calcium oxalate monohydrate crystals (COM) or calcium oxalate dihydrate crystals (COD) are added to the monolayer of RPCT cells, the crystals bind on or about these clumps of rounded-up cells. The use of this system as a model for the study of crystal membrane interactions in crystalluria and urolithiasis is discussed. (J. Urol., 138: 640–643, 1987)

We report a case of primary oxalosis in a 4-year-old boy with intensive deposition of calcium oxalate monohydrate crystals in the kidney and the myocardium. In addition severe fibroplastic inflammatory reaction in form of intensive myocarditis was found. It is an extremely rare complication at this age and represents a particularly rare case of oxalosis. Disorders of oxalate metabolism are discussed in relation to extrarenal deposition of oxalate crystals.