Presentation
In ICU for 1 week with acute confusional state, altered gait, found to have lactate of 33 mmol/L and abdominal pain, which resolved. No ischemic bowel. No clear hypotensive/hypoxic event. Normal initial CT brain.
Patient Data
Prominent bilateral and symmetric swelling and increase T2 signal, with no enhancement and only facilitated diffusion on ADC, is demonstrated. ADC findings presumably are due to subacute imaging.
Case Discussion
The differential on imaging is essentially that of increased T2 signal of the basal ganglia. Of these, toxic and metabolic seem most likely. A CT venogram was also normal.
The patient had developed acute renal impairment. Urine protein 3.7g/L, RBC 50. GN screen: ANCA+ but titer negative. They went on to have a renal biopsy.
Histology:
MICROSCOPIC DESCRIPTION: Light microscopy: The biopsy consists of cortex, with 12 glomeruli in one level, none of which is globally sclerosed. The glomeruli show mild ischemic effects, including mild retraction of the tuft, thickening and wrinkling of glomerular basement membranes. The glomeruli are otherwise unremarkable, with no mesangial expansion, no segmental proliferation, necrosis or sclerosis and no immune type or other deposits. The glomerular basement membranes appear normal, with no reduplication or membranous transformation. There is mild acute tubular injury, with some tubular dilatation, thinning of epithelium, mild reactive changes and occasional sloughed cells. There is also nonspecific cytoplasmic vacuolation in some tubules. Prominent birefringent calcium oxalate crystal deposition in tubules is present. There is no significant inflammatory or giant cell reaction and no interstitial inflammation. There is no interstitial fibrosis / tubular atrophy. A small artery shows minor fibroelastic intimal thickening, without inflammation or acute changes, and arterioles are normal.
Immunoperoxidase: IgG, IgA, IgM, Fibrinogen, C3c, C1q: negative
Conclusion: The features are of acute tubular injury with prominent oxalate deposition. While there is some evidence of glomerular ischemia, the amount of crystal deposition is unusual for ischemic type ATN and toxic etiology is favored. Elucidation of possible causes, including ethylene glycol ingestion, requires clinical correlation. There is no evidence of glomerulonephritis or inflammatory tubulointerstitial process. There is no significant chronic parenchymal damage.
Further collateral history was obtained which confirmed ingestion of ethylene glycol.