Biomedical subjects
Publications and source records attributed to E Bourke.
Mesangiocapillary glomerulonephritis due to mixed essential cryoglobulinaemia is reported in association with unilateral renal papillary necrosis. This previously unreported manifestation of cryoglobulinaemia supports the vascular theory of aetiology of papillary necrosis.
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The renal papilla has a double blood supply - from both the vasa recta and the calyceal arteries. The importance of the latter supply is not established. A case of polyarteritis associated with papillary necrosis is reported, in which the calyceal vessels, supplying the area, show acute necrotizing arteritis and occlusion. The pathophysiological and clinical implications are discussed.
A simple method is described for the measurement of urinary oxalate. Oxalate decarboxylase is coupled with NAD+ requiring formate dehydrogenase and the result recorded spectrophotometrically. Accurate determination can be carried out either on urine or a citrate extract or urine. Using the citrate extract procedure, the urinary samples can be stored for at least 3 months without any effect on the oxalate content.
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1. The effects of oral hydrochloric acid, ammonium chloride, sodium bicarbonate and ammonium bicarbonate on urea and ammonium excretion in rats on a constant diet were studied. 2. Hydrochloric acid acidosis significantly reduced urea excretion in the rat, with an equimolar increase in NH+4 excretion and no change in their sum. In ammonium chloride acidosis, most of the additional nitrogen intake is excreted as NH+4 and a small percentage as urea. The converse holds true after administration of ammonium bicarbonate. The physiological significance of this is discussed. 3. The shift in nitrogen excretion from urea to NH+4 in acidosis is interpreted on the basis of bicarbonate production and utilization. Urea formation utilizes HCO-3. For amino acid sources, this utilization is offset by the metabolism of the carbon skeleton, which gives rise to HCO-3. When waste nitrogen is excreted as NH+4, no bicarbonate is utilized and the new HCO-3, generated by the carbon skeleton, hels to maintain hydrogen ion homeostasis.
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Hydrochloric-acid induced acidosis reduced urea excretion in the rat, with an equimolar increase in NH+4 excreation and no change in their sum. By contrast, in the guinea pig, where ammonium excretion is small, HC1 administration did not effect urea excretion. Ammonium administered as NH4HCO3 was excreted mainly in the form of urinary urea, whereas that administered as NH4C1 was mainly in the form of ammonium. Methionine sulphoximine did not impair the increased ammonium excretion induced by acidosis, but did lead to a marked decrease in plasma glutamine levels and an overall increase in total urinary urea and ammonium nitrogen excretion. A reinterpretation of some aspects of the adaptations to metabolic acidosis is made based on these findings.
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