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Renal Accumulation of Ammonia: The Cause of Post‐lschaemic Functional Loss and the “Blue Line”
Author(s) -
FITZPATRICK J. M.,
MONSON J. R. T.,
GUNTER P. A.,
WATKINSON L. E.,
WICKHAM J. E. A.
Publication year - 1982
Publication title -
british journal of urology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.773
H-Index - 148
eISSN - 1464-410X
pISSN - 0007-1331
DOI - 10.1111/j.1464-410x.1982.tb13606.x
Subject(s) - kidney , renal function , bicarbonate , chemistry , endocrinology , ischemia , medicine , creatinine , ammonia , biochemistry
Summary— The “blue line”, a dark discoloration at the corticomedullary junction, is a constant finding after a significant period of renal ischaemia. In this study, it has been shown to be caused by packing of all of the peritubular capillaries at the corticomedullary junction with red blood cells. Five rats and 10 dogs were alkalinised by replacing their drinking water with 2% sodium bicarbonate for 2 weeks pre‐operatively, in order to inhibit the glutaminase enzyme system and thereby decrease ammonia accumulation during ischaemia. Five rats and 6 dogs were used as unprotected controls. All animals were subjected to 60 min warm ischaemia. Renal function was significantly protected in the alkalinised rats (P<0.002) and dogs (P<0.001), with the serum creatinine rising to a maximum of 0.21 ± 0.03 mmol/l in the alkalinised rats and 0.18 ± 0.04 mmol/l in the alkalinised dogs. There was no “blue line” in the alkalinised animals. It is suggested that the “blue line” plays a central role in post‐ischaemic renal failure. Prevention of ammonia formation by alkalinisation protects against ischaemic renal damage and the formation of the “blue line”.