CHAP. III.] THE BLOOD IN DISEASE. 173 



followed very closely the masterly memoir in which Dr Bright 1 had 

 first announced the connexion between albuminuria and morbid 

 changes in the kidney. 



Christison pointed out that in the early stages of kidney disease 

 the blood presents the following characters ; the density of the serum 

 is low (1020 or even 1019), the proportion of albumin diminishes, 

 the fibrin of the blood may be increased, the proportion of blood- 

 colouring matter is unaffected, but, above all, the serum frequently con- 

 tains urea. He shewed that as the disease became chronic some of 

 these changes in the blood became less distinct, e.g. the diminution 

 in the amount of albumin, and the presence of urea, but that a very 

 constant and considerable diminution of the blood-colouring matter 

 was a characteristic occurrence. 



Subsequent researches have thoroughly confirmed the statements 

 of Christison as to the excess of urea which is present in the blood of 

 Bright's disease. Although there is no longer any difference of opinion 

 as to the accumulation of urea in the blood in cases of Bright's disease 

 in which there is a marked suppression of urine or a very obvious 

 deficiency in the elimination of urea, facts have hitherto been 

 wanting to decide whether after the establishment of any of the 

 chief lesions of the kidney there is a permanent impairment of the 

 normal power which the kidneys possess of eliminating urea. This 

 question has occupied the attention of the Author, and he is inclined 

 to believe that in most cases of chronic Bright's disease, even whilst 

 the patient is in the apparent enjoyment of fair health, there is a per- 

 sistent excess of urea in the blood. 



The convulsions and coma which are apt to supervene when the 

 elimination of urea is defective have been designated as 'uraemic' 

 or as evidences of ' uraemic ' poisoning. At first it was held as 

 certain that these nervous phenomena were occasioned by the 

 accumulation of urea in the blood acting as a poison on the 

 great nerve centres. There can be no doubt, however, that this 

 simple explanation is not sufficient ; the condition of uraemia is 

 one which depends upon many factors. It must not be for- 

 gotten, that before the condition of uraemia is induced, the blood 

 has usually become rich in water, poor in albumin, poor in corpuscles, 

 and that in addition to an accumulation of urea and uric acid it 

 probably contains an excess of other proximate principles which may 

 exert a specially poisonous action. 



It was suggested by FrerichsHhat uraemic phenomena are due to 

 the conversion of urea into ammonium carbonate in the blood, 

 but there is no ground for believing that such a conversion actually 

 does occur during life. 



1 Bright, " Cases illustrative of some of the appearances observable on the examina- 

 tion of diseases terminating in dropsical effusion, and first of the kidney." Bright's 

 Beporte. London, 1827. 



2 Frerichs, Archiv f. phys. HeilJc., 1852, Vol. xi. p. 88. 



