Goulstonian Lectures on the Natural History of Pulmonary Consumption
Authors: A. B. Shepherd
Journal: BMJ (1876)

of the disor(der, are such as to show that it is the result of local disturb- ance, not genieral deterioration.And it has been further shown, both by Dr. Galabin and by Dr. Sibson, that simnple hypertrophy of the heart, which may probably be taken without error as an index of the cardio-vascular change, may re- sult from tlle incapacitation of one or both kidneys by calculous dis- ease.I can see no escape from the conclusion that disease, at first local to the kidneys, may be attended by, or, in other words, may pro- duce, the vascular and cardiac thickening.And, as to the modus operandi, none other can be suggested than functional disturbance of the gland.'To take note in passing of a prominent clinical landmark which opens to our view, it may be accepted as a general truth, that hyper.trophy of the heart in connection with albuminuria is a sign that the kidneys, hIowever affected originally, have become the subjects of fibrotic and irrevocable disease.The association is, no doubt, partly one of time.When the disorder has lasted long enough to thicken the ventricle, it will almost invariably have extended to the interstices of the gland.To speculate on the essential nature of the cardio-vascular change, it hlas beeni slhown-i that, though differing in degree, it is similar in kind, whether the renal affection be of inflammatory origin or have begun, however obscurely, as granular degeneration.The change is com- pounded of muscular thickening, arterial and ventricular, which de- serves in both situations to be called hypertrophy, notwithstanding its admixture in the arteries with degenerative changes, and, as coincident witlh or successive upon it, an exaggeration of the outer or fibroid sheath w-hiclh is as truly as the muscular coat hypertrophied.These structural alterations are concurrent during life with increased tension or tight.ness of the arterial system.Where there is no increase of tension, to anticipate a fact with regard to the lardaceous disorder, there is no arterial or cardiac thickening.When both ensue, and the time of their accession can be observed, as happens when they succeed upon an inflammatory attack, the tension appears early, the hypertrophy late, in the di ease.Thus, it is impossible to attribute the tension to change of structure; but, on the other hand, the two may be the con- secutive results of a common cause, or the change of structure may be directly due to the increased tension.Whether we seek the cause of the cardiac hypertrophy or of the arterial tension, we can find it only in obstruction.After what has been recently brought before the Col- lege, I need not recur to the evidences that the increased tension of Bright's disease depends upon retardation of the arterial outflow.Bright, with a sagacity which served him in the place of microscope and, sphlygmograph, was led by the cardiac hypertrophy to infer the existen-ce of this condition, and to attr-ibute it to a difficulty with which the imiipure blood penetrated the capillary vessels.And at present the only question which calls for consideration is, whether we are to place the difficultywith Bright in the capillaries, or with Johnson in the arterioles.In the view of the later pathologist, one to whose observa- tions, however we interpret them, a large importance must be attached, the circulating system is the seat of divided councils.The arteries