Vius showed 14hypertrophies out of 20 cases of parenchymatous nephritis; Ewald (not cited in the paper), 5 out of 10. Thus, according to the statistics appealed to, fully one-half the cases of chronic parenchymatous nephritis had cardiac hypertrophy. If, now, with this correction, we accept Labadie-Lagrave’s assertion that dilatation is the rule in parenchymatous nephritis, we arrive at the conclusion that either dilatation or hypertrophy, or both, obtain more commonly than a heart of normal size in chronic parenchymatous nephritis. This is substantially the conclusion of Lecorche and Salamon.
Familiarity with their work makes it difficult for me to conceive how the author of the paper could have so misconceived their meaning as to write that “they plainly exaggerate when they speak of hypertrophy of the heart as a constant lesion in this disease” (parenchymatous nephritis). I have been unable to find anywhere in this book any such assertion, and such exaggeration as there maybe is on the side that claims that it is exceptional. What lecorche and Salamon have stated is exemplified in the following extract from their work (pp. 624, 625):.
“In the question of diagnosis, determination of the state of the heart is one of the principal points. In a general way, it can be said that the degree of hypertrophy measures the degree of atrophy of the kidney. When the left ventricle only is increased in size, it can be affirmed that the bright’s disease is old, whatever may be the acute appearances revealed by the actual episode, and that a slow and latent phase of atrophy has preceded the acute attack under observation. Two great categories of Bright’s disease can be established according to whether or not cardiac hypertrophy is associated with the symptoms of Bright’s, whatever may be these symptoms, and, in particular, the physical and chemical character of the urine.
“If the heart is normal, or simply dilated, it is surely a matter of a large kidney, soft, red, mottled or white.
“If a middling (moderate) hypertrophy of the heart exist, the anatomical characters of the kidney are those of one of the forms which we have described under the name of intermediate evolutionary forms, or a small kidney atrophied rapidly by successive attacks close together-this kidney showing the appearance of a red granular kidney, and more often of a white contracted kidney.
“If, finally, the cardiac hypertrophy is enormous, there is no doubt of the small red kidney, contracted by slow and progressive atrophy.
“These rules are true, and ought to guide in the immense majority of cases. But, as with every pathological law, one should not lose sight of exceptions. Cardiac hypertrophy can develop rapidly in the course of acute and subacute nephritis, as has been noted apropos of scarletinal nephritis. In these precocious hypertrophies dilatation outweighs the hypertrophy, properly speaking; but clinically it is not easy to make the distinction, and by relying on observation of the heart, it is easy to deceive one’s self upon the duration and real appearance of the renal lesions.
“In the second place, there may be the following ensemble of symptoms: considerable hypertrophy of the heart without valvular lesions; generalized atheroma-traces of albumin in the urine, which is pale, poor in urea and solids. Clinically, it is difficult to avoid error.
There are the symptoms of the small, contracted kidney by progressive atrophy, and yet the autopsy shows large red kidneys, smooth and of normal appearance. Shall it be said that because the microscope shows a few glomerulic and tubular lesions, that it is bright’s disease? No; we must recognize that the clinician has been deceived, and that it is only a slight nephritis and an albuminuria, which has nothing to do with Bright’s disease in an atheromatous subject whose cardiac hypertrophy is explained by generalized arterio- sclerosis, and which has no connection with the state of the kidneys.
“Finally, hypertrophy of the heart may rarely be absent in very pronounced granular atrophy”.
The points which I have intended to suggest in discussion have been the following: 1. That the field of Bright’s disease is larger than so-called parenchymatous nephritis: 2. That it includes so-called interstitial nephritis; 3. That Bright’s disease is more plural than duel or single in its anatomical forms of kidneys; 4. That its fundamental process or processes maybe essentially single rather than dual or plural, its evolution and varieties depending upon the aetiological factors at work in the individual case; 5. That interstitial nephritis is not commonly a late episode of a general arterio-sclerosis; 6. That arterio-sclerosis is itself a result of the nephritic lesion of Bright’s disease. 7. That the heart and vascular tension are altered in all the forms of bright’s disease.
I should also like to emphasize the thought, which has grown upon me with experience, that behind the cases which we diagnosed as parenchymatous nephritis, acute or chronic, appearing without assignable cause, there has been a silent, latent period of renal atrophy similar to that demonstrated in experimental lead- poisoning, though not necessarily confined in its causes to lead, syphilis or gout; that there has been, in reality, a disease of long duration,
which has been evolving by minor localized attacks of slight nephritis, remitting, renewing, slowly progressing, gradually disabling the kidneys part by part, yet without apparent disturbance of the general health, until, through some new exciting factor or an intensification of some cause previously existing, the remaining healthy portions of the renal parenchyma are extensively invaded by a more intense inflammation, when renal obstruction becomes manifest by circulatory symptoms, often including dropsy, and renal inadequacy shows itself in some of the manifold phenomena of uraemia.
In thus suggestion that the so-called interstitial process may oftentimes precede the so-called parenchymatous process, and that the complex results of both processes, either singly or variously combined, is what we call Bright’s disease, there is the clinical inference that attentive examination of the urine for renal inadequacy and close observation of the cardio- vascular system should go hand in hand for correct diagnosis in all the forms of the disease.
