Ever since Traube established the close relationship between chronic nephritis and cardiac hypertrophy and the recognition of arterial hypertension as the cause of the latter, there has been an increasing tendency to see in a left ventricular hypertrophy presumptive evidence of an underlying chronic nephritis, in the absence of some other cause to explain it. Whether we follow the school of Romberg, which makes arterial hypertension the consequence of a glomerular lesion, or adhere to the opinion of Jores,1 that high pressure results from a fibrosis of the smaller vessels, including those of the kidney, it seems agreed that the occurrence of high blood-pressure and its corollary, cardiac hypertrophy, point to a lesion in the vascular component of the kidney. It is, however, not only in the outspoken cases of nephritis that we expect to find cardiovascular changes. Even in those not uncommon cases of nephritis in