366 DISEASES OF THE URINARY APPARATUS. 



thelial cells. The œdemas often diminish gradually, then disappear 

 entirely. The modifications of the urine and the resorption of the 

 transudates are results of the increased activity of the heart and 

 elevation of arterial pressure. 



As long as the cardiac activity compensates the renal alteration 

 the affection remains stationary ; this condition mçiy last for years, 

 but sooner or later the period of fatigue appears, with atony of the 

 heart. The pulse becomes more feeble and irregular : blood stag- 

 nations are produced ; we observe the appearance of bronchial and 

 gastro-intestinal catarrh, extended œdema, symptoms of heaves, 

 cardiac palpitations, vertigo, pneumonia, pleurisy, pericarditis, and 

 hemorrhages; the quantity of urine is reduced, its specific gravity 

 increases, and it contains albumin. Death occurs through acute 

 or chronic uremia. 



Treatment. The treatment of chronic nephritis is nearly the 

 same as that of acute nephritis; but the chances of success are even 

 less than in the acute form. In chronic nephritis we should seek 

 to influence the general nutrition, to combat anemia, and to relieve 

 vascular pressure in cases of cardiac insufficiency. It is essential 

 to administer cardiac tonics and also diuretics : digitalis, caffeine, 

 strophanthus, etc. 



[The mercurial preparations exert a very powerful influence upon 

 connective tissue indurations. The iodide of potassium also exerts 

 a similar influence, whilst arsenous acid diminishes arterial tension. 

 These are all valuable agents in the treatment of this disease, either 

 alone or in combination in the form of Donovan's solution. Spirits 

 of turpentine in small and continued doses often gives good results. 

 — w. L. z.] 



If there is any œdema or dropsy pilocarpine may be used. 

 Several hypotheses have been advanced on the pathology of car- 

 diac hypertrophy which appears during the course of nephritis.^ 



1 The pathology of cardiac hypertrophy occurring in the course of interstitial 

 nephritis of the human race is variously interpreted by different authors. By some 

 hypertrophy of the heart is considered tributary to the renal lesion; by others, the 

 cardiac and renal lesions are regarded as independent but to be traced back to a 

 common cause (Dieulafoy). Upon the first hypothesis the cardiac hypertrophy is 

 explained either by an excess of arterial tension (Bright, Potain, Senator), or by this 

 influence together with the vascular alterations of the kidney (Traube). The second 

 hypothesis asserts that the cardiac and renal lesions are produced simultaneously by 

 arteriosclerosis. The sclerous thickening of the walls of a number of small vessels 

 of the parenchyma would hinder the general circulation, elevate the arterial tension 

 and produce hypertrophy of the heart, necessitating increased activity. — n. d. t. 



