CHRONIC INFLAMMATION OF THE KIDNEYS 185 



nephritis), and the atrophic or hard kidney (chronic interstitial nephritis). 

 The first contlition is generally the forerunner of the second, but, as the 

 hard kidney is most frequently found in post-mortem, it is possible 

 that it niaj' develop as a primary condition. The white kidney is en- 

 larged from the normal size, and has a smooth yellow or irregular yellow- 

 colored surface. The cortical portion is yellowish in color, while the 

 pyramids are red. In some cases we find the kidney large and red, or al- 

 ternated red and yellow, or covered with hsemorrhagic spots. The 

 atrophic kidney (shrunken or contracted kidney) results from an increase 

 of the interstitial substance and atrophy of the parenchymatous substance. 

 It is hard and tough on its surface, and has small, wart-like irregularities 

 and granulations. The capsule is thickened and it is hard to strip from the 

 body of the kidney; here and there we find small cysts of various sizes. 

 The cortical substance is lessened in diameter and striated wdth layers of 

 dark colored tissue. The pyramids are smaller and deep red in color. 



Clinical Symptoms and Course. — As a rule, very little that can be recog- 

 nized in the clog during life. The quantity of urine passed is greatly in- 

 creased and at much shorter intervals; this increase of the amount of 

 urine passed is one of the first symptoms to attract the attention of the 

 owner. The urine is very light in color, almost like water, the specific grav- 

 ity being much lessened. Microscopically examined, we may find iso- 

 lated hyaline cylinders, and a few blood corpuscles; albumin is never present 

 in any great amount, frequently for a certain period small quantities of 

 albumin may be present and then it entirely disappears. Palpation of the 

 kidney may find it hard, and uneven on the surface. In such cases there 

 is generally hj-pcrtrophy of the left ventricle, which can be recognized 

 by palpitation of the heart (loud pulsations and a hard, full pulse). It 

 is presumed that this high arterial pressure tends to keep up the action 

 on the impaired kidney and prevent any serious disturbance in the secre- 

 tion of the kidney. As the disease advances we soon recognize a change: 

 the heart becomes weaker in its action, the pulse is small and frequent, the 

 urine is scant, dark and very albuminous. This is followed by chronic 

 inflammatory processes in various organs, especially the bronchia, and in 

 the intestinal canal; and finally we have symptoms of uraemia. In the 

 majority of cases the parenchymatous form can be recognized by the 

 urine. This is very similar to acute nephritis. It contains much albu- 

 min, and the urine is scant in quantity, and there are certain dropsical 

 symptoms in the dependent regions; death may occur as a result of gen- 

 eral dropsy or uraemia, or such complications as pneumonia, pleurisy, or 

 pericarditis. There is also loss of appetite, great fatigue on taking any 

 exercise, hypertrophy of the heart, which finally becomes weak, and then 

 symptoms of ursmia follow as stated above. In rare cases the condition 

 may change and the active symptoms cease; the urine gradually becomes 



