Active hyperemia is caused by dilatation of the renal arteries. This may be from traumatic injury to the vasomotor centre in the medulla oblongata. In a case of this kind observed by the author there was the most intense hyperemia with enlargement of both kidneys, the injection affecting all the vessels. During the few hours that the patient survived large quantities of urine were twice removed by the catheter, and after death the bladder was again found distended by a watery urine. Again, we may have an active hyperemia from removal of pressure, as after excision of large tumours from the abdomen or tin-removal of ascitic fluid, or even the removal of fluid from the pleura. Under these circumstances there is often for a day or two excessive secretion of urine lasting till the renal vessels resume their normal state of contraction.

The hyperemia which follows on the administration of certain poisons, such as cantharides, arsenic, and carbolic acid, is to be regarded as really inflammatory.

Passive hyperaemia results from obstruction to the venous circulation, and is most frequently met with in valvular disease of the heart and in diseases of the lungs in which the circulation is seriously interrupted, as in severe emphysema.

If the obstruction take place suddenly there may be very intense engorgement of the renal vessels and considerable haemorrhage from the glomeruli, so that their capsules and the tubules contain blood.

In the more usual chronic cases, such as occur so frequently in cases of heart disease, the kidneys present an increase in density due to Cyanotic induration (see ante, p. 90). There is also a general redness, but this is usually most manifest in the pyramids where the arteriae rectse often show very special dilatation, indicated by exaggeration of the red streaks which pass from the bases of the pyramids in the direction of the apices. The glomeruli are also visible in the cortex as small red spots.

Microscopic examination shows great overfilling of the vessels, accompanied in many cases with atrophy of the epithelium of the tubules, which is not infrequently fatty. There is often blood in the glomeruli and tubules, and sometimes brown pigment which has formed from blood. This pigment may be partly crystalline. The tubules also frequently contain hyaline tube-casts.

Thrombosis of the renal veins is sometimes a result of passive hyperaemia, but it usually occurs just before death and when the patient is very much debilitated. The author met with it in a case of amyloid disease which had followed on an attack of gonorrhoeal rheumatism.

Embolism of the kidney is very frequent. Remembering that the renal arteries are strictly end arteries, it will be understood that when one of them is obstructed the Infarction virtually always occurs. The arteries of the kidney being distributed primarily to the cortex, the infarction is more or less wedge-shaped (Fig. 420)with the base of the wedge at the surface. If the wedge be of larger size it will extend also into the pyramids.

As a rule the infarction is of a pale colour and of dense consistence, the tissue having undergone Coagulation-necrosis. There is not generally much haemorrhage, but usually at the margin there is some, and if the infarction be small the haemorrhage may extend throughout it. Around the infarction there is a zone of hyperaemia.

Embolic infarction of kidney. The white appearance and wedge shape of the infarction are represented. (After Rayer).

Fig. 420. - Embolic infarction of kidney. The white appearance and wedge shape of the infarction are represented. (After Rayer).

The kidney tissue seems to undergo necrosis very readily when deprived of blood. Litten found that when the renal artery was ligatured for two hours the renal epithelium was already necrosed. This is probably the reason why the infarction seldom takes the hipmorrhagic form. The readiness with which the renal epithelium dies is frequently shown in infarctions of the kidneys, and is illustrated in Figs. 37 and 38, pp. 127, 128. At the peripheral parts of the infarction, and in small ones throughout it, the epithelium may be found dead, as evidenced by the absence of nuclear staining, whilst the connective tissue remains alive, having its nuclei fully stained.

The infarction gradually undergoes absorption, and is replaced by;t cicatrix. In this way deep depressions of the kidney may occur, and if there are several of them the kidney may assume a lobed appearance. In cases of old mitral or aortic disease it is very common to find deep cicatrices, indicating that, probably at the time of acute endocarditis, embolism of the kidney had occurred.

The kidney is not infrequently the seat of Septic embolism in pyaemia, ulcerative endocarditis, etc. The result is the formation of miliary abscesses, which will come up for consideration hereafter.

Haemorrhage from the kidney is very frequent and important. It is of common occurrence in acute nephritis, and is not infrequent in chronic. It is a frequent symptom in tumours of the kidney, especially in cancers and cystic degeneration, and it results from calculi in the pelvis of the organ.

Purpura and scurvy seem to have a special tendency to affect the pelvis of the kidney, causing bleeding from its mucous membrane. A peculiar and interesting form is met with in infants, in whom a scorbutic condition has been induced by artificial feeding without sufficient fresh milk. In this case blood in the urine may be the only direct symptom of scurvy. (See Dickinson).

When the haemorrhage is from the kidney proper the blood is intimately mixed with the urine, as in Bright's disease and scurvy. When the bleeding is from the pelvis as from calculi, tumours, etc., the blood is often coagulated, and when found in the urine it sometimes has an elongated worm-like form acquired in passing through the ureter. This passage causes much pain. Haemorrhage into the parts around the kidney will only occur in cases of rupture from injury of the organ.


Cohnheim, Die embol. Process, 1872, and Allg. Path., ii.; Litten, Hwmorrh. Infarc, 1877, and Virch. Arch., lxxxviii., 1882; Reiklinohausen, (Retrograde embol. of renal vein) ibid., c. 1885; Dickinson, Renal and urinary affections, part iii., 1885.