Patients suffering from the association of chronic nephritis with hypertension die slowly, usually. There is gradual development of anasarca. Headache is frequent and severe. Pains all over the body may occur. The sight may suddenly become dim or may even be lost. Dizziness may be complained of and dyspnea is usually marked. Cyanosis comes on, the pulse becomes weak, irregular or intermittent, heart failure sets in, and the patient dies with edema of the lungs.
Another class of renal arteriosclerosis is characterized by a small granular kidney in which fibrous changes of a patchy character have taken place. These scattered areas are the result of obliterating endarteritis of renal arteries here and there with consequent anemia, death of cells, and replacement by fibrous tissue. It occurs as part of a generalized arteriosclerosis in which the whole arterial system is the seat of diffuse (senile) sclerosis. The palpable arteries are usually beaded or even encircled with calcareous deposits and the aorta is the seat of an extensive nodular and ulcerating sclerosis. The heart is usually small, shows extensive fibrous and fatty changes and possibly the condition known as "brown atrophy;" the blood pressure is low. Such cases do not show any special symptoms. They are anemic, short of breath on exertion, have the appearance and show the signs of senility.
In the first group it is, at times, difficult to say whether the kidney disease or the arterial disease is the most important. From a clinical standpoint the decision is not essential as the end results are much the same in both. However, when actual uremic symptoms dominate the picture, it becomes evident that the disease of the kidney is the chief feature in the causation of the symptoms.
Abdominal or Visceral
There is an important group of cases to which but little attention has been paid until quite recently. This is the abdominal or visceral type of arteriosclerosis. It has been stated that arteriosclerosis of the splanchnic vessels almost invariably causes high tension. Among others, Janeway has shown that general arteriosclerosis without marked disease of the splanchnic vessels does not cause as a rule increase of blood pressure.
There are cases in which the brunt of the lesion falls upon the abdominal vessels. Such cases have been called "angina abdominalis." It has been suggested (Harlow Brooks) that this type of arteriosclerosis may be determined by constant overloading of the stomach with food, especially rich and spiced food. This causes overwork of the special arteries connected with digestion and so leads to sclerosis of the vessels of the stomach, pancreas, and intestines. Personal habits probably influence to great extent the production of this more or less localized condition.
The organs supplied by the diseased arteries suffer from changes analogous to those occurring in general or local malnutrition, such as starvation, old age, or local anemias. These changes are atrophy with hemachromatosis (brown atrophy) or fatty infiltration and degeneration. Following the degenerative changes there result connective tissue growth and further limitation of the functionating power of the affected organs.
Pain is a more or less constant symptom of visceral sclerosis. In the early stages there may be only a sense of oppression, of weight, or of actual pressure in the abdomen or pit of the stomach. There may be only recurring attacks of violent abdominal pain accompanied by vomiting. In some cases symptoms of tenderness in the epigastrium, pains in the stomach after eating, vomiting and backache may suggest gastric ulcer. There may be dyspnea and a sense of anguish accompanied with a rapid and feeble pulse. Hematemesis may make the symptom group even more like ulcer of the stomach, and only the course of the disease with the failure of rigid ulcer treatment and the substitution of treatment directed toward relief of the arterial spasm with resulting betterment, enables one to make a diagnosis. The condition may be present for years and the symptoms only epigastric tenderness with dizziness and sweating on lying down after dinner, as in one of Perutz's patients. The attacks are probably due to spasmodic contraction of the sclerosed intestinal vessels with a resulting local rise in blood pressure. The pains are most probably due to the spasm of the intestinal muscles, and some think they are located in the sympathetic and mesenteric plexuses.
This result of arteriosclerosis is not so uncommon, and by keeping this cause of obscure abdominal pain in mind we are now and then enabled to save a patient from operation.
An autopsy on a case which for many years had attacks of abdominal pain and cramp-like attacks, with high blood pressure and heart hypertrophy, showed extensive sclerosis of the abdominal aorta, superior mesenteric and iliacs. These vessels were calcified. Hypertrophy of the left ventricle was found. The kidneys were microscopically normal. There were no changes in the ascending aorta but in the descending portion there were scattered nodules and small calcified plaques.