Text “Acute nephritis”

Etiology . Acute infections practically always precede the onset of acute nephritis. Diphtheria, measles, chickenpox, suppurative lymph glands, chills, appendiceal abscess or almost any infection in the body may responsible for nephritis, but tonsillitis, septic sore throat, and otitis media ear the main predisposing diseases.

Pathology . Acute glomerular nephritis is not merely a disease of the kidney. The term «acute glomerular nephritis» is used because the capillaries of the glomeruli are practically always the site of the initial lesion. It is known that infection by streptococci plays the predominant role in the cause of acute glomerular nephritis. The kidney is large and ischemic, and the capsule is usually under tension greater than normal.

Symptoms. Following an acute infection, for example, an upper respiratory infection, the patient may develop the clinical picture of acute nephritis within a period of from two to eight days. The classical textbook picture of hematuria, hypertension, edema and nitrogen retention is not always present. More often the patient has only evidences of renal inflammation as shown by the urine examination. Albuminuria, red blood cells, pus cells and casts in the urine are frequently the only signs and are often overlooked if symptoms are absent. Disturbances of urination characterized by a scanty outflow of urine or even complete anuria may be present.

The severity or mildness of the kidney disease cannot always be measured by the examination of the urine or any other tests. In the course of the first days of the disease there may appear fatal symptoms of heart insufficiency or kidney eclampsia, which are indicative of the severity of the disease. Hypertension is the most characteristic symptom. Sometimes the blood pressure rises rapidly to 200/120 mm Hg. Edema is very mild and hardly recognized by the examining.

The rise in the nonprotein nitrogen is a sign of renal insufficiency. Frequently the rise is rapid in the early stages of acute anuria. Then, after four or five days, when urine output is restored to normal, the blood NPN drops to normal. While the initial rise in NPN in the acute episode is not of great importance, it does point out to the physician that he must establish urinary flow as soon as possible. As a rule, if this condition is allowed to go uncorrected for seven or eight days genuine fatal uremia sets in.

Cerebral complications. Headache, visual disturbances, vomiting, convulsions and loss of consciousness occur in the course of acute nephritis. These complications were at one time thought to be the result of edema of the brain, and, although edema of the brain may be present, it is the hypertension that behind these features which is to blame, as they practically never occur without high blood pressure.

Remissions and relapses. After the first two weeks of acute nephritis patients usually appear to make a complete recovery and in some cases they do. In others the recovery is more apparent than real. Frequently the patient that seems to have recovered completely is only partly cured, and the cure is more on the surface then underneath. These patients may feel quit well, but in fact only the more acute, severe phase has ceased. In some of these cases a low grade, smouldering inflammation continues. This may be called the latent stage of acute nephritis, where nothing appears to be wrong unless careful urinary examination is carried out. Then the truth comes to light and it is found that an excessive amount of red blood cells, pus cells and casts are present in the urine. There may be no high blood pressure, headache, edema or other disturbances.

Sometimes these latent cases go on to recovery, while others continue and finally terminate with chronic glomerular nephritis. Perhaps the greatest problem in the management of acute nephritis is to recognize this latent stage and to deal with it satisfactorily.