nephritis(redirected from salt-losing nephritis)
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nephritis(nəfrī`təs), inflammation of the kidney. The earliest finding is within the renal capillaries (glomeruli); interstitial edema is typically followed by interstitial infiltration of lymphocytes, plasma cells, eosinophils, and a small number of polymorphonuclear leukocytes. The disease is thought to be immunological, but immunoglobulins and drug antigens have been found in only a few cases. The damage is usually reversible when the cause is recognized and removed, but severe cases can progress to fibrosis and renal failure. The disease can take several forms. Pyelonephritis is usually associated with a bacterial infection transmitted from the bladder or blood; it affects the renal pelvis and is treated with antibiotics. Glomerulonephritis, or Bright's disease, causes degenerative changes in the glomeruli and is believed to be an allergic response to infection elsewhere in the body. Symptoms include headache, mild fever, puffiness of the eyes and face, high blood pressure, and discoloration of the urine. Treatment includes bed rest and limiting the intake of water, sodium, and proteins, and, if necessary, dialysis; antibiotics are given to halt infections (e.g., streptococcal) invasion. The disease occurs more frequently among the young. About 95% of patients recover from the acute phase of the disease; however, if glomerulonephritis becomes chronic, renal damage results after many years, causing kidney failure.
the principal disease of the kidneys. Nephritis was described by R. Bright in the first half of the 19th century.
During the pathogenesis of nephritis, a decisive role is played by such immune disorders as the inadequate formation of antibodies and immune lymphocytes in response to streptococcal or other types of infections or in response to the body’s own denatured tissues. Inadequate antibody and lymphocyte formation in response to extrarenal antigens is recognized as the primary mechanism by which the onset of nephritis takes place. Once an antigen-antibody complex is formed, it circulates freely in the blood and becomes entrapped in the narrow capillaries of the renal glomeruli, which become the focus of an inflammatory process. A less common mechanism is the formation of antibodies against antigens that are from a renal source, such as the membrane of the glomerular capillaries.
Two independent types of nephritis are recognized: acute and chronic. As a rule, acute nephritis arises during the recovery period from tonsillitis, or pharyngitis caused by certain types of streptococci. Acute nephritis can have an epidemic character, especially in wartime among service personnel living in the cold under conditions that foster the spread of infection. Symptoms of acute nephritis include the sudden onset of edema and dyspnea as a result of the overloading of the circulatory system by retained fluids; a decrease in the volume of urine, accompanied by an excess of urinary protein and blood; and the appearance under the microscope within the urinary sediment of renal epithelium, leukocytes, erythrocytes, and protein casts of the renal tubules. Acute poststreptococcal nephritis is rare and usually results in complete recovery. In some patients nephritis is only a component of a multisystem disease, such as collagen disease, serum sickness, or drug disease; in such cases, its course most often becomes subacute or chronic.
Chronic nephritis is often encountered as a primary disease: it need not necessarily occur as a consequence of acute streptococcal nephritis. Primary chronic nephritis can take several clinical forms and can develop at various rates. Renal insufficiency and uremia develop within one year if the course is rapid and accompanied by edema, increased arterial pressure, a char acteristic semilunar proliferation of the capsular epithelium of the glomerulus, and proteinuria (the excess excretion of protein in the urine). Less frequently, renal insufficiency and uremia develop over the course of 1½ to two years. In another form of chronic nephritis the nephrotic syndrome predominates. In the hypertensive and latent forms of chronic nephritis, hypertension and reduced proteinuria may persist for years or even decades. All forms of chronic nephritis result in renal insufficiency and uremia, if death does not occur earlier from cardiac insufficiency or other causes.
Corticosteroids, cytostatics, indole derivatives, and 4-aminoquinolines are used in treatment to suppress the formation of antibodies or to destroy pathogenic lymphocytes. When nephritis occurs in conjunction with streptococcal infection, antibiotics are used. Bed rest is recommended in cases of acute nephritis or aggravated chronic nephritis. The intake of table salt is restricted and even prohibited when serious dyspnea arises or when acute edema of the lungs or brain develops. Diuretics and other remedies are employed, depending on the nature of the specific case and the stage of the disease. With the exception of aggravated chronic nephritis, all nephritides may be treated with climatotherapy under a physician’s observation on the Southern Crimean Shore or in Bairam-Ali. Nephritis patients should avoid infections, vaccination, and unnecessary exposure to the sun and should be especially cautious in their use of medications.
REFERENCEOsnovy nefrologii, vols. 1–2. Edited by E. M. Tareev. Moscow, 1972.
E. M. TAREEV