Apostematous Nephritis

APOSTEMATOUS NEPHRITIS, one of the patho-anatomical varieties of suppurative nephritis. A. nephritis is the name for a disease of the cortical layer, when irregularly shaped and various-sized hemorrhages are clearly outlined on the surface under the capsule, dotted with small yellowish-white beads—miliary pustular lesions of the kidney cortex; the medullary layer, papillae, and pelvis usually appear microscopically relatively healthy. A. n. is contrasted with the patho-anatomical other form of suppurative nephritis—papillary metastatic nephritis or "Ausscheidungs-nephritis" (according to Aschoff's nomenclature). This distinction is found in the early stages of acute cases; in chronic cases, both forms pass into one another and give a mixed picture of purulent lesion of the entire kidney, pyelo-nephritis apostematosa (Israel). Purulent inflammation of the kidneys is the result of penetration of infection into the kidney either through the blood, or by introducing it into the pelvis of the kidney by a ureteral catheter, or by direct transition from a purulent focus in the lower parts of the urinary tract or neighboring organs, or finally by lymphatic pathways from the intestine, as well as from the lower part of the urinary sphere. In the presence of a number of predisposing factors (mobility of the kidney, stagnant phenomena in it, delays in urination, stones, injuries, etc.), various microbial diseases, such as: furuncle, carbuncle, eczema, panaritium, mastitis, diseases of the nose, teeth, angina, postpartum complications, as well as general diseases (pyemia, typhoid, scarlet fever, diphtheria, endocarditis, etc.), can cause purulent inflammation of the kidneys in acute form of purely metastatic character. Microorganisms that have entered the kidney through the blood get stuck in the vessels of the cortex and glomeruli; in most cases, these are staphylococci and streptococci. The tissue reaction of the kidney is expressed in the swelling of the glomerular endothelium, accumulation of leukocytes in the capillaries and in Bowman's capsule of the glomeruli and their transformation into a pustule. At the same time, edema of the interstitial tissue occurs and formation of similar pustules on the surface of the kidney. Unlike tubercular tubercles, the pustules in A. n. are located either against the background of flat hemorrhage or surrounded by a reactive red halo, while a tubercular tubercle is found among macroscopically unchanged kidney tissue. A. n. with low-grade infection may stop in its development; in this case, the tissue of the kidney cortex heals, recovery occurs; in other cases, individual areas of the pustular rash merge into a large abscess, forming a carbuncle (Israel) of the kidney; or the purulent infiltration involves the medullary layer, pyramids, and pelvis, giving a picture of descending pyelonephritis. Acute A. n. should be considered in most cases as a hematogenous metastatic process of embolic type, although Israel described two cases of ascending infection after gynecological operations. The kidney capsule does not remain without participation in the process: at first, its edema is observed, and then purulent inflammation also passes to it, forming peri- and pararenal changes up to large purulent pararenal collections. Sometimes along lymphatic pathways, infection penetrates into the pleura, which reacts with abundant exudate. It was previously believed that A. n. must necessarily be bilateral, but observations of recent years confirm the existence of unilateral lesions. - According to clinical course, acute A. n. gives a picture of a severe disease: shaking chills, nausea, vomiting, high temperature up to 40°, headaches, pains in the kidney area, tension of muscles and acute sensitivity in the area of the triangle of Grünfeld; pains often radiate along the course of the ureter to the groin and may be accompanied by dysuric phenomena. If the capsule of the kidney is also involved in the inflammatory process, then the protective tension of the muscles of the lumbar region and anterior abdominal wall clearly appears. In cases where the process passes into the chronic stage, subjective complaints are negligible: patients pay attention to pulling or dull pains in the hypochondrium of the corresponding side, to turbid, purulent urine. Objectively, one can note an increase in the kidney and its tenderness on deep palpation of the abdomen, the presence in the urine of a significant amount of protein and leukocytes and single erythrocytes. The chronic stage of the disease proceeds, giving periodic exacerbations with sharp increases in temperature. The general condition of patients sharply worsens, there is a decline in general nutrition, headaches and diarrhea, which, mainly, forces patients to seek medical help. The prognosis for acute A. n. is poor: in some cases (more often) the disease develops very rapidly and, affecting both kidneys, can quickly lead to death with symptoms of sepsis, if energetic intervention is not undertaken; in other cases, the development of A. n. proceeds more slowly, but still the inflammatory process gradually involves both kidneys and finally puts them out of action. In individual cases, the process can stop and lead to recovery even without surgical intervention. Diagnosing acute A. n. is not always easy, since with rapid development of the disease, local phenomena are either absent or slightly expressed. Pains, protective tension of the muscles of the abdominal wall, increase in the kidney, temperature and change in urine make it possible to suspect a purulent process in the kidneys. In differential diagnosis, pararenalitis and pyelitis should be kept in mind. If in pyelitis there are always present in the urine a large number of pus globules and pelvic epithelium, then for purulent nephritis the presence of a significant number of microbes (bacteriuria) with a small number of pus globules and erythrocytes is characteristic. Furthermore, in pyelitis, the protective tension of the muscles of the lumbar region and anterior abdominal wall, characteristic of acute A. n., is not always observed. In case of suspicion of pararenalitis, one should be guided by clinical analysis of urine. In A. n., the amount of urine decreases with an increase in specific gravity and an increase in the amount of protein. Catheterization of the ureters, however, reveals a relatively good condition of the bladder and gives an idea of the degree of kidney damage. In connection with these data, functional tests shed even more light on the differential diagnosis of A. n. from pararenalitis, in which the function of the kidneys, as a rule, does not suffer. The phloridzin test gives a satisfactory idea of the degree of exclusion or decrease in function of one or the other kidney. Phenol-sulfonphthalein and indigo carmine, introduced into the blood, give a clear picture in the case of a unilateral process, when intensely colored urine appears from one ureteral catheter, and clear urine from the other. However, judging by the intensity of the color of the urine about the degree of involvement in the purulent process of one or the other kidney is not always a correct and precise diagnostic method. Only in connection with clinical phenomena, the course of the disease, the general condition of the patient and the data of urine analysis does instrumental research acquire value for establishing a differential diagnosis and for developing measures of therapy for A. n. In the chronic stage of A. n., it should be differentiated from calculous pyonephrosis—on the basis of X-ray examination, from infected hydronephrosis—on the basis of pyelogram—and tubercular lesion of the kidney, in which, as a rule, the urinary bladder is also involved in the process. The treatment of acute A. n. is surgical, and only in some exceptional cases autovaccination, intravenous therapy (urotropin, electragol, neosalvarsan, etc.) and autogenous hemotherapy can lead to recovery. In A. p., removal of the kidney, its incision and exposure of the kidney from its fibrous capsule (decapsulation) are applied. Nephrectomy is indicated in unilateral lesions, and the other operations in bilateral disease. Sometimes after decapsulation or nephrotomy, a secondary nephrectomy has to be done (non-healing fistulas, progressive weakness of the patient and further development of the process in one kidney with complete recovery of the other).