To clarify the significance of mononuclear phagocytes in IgA nephropathy, renal biopsied materials from 45 patients with the disease were examined by the indirect immunoperoxidase method using anti-human monoclonal antibodies and by ultrastructural peroxidase (PO) cytochemistry. The monoclonal antibodies were FMC32, S-100 (alpha), My4, and LeuM5 for detection of mononuclear phagocytes and HLA-DR for Ia antigens. Mesangial hypercellularity in IgA nephropathy was divided into three grades. The number of monocyte/macrophages per glomerulus differed significantly among the grade of mesangial hypercellularity. In the capillary lumen, monocytes were more numerous in the group with slight mesangial hypercellularity. By contrast, macrophages were often found in the Bowman's space and mesangial area of the glomeruli in the advanced group. In the renal interstitium, the number of monocyte/macrophages per 100 interstitial cells differed significantly among the degree of interstitial damage, and they were observed mainly around sclerotic glomeruli. Ultrastructural PO cytochemistry revealed infiltration of monocytes, exudate macrophages, and/or PO-negative macrophages. Clinicopathological study showed a relationship between the number of monocyte/macrophages per glomerulus and the number of glomerular crescents and the degree of proteinuria. The constancy of the percentage of exudate macrophages and polymorphonuclear leukocytes were observed irrespective of the grade of mesangial hypercellularity. On the other hand, the increasing percentage of PO-negative macrophages and decreasing percentage of monocytes were observed over the grade. These results suggest that mononuclear phagocytes might play an important role in the pathogenesis of mesangial hypercellularity, and irreversible glomerular damage and interstitial tissue injury in IgA nephropathy.
The occurrence of rhabdomyolysis and acute renal failure associated with cytomegaloviral infection is rare. A 27-year-old housewife was admitted to our hospital with complaints of thirst, muscle weakness, abdominal pain and oliguria. There was no past history of diabetes, drinking, fever or drug habituation and a negative family history. Laboratory tests revealed myoglobi nuria, hyper-pancreatic type amylaseuria, hyperglycemia, azotemia and highly increased creatine phosphokinase in the plasma. She was treated with hemodialysis and insulin therapy. Serological studies showed a 4-fold increase in cytomegalovirus antibody titers 4 weeks after admission. Muscle biopsy specimens showed hyaline degeneration and infiltration of T cell lymphocytes in the muscle. Renal biopsy specimens showed acute tubular necrosis and some myoglobin casts. No cytomegalovirus antigen was found in renal specimens by immunofluorescence study. From these results, it was determined that a systemic cytomegalovirus infection triggered pancreatitis which caused diabetic ketoacidosis, rhabdomyolysis and acute renal failure. (Internal Medicine 31: 426-430, 1992)
Batter's syndrome characteristically exhibits the constellation of hypokalemic alkalosis, normotensive hyperreninism, hyperalodosteronism, hyporesponsiveness to pressor agent and juxtaglomerular cell hyperplasia. Recently, metabolic mimicry of Batter's syndrome by vomiting, diarrhea, laxatives and diuretics abuse has been reported. We had a 30 year-old female patient whodeveloped so-called pseudo-Bartter's syndrome as the result of surreptitious self-administration of furosemide for about six years. In this case, calcification of bilateral renal medulla was demonstrated. Such adverse reaction has not been reported to date. Moreover, a total 14 cases of pseudo-Bartter's syndrome reported in Japanese literature is reviewed.
A 54-year-old womanwho had proteinuria due to stage II membranous nephropathy is reported. She was treated with indomethacin for proteinuria and developed drug-induced
SUMMARYSerum angiotensin converting enzyme (ACE) activity in patients with chronic renal failure (CRF) on regular hemodialysis (HD) was measured. The enzyme activity of these patients was significantly higher than that of an age-matched control group. Additionally, we found that an elevated activity was observed in patients who had a longer history of HD. The enzyme activity in patients with CRF caused by diabetic nephropathy was higher than that in patients with CRF caused by chronic glomerulonephritis, though this difference was not significant. We conclude that diffuse vascular damage might be the cause of the increased ACE activity seen in CRF.Additional Indexing Words: Angiotensin converting enzyme Diffuse vascular damage Chronic renal failure NGIOTENSIN converting enzyme (ACE), an endopeptidase, catalyzes the formation of the octapeptide angiotensin II by splitting the dipeptide histidyl-leucine from the decapeptide angiotensin I. Moreover, it degrades the nonapeptide bradykinin which acts as a potent vasodilator. ACE is known to be distributed widely in the body. The activity of the enzyme is especially high in lung and kidney tissue1) and is also detectable in serum.It has been known that elevated ACE activity is frequently detectable in the serum and in granulomatous lymph nodes obtained from patients with sarcoidosis. The enzyme activity seems to be a sensitive index for evaluating the clinical course and effectiveness of therapy for this disease.2)-4) Furthermore, the enzyme activity is found to be increased in Gaucher's disease, leprosy, liver cirrhosis, and in diabetes mellitus,5)-7) and conversely decreased in
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