[Aldosteronuria and the state of partial functions of the kidneys in diffuse glomerulonephritis, nephritis-like syndrome and hereditary nephritis in children].
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Aldosterone↗
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Comparative ultrastructural studies on endemic (Balkan) nephropathy and chicken embryo nephritis caused by infectious bronchitis virus. II. Chick embryo nephritis.
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Animals↗
[Glycoprotein nephritis-some problems in the existing experimental model of nephritis].
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Animals↗
[Radiology of bacterial and abacterial interstitial nephritis (author's transl)].
The x-ray findings of 727 patients with chronic interstitial nephritis are evaluated; these patients have been controlled over a period of several years: 594 suffer from chronic bacterial interstitial nephritis (pyelonephritis) and 133 patients from chronic abacterial interstitial nephritis of different etiology. The causes for the abacterial type of nephritis are phenacetin and primary gout. The radiological signs of the two forms of chronic interstitial nephritis in different degrees of involvement are pointed out. Whereas with the chronic abacterial interstitial nephritis symmetrical affection is typical, the chronic bacterial interstitial nephritis shows asymmetrical findings, especially in ascending pyelonephritis. Differentiation between the chronic bacterial nephritis and the chronic abacterial nephritis can be achieved in most cases by radiological signs, (morphological findings). The microscopic evaluation does not always allow a differentiation; because there are mixed forms and secondary bacterial infections are associated with primary chronic abacterial interstitial nephritis in the late stages. The multiple causes for chronic abacterial interstitial nephritis is radiologically reflected mostly by uniform signs during the different degrees of involvement.
Chronic Disease↗
Primary IgA glomerulonephritis and Schönlein-Henoch purpura nephritis: Clinicopathological and immunohistological characteristics.
A comparative analysis on clinicopathological and immunohistological characteristics was performed of 205 cases with primary IgA nephritis and 35 with Schönlein-Henoch purpura nephritis (purpura nephritis). Diagnostic criteria for primary IgA nephritis were set out so that IgA was either the most prominent immunoglobulin or, at least, equal to IgG and/or IgM, if present, irrespective of mesangial or peripheral localization. In primary IgA nephritis, one half of the cases were discovered by asymptomatic proteinuria, and one-third presented recurrent upper respiratory tract infection and gross hematuria, one-fourth abdominal pain and a few cases joint pain, while purpura nephritis was associated with a significantly higher incidence of such systemic symptoms as abdominal and joint pains, in addition to purpura. Both diseases shared a tendency toward conspicuous hematuria in contrast to the modest proteinuria, with normal renal function in three-fourths to two-thirds. Moreover, four of 35 with purpura nephritis showed preceding proteinuria and had been regarded as primary IgA nephritis until purpura appeared. The glomerular pathology had a common feature in that there was frequent occurrence of mesangial proliferative and focal and segmental lesions. The immunohistology in the two diseases was indistinguishable with regard to the glomerular immunoglobulins and mediators, whether purpura was present or absent. Thus, we propose a unifying concept that, by analogy with SLE, primary IgA nephritis may be regarded as 'sine lupo,' lying on one side of the nosological spectrum with less systemic symptoms, whereas purpura nephritis may occupy the other side with more systemic aspects. Furthermore, we confirmed the epimembranous granular deposition of IgA in both diseases as the most characteristic morphological expression of circulating immune complexes.
Adolescent↗
Lupus nephritis. Clinical course as related to morphologic forms and their transitions.
An intensive study of the course of lupus nephritis has been undertaken in 88 patients in whom strict morphologic criteria were utilized in classification. All were treated with steroid, and 17 received cytotoxic drugs in addition. Focal proliferative lupus nephritis generally follows a benign course except in the occasional instances when transition to the diffuse proliferative or membranous forms occurs. Membranous lupus nephritis, when characterized by persistent nephrotic syndrome, leads slowly to renal failure, but this progression is aborted in the one-third in whom remission of the nephrotic syndrome can be achieved. A fatal outcome occurs within five years in the majority of those with diffuse proliferative lupus nephritis and the nephrotic syndrome, often in association with necrotizing renal vasculitis, severe hypertension and accelerated renal failure. A small number with the diffuse proliferative form have a remission and then show only mesangial abnormalities, usually, however, with the appearance of glomerular sclerosis. Progressive glomerular sclerosis is observed in some patients and may be a sequel of the remission of the diffuse or focal proliferative lesions, or it may represent still another form of lupus nephritis. Mesangial immune deposits with or without proliferation, at times in the absence of clinical renal disease, are observed early in the course of systemic lupus erythematosus (SLE) and may proceed to the diffuse proliferative or membranous forms. The present observations serve to emphasize the importance of strict morphologic classification in the comparison of different treatment regimens for lupus nephritis. In view of the grave prognosis of established diffuse proliferative lupus nephritis, which probably evolves from a mesangial involvement common to all patients with SLE from its onset, early therapy may be the key to the management of lupus nephritis.
Adolescent↗
Autoimmunity to glomerular antigens in Henoch-Schoenlein nephritis.
1. Henoch-Schoenlein nephritis and IgA nephropathy share clinical and immunological features, but the pathogenesis of neither condition is established. We have recently described IgG autoantibodies to glomerular components in active IgA nephropathy and have now sought evidence for a similar autoimmune component in Henoch-Schoenlein purpura. 2. Sera from 26 patients with Henoch-Schoenlein nephritis and six patients with Henoch-Schoenlein purpura without accompanying nephritis were studied and compared with sera from 20 patients with other forms of glomerulonephritis and 40 normal subjects. E.l.i.s.a.s were developed to detect IgA and IgG binding to the ligand from whole human glomeruli previously described, laminin, DNA, cardiolipin (diphosphatidylglycerol) and a panel of dietary constituents (BSA, alpha-caesin, beta-lactoglobulin, ovalbumin and wheat gliadin). 3. Sera from 16 of the 26 patients with Henoch-Schoenlein nephritis displayed increased IgG binding to the human glomerular extract compared with the normal control group (P < 0.001), whereas IgG binding was not significantly raised in the patients with Henoch-Schoenlein purpura without evidence of renal involvement. IgA binding was not raised compared with control subjects. Serum IgA and IgG binding to other potential autoantigens or antigens present on dietary constituents was not significantly different in patients with Henoch-Schoenlein nephritis or patients with Henoch-Schoenlein purpura without nephritis compared with control subjects. 4. Western blotting of the denatured and reduced glomerular extract revealed binding of IgG, from the sera of patients with active Henoch-Schoenlein nephritis, to glomerular components of M(r) 48,000 and 58,000, similar to the M(r) of the glomerular antigens identified in IgA nephropathy.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
Poststreptococcal nephritis--a rare disease?.
Forty-three children presenting with acute nephritis were studied for evidence of preceeding steptococcal infection. They were compared with a group of control children of similar age. Two-thirds of those with nephritis gave a history of a preceeding respiratory infection (compared with one-third of the controls). A significant rise of antistreptolysin O tire occurred in only 16 children with nephritis and within this minority several did not show a fall of serum C3 level. It is probable that only one-third of the children with acute nephritis had poststreptoccoccal glomerulonephritis. Poststreptococcal glomerulo-nephritis is no longer the main cause of childhood acute nephritis in the Leeds area. There may be many different aetiological factors and this diversity calls for more rigorous investigations and a more guarded prognosis.
Acute Disease↗
Correlation between reduction of polymorphonuclear leucocytes in glomeruli injected with a newly developed monoclonal antineutrophil antibody and proteinuria in Masugi nephritis.
The effects of the reduction of neutrophils in glomeruli on the improvement of proteinuria and glomerular injuries were determined in the first (heterologous) phase of Masugi (nephrotoxic) nephritis. Male (6-week-old) WKA/Hkm rats were initially injected with 2.0 ml of a newly developed monoclonal antineutrophil antibody and then injected with 1.0 ml of nephrotoxins. This monoclonal anti-neutrophil antibody was found to have selectively reduced the number of neutrophils in the glomerular capillary lumen in cases of Masugi nephritis by light microscopy. Malondialdehyde (MDA) levels or superoxide dismutase (SOD) activities in renal tissues of such rats were also examined. However, there were no significant differences in the levels of proteinuria and the number of glomerular cells containing resident cells and infiltrated mononuclear cells in the first phase of Masugi nephritis with or without pretreatment with antineutrophil antibody. No significant differences were observed in the levels of MDA or SOD activities in renal tissues of Masugi nephritis with or without pretreatment with such an antibody either. It appeared that infiltration of neutrophils in the glomeruli might not be related to proteinuria and glomerular injuries in the first phase of Masugi nephritis. It was postulated that the massive proteinuria in the first phase of Masugi nephritis might be correlated with the activities of reactive oxygen species induced by the glomerular cells, i.e. glomerular resident cells and infiltrated mononuclear cells.
Animals↗
Soluble interleukin-2 receptor levels in lupus nephritis.
Soluble interleukin-2 receptor (IL-2R) levels were measured and correlated prospectively with clinical, histologic and serologic findings over a 9-month period in 62 lupus patients. Initially, 39 patients had clinical nephritis and 23 patients did not have nephritis. The 62 lupus patients has significantly higher IL-2R than 15 normal controls, most of this difference attributable to patients with nephritis. During lupus nephritis flare 9 of 10 patients showed significant elevations of IL-2R while only 6 of the 10 patients showed either elevation of anti-DNA antibody or decrease in CH50. During disease remission or stable clinical activity changes in IL-2R levels paralleled changes in anti-DNA antibody and CH50. Nephritis patients with cellular proliferative histology had significantly higher IL-2R levels than those with membranous or mesangial nephropathy. IL-2R correlated strongly with histologic activity and chronicity indices, IgG and C3 deposition whereas anti-DNA antibody and CH50 levels did not. IL-2R levels did not correlate with serum creatinine suggesting that elevations of IL-2R were not simply due to decreased clearance. These observations suggest that serum IL-2R level is a useful marker of disease activity in lupus nephritis and may serve as a helpful adjunct in management of this disorder.
Adult↗
Comparison of the complement-fixing activity of antinuclear antibodies in lupus nephritis, mixed connective tissue disease, and scleroderma.
Complement-fixing antinuclear antibody (CFANA) titers were measured in 18 patients with lupus nephritis and were compared to titers in 22 patients with scleroderma and mixed connective tissue disease (MCTD) who had comparable ANA titers but lacked nephritis. CFANA titers were higher in SLE patients with nephritis than in a control group of SLE patients without nephritis but were no higher than in scleroderma or MCTD. Thus the striking differences in the prevalence of nephritis among these patients with high titer ANA cannot be explained by differences in complement fixation by these antibodies.
Antibodies, Antinuclear↗
Intrarenal platelet consumption in the diffuse proliferative nephritis of systemic lupus erythematosus.
1. Platelet survival and an index of the localization of platelets in the kidney were studied in patients with the proliferative nephritis of systemic lupus erythematosus, either focal or diffuse, and in control subjects. Platelet survival was reduced in patients with proliferative lupus nephritis, more in those with diffuse rather than focal renal involvement. 2. The index of renal platelet localization in patients with diffuse proliferative nephritis suggested an intrarenal platelet consumption not found in other groups. 3. A patient with the classical platelet autoantibody disease, idiopathic thrombocytopenic purpura, also showed reduced platelet survival but localization of platelets was in the spleen rather than the kidney. 4. Intrarenal platelet consumption in diffuse proliferative lupus nephritis may be an epiphenomenon of pre-existing scarring or platelet aggregation secondary to immune complex-formation, which contributes to the progressive sclerosing lesions of this form of nephritis.
Adult↗
Antibody avidity for native DNA in lupus nephritis.
To study the participation of the antibody avidity in the pathogenesis of lupus nephritis, we measured the antibody avidity to native DNA by the method of Minden and Farr (14) in patients with SLE. The avidity to native DNA was almost less than 40%. The avidity and the histological activity of lupus nephritis were well correlated; the antibody avidity of the active-group sera was higher than that of the inactive-group sera and the group without nephritis. In the group with antibodies of relatively high avidity, the complexes were deposited mainly in the subendothelial side of GBM and in the mesangium. On the other hand, in the group with low-avidity antibodies, the complexes were localized in the subepithelial side of GBM. On investigating the quality of the complexes, we noted that the complexes composed of high-avidity antibodies prepared in vitro were larger than those of low avidity and the former were larger than 19S. If the native-DNA-anti-native DNA system is the mechanism basic to lupus nephritis, the differences in immune response of the host, namely the degree of antibody avidity may greatly affect complex formation and influence the histological activity and nephritogenicity of lupus nephritis.
Adult↗
[A case of acute interstitial nephritis and nonoliguria acute renal failure induced by cimetidine].
Cimetidine is a histamine H2-receptor antagonist. Widely it is prescribed, and then various side effects have been increasingly recognized. Acute renal failure as a result of acute interstitial nephritis is one of the most important adverse effect. We report a case of biopsy-proven acute interstitial nephritis following cimetidine therapy. Farther more, we review other reported cases of cimetidine-induced acute interstitial nephritis, and discuss the clinical features and a role of immunological mechanisms of these cimetidine-induced disorders. A 52-year-old woman was admitted because of fever and protenuria. A month before admission, she developed gastric ulcer and was given cimetidine 600mg orally a day by a near physician. Laboratory data on admission included the following: white blood cell count, 14700/microliters; eosinophils, 6%; BUN, 50.7mg/dl; Cr, 7.6mg/dl; CRP, 34.0mg/dl. All drugs were discontinued because we suspected drug-induced acute renal failure, especially by cimetidine. Renal biopsy performed on day 3 showed interstitial nephritis with lymphocyte infiltration which was composed mainly of T cell. T4/T8 ratio was determined to be 1. There was neither predominance of helper nor cytotoxic cells in T cell subpopulation. We reviewed 22 cases reported and discussed the features of cimetidine-induced interstitial nephritis. The most important thing is to monitor renal function periodically with the suspicion of this disorder. On the detection of abnormality of laboratory data, cimetidine should be discontinued.
Acute Kidney Injury↗
Clinical prognostic factors in lupus nephritis. The importance of hypertension and smoking.
BACKGROUND: Many previous studies of the influence of sociodemographic and clinical factors on the development of renal failure in patients with lupus nephritis have been based on selected subgroups of patients and have yielded conflicting results. We sought to determine the prognostic importance of patient demographic characteristics (age, gender, race, and socioeconomic status), smoking status, and hypertension in the development of end-stage renal disease (ESRD) among patients with lupus nephritis. METHODS: This retrospective cohort study followed an inception cohort of 160 adults with lupus nephritis. The outcome measure was the development of ESRD, defined as the institution of maintenance dialysis or measurement of a creatinine clearance of 10 mL/min or less. Life-table analysis was used to determine differences between patient subgroups in the time to development of ESRD. RESULTS: End-stage renal disease developed in 41 (26%) of 160 patients followed up for a median of 6.4 years. Hypertension and smoking status at the onset of nephritis were strongly associated with differences in the time to development of ESRD. The median time to ESRD among patients with moderate to severe hypertension (diastolic blood pressure, greater than or equal to 105 mm Hg) was 7 months, among patients with mild hypertension (diastolic blood pressure, 90 to 104 mm Hg) it was 146 months, and among normotensive patients it was greater than 273 months. The median time to ESRD among smokers was 145 months and among nonsmokers it was greater than 273 months. These effects persisted in multivariable analyses adjusting for differences among patients in age, gender, socioeconomic status, renal histology, and immunosuppressive treatment. The independent effects of hypertension and smoking resulted in shorter times to renal failure among patients who were both hypertensive and smoking, compared with nonsmoking hypertensive patients. The development of ESRD did not differ among patient demographic subgroups. CONCLUSION: Patient demographic characteristics had no detectable impact on the rate of progression to ESRD in this cohort. Hypertension and smoking appear to be important, potentially modifiable, factors influencing the prognosis of patients with lupus nephritis.
Adult↗
Single and multiple drug therapy in autologous immune complex nephritis in rats.
Autologous immune complex (AIC) nephritis is a form of chronic renal disease with remarkable similarities to idiopathic membranous nephropathy occurring in man. AIC nephritis was induced in 160 gram Lewis rats with a single footpad injection of tubular brush-border antigen (FxIA) in complete Freund's adjuvant. When killed at 8 weeks, 85 per cent of the rats demonstrated typical diffuse glomerular deposits of immunoglobulin G and B1C (C1/3 component of complement) by immunofluorescent microscopy, and subepithelial electron-dense deposits by electron microscopy. Both immune complex disease and significant proteinuria occurred in two-thirds of these animals. An attempt to modify the natural course of established AIC nephritis using large doses of potent glucocorticoids (methyl-prednisolone), anti-inflammatory agents (acetylsalicylic acid, indomethacin, and cyproheptadine), and immunosuppressive drugs (cyclophosphamide, azathioprine) was begun 4 weeks after initial immunization and continued for 4 more weeks. None of the single drug nor multiple drug protocols employed was of demonstrable benefit in ameliorating the immune events operating in AIC nephritis. Cyclophosphamide and indomethacin, when used singly, were associated with significant mortality in the animals studied. All combined drug protocols involving glucocorticoids and antimetabolites were associated with unacceptable mortality as well. Of interest, immune complexes could not be demonstrated in the vascular choroid plexus of any rat with AIC nephritis. This failure to modify the course of established renal disease (AIC) in an experimental animal with generally available pharmacologic agents, is similar to the usual results of such treatment in chronic renal disease (idiopathic membranous nephropathy) in man. It is possible that new and more potent anti-inflammatory agents employed singly or in various combinations, will permit more successful manipulation of the host's immunologic system to prevent or modify immune injury of the renal glomerulus.
Animals↗
[Treatment of experimental immune complex nephritis with indomethacin].
Functional, histological and immune-histological examination were performed in altogether 64 Wistar-rats, in order to control the effect of a therapy with 2 mg/kg per body weight indomethazine lasting 2 months at the model of an experimental immune complex nephritis. In 44 rats after presensibilisation an immune complex nephritis was performed by intraperitoneal injections with human serum albumin which were repeated three times a week. 24 glomerulonephritis animals and other 20 animals without glomerulonephritis were daily administered indomethazin through a tube probe, the remaining 20 animals with glomerulonephritis served as untreated control groups. The excretion function of the kidney was tested before the beginning of the experiment, 2 weeks after the beginning of the therapy and the regular serum injections, respectively, and before the end of the experiment by determination of the biological half-life period of 131J-hippuran. In every case one day before this the proteinuria during 24 hours was determined. At the end of the experiment the kidneys were examined histologically and immune-histologically. The results showed that indomethazin does not lead to a clear influence on the proteinuria in the immune complex nephritis of the rat. The excretion of 131J-hippuran was significantly restricted, whereas the histological and immune-histological preparations in the animals with foreign serum injections showed clear changes of the glomeruli in the sense of an early stage of the immune complex nephritis, however, they did not show any essential influence by indomethazin. That is, indomethazin had altogether no favourable effect on the immune complex nephritis of the rat.
Animals↗
[Dysembryogenesis in hereditary nephritis].
In 75 children with hereditary nephritis, in 27 ones with hematuric form of acquired nephritis and in 55 parents dysplastic symptoms were investigated. A high differential and diagnostic value of disembriogenetic stigmata for hereditary nephritis is demonstrated. It is considered that connective tissue stigmata are one of the symptoms of hereditary nephritis. Some genetic and ontogenetic aspects of displastic symptoms formation in this case are discussed.
Adolescent↗