Course Of Chronic Glomerulonephritis Research Articles

Clinical and Biochemical Aspects of the Development of Chronic Viral Hepatitis with A Comorbid Course of Chronic Glomerulonephritis

In viral hepatitis, secondary glomerular lesions are slow, but in one third of patients, this process develops steadily and manifests itself as a nephrotic syndrome, worsening the patient’s condition with the manifestation of renal failure. The purpose of this study is to examine the clinical and biochemical aspects of damage to the functional state of the kidneys in chronic viral Hepatitis B and C. The study involved 198 patients with positive HBV and HCV serological markers and clinical and laboratory syndromes of kidney damage.

Clinical and Biochemical Aspects of the Development of Chronic Viral Hepatitis with A Comorbid Course of Chronic Glomerulonephritis

Clinical and Biochemical Aspects of the Development of Chronic Viral Hepatitis with A Comorbid Course of Chronic Glomerulonephritis

Clinical and Biochemical Aspects of the Development of Chronic Viral Hepatitis with A Comorbid Course of Chronic Glomerulonephritis

Clinical and Biochemical Aspects of the Development of Chronic Viral Hepatitis with A Comorbid Course of Chronic Glomerulonephritis

Heat shock protein 90 and NFkB levels in serum and urine in patients with chronic glomerulonephritis.

Heat shock proteins play an important role in immune inflammation and the formation and restoration of proteins. In recent years, the importance of heat shock protein 90 (Hsp90) in the activation of immune inflammation through nuclear factor kB (NFkB) has been discussed. To assess the activation of the Hsp90-NFkB system by measuring serum and urinary levels in patients with chronic glomerulonephritis (CGN). This study included 32 patients with active forms of CGN and 14 patients with Fabry nephropathy. The control group included 10 healthy individuals. Twenty-one out of 32 CGN patients had nephrotic syndrome (NS). Eleven out of 32 CGN patients had proteinuria levels from 1 to 3g/day without nephrotic syndrome. A total of 17 patients had renal dysfunction (estimated glomerular filtration rate < 60ml/min/1.73m2). Fourteen patients with Fabry nephropathy had proteinuria without nephrotic syndrome. Serum and urine HSP-90 and NFkB p65 levels were determined using an enzyme-linked immunosorbent assay. The levels of HSP-90 and NFkB in the serum of patients with CGN were significantly higher than in healthy individuals and patients with Fabry nephropathy. In patients with Fabry nephropathy, the HSP-90 and NFkB levels in the urine and serum did not significantly differ from those in the control subjects. Serum Hsp90 levels were significantly higher in the CGN patients with NS than in patients without NS, as well as in patients with normal renal function compared with patients with an eGFR < 60ml/min/1.73m2 and patients with tubulo-interstitial fibrosis. Higher levels of HSP-90 and NFkB in serum were observed in patients with nephrotic forms of CGN, including focal segmental glomerulosclerosis, minimal change disease and membranous nephropathy. There were no correlations between the clinical signs of CGN and urinary HSP90/NFkB levels. Activation of the HSP-90-NFkB system, which is directly involved in the development of immune inflammation in CGN, was found in patients with an active course of CGN, especially in those with nephrotic syndrome.

THE INFLUENCE OF HEMERIN ON THE COURSE OF CHRONIC GLOMERULONEPHRITIS

Objective: determination of the infl uence of hemerin on the features of the course of chronic glomerulonephritis. Materials and method: the study included 80 patients with chronic glomerulonephritis. Th e criterion for including patients in the study was the presence of indications for nephrobiopsy and the patient’s consent to perform it. All patients underwent general clinical examination with establishment of anamnesis of the disease, creatinine level, urea, calculation of GFR, determination of the general blood test, general urine analysis, daily proteinuria. Venous blood sampling was used to determine the level of hemerin. Twelve months aft er the patients were admitted to the study and treated according to standard therapy, several indicators were re-recorded. Results: positive correlation associations of hemerin and sedimentation rate of erythrocytes, total cholesterol and negative - with the level of protein in the blood have been established. It was shown that significantly more significant improvement in the clinical manifestations of renal remodeling was observed in patients with a high level of hemerin (≥ 297 pg / ml) 12 months aft er treatment in comparison with the group of patients with lower values of Hemerin (<297 pg / ml) - the hyperhydration Syndrome, the proteinuria of a single and daily portion, total cholesterol, fibrinogen decreased to a greater extent. Conclusion: based on the presented results of statistical analysis, it is possible to judge the severity of clinical manifestations associated in patients with elevated values of hemerin. However, aft er the standard therapy of chronic glomerulonephritis, these patients have better dynamics in stabilizing clinical parameters. It is possible to assume some protective function of hemerin in patients with glomerulonephritis.

Association of Retinoid X Receptor Alpha Gene Polymorphism with Clinical Course of Chronic Glomerulonephritis

BackgroundVitamin D (VD), VD binding protein, VD receptor (VDR), and retinoids are involved in pathogenesis of chronic glomerulonephritis (ChGN). We aimed to compare distribution of VD pathway gene polymorphisms in ChGN patients showing glomerular filtration rate (GFR) category 1–3, GFR category 5D, and healthy controls in order to elucidate the role of VD-related polymorphisms in the course of ChGN.Material/MethodsGFR category 1–3 ChGN patients (n=195), GFR category 5D ChGN patients (n=178), and controls (n=751) underwent testing for polymorphisms of genes encoding VD binding protein (GC, rs2298849, rs7041, rs1155563), VDR (VDR, rs2228570, rs1544410), and retinoid X receptor alpha (RXRA, rs10776909, rs10881578, rs749759).ResultsAmong GFR 1–3 subjects possessing TT genotype of RXRA rs10776909, 75% of patients had nephrotic syndrome, and 37.5% had glomerular hyperfiltration defined as GFR >140 ml/min/1.73 m2, and, consequently, serum creatinine was lower in these patients compared to the remaining subjects (0.67±0.26 vs. 0.94±0.34, P=0.014). In GFR category 5D ChGN patients, frequencies of RXRA rs10776909 allele T (25% vs. 19%) and CT+TT (46% vs. 34%) were higher compared to frequencies of respective variants in controls (Ptrend=0.004, Pgenotype=0.008).ConclusionsRXRA rs10776909 allele T is specifically involved in the pathogenesis of ChGN. This risk allele may be also associated with worse clinical course of ChGN.

Urinary biomarkers for podocyte injury: Significance for evaluating the course and prognosis of chronic glomerulonephritis

To estimate the degree of podocyte injury in patients with different types of chronic glomerulonephritis (CGN) from the urinary level of podocyte markers and to determine the significance of these indicators as criteria for disease activity and prognosis. Seventy-three patients with CGN, including 20 with inactive nephritis (Group 1), 23 with obvious urological syndrome (Group 2), 30 with nephrotic syndrome (NS) (Group 3), among them there were 7 patients with severe NS and 7 with NS concurrent with acute nephritic syndrome, were examined. A control group consisted of 8 healthy individuals. In the examined groups, the degree of podocyturia (PCU) was investigated by flow cytometry using podocalyxin-labeled antibodies and the levels of nephrinuria (NU), heat shock protein 27 (HSP27) in urine, interleukin 6 (IL-6), caspase 9, and vascular endothelial growth factor (VEGF) were estimated by ELISA. The patients with active CGN were found to have a high level of markers for podocyte injury: PCU and NU, which correlate with the magnitude of proteinuria, severity of NS, and degree of podocytopenia. Those with the severest NS, that concurrent with renal dysfunction in particular, were observed to have a progressive imbalance of inflammatory (IL-6), apoptotic (caspase-9), and defensive (HSP27 and VEGF) factors, which displays the incompetence of self-defense mechanisms in podocytes and contributes to the torpid course of CGN. Progressive PCU and NU are a poor prognostic sign indicating the risk of glomerulonephritis. The indicators considered are universal for all patients with CGN running with proteinuria and may be used to monitor the course of the disease; moreover, the damaging factors should be considered in conjunction with the defensive factors.

Influences of pregnancy on the natural course of chronic glomerulonephritis with impaired renal function

In an attempt to clarify the influence of pregnancy on the natural course of the chronic glomerulonephritis with impaired renal function (glomerular filtration rate: GFR less than or equal to 70 ml/min), the courses of 14 pregnancies occurring in 10 patients (seven with IgA nephropathy, one with membranoproliferative glomerulonephritis, one with membranous nephropathy and one with hereditary nephropathy) were studied. In 8 patients GFR measured before pregnancies ranged from 46 to 70 ml/min and in the other two creatinine clearance estimated in the first trimester of pregnancies was 62 and 49 ml/min, respectively. The pregnancies resulted in 10 live births, one spontaneous abortion, one artificial abortion and 2 neonatal deaths. In 2 out of 10 live births fetal weight was less than 2500 g. In 3 of 11 pregnancies there was neither increase in urinary protein nor elevation of blood pressure during pregnancies, while seven (64%) had increased proteinuria during the third trimester, and 4 of them were also complicated with hypertension. In 6 of 10 patients, there was no decrease in GFR during pregnancies. In three patients GFR was decreased from 70 to 36 ml/min, 70 to 58 ml/min and 62 to 48 ml/min, respectively. However, these reductions were considered to go with the natural course of respective patients because the reduction slopes were almost the same or rather mild in comparison with those estimated before or after pregnancies. The other patient also had a transient increase in serum creatinine level during two pregnancies, but the reciprocals of serum creatinine concentration before and after the pregnanciesdeclined linearly with time. These data suggest that pregnancy might have little influence on the natural course of the chronic glomerulonephritis even if complicated with renal functional impairment defined as GFR of 70 ml/min or less.

THE NEPHROTIC PHASE: ITS FREQUENCY OF OCCURRENCE AND ITS DIFFERENTIAL DIAGNOSTIC VALUE IN DETERMINING THE NATURE OF THE RENAL LESION IN 120 PATIENTS WHO DIED OF RENAL FAILURE

Article1 July 1946THE NEPHROTIC PHASE: ITS FREQUENCY OF OCCURRENCE AND ITS DIFFERENTIAL DIAGNOSTIC VALUE IN DETERMINING THE NATURE OF THE RENAL LESION IN 120 PATIENTS WHO DIED OF RENAL FAILUREWALTER L. BLOOM, DAVID SEEGALWALTER L. BLOOMSearch for more papers by this author, DAVID SEEGALSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-25-1-15 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptINTRODUCTIONThe term "nephrotic phase" is used to describe a syndrome occurring during the course of chronic glomerulonephritis and characterized by albuminuria, hypoproteinemia, hypercholesterolemia and edema. In general, these features have served as the criteria for diagnosis.1, 2 The degrees of hypoproteinemia, proteinuria, edema and lipemia necessary for the diagnosis have not been clearly defined.There is agreement over the occurrence of the nephrotic phase in particular types of renal diseases which terminate in renal failure. Baehr3noted that "every case of glomerulonephritis has a nephrotic element." Christian4agrees with this opinion. The rarity of the nephrotic phase in arteriolarnephrosclerosis...Bibliography1. LEITER L: Nephrosis, Medicine, 1931, x, 221-225. Google Scholar2. ATCHLEY DW: The nephroses, Textbook of Medicine, Cecil, 1943, 6th edit, W. B. Saunders Co., Philadelphia, 924-925. Google Scholar3. BAEHR G: Discussion of "Nephrosis with glomerulonephritis," (case report) Margaret Worwick. Presented at Scientific Proceedings of the Twenty-Eighth annual meeting of the American Association of Pathologists and Bacteriologists, Am. Jr. Path., 1928, iv, 632. Google Scholar4. CHRISTIAN HA: Nephrosis: A critique, Jr. Am. Med. Assoc., 1929, xciii, 23-25. CrossrefGoogle Scholar5. LOEB RF: Nephritis, Textbook of Medicine, Cecil, 6th Ed., 1943, W. B. Saunders, Philadelphia, p. 903-924. Google Scholar6. WEISSPARKER SF: Pyelonephritis: Its relation to vascular lesions and to arterial hypertension, Medicine, 1939, xviii, 221-315. CrossrefGoogle Scholar7. FISHBERG AM: Hypertension and nephritis, 1939, Lea and Febiger, Philadelphia. CrossrefGoogle Scholar8. PETERSVAN SLYKE JPDD: Quantitative Clinical Chemistry. Interpretations, 1935, Williams and Wilkins, Baltimore. Google Scholar9. LINDERLUNDSGAARDVAN SLYKE GCCDD: The concentration of the plasma proteins in nephritis, Jr. Exper. Med., 1924, xxxix, 887-955. CrossrefGoogle Scholar10. PETERSBRUCKMANEISENMANHALDWAKEMAN JPFSAJPMAM: The plasma proteins in relation to blood hydration. VII. A note on the proteins in acute nephritis, Jr. Clin. Invest., 1932, xi, 97-102. PAYNE S. A. PETERS J. P.: The plasma proteins in relation to blood hydration. VIII. Serum proteins in heart disease, Jr. Clin. Invest., 1932, xi, 103-112. PETERS J. P. BRUCKMAN F. S. EISENMAN A. J. HALD P. M. WAKEMAN A. M.: The plasma proteins in relation to blood hydration. IX. Serum proteins in the terminal stages of renal disease, Jr. Clin. Invest., 1932, xi, 113-122. CrossrefGoogle Scholar11. VAN SLYKESTILLMANMÖLLEREHRICHMCINTOSHLEITERMACKAYHANNONMOOREJOHNSTON DDEEWJFLEMRRNSC: Observations on the courses of different types of Bright's disease, and on the resultant changes in renal anatomy, Medicine, 1930, ix, 257-386. CrossrefGoogle Scholar12. BLOOR WR: The distribution of the lipoids ("fats") in human blood, Jr. Biol. Chem., 1916, xxv, 577-599. CrossrefGoogle Scholar13. DENIS W: Cholesterol in human blood under pathological conditions, Jr. Biol. Chem., 1917, xxix, 93-110. CrossrefGoogle Scholar14. PAGEKIRKVAN SLYKE IHEDD: Plasma lipids in essential hypertension, Jr. Clin. Invest., 1936, xv, 109-113. CrossrefGoogle Scholar15. STEINERDOMANSKI AB: Serum cholesterol and atherosclerosis in chronic glomerulonephritis, Am. Jr. Med. Sci., 1942, cciv, 79-84. CrossrefGoogle Scholar16. MANSFIELDMALLORYELLIS JSGKLB: The differential diagnosis of chronic Bright's disease, New England Jr. Med., 1943, ccxxix, 387-395. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: New York, N. Y.*Received for publication October 30, 1945.From the Research Service, First (Columbia) Division, Goldwater Memorial Hospital, Department of Hospitals, and the College of Physicians and Surgeons, Columbia University, New York City. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byMASSIVE PROTEINURIA ASSOCIATED WITH VESICO-URETERAL REFLUXHistopathologie des nephrotischen Syndroms beim KindeThe General Appearance (Habitus)Uropoietic SystemThe nephrotic syndromeVergleichende pathologisch-anatomische und klinische Untersuchungen an 100 F�llen von diffuser GlomerulonephritisSTUDIES OF POSTSTREPTOCOCCAL NEPHRITIS AND OTHER GLOMERULAR DISEASES*†DAVID P. EARLE, M.D., F.A.C.P., ROBERT B. JENNINGS, M.D.THE NEPHROTIC SYNDROME IN ADULTS: A COMMON DISORDER WITH MANY CAUSES*ROBERT M. KARK, F.A.C.P., F.R.C.P. (Lond.), CONRAD L. PIRANI, M.D., VICTOR E. POLLAK, M.B., M.R.C.P.E., ROBERT C. MUEHRCKE, M.D., JOHN D. BLAINEY, M.D., M.R.C.P.Polycyclic nephrotic syndromeNatural history of glomerulonephritisGlomerular nephritis and lipid nephrosis: Identities and mechanismsGlomerulonephritisThe nephrotic syndromeThe Nephrotic Syndrome in ChildrenThe Nephrotic Syndrome 1 July 1946Volume 25, Issue 1Page: 15-21KeywordsEdemaGlomerulonephritisHyperlipidemiaHypoproteinemiaLesionsProteinuriaRenal diseasesRenal failureSurgeons ePublished: 1 December 2008 Issue Published: 1 July 1946 PDF downloadLoading ...

CHRONIC GLOMERULONEPHRITIS FOR FORTY YEARS: REPORT OF CASE

Case Reports1 April 1944CHRONIC GLOMERULONEPHRITIS FOR FORTY YEARS: REPORT OF CASENORMAN M. KEITH, M.D., HOWARD M. ODEL, M.D., F.A.C.P., ARCHIE H. BAGGENSTOSS, M.D.NORMAN M. KEITH, M.D.Search for more papers by this author, HOWARD M. ODEL, M.D., F.A.C.P.Search for more papers by this author, ARCHIE H. BAGGENSTOSS, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-20-4-695 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe course of chronic glomerulonephritis has been a subject of interest since Bright1considered it in a paper published in 1840. His appraisal of the course was necessarily limited to a period of 10 to 15 years; however, Mann2in 1895 reported a case which he had followed for 28 years. Recently two factors have stimulated a renewed interest in the subject. The first is that clinicians have made a more intensive application of physiologic principles to the immediate problem of the patient and their findings created a desire for the second factor, namely, an accurate record of the whole...Bibliography1. BRIGHT R: Cases and observations illustrative of renal disease accompanied with the secretion of albuminous urine. Memoir the second, Guy's Hosp. Rep., 1840, v, 101-161. Google Scholar2. MANN JD: On granular kidney following scarlatinal nephritis, Lancet, 1895, ii, 670-671. CrossrefGoogle Scholar3. VAN SLYKESTILLMANMÖLLEREHRICHMCINTOSHLEITERMACKAYHANNONMOOREJOHNSTON DDEEWJFLEMRRNSC: Observations on the courses of different types of Bright's disease, and on the resultant changes in renal anatomy, Medicine, 1930, ix, 257-386. CrossrefGoogle Scholar4. ADDISOLIVER TJ: The renal lesion in Bright's disease, 1931, Paul B. Hoeber, Inc., New York. Google Scholar5. VOLHARDSUTER FF: Nieren und ableitende Harnwege. In von Bergmann, G. Staehelin R.: Handbuch der inneren Medizin (2nd ed.), vol. VI, pt. 2, 1931, Julius Springer, Berlin. CrossrefGoogle Scholar6. ELLIS A: Natural history of Bright's disease; clinical, histological and experimental observations, Lancet, 1942, i, 1-7; 34-36; 72-76. CrossrefGoogle Scholar7. WAKEFIELDPOWERKEITH EGMHNM: Inorganic sulphates in the serum in early renal insufficiency. Significance of determinations, Jr. Am. Med. Assoc., 1931, xcvii, 913-917. CrossrefGoogle Scholar8. GRAHAM RW: Opthalmoscopically visible retinal lesions in chronic glomerulonephritis. Occurrence and characteristics, Arch. Ophth., 1941, xxvi, 435-465. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Rochester, Minnesota*The patient was presented before a clinic on glomerulonephritis at the annual meeting of the American College of Physicians, St. Paul, Minnesota, April 23, 1942. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byApplication of Tests of Renal Function to Renal DiseaseChronic Glomerulonephritis: Report of a Case Followed from Onset to Termination During a Period of Nine Years 1 April 1944Volume 20, Issue 4Page: 695-709KeywordsGlomerulonephritis Issue Published: 1 April 1944 PDF downloadLoading ...