Relevant bibliographies by topics / Glomerulonephriti

Academic literature on the topic 'Glomerulonephriti'

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Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Glomerulonephriti"

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Mukhtarova, A. V. Mukhtarova, M. M. Batyushin Batyushin, E. А. Sinelnik Sinelnik, N. V. Antipova Antipova, and A. V. Razina Razina. "Effect of VEGF a on the development of tubulointerstitial fibrosis and the probability of achieving complete remission in patients with primary chronic glomerulonephriti." Nephrology 4_2021 (December 29, 2021): 48–52. http://dx.doi.org/10.18565/nephrology.2021.4.48-52.

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Vanga, Amaresh, Sandeep Magoon, Jolanta Kowalewska, and Saad Mussarat. "Fibrilo-Tactoid Glomerulonephritis: A Possible Novel Morphological Variant." Case Reports in Nephrology and Dialysis 10, no. 3 (November 17, 2020): 154–62. http://dx.doi.org/10.1159/000510871.

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Fibrillary and immunotactoid glomerulonephritis are infrequent causes of primary nephrotic range proteinuria and are poorly understood. Recent significant developments include the discovery of DNA JB9 antigen in fibrillary glomerulonephritis. Here, we present a case of a middle-aged woman who presented with nephrotic range proteinuria, hematuria, and normal renal function. Renal biopsy revealed fibrils that were randomly arranged on electron microscopy. They were of small size and congo red negative similar to the ones found in fibrillary glomerulonephritis, but were also DNA JB 9 negative, and had a hollow core like in immunotactoid glomerulopathy. Though we try to classify these conditions into either immunotactoid glomerulonephropathy (ITGN) or fibrillary glomerulonephritis (FGN), there are scenarios such as this case where it does not fit into either and is probably an overlap or intermediate variant of these two conditions. Pathological features of these glomerulonephrites are discussed together with their clinical implications, treatment choices, and diagnostic importance.
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Manitius, J., B. Biedunkiewicz, J. Kustosz, and B. Rutkowski. "The Relationship between Insulin, Glucose and Serum Uric Acid and Their Contribution to the Progression of Renal Damage in Patients with Primary Glomerulonephritis." Journal of International Medical Research 24, no. 6 (November 1996): 449–53. http://dx.doi.org/10.1177/030006059602400601.

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It is known that some metabolic disturbances may modify the progression of renal disease including primary glomerulonephritis, but the role of purines in this process is still unknown. To investigate this, 13 untreated patients with primary glomerulonephritis were followed up for a mean of 17.6 months to analyze the changes in proteinuria and glomerular filtration rate. On entering the study, each patient was given an oral glucose tolerance test and an oral fructose load test. The areas under the glucose (PGA), insulin (PIA) and uric acid (PUAA, post-fructose) curves were calculated. Glomerulonephritic patients were found to have a statistically higher response to fructose than controls (782 ± 219 vs 518 ± 154, P < 0.005). Multiple regression analysis showed that PGA, PIA and PUAA were independently related to changes in proteinuria and glomerular filtration rate during the natural course of the disease. This preliminary study suggests that purine metabolism may modulate the progression of renal disease in proteinuric patients.
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Alaridhee, Hasanain, Azzah Alharbi, Zeayd Saeed, Róisín C. Thomas, and Cordula M. Stover. "Complement Properdin Determines Disease Activity in MRL/lpr Mice." Medicina 56, no. 9 (August 27, 2020): 430. http://dx.doi.org/10.3390/medicina56090430.

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Background and objects: In systemic lupus erythematosus, circulating immune complexes activate complement and, when trapped in renal capillaries, cause glomerulonephritis. Mouse models have been used in the preclinical assessment of targeting complement activation pathways to manage chronic inflammation in lupus. Properdin is the only known positive regulator of complement activation, but its role in the severity of lupus nephritis has not been studied yet. Materials and Methods: Fully characterized properdin-deficient mice were crossed with lupus prone MRL/lpr mice on C57Bl/6 background. Results: Compared to MRL/lpr properdin wildtype mice, MRL/lpr properdin-deficient mice had significantly lower anti-DNA antibody titres, TNFα and BAFF levels in serum. The qualitative glomerulonephritic score was less severe and there was significantly less serum creatinine in MRL/lpr properdin-deficient mice compared to MRL/lpr properdin wildtype littermate mice. Conclusion: Properdin plays a significant role in the severity of lupus overall and specifically in the extent of glomerulonephritis observed in MRL/lpr mice. Because MRL/lpr properdin-deficient mice had lower levels of anti-DNA antibodies, inflammatory mediators and markers of renal impairment, the study implies that properdin could constitute a novel therapy target in lupus disease.
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Wagner, J., S. Volk, C. C. Haufe, A. Ciechanowicz, M. Paul, and E. Ritz. "Renin gene expression in human kidney biopsies from patients with glomerulonephritis or graft rejection." Journal of the American Society of Nephrology 5, no. 7 (January 1995): 1469–75. http://dx.doi.org/10.1681/asn.v571469.

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The expression of renin mRNA was determined by a quantitative polymerase chain reaction assay in 27 human kidney samples: (1) 15 biopsies of patients with glomerulonephritis with or without angiotensin-converting enzyme inhibitor (ACEI) treatment; (2) biopsies of six renal allografts with graft rejection; and (3) six biopsy samples from unaffected parts of tumor nephrectomy specimens as controls. After isolation of RNA, 0.5 to 1 microgram of total RNA was used for reverse transcription to generate cDNA. The human renin gene was subsequently amplified by the use of two primers spanning the second and third exons. Renin expression was quantified with a renin cDNA mutant as the internal standard. It exhibited the same primer binding sites as the endogenous gene but carried a 155-basepair deletion, thus yielding a shorter amplification product. The number of glomeruli was counted by microscopic transillumination immediately after biopsy (median, 9 per biopsy; range, 2 to 23). Renin mRNA was expressed as femtograms of renin mRNA per glomerulus. Renin gene expression was lower in glomerulonephritic patients without ACEI treatment compared with that in control tumor nephrectomy samples, i.e., 63 +/- 20 (N = 7) versus 250 +/- 50 fg (N = 6) of renin mRNA/glomerulus, (P < 0.02), although plasma renin concentration in the glomerulonephritic patients was in the normal range. Significantly higher renin mRNA expression was found in glomerulonephritic patients treated with ACEI, i.e., 210 +/- 50 (N = 8) compared with 63 +/- 20 (N = 7) fg of renin mRNA/glomerulus in patient not treated with ACEI (P < 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
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Werber, H. I., S. N. Emancipator, M. L. Tykocinski, and J. R. Sedor. "The interleukin 1 gene is expressed by rat glomerular mesangial cells and is augmented in immune complex glomerulonephritis." Journal of Immunology 138, no. 10 (May 15, 1987): 3207–12. http://dx.doi.org/10.4049/jimmunol.138.10.3207.

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Abstract Cultured rat mesangial cells have features of immune effector cells that may contribute to the derangements in glomerulonephritis. Recent reports have demonstrated that mesangial cells produce a cytokine similar to interleukin 1 (IL 1). We predicted rat mesangial cells could express a gene homologous to murine macrophage IL 1. Mesangial cells were cultured by explant and were used in the fourth through sixth passages. Antibodies to desmin and fibronectin but not cytokeratin stained the cytoskeleton of all mesangial cells examined; no Ia+, leukocyte common antigen+ mononuclear phagocytes were present. RNA from mesangial cells and P388D macrophages hybridized in dot blots with a 32P-probe nick-translated from the murine IL 1 cDNA. Mesangial cells but not Swiss 3T3 fibroblasts contained IL 1 mRNA transcripts that co-migrated with the 2.0 kb message from murine P388D macrophages by Northern analysis of poly(A) RNA. In situ hybridization of cultured cells demonstrated specific hybridization of 3H-IL 1 probe to cells with the morphology of contractile mesangial cells and P388D cells but not 3T3 cells. IL 1 release is an important mediator of local inflammation and injury. Therefore we compared the expression of the IL 1 gene in total RNA from kidneys of rats with immune complex glomerulonephritis with that extracted from kidneys of healthy rats. Glomerulonephritic kidneys contain a twofold to threefold increase in IL 1 mRNA compared with normals. We conclude that rat mesangial cells express mRNA with significant homology to murine macrophage IL 1 mRNA and further suggest that local production of the potent phlogistic mediator IL 1 may be important in the pathogenesis of glomerulonephritis.
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Peterson, O. W., L. C. Gushwa, C. B. Wilson, and R. C. Blantz. "Tubuloglomerular feedback activity after glomerular immune injury." American Journal of Physiology-Renal Physiology 257, no. 1 (July 1, 1989): F67—F71. http://dx.doi.org/10.1152/ajprenal.1989.257.1.f67.

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Tubuloglomerular feedback responses were examined in control euvolemic and glomerulonephritic rats 4 wk after administration of antiglomerular basement membrane antibody (AGBM). Single-nephron glomerular filtration rate (SNGFR) was reduced approximately 30% in AGBM rats. Tubuloglomerular feedback responses were also tested with both artificial and native tubular fluid. SNGFR was evaluated at 0, 10, 20, 30, and 40 nl/min. Tubuloglomerular feedback response was present in both control and AGBM rats, although there was a shift in turning point or perfusion rate down and leftward at which SNGFR decreased in the AGBM rats. No difference in tubuloglomerular feedback responses was observed between artificial and native tubular fluids. In this model of moderate glomerulonephritis, tubuloglomerular feedback activity appears to be appropriate and intact, and the composition of the fluid entering the loop of Henle does not appear to determine or to be a condition for the presence or absence of tubuloglomerular feedback activity.
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Horino, Taro, and Yoshio Terada. "5. Mesangial Proliferative Glomerulonephritis, Endocapillary Proliferative Glomerulonephritis, Crescentic Glomerulonephritis." Nihon Naika Gakkai Zasshi 98, no. 5 (2009): 1036–41. http://dx.doi.org/10.2169/naika.98.1036.

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Zarconi, Joseph, and Michael C. Smith. "Glomerulonephritis." Postgraduate Medicine 84, no. 1 (July 1988): 239–51. http://dx.doi.org/10.1080/00325481.1988.11700351.

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Dittrich, K. "Glomerulonephritis." Kinder- und Jugendmedizin 10, no. 04 (2010): 195–202. http://dx.doi.org/10.1055/s-0038-1628975.

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ZusammenfassungGlomerulonephritiden sind relativ seltene Erkrankungen im Kindesalter, die resultierenden chronischen glomerulären Veränderungen führen jedoch dazu, dass in Deutschland jedes fünfte Kind mit chronischem Nierenersatzverfahren eine Glomerulonephritis als Grunderkrankung hat.Glomerulonephritiden manifestieren sich in dieser Altersgruppe überwiegend als akute Erkrankungen. Auch rapid progressive Verläufe mit plötzlicher Verschlechterung der Nierenfunktion sind bekannt, während schleichende Verläufe mit chronischer Hämaturie und/oder Proteinurie wesentlich seltener beobachtet werden.Die Langzeitprognose hängt stark von der rechtzeitigen Diagnosestellung und gezielten Behandlung ab. Deshalb sollte jeder Kinderarzt die klinischen Zeichen einer möglichen Glomerulonephritis kennen und die notwendigen diagnostischen Maßnahmen einleiten. Die rationale Diagnostik und die Besonderheiten typischer, im Kindesalter auftretender Glomerulonephritisformen werden in diesem Beitrag vorgestellt. Da die glomeruläre Entzündungsreaktion überwiegend immunologisch bedingt ist, besteht die Therapie neben symptomatischen auch aus immunsuppressiven Maßnahmen. Die Art der Behandlung ist jedoch von den in der Nierenbiopsie festgestellten spezifischen Veränderungen abhängig. Die kindernephrologische Mitbetreuung der betroffenen Kinder ist nicht nur bei chronischen Systemerkrankungen, sondern auch nach akuten Glomerulonephritiden notwendig.
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Dissertations / Theses on the topic "Glomerulonephriti"

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IVANOVA, MARIIA. "Advanced proteomics MALDI-MSI imaging in chronic glomerulonephrites: from diagnostics to precision medicine." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2020. http://hdl.handle.net/10281/263391.

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Chronical kidney disease (CKD) is a worldwide health problem with increasing incidence, where the major part accounts for chronic glomerulonephrites (GN). It is a group of diseases of various aetiology and multiform clinical course, having various prognosis which is often hardly predictable as well as existing prognostic markers are not always certain. There is an urging need of new reliable and specific prognostic and therapeutic markers research. A modern proteomic technology - Matrix-assisted laser desorption/ionization mass spectrometry imaging (MALDI-MSI) has been employed in many GN studies showing promising results. We aimed to study several forms of primary and secondary glomerulonephrites (membranous nephropathy, IgA nephropathy, diabetic nephropathy) to enlighten possible molecular alterations significant of diseases’ progression. The studies were performed on renal tissue biopsies, analysing them with high spatial resolution MALDI-MSI to get better visualisation of signals’ co-localisation on tissue. We performed a comparison of molecular profiles of various forms of GN. As a result, we were able to generate and distinguish specific tryptic peptides profiles of different cell regions (tubules, glomeruli, interstitium, connective tissue) and detect proteins with an altered intensity, implicated in inflammatory and healing pathways. MALDI-MSI, being able to define renal structures, could provide additional diagnostic and prognostic information. Generation of collective diagnostic panels may fulfil our pathogenesis understanding and assist clinical prognostic assessment.
Chronical kidney disease (CKD) is a worldwide health problem with increasing incidence, where the major part accounts for chronic glomerulonephrites (GN). It is a group of diseases of various aetiology and multiform clinical course, having various prognosis which is often hardly predictable as well as existing prognostic markers are not always certain. There is an urging need of new reliable and specific prognostic and therapeutic markers research. A modern proteomic technology - Matrix-assisted laser desorption/ionization mass spectrometry imaging (MALDI-MSI) has been employed in many GN studies showing promising results. We aimed to study several forms of primary and secondary glomerulonephrites (membranous nephropathy, IgA nephropathy, diabetic nephropathy) to enlighten possible molecular alterations significant of diseases’ progression. The studies were performed on renal tissue biopsies, analysing them with high spatial resolution MALDI-MSI to get better visualisation of signals’ co-localisation on tissue. We performed a comparison of molecular profiles of various forms of GN. As a result, we were able to generate and distinguish specific tryptic peptides profiles of different cell regions (tubules, glomeruli, interstitium, connective tissue) and detect proteins with an altered intensity, implicated in inflammatory and healing pathways. MALDI-MSI, being able to define renal structures, could provide additional diagnostic and prognostic information. Generation of collective diagnostic panels may fulfil our pathogenesis understanding and assist clinical prognostic assessment.
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Segelmark, Mårten. "Pathogenic aspects of rapidly progressive glomerulonephritis." Lund : Dept. of Nephrology, Lund University, 1995. http://catalog.hathitrust.org/api/volumes/oclc/39160027.html.

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Westman, Kerstin. "Autoimmuity in glomerulonephritis serological diagnosis and clinical outcome with special reference to Wegener's granulomatosis and microscopic polyangiitis /." Lund : Dept. of Nephrology, University Hospital, 1997. http://catalog.hathitrust.org/api/volumes/oclc/39116623.html.

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Condon, Marie. "Improving outcomes in glomerulonephritis." Thesis, Imperial College London, 2015. http://hdl.handle.net/10044/1/41079.

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INTRODUCTION: Lupus Nephritis (LN) and Idiopathic Membranous Nephropathy (IMN) are immune mediated kidney diseases. The gold standard test for diagnosis and monitoring is kidney biopsy. Current treatment regimens for both diseases can be toxic with long-term effects. AIMS: Assess the outcomes of less toxic steroid sparing regimens in both diseases. To validate urinary biomarkers in LN. Assess the indirect immunofluorescence test (IIFT) for identification of anti-PLA2R antibodies in IMN. METHODS: Prospectively data was collected on 50 consecutive patients with Lupus Nephritis (LN) were treated with the steroid sparing RITUXILUP regimen. Retrospectively data was collected on 43 patients with Idiopathic Membranous Nephropathy (IMN) who received >12 months of treatment with Tacrolimus Monotherapy (Tac). Enrolment and data monitoring of the IMN induction trial 'MTac' is described. The urine biomarker MIF was measured in 586 urine samples from 59 patients; results were correlated with disease activity. A Multiplex cytokine array identified Angiogenin (ANG) as a novel cytokine. ANG was measured in 342 urine samples from 34 patients treated with RITUXILUP regimen. IIFT was used to identify anti-PLA2R antibodies in 59 plasma samples from 24 patients in the MTac trial. RESULTS: RITUXILUP and Tac regimens were safe and effective with 86% response rate at 1 year (52% CR and 34% PR) and 98% response rate respectively. Tac can be valuable in relapsing or resistant disease to maintain remission. uMIF reflected the change in disease activity, baseline uMIF did not predict time to CR. ANG was identified in urine from patients with active LN. Levels were significantly lower when in remission. An association between uANG and the degree of renal impairment but not with proteinuria was shown. IIFT is effective and reproducible for the qualitative assessment of anti-PLA2R antibodies, however it is laborious and can have subjective variability when used in a quantitative manner. CONCLUSIONS: Steroid sparing treatment may be possible in both LN and IMN; but this needs to be validated in RCTs. uMIF and uANG both reflect disease activity in LN, more work is needed to assess if they have a unique role as a biomarker in LN or as a therapeutic target. The clinical application of anti-PLA2R antibodies is being investigated widely. The IIFT is sufficient for current research use, however probably not for a high throughput use.
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Ringsted, S. "Pathogenic mechanisms in glomerulonephritis." Thesis, University of Oxford, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.670361.

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Hägele, Holger. "Molekulare Mechanismen viral getriggerter Glomerulonephritis." Diss., lmu, 2013. http://nbn-resolving.de/urn:nbn:de:bvb:19-155778.

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Pickering, Matthew Caleb. "Glomerulonephritis and factor H deficieny." Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252096.

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Tam, Wai Keung. "Cytokine gene expression in glomerulonephritis." Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.363081.

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Owen, Elizabeth Louise. "Endothelin-1 antagonism in glomerulonephritis." Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/23564.

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A common feature of glomerular disease is a protein leak into the urine. Proteinuria occurs in kidney disease and is an important risk factor for cardiovascular disease (CVD). ET‐1 is a potent vasoconstrictor/pressor peptide that is up‐regulated in CVD and many forms of inflammatory renal diseases. The actions of ET‐1 are mediated via two G‐protein coupled receptors, the ETAR which serves primarily in the pro‐hypertensive actions of ET‐1 and is often considered as the main pathological receptor subtype, with the ETBR serving to clear circulating ET‐1. Antagonism of one or both of receptors has been shown to be of clinical benefit in the treatment of hypertension. This research demonstrated a beneficial effect of selective ETAR antagonism using Sitaxsentan in a rat model of GN. ETAR blockade reduced blood pressure and importantly reduced glomerular inflammation as assessed by glomerular macrophage (Mϕ) infiltration. Further, we aimed to demonstrate that Mϕ, key mediators of inflammation are activated by ET‐1 to adopt a pro‐inflammatoy phenotype. However, early studies demonstrated that ET‐1 does not activate Mϕ as hypothesised. Mϕ were more phagocytic, and ET‐1 was chemokinetic for macrophages, an ETBR medicated event. ET‐1 was also removed by Mϕ, suggesting a potential regulatory role of Mϕ in the ET system. This phenomenon led to inclusion of additional in vivo studies to investigate the role of Mϕ in the regulation of ET‐1 and its pressor effects. These effects were investigated in a murine model of Mϕ ablation using CD11b‐DTR mice. These experiments determined in vivo that Mϕ ablation augments pressor responses to ET‐1, suggesting that Mϕ are required to regulate ET‐1. In vitro, Mϕ remove ET‐1 by several mechanisms involving proteolytic degradation of the peptide and ETBR mediated clearance, demonstrating a potential mechanism for the in vivo observation. Furthermore, proteinuria is believed to be due to damage or effacement of specialized visceral glomerular epithelial cells or podocytes. We identified in vitro that the ETAR mediates ET‐1 induced human podocyte cell effacement by actin cytoskeleton aberrations and slit‐diaphragm protein down-regulation, ET‐1 and pro‐inflammatory cytokine production. This thesis provides evidence to support our initial hypotheses that selective ETAR antagonism ameliorates proteinuric renal disease via its effects on podocytes and macrophages. Continued studies both in vitro and in vivo will strengthen the body of evidence to promote the therapeutic use of ETR antagonists in inflammatory renal disease.
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GOBERT, REGIS. "Glomerulonephrite membranoproliferative et cancer bronchique." Lille 2, 1988. http://www.theses.fr/1988LIL2M210.

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Books on the topic "Glomerulonephriti"

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IgA nephropathy: From molecules to men. Basel: Karger, 1999.

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R, Clarkson A., and Woodroffe A. J, eds. IgA nephropathy: Pathogenesis and treatment. Basel: Karger, 1995.

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Catto, Graeme R. D., ed. Glomerulonephritis. Dordrecht: Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-2225-9.

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Trachtman, Howard, Jonathan J. Hogan, Leal Herlitz, and Edgar V. Lerma, eds. Glomerulonephritis. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-27334-1.

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D, Catto Graeme R., ed. Glomerulonephritis. Dordrecht: Kluwer Academic Publishers, 1990.

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D, Pusey C., and Rees A. J, eds. Rapidly progressive glomerulonephritis. Oxford: Oxford University Press, 1998.

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Ponticelli, Claudio, Luigi Minetti, and Giuseppo D’Amico, eds. Antiglobulins, cryoglobulins and glomerulonephritis. Dordrecht: Springer Netherlands, 1986. http://dx.doi.org/10.1007/978-94-009-4289-9.

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Pusey, C. D., ed. The Treatment of Glomerulonephritis. Dordrecht: Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-0-585-37972-2.

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A, Sessa, ed. Glomerulonephritis in the elderly. Basel: Karger, 1993.

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D, Pusey C., ed. The treatment of glomerulonephritis. Dordrecht: Kluwer Academic, 1999.

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Book chapters on the topic "Glomerulonephriti"

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Yau, Timothy. "Approach to Renal Biopsy." In Glomerulonephritis, 1–15. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-49379-4_1.

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Crawford, Brendan D., Matt G. Sampson, Jeffrey B. Hodgin, and Kevin V. Lemley. "Focal Segmental Glomerulosclerosis, Pediatric." In Glomerulonephritis, 169–92. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-49379-4_10.

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Rheault, Michelle N. "Alport Syndrome and Other Collagen Disorders." In Glomerulonephritis, 193–214. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-49379-4_11.

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Rheault, Michelle N., and Mark Birkenbach. "Other Genetic Glomerular Disorders." In Glomerulonephritis, 215–30. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-49379-4_13.

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Anvari, Evamaria, Laura Ferreira Provenzano, Alana Nevares, Leal C. Herlitz, and Howard Smith. "Lupus Nephritis (Including Antiphospholipid Antibody Syndrome), Adult." In Glomerulonephritis, 231–63. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-49379-4_14.

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Wenderfer, Scott E., and Natasha M. Ruth. "Lupus Nephritis (Including Antiphospholipid Antibody Syndrome), Pediatric." In Glomerulonephritis, 265–300. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-49379-4_15.

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Toth-Manikowski, Stephanie, and Laurence H. Beck. "PLA2R- and THSD7A-Associated Primary Membranous Nephropathy." In Glomerulonephritis, 301–31. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-49379-4_16.

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Nachman, Patrick H., and Shannon L. Murphy. "ANCA-Associated Vasculitis, Adult." In Glomerulonephritis, 333–48. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-49379-4_17.

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Gibson, Keisha, and Dorey Glenn. "ANCA-Associated Vasculitis, Pediatric." In Glomerulonephritis, 349–57. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-49379-4_18.

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Benchimol, Corinne. "Anti-glomerular Basement Membrane Disease." In Glomerulonephritis, 359–66. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-49379-4_19.

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Conference papers on the topic "Glomerulonephriti"

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Tadjibayeva, K., and T. R. Romanovskaya. "REGULATORY ROLE OF INTERLEUKINS-4, 5 AND 6 IN THE DEVELOPMENT OF GLOMERULONEPHRITIS OF VARIOUS ETIOLOGIES." In SAKHAROV READINGS 2022: ENVIRONMENTAL PROBLEMS OF THE XXI CENTURY. International Sakharov Environmental Institute of Belarusian State University, 2022. http://dx.doi.org/10.46646/sakh-2022-2-24-27.

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The relationship between the concentration of interleukin-4, 5, and 6 with the content of eosinophils and the level of C-reactive protein in patients with chronic glomerulonephritis was established. An increase in eosinophils was found in patients with chronic glomerulonephritis with a predominance of interleukin-4 compared with patients with a predominance of interleukin-5 and 6, which may be an important diagnostic marker of glomerulonephritis.
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Lee, S. S., J. Deangelis, B. ElBebawy, and L. J. Riley. "Rapidly Progressive Glomerulonephritis Secondary to Pauci-Immune Glomerulonephritis Andanti-Neutrophil Cytoplasmic Antibodies Vasculitis." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a5168.

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Almeida, Helton Kazuhiro Sakakibara de, THIAGO ALBERTO FERNANDES GOMES SANTOS, CLAUDINE JULIANA CRISTINA CAZNOCH, THELMA LAROCCA SKARE, ANA PAULA CRUPZACKI, and ELISA ELISA FRANZOI. "Adherence to treatment in lupus glomerulonephritis." In XXXIX Congresso Brasileiro de Reumatologia. Sociedade Brasileiro de Reumatologia, 2022. http://dx.doi.org/10.47660/cbr.2022.1812.

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"Clinical and Pathological Features of C3 Glomerulonephritis." In 2018 International Conference on Medicine, Biology, Materials and Manufacturing. Francis Academic Press, 2018. http://dx.doi.org/10.25236/icmbmm.2018.53.

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Milosevic, Danko. "363 Two boys with C3/DDD glomerulonephritis." In 10th Europaediatrics Congress, Zagreb, Croatia, 7–9 October 2021. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2021. http://dx.doi.org/10.1136/archdischild-2021-europaediatrics.363.

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LOURENÇO, LARISSA ANDRADE, Cezar Gonçalves de Carvalho, Beatriz Mota Tiburcio, Úrsula da Silva Teixeira, Evelyn Joyce Corgosinho, Camila Martins Lopes, and Eduardo José do Rosário e. Souza. "Pauci-immune Glomerulonephritis in Systemic Lupus Erythematosus." In XXXIX Congresso Brasileiro de Reumatologia. Sociedade Brasileiro de Reumatologia, 2022. http://dx.doi.org/10.47660/cbr.2022.1983.

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Ferreira, William Barros Hyppolito, Carolina Pellisson Carvalho, Nayara Mota Carvalho, Daniela Vieira, José Victor Martinez, Rebeca Barbosa Carbinatto, Rubens Bonfiglioli, et al. "ACUTE DIFFUSE GLOMERULONEPHRITIS: DIFFERENTIAL DIAGNOSIS OF LUPUS NEPHRITIS." In XXXIX Congresso Brasileiro de Reumatologia. Sociedade Brasileiro de Reumatologia, 2022. http://dx.doi.org/10.47660/cbr.2022.1837.

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Tsuruno, Kosuke, Kazunori Tobino, Kazuhito Takeda, Norikazu Matsuo, Yoko Takahashi, Yukihiro Sugimoto, Noriyuki Ebi, and Hidehiko Yamamoto. "Chest Computed Tomographic Findings In Rapidly Progressive Glomerulonephritis." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4585.

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Padmavathi, K., A. V. Senthil Kumar, and Ismail Bin Musrin. "Feature Sequential Selection Process for Predicting Disease Glomerulonephritis." In 2022 International Conference on Computer Communication and Informatics (ICCCI). IEEE, 2022. http://dx.doi.org/10.1109/iccci54379.2022.9740865.

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Atmiş, Bahriye, Aysun Karabay Bayazit, Engin Melek, Çağla Çağli, and Ali Anarat. "P309 Is the incidence of postinfectious glomerulonephritis increasing?: 13 cases with postinfectious glomerulonephritis from a single centre in november-december 2016." In 8th Europaediatrics Congress jointly held with, The 13th National Congress of Romanian Pediatrics Society, 7–10 June 2017, Palace of Parliament, Romania, Paediatrics building bridges across Europe. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2017. http://dx.doi.org/10.1136/archdischild-2017-313273.397.

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Reports on the topic "Glomerulonephriti"

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Zhang, LiBo, GuangZhen Liu, and YanChuang Liang. Meta-analysis of Buzhong-Yiqi Decoction for chronic glomerulonephritis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2020. http://dx.doi.org/10.37766/inplasy2020.5.0048.

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Guerguinova, Nevena, Boris Bogov, Milena Nikolova, Mila Liubomirova, and Todor Kundurzhiev. Evolution of Membranous Glomerulonephritis in Relation to Treatment – Retrospective and Prospective Assessment. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, December 2018. http://dx.doi.org/10.7546/crabs.2018.12.16.

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Tilkiyan, Eduard E., Emil P. Kumchev, and Violina A. Minkova. Clinical Investigation of Crescentic Glomerulonephritis in Elderly Patients in a Single Centre in Bulgaria. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, March 2019. http://dx.doi.org/10.7546/crabs.2019.03.17.

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Wang, Zhendong, He Yu, Yang Wang, Bochuan Wang, and Xiaohong Gu. Effectiveness and Safety of Traditional Chinese Medicine in the Treatment of Chronic Glomerulonephritis: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2021. http://dx.doi.org/10.37766/inplasy2021.8.0108.

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You might also be interested in the extended bibliographies on the topic 'Glomerulonephriti' for particular source types:
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