In einer Beobachtungsstudie an 20 Patienten mit fokal sklerosierender und membranöser Glomerulonephritis wurde der Effekt einer Therapie mit ACE- Hemmer, Methylprednisolon und Ciclosporin A über einen Zeitraum von bis zu 10 Jahren verfolgt. Die Effektivität der genannten Therapie ist in der Literatur gut dokumentiert. Die Studie beobachtet folgende neue, bislang nicht beschriebene Ergebnisse: 1. Das Ausmaß der Proteinurie beim nephrotischen Syndrom unterliegt einem 28-Tage-Zyklus. Als Arbeitshypothese nehmen wir zyklische Schwankungen in der Aktivität des Immunsystems an. 2. Die bislang gängige Praxis, das nephrotische Syndrom ein halbes Jahr lang oder allenfalls bis zur ersten Abnahme der Proteinurie zu therapieren bedarf einer Korrektur. Erst wenn die Periodizität der Proteinurie sistiert, kann die Therapie ausgeschlichen werden, ohne ein Rezidiv befürchten zu müssen. Auf jeden Fall muss wesentlich länger therapiert werden als gegenwärtig in der Literatur berichtet. 3. Vor allem Patienten der Kategorie mit sehr langem Intervall zwischen Erstmanifestation und Therapiebeginn bedürfen einer möglicherweise lebenslangen Therapie um kein Endstage Renal Failure zu erleiden. 4. Das bislang gültige therapeutische Fenster der Ciclosporin-A-Therapie von 80 – 120 ng/ml Talspiegel kann bei gutem Ansprechen auf 60 – 80 ng/ml reduziert werden ohne hohes Rezidivrisiko. / 20 patients with focal segmental glomerulosclerosis (FSGS) and membranous nephropathy (mGN) are examined in a clinical trial, concerning the effect of a combined therapy with ACE inhibitor, prednisolone and cyclosporine A in a period of 10 years. The efficiency of this therapy is well documented in literature. The trial recognizes the following yet unknown facts: 1. The level of proteinuria in nephrotic syndrome describes a 28 days cycle. We suppose a connection to the cyclic change of the immune system. 2. The common therapy of the nephrotic syndrome lasting a half year needs a change. The immunsuppressive therapy may only be reduced after the suspending of the cycles of the proteinuria, without risking a relapse. 3. A long period between the first symptoms and the beginning of the therapy is a bad prediction. 4. The common blood level of cyclosporine A of 80 - 120 ng/ml may be reduced to 60 - 80 ng/ml without risking a higher relapse rate.

To Wah Yuen. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1994. / Includes bibliographical references (leaves 118-142). / Acknowledgements --- p.1 / Summary --- p.3 / List of Abbreviations --- p.7 / Chapter Part I --- Alpha2-HS glycoprotein: Identification and Characterization of the Jacalin Binding Properties --- p.8 / Chapter Chapter 1 --- Introduction --- p.9 / Chapter 1.1 --- Jackfruit and jacalin --- p.10 / Chapter 1.2 --- Biochemical and immunological properties of jacalin --- p.11 / Chapter 1.2.1 --- Molecular Weight of Jacalin --- p.11 / Chapter 1.2.2 --- Molecular structure of jacalin --- p.11 / Chapter 1.2.3 --- Specificity of jacalin to Thomsen-Fredenreich- antigen (T-antigen) --- p.13 / Chapter 1.2.4 --- The internal repeated sequence in the jacalin --- p.13 / Chapter 1.2.5 --- Jacalin-Bound Proteins (JBP) --- p.15 / Chapter 1.2.6 --- Interaction of jacalin to JBP --- p.15 / Chapter 1.2.7 --- Immunological properties of jacalin --- p.16 / Chapter 1.3 --- Application of jacalin in medical research --- p.17 / Chapter 1.4 --- Background knowledge of α2HSG --- p.18 / Chapter Chapter 2 --- Materials and Methods --- p.20 / Chapter 2.1 --- Design of experiment --- p.21 / Chapter 2.2 --- Identification of the Unknown JBP --- p.21 / Chapter 2.2.1 --- Sera --- p.21 / Chapter 2.2.2 --- Isolation of JBP by Affinity Chromatography --- p.22 / Chapter 2.2.3 --- Fast protein liquid chromatography (FPLC) of JBP --- p.22 / Chapter 2.2.4 --- Affinity chromatography with anti-human IgA column --- p.23 / Chapter 2.2.5 --- Preparation of non-IgA JBP fraction --- p.24 / Chapter 2.2.6 --- N-terminal sequencing of the non-IgA JBP fraction --- p.24 / Chapter 2.2.7 --- SDS-PAGE and immunoblot of gel filtration fractions --- p.25 / Chapter 2.2.8 --- ELISA of FPLC fractions of JBP --- p.26 / Chapter 2.2.9 --- Immunochemical analysis --- p.27 / Chapter 2.3 --- α2HSG: the property of jacalin binding --- p.28 / Chapter 2.3.1 --- α2HSG -jacalin binding curve and competitive ELISA --- p.28 / Chapter 2.3.2 --- Purification of jacalin-crude extract (JCE) --- p.28 / Chapter 2.3.3 --- Characterization of JCE and ASJ --- p.29 / Chapter 2.3.4 --- Comparison of jacalin from different sources for binding to α2HSG by competitive ELISA --- p.29 / Chapter Chapter 3 --- Results --- p.31 / Chapter 3.1 --- Identification of the unknown JBP --- p.32 / Chapter 3.1.1 --- Isolation and FPLC of JBP --- p.32 / Chapter 3.1.2 --- Identification of non-IgA JBP by anti-human IgA affinity column --- p.32 / Chapter 3.1.3 --- Identification of the known JBP in the FPLC fractionated JBP --- p.36 / Chapter 3.1.4 --- Characterization and confirmation of non-IgA JBP --- p.36 / Chapter 3.2 --- α2HSG: the property of jacalin binding --- p.42 / Chapter 3.2.1 --- Characterization of α2HSG-jacalin binding --- p.42 / Chapter 3.2.2 --- Characterization of the purified jacalin --- p.45 / Chapter 3.2.3 --- Comparison of different batches of jacalin to interact with α2HSG --- p.45 / Chapter Chapter 4 --- Discussion --- p.53 / Chapter Part II --- Jacalin-α2HSG binding: the Clinical Values --- p.57 / Chapter Chapter 5 --- Introduction --- p.58 / Chapter Chapter 6 --- Materials and Methods --- p.61 / Chapter 6.1 --- Preparation of IgA-specific jacalin (ASJ) by IgA-Sepharose 4B affinity column --- p.62 / Chapter 6.2 --- Preparation of JCE- and ASJ-Sepharose-4B affinity column --- p.62 / Chapter 6.3 --- Factors affecting the yield of α2HSG --- p.62 / Chapter 6.4 --- Miscellaneous methods --- p.63 / Chapter Chapter 7 --- Results and Discussion --- p.65 / Chapter Part III --- Application of Jacalin for Studying the Pathogenesis of IgA Nephropathy --- p.77 / Chapter Chapter 8 --- An Overview of IgA Nephropathy --- p.78 / Chapter 8.1 --- Clinical manifestation of IgA nephropathy --- p.79 / Chapter 8.2 --- Mesangial deposits in IgAN --- p.80 / Chapter 8.3 --- Human IgA system --- p.81 / Chapter 8.4 --- The role of circulating IgA in the pathogenesis of IgA nephropathy --- p.84 / Chapter 8.5 --- Pathogenesis of primary IgA nephropathy --- p.86 / Chapter 8.6 --- Interaction between circulatory IgA and fibronectin (FN) in primary IgAN --- p.87 / Chapter Chapter 9 --- Materials and Methods --- p.90 / Chapter 9.1 --- Design of experiment --- p.91 / Chapter 9.2 --- Sera --- p.91 / Chapter 9.3 --- Analysis of IgAl/IgA ratio in sera and JBP --- p.91 / Chapter 9.4 --- Purification and Fast protein liquid chromatography (FPLC) of jacalin-bound protein (JBP) --- p.92 / Chapter 9.5 --- Analysis of FPLC-fractionated JBP --- p.93 / Chapter 9.5.1 --- ELISA of IgA-containing immune complexes (IgA-IC) --- p.93 / Chapter 9.5.2 --- "Quantitative ELISA of IgA, K-IgAl, and λ-IgAl" --- p.94 / Chapter 9.5.3 --- "Measurement of sIgA,dIgA and IgA containing immune complex (IgA-IC)" --- p.95 / Chapter 9.5.4 --- SDS-PAGE analysis --- p.95 / Chapter 9.6 --- Statistics --- p.95 / Chapter Chapter 10 --- Results --- p.96 / Chapter 10.1 --- IgA1/IgA ratio of serum and JBP --- p.97 / Chapter 10.2 --- Isolation and FPLC of JBP --- p.97 / Chapter 10.3 --- SDS-PAGE analysis of FPLC fractionated JBP --- p.97 / Chapter 10.4 --- ELISA of the FPLC fractionated JBP --- p.99 / Chapter 10.4.1 --- "Distribution of IgA, secretory IgA (sIgA) and dimeric IgA (dIgA) in the FPLC fractions" --- p.99 / Chapter 10.4.2 --- Distribution of IgA containing immune complex (IgA-IC) in the FPLC fractions --- p.99 / Chapter 10.4.3 --- Quantitation of IgA --- p.106 / Chapter 10.4.4 --- "Quantitation of K-IgAl and λ-IgA1, and determination of k/λ ratio of IgAl" --- p.106 / Chapter 10.4.5 --- "Quantitation of sIgA,dIgA, and IgA-containing immune complex (IgA-IC)" --- p.109 / Chapter Chapter 11 --- Discussion --- p.112 / References --- p.118

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.

Thesis (Ph. D.)--University of Adelaide, 1986. / Includes bibliographical references (leaves 119-136).

Thesis (Ph. D.)--University of Hong Kong, 2008. / Includes bibliographical references (leaves 263-321) Also available in print.

Orientadora: Julieta Rodini Engrácia de Moraes / Banca: Marileda Bonafim Carvalho / Banca: Silvia Regina Catharino Sartori Barraviera / Resumo: Os estudos do tecido renal de cães com insuficiência renal são raros e em sua maioria estão relacionados aos quadros de doença renal familial ou de doenças específicas. Nestes casos, a estrutura morfológica dos rins pode ser alterada por vários fatores no curso de doenças sistêmicas, podendo ser diagnosticadas por meio da histopatologia. A doença glomerular é classificada de acordo com o padrão histológico das alterações visualizadas no tecido renal, e portanto o conhecimento deste aspecto da histopatologia é necessário para a sua compreensão. Análise morfológica de 11 casos de cães com insuficiência renal foi descrita. As alterações foram caracterizadas e classificadas morfologicamente, de acordo com os padrões estabelecidos pela Organização Mundial de Saúde para seres humanos. Glomerulonefrite esclerosante difusa foi diagnosticada em 82% dos animais e Nefrite intersticial crônica nos 18% restantes. Os tipos de lesões identificadas neste estudo, e suas freqüências, foram similares aos encontrados na literatura, onde alterações glomerulares são mais freqüentes na insuficiência renal crônica. / Abstract: The studies of the renal tissue of dogs with renal failure are rare and in most of cases are related to the familial renal disease or of specific diseases. In these cases, the morphologic structure of the kidneys may be changed by several factors in the course of systemic diseases, could be diagnosed by means of histopatology. The glomerular disease is classified as for the histological pattern of the alterations visualized in the renal tissue, and therefore the knowledge of this histopatologic aspect is necessary for his comprehension. Morphologic analysis of 11 cases of dogs with renal failure was described. The alterations were characterized and classified morphologically, as for the patterns established by the World Health Organization for human beings. Glomerulonephritis diffuse sclerosing was diagnosed in 82% of the animals and chronic interstitial nephritis in the remaining 18%. The types of lesions identified in this study, and their frequencies, were similar to the noticed in the literature, in which glomerular alterations are more frequent in the chronic renal failure. / Mestre

Made available in DSpace on 2014-06-11T19:27:58Z (GMT). No. of bitstreams: 0 Previous issue date: 2002-08-30Bitstream added on 2014-06-13T20:17:36Z : No. of bitstreams: 1 camargo_mhb_me_jabo.pdf: 948018 bytes, checksum: c97b9fdef07dcd51c130069083d377af (MD5) / Os estudos do tecido renal de cães com insuficiência renal são raros e em sua maioria estão relacionados aos quadros de doença renal familial ou de doenças específicas. Nestes casos, a estrutura morfológica dos rins pode ser alterada por vários fatores no curso de doenças sistêmicas, podendo ser diagnosticadas por meio da histopatologia. A doença glomerular é classificada de acordo com o padrão histológico das alterações visualizadas no tecido renal, e portanto o conhecimento deste aspecto da histopatologia é necessário para a sua compreensão. Análise morfológica de 11 casos de cães com insuficiência renal foi descrita. As alterações foram caracterizadas e classificadas morfologicamente, de acordo com os padrões estabelecidos pela Organização Mundial de Saúde para seres humanos. Glomerulonefrite esclerosante difusa foi diagnosticada em 82% dos animais e Nefrite intersticial crônica nos 18% restantes. Os tipos de lesões identificadas neste estudo, e suas freqüências, foram similares aos encontrados na literatura, onde alterações glomerulares são mais freqüentes na insuficiência renal crônica. / The studies of the renal tissue of dogs with renal failure are rare and in most of cases are related to the familial renal disease or of specific diseases. In these cases, the morphologic structure of the kidneys may be changed by several factors in the course of systemic diseases, could be diagnosed by means of histopatology. The glomerular disease is classified as for the histological pattern of the alterations visualized in the renal tissue, and therefore the knowledge of this histopatologic aspect is necessary for his comprehension. Morphologic analysis of 11 cases of dogs with renal failure was described. The alterations were characterized and classified morphologically, as for the patterns established by the World Health Organization for human beings. Glomerulonephritis diffuse sclerosing was diagnosed in 82% of the animals and chronic interstitial nephritis in the remaining 18%. The types of lesions identified in this study, and their frequencies, were similar to the noticed in the literature, in which glomerular alterations are more frequent in the chronic renal failure.

Made available in DSpace on 2016-07-01T13:10:36Z (GMT). No. of bitstreams: 0 Previous issue date: 2015-11-13. Added 1 bitstream(s) on 2016-07-01T13:14:18Z : No. of bitstreams: 1 000866867.pdf: 2330149 bytes, checksum: 96dff1e0184e3c0fb472e739765d613e (MD5) / Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) / A ehrlichiose monocítica canina (EMC), é doença infecciosa de alta incidência na clínica veterinária, causada por Ehrlichia canis, bactéria gram-negativa intracelular obrigatória e transmitida pelo carrapato Rhipicephalus sanguineus. O trabalho teve como objetivo avaliar as lesões histopatológicas em rins e baço causadas pela EMC, assim como os parâmetros da bioquímica sérica, ureia, creatinina, albumina e globulina. Para tanto, 16 cães apresentaram valores médios de ureia (90,18mg/dl) e creatinina (1,62mg/dl) acima dos valores de referência normal para cães; a albumina apresentou valores abaixo do normal com média de 2,01g/dl, enquanto a globulina permaneceu dentro da média com 3,58g/dl. A análise histopatológica constituiu na avaliação da região cortical e medular dos rins e do parênquima esplênico. As alterações morfológicas mais prevalentes foram o espessamento da membrana basal, formação de sinéquias, degeneração e necrose tubular. Quanto às glomerulonefrites a que apresentou maior ocorrência foi a do tipo mesangial em 62,5% (10/16) dos cães. Quanto às alterações esplênicas 43,7% (7/16) dos cães desenvolveram hipoplasia dos folículos linfóides, e 87,5% destes (14/16) apresentaram acúmulo de plasmócitos no parênquima. A análise estatística de correlação entre as variáveis, evidenciou correlação positiva entre a concentração de ureia e hiperplasia de células epiteliais glomerulares, e correlação positiva entre a creatinina e hiperplasia de células mesangiais e dilatação tubular; e entre a concentracão de globulina e o infiltrado de plasmócitos. Correlação negativa foi observada para albumina e infiltrado plasmocitário. Em baço, hipertrofia de folículos linfoides e ureia tiveram correlação positiva, enquanto albumina e infiltrado plasmocitário apresentaram correlação negativa. Houve predomínio de glomerulonefrite mesangial, e o infiltrado plasmocitário parece ter papel... / Canine monocytic ehrlichiosis (CME), is an infectious disease of high incidence in clinical routine, caused by Ehrlichia canis, an obligate intracellular gram-negative bacterium and transmitted by the tick Rhipicephalus sanguineus. This work aimed to evaluate the histopathological lesions in kidneys and spleen caused by CME, as well as the parameters of serum biochemistry urea, creatinine, albumin and globulin. To this end, 16 dogs showed mean values of urea (90,18mg / dl) and creatinine (1,62mg / dl) were above the normal reference values for dogs; albumin showed values below normal averaging 2.01g / dl, while globulin remained within the average with 3,58g / dl. The histopathological analysis consisted of the evaluation of cortical and medullary region of the kidney and splenic parenchyma. The most prevalent morphological changes were the thickening of the basement membrane, synechia formation, tubular degeneration and necrosis. As for glomerulonephritis the one that presented the highest occurrence was the mesangial type in 62.5% (10/16) of dogs. As for the splenic changes 43.7% (7/16) of the dogs developed hypoplasia of lymphoid follicles, and 87.5% of them (14/16) had plasma accumulation in the parenchyma. The statistical analysis of correlation between the variables, showed positive correlation between the urea concentration and hyperplasia of the glomerular epithelial cells, and also a positive correlation between creatinine and hyperplasia of mesangial cells and tubular dilation; and between the concentration of globulin and infiltrate of plasma cells. Negative correlation was observed for albumin and plasma cell infiltration. In spleen, enlarged lymphoid follicles and urea had positive correlation, whereas albumin and plasma cell infiltrates showed a negative correlation. There was a predominance of mesangial glomerulonephritis, and the plasma cell infiltrate probably plays an essential role in the immunopathology of injuries

Orientador: Antonio Calos Paes / Coorientador: Osimar de Carvalho Sanches / Banca: Noeme Souza Rocha / Banca: Rogério Giuffrida / Resumo: A ehrlichiose monocítica canina (EMC), é doença infecciosa de alta incidência na clínica veterinária, causada por Ehrlichia canis, bactéria gram-negativa intracelular obrigatória e transmitida pelo carrapato Rhipicephalus sanguineus. O trabalho teve como objetivo avaliar as lesões histopatológicas em rins e baço causadas pela EMC, assim como os parâmetros da bioquímica sérica, ureia, creatinina, albumina e globulina. Para tanto, 16 cães apresentaram valores médios de ureia (90,18mg/dl) e creatinina (1,62mg/dl) acima dos valores de referência normal para cães; a albumina apresentou valores abaixo do normal com média de 2,01g/dl, enquanto a globulina permaneceu dentro da média com 3,58g/dl. A análise histopatológica constituiu na avaliação da região cortical e medular dos rins e do parênquima esplênico. As alterações morfológicas mais prevalentes foram o espessamento da membrana basal, formação de sinéquias, degeneração e necrose tubular. Quanto às glomerulonefrites a que apresentou maior ocorrência foi a do tipo mesangial em 62,5% (10/16) dos cães. Quanto às alterações esplênicas 43,7% (7/16) dos cães desenvolveram hipoplasia dos folículos linfóides, e 87,5% destes (14/16) apresentaram acúmulo de plasmócitos no parênquima. A análise estatística de correlação entre as variáveis, evidenciou correlação positiva entre a concentração de ureia e hiperplasia de células epiteliais glomerulares, e correlação positiva entre a creatinina e hiperplasia de células mesangiais e dilatação tubular; e entre a concentracão de globulina e o infiltrado de plasmócitos. Correlação negativa foi observada para albumina e infiltrado plasmocitário. Em baço, hipertrofia de folículos linfoides e ureia tiveram correlação positiva, enquanto albumina e infiltrado plasmocitário apresentaram correlação negativa. Houve predomínio de glomerulonefrite mesangial, e o infiltrado plasmocitário parece ter papel... / Abstract: Canine monocytic ehrlichiosis (CME), is an infectious disease of high incidence in clinical routine, caused by Ehrlichia canis, an obligate intracellular gram-negative bacterium and transmitted by the tick Rhipicephalus sanguineus. This work aimed to evaluate the histopathological lesions in kidneys and spleen caused by CME, as well as the parameters of serum biochemistry urea, creatinine, albumin and globulin. To this end, 16 dogs showed mean values of urea (90,18mg / dl) and creatinine (1,62mg / dl) were above the normal reference values for dogs; albumin showed values below normal averaging 2.01g / dl, while globulin remained within the average with 3,58g / dl. The histopathological analysis consisted of the evaluation of cortical and medullary region of the kidney and splenic parenchyma. The most prevalent morphological changes were the thickening of the basement membrane, synechia formation, tubular degeneration and necrosis. As for glomerulonephritis the one that presented the highest occurrence was the mesangial type in 62.5% (10/16) of dogs. As for the splenic changes 43.7% (7/16) of the dogs developed hypoplasia of lymphoid follicles, and 87.5% of them (14/16) had plasma accumulation in the parenchyma. The statistical analysis of correlation between the variables, showed positive correlation between the urea concentration and hyperplasia of the glomerular epithelial cells, and also a positive correlation between creatinine and hyperplasia of mesangial cells and tubular dilation; and between the concentration of globulin and infiltrate of plasma cells. Negative correlation was observed for albumin and plasma cell infiltration. In spleen, enlarged lymphoid follicles and urea had positive correlation, whereas albumin and plasma cell infiltrates showed a negative correlation. There was a predominance of mesangial glomerulonephritis, and the plasma cell infiltrate probably plays an essential role in the immunopathology of injuries / Mestre

Background Glomerulonephritis is a major cause of end-stage kidney disease (ESRD) in Africa. There is scanty data on the clinico-pathological characteristics and outcome of the mesangioproliferative glomerulonephritides in Africa, despite the non-IgA subtype being reported as a common cause of nephrotic syndrome. This study will assess the outcome of patients with biopsy proven mesangioproliferative glomerulonephritis (MesPGN) from a single centre in Cape Town, South Africa. Methods The study is designed as 10-year retrospective analysis of patients with biopsy proven MesPGN. The MesPGN patterns were divided into non-IgA MesPGN and IgA nephropathy (IgAN), depending on the predominant type of immune deposit. Univariate cox regression analysis was used to determine factors associated with ESRD. Results Data of 109 patients with renal biopsy-proven MesPGN were included for the period between 2005-2014. The mean age at biopsy was 33.8 ±14.9 years, 53.2% were males, and 39.4% were black Africans. Clinically, 58.7% presented with nephrotic syndrome. On histology 79.8% had non-IgA MesPGN, and 20.2% had IgAN. Compared to the non-IgA group, most patients with IgAN were not treated with immunosuppression (72.7% vs. 40.2%; p=0.006). At the last visit, 10.1% reached ESRD (40.9% vs. 2.3%; p<0.0001) and 30.2% achieved complete remission (9.1% vs. 35.7%; p=0.015) for IgAN and non-IgA MesPGN respectively. The 5-year renal survival for IgAN and non-IgA MesPGN respectively, were: 63.3% vs. 97.6%, log rank p=0.001. Overall, hypertension (p=0.019), not receiving immunosuppression (p=0.046) and having IgAN (p=0.007) were independent predictors of progression to ESRD. Conclusion There is a significantly higher ESRD-free survival of patients with biopsy proven non-IgA MesPGN than IgAN. Whether this is related to the limited use of immunosuppressive therapy in IgAN patients or represents a true nature of the disease still requires further research.