Non-visible haematuria in a military setting

AbstractAsymptomatic non-visible haematuria is a common finding at routine military medical examinations. This article briefly reviews the possible causes, which include malignancy, structural causes, exertion haematuria, hereditary nephritis, thin basement membrane disease (TBMD), immunoglobulin A nephropathy (IgAN), tuberculosis (TB) and schistosomiasis. This paper discusses how these conditions may affect potential military recruits as well as currently serving members of the Armed Forces, and offers a general approach to the management of a patient with non-visible haematuria.

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The significance of Goodpasture antigen in hereditary nephritis

Srpski arhiv za celokupno lekarstvo ◽

10.2298/sarh08s4282b ◽

2008 ◽

Vol 136 (Suppl. 4) ◽

pp. 282-286

Author(s):

Gordana Basta-Jovanovic ◽

Sanja Radojevic-Skodric ◽

Milena Jovanovic ◽

Ljiljana Bogdanovic ◽

Radovan Bogdanovic ◽

...

Keyword(s):

Basement Membrane ◽

High Titer ◽

Antigen Detection ◽

Antigenic Determinants ◽

Phase Method ◽

Tubular Basement Membrane ◽

Electron Microscopic ◽

Hereditary Nephritis ◽

Thin Basement Membrane Disease ◽

Goodpasture Antigen

INTRODUCTION. Two types of hereditary nephritis, nonprogressive and progressive, clinically present as asymptomatic haematuria, sometimes combined with proteinuria. At the onset, in both types, light microscopic changes are minimal, immunofluorescence findings are negative, and diagnosis can be made only upon electron microscopic findings that are considered to be specific. OBJECTIVE. The aim of this study was to determine the significance of Goodpasture antigen detection in diagnosis of progressive and nonprogressive hereditary nephritis in its early phase. METHOD. Analysis of renal biopsy specimens was done in patients with hereditary nephritis that were followed from 1990 to 2005. Progression of renal disease was examined in 14 patients with Alport?s syndrome, 10 patients with thin basement membrane disease, and 6 patients with unclassified hereditary nephritis diagnosed. For all these cases, indirect immunofluorescence study with serum from a patient with high titer of Goodpasture autoantibodies that recognize the antigenic determinants in human glomerular and tubular basement membrane was performed. RESULTS. In 11 out of 14 cases diagnosed as Alport?s syndrome, there was negative staining with Goodpasture serum, and in 3 additional cases with Alport?s syndrome, expression of Goodpasture antigen in glomerular basement membrane and thin basement membrane was highly reduced. In all 10 patients with thin basement membrane disease, immunofluorescence showed intensive, bright linear staining with Goodpasture serum along glomerular and tubular basement membrane. In 2 out of 6 patients with unclassified hereditary nephritis, Goodpasture antigen expression was very strong, in one patient it was very reduced, and in 3 patients it was negative. CONCLUSION. The results of our study show that Goodpasture antigen detection plays a very important role in differential diagnosis of progressive and nonpregressive hereditary nephritis, particularly in early phases of the disease.

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Clinicopathologic and ultrastructural findings of hereditary nephritis; a 16-year single center survey in Iran

Journal of Renal Injury Prevention ◽

10.34172/jrip.2020.17 ◽

2020 ◽

Vol 9 (2) ◽

pp. e17-e17

Author(s):

Seyed Mohammad Owji ◽

Hadi Raeisi Shahraki ◽

Naser Pajouhi ◽

Seyed Hossein Owji ◽

Farshad Dehghani

Keyword(s):

Electron Microscopy ◽

Basement Membrane ◽

Light Microscopy ◽

Fabry Disease ◽

Toluidine Blue ◽

Alport Syndrome ◽

Blue Staining ◽

Toluidine Blue Staining ◽

Hereditary Nephritis ◽

Thin Basement Membrane Disease

Introduction: Hereditary nephritis is an umbrella term for a group of congenital childhood diseases including but not limited to Alport syndrome, thin basement membrane disease, and Fabry disease. Objectives: The purpose of this study was a clinicopathologic investigation of Alport syndrome, thin basement membrane disease, and Fabry disease with a focus on the role of electron microscopy and toluidine blue staining in diagnosis. Patients and Methods: In this cross-sectional study, we investigated kidney biopsies with a final diagnosis of either Alport syndrome, thin basement membrane disease or Fabry disease from 2001 to 2016. Electron microscopy and light microscopy were done and the clinical and paraclinical data were extracted from the patients’ medical charts. Electron microscopy role was assessed in terms of necessary, helpful or non-necessary, while correlations between clinical and para-clinical data were determined using appropriate statistical tests. Results: Among the 2865 kidney biopsies, there were 22 patients of hereditary nephritis including 15 (0.52%) Alport syndrome, 5 (0.17%) thin basement membrane disease and 2 (0.07%) Fabry disease diagnosed by electron microscopy. Electron microscopy was essential for the diagnosis of 19 (86.4%) cases, helpful for 3(13.6%) and there was no case for which electron microscopy was non-necessary. The patients’ mean age was 16.1 ± 9.0 years. The most common finding in Alport syndrome was proteinuria (86.7%) followed by hematuria (60.0%). Conclusion: Considering the rate of misdiagnosis of hereditary nephritis using light microscopy and clinical findings alone, electron microscopy study and toluidine blue staining has an essential role in the precise diagnosis in these patients. With regard to the progressive nature of these diseases, prompt diagnosis using electron microscopy is pertinent for therapeutic decisions.

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Plasma CXCL16 May Predict Renal Inflammation and the Progression of Immunoglobulin a Nephropathy

SSRN Electronic Journal ◽

10.2139/ssrn.3424178 ◽

2019 ◽

Author(s):

Ran Luo ◽

Yi-Chun Chen ◽

Dan Chang ◽

Ting-Ting Liu ◽

Yue-Qiang Li ◽

...

Keyword(s):

Immunoglobulin A ◽

Immunoglobulin A Nephropathy ◽

Renal Inflammation

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Immunostaining of galactose-deficient IgA1 by KM55 is not specific for immunoglobulin A nephropathy

Clinical Immunology ◽

10.1016/j.clim.2020.108483 ◽

2020 ◽

Vol 217 ◽

pp. 108483 ◽

Cited By ~ 1

Author(s):

Lu Zhao ◽

Liang Peng ◽

Danyi Yang ◽

Shi Chen ◽

Zhixin Lan ◽

...

Keyword(s):

Immunoglobulin A ◽

Immunoglobulin A Nephropathy

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Immunoglobulin A Nephropathy in Blacks and Homozygosity for the Genetic Marker A2m

Annals of Internal Medicine ◽

10.7326/0003-4819-104-2-287_2 ◽

1986 ◽

Vol 104 (2) ◽

pp. 287 ◽

Cited By ~ 8

Author(s):

KOTRESHA NEELAKANTAPPA

Keyword(s):

Genetic Marker ◽

Immunoglobulin A ◽

Immunoglobulin A Nephropathy

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Podocytopathy in the mesangial proliferative immunoglobulin A nephropathy: new insights into the mechanisms of damage and progression

Nephrology Dialysis Transplantation ◽

10.1093/ndt/gfy413 ◽

2019 ◽

Vol 34 (8) ◽

pp. 1280-1285 ◽

Cited By ~ 9

Author(s):

Hernán Trimarchi ◽

Rosanna Coppo

Keyword(s):

Mesangial Cells ◽

Immunosuppressive Treatment ◽

Immunoglobulin A ◽

Primary Site ◽

New Drugs ◽

Immunoglobulin A Nephropathy ◽

Inflammatory Reactions ◽

Persistent Proteinuria ◽

Mesangial Area ◽

Function Loss

Abstract Immunoglobulin A nephropathy (IgAN) was defined as a mesangiopathic disease, since the primary site of deposition of IgA immune material is the mesangium, and proliferation of mesangial cells and matrix excess deposition are the first histopathologic lesions. However, the relentless silent progression of IgAN is mostly due to the development of persistent proteinuria, and recent studies indicate that a major role is played by previous damage of function and anatomy of podocytes. In IgAN, the podocytopathic changes are the consequence of initial alterations in the mesangial area with accumulation of IgA containing immune material. Podocytes are therefore affected by interactions of messages originally driven from the mesangium. After continuous insult, podocytes detach from the glomerular basement membrane. This podocytopathy favours not only the development of glomerular focal and segmental sclerosis, but also the progressive renal function loss. It is still debated whether these lesions can be prevented or cured by corticosteroid/immunosuppressive treatment. We aimed to review recent data on the mechanisms implicated in the podocytopathy present in IgAN, showing new molecular risk factors for progression of this disease. Moreover, these observations may indicate that the target for new drugs is not only focused on decreasing the activity of mesangial cells and inflammatory reactions in IgAN, but also on improving podocyte function and survival.

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