Histopathology Interstitial Severity Index Associated with Glomerular and Tubular Severity Index in Nephrotic Syndrome Patients

Introduction: Nephrotic syndrome is characterized by massive proteinuria due to leakage of glomerular basal membrane, and subsequent process in tubular and interstitial tissue. It should be elucidated whether the severity of histopathological lesions in compartments of kidney tissue play a role and whether lesion in those compartments associated one to another. Aim: The study aims to correlate severity histopathologic lesions among compartments in kidney tissue. Method: All patients with nephrotic syndrome were biopsied and the cores were stained with Hematoxylin-Eosin, PAS, Masson’s Trichrome to look at glomerular, tubular, interstitial and vascular involvements. Glomerular abnormalities including mesangial hypercellularity, endocapillary hypercellularity, membranous; tubular, interstitial, and vascular severities were scored according to type, activity, severity and distribution in histopathologic features. Results: This study included 46 patients consisted of 16 (34.8%) males and 30 (65.2%) females, aged 26 ± 10 years, SBP 121.7 ± 13.10 and DBP 78.21 ± 7.80 mmHg, diagnosed with 14 lupus and 32 non-lupus nephrotic syndrome. Histopathologic abnormalities showed glomerular index was 4.26 ± 2.34, tubular index was 3.09 ± 1.90, interstitial index was 3.02 ± 1.48, vascular index was 0-3, pathologic index was 10.56 ± 4.54. There was significant correlation of severity index between interstitial and glomerular lesions (R=0.49, P=0.001), and between interstitial and tubular lesions (R=0.45, P=0.002). However, there were no significant correlations of severity index between interstitial and vascular lesions, and glomerular and tubular lesions. Conclusion: There are significant correlations of severity index between interstitial with glomerular and tubular lesions. It may implicate that histopathological process in interstitial tissue plays a central role in the pathogenesis of proteinuria in nephrotic syndrome.

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ARF in children with minimal change nephrotic syndrome may be related to functional changes of the glomerular basal membrane

American Journal of Kidney Diseases ◽

10.1053/j.ajkd.2003.10.039 ◽

2004 ◽

Vol 43 (3) ◽

pp. 399-404 ◽

Cited By ~ 29

Author(s):

Johan Vande Walle ◽

Reiner Mauel ◽

Ann Raes ◽

Kristof Vandekerckhove ◽

Raymond Donckerwolcke

Keyword(s):

Nephrotic Syndrome ◽

Basal Membrane ◽

Minimal Change Nephrotic Syndrome ◽

Minimal Change ◽

Functional Changes ◽

Glomerular Basal Membrane

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Green tea and bilberry protective effect against gentamicin-induced nephrotoxicity in rats

Acta Facultatis Medicae Naissensis ◽

10.5937/afmnai2003261v ◽

2020 ◽

Vol 37 (3) ◽

pp. 261-266

Author(s):

Milica Veljković ◽

Dragana Pavlović ◽

Ivan Ilić ◽

Dušan Sokolović

Keyword(s):

Protective Effect ◽

Green Tea ◽

Biochemical Analysis ◽

Histological Analysis ◽

Basal Membrane ◽

Bactericidal Effect ◽

Proximal Tubules ◽

Glomerular Basal Membrane ◽

Complete Disruption ◽

Distal Tubules

The aim of our study was to investigate if green tea and bilberry have protective effect on gentamicin-induced kidney damage, when applied together, and to make a connection between their effects. GM group of rats received only gentamicin, GT group received green tea only, B group received only bilberry, whereas control (C) group received saline only. GT+GM group received green tea together with gentamicin, and B+GM group received bilberry together with gentamicin. Biochemical analysis showed significantly increased urea and creatinine levels in GM group when compared to groups that also received bilberry or green tea. Histological analysis showed complete disruption of glomerular basal membrane as well as basal membranes of both proximal and distal tubules in GM group. These destructive effects were significantly milder and limited only to proximal tubules when bilberry or green tea was applied simultaneously with gentamicin. Both green tea and bilberry protective effect on gentamicin-induced nephrotoxicity is manifested because of their strong antioxidant activity. Since they are strong antioxidants, widely distributed in nature, they can offer available and inexpensive adjuvant therapy in Gram-negative infections, which can relieve gentamicin nephrotoxicity, but will not affect its bactericidal effect.

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AN UNUSUAL CASE OF NEW ONSET NEPHROPATHY IN A PATIENT OF PSORIASIS: CASE REPORT AND REVIEW OF LITERATURE

10.36106/ijsr/8400474 ◽

2021 ◽

pp. 13-14

Author(s):

VPS Punia ◽

Apoorva Shetty ◽

Prashant Prashant ◽

Akash Bharti ◽

Praveen Raman Mishra ◽

...

Keyword(s):

Nephrotic Syndrome ◽

Case Report ◽

Male Patient ◽

Renal Damage ◽

Unusual Case ◽

Review Of Literature ◽

Immune Mediated ◽

Different Types ◽

Glomerular Lesions ◽

New Onset

Psoriasis is known to cause chronic inammatory disorder of the skin through an immune mediated mechanism, it may be complicated by different types of glomerular lesions. Three different mechanisms have been implicated by which psoriasis can cause renal damage: immune-mediated renal damage, drug-related renal damage and chronic renal damage. This report presents a case of 35 years old male patient with extensive psoriasis, who presented to our hospital with nephrotic syndrome

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P0022INNATE IMMUNE RESPONSES ELICITED BY TOLL-LIKE RECEPTORS ARE POSSIBLY INVOLVED IN THE PATHOGENESIS OF NEPHROTIC SYNDROME

Nephrology Dialysis Transplantation ◽

10.1093/ndt/gfaa142.p0022 ◽

2020 ◽

Vol 35 (Supplement_3) ◽

Author(s):

Eriko Tanaka ◽

Ichiro Hada ◽

Naoaki Mikami ◽

Kunimasa Yan

Keyword(s):

Innate Immunity ◽

Nephrotic Syndrome ◽

Immune System ◽

Innate Immune System ◽

Expression Profiles ◽

Kidney Tissue ◽

Innate Immune ◽

Rna Expression ◽

Toll Like Receptors ◽

Tissue Samples

Abstract Background and Aims Pathogenesis of idiopathic nephrotic syndrome (INS) is yet to be fully elucidated. Immunological disorders are reported to be involved in the etiology of INS. Due to the efficacy of immunosuppressant agents such as calcineurin inhibitor and rituximab in treating nephrotic syndrome, aberrant activation of the acquired immune system through T and B cells are considered to be the underlying pathogenic mechanisms of INS. Nevertheless, there is a possibility that the innate immune system plays a key role in INS pathogenesis. This study aims to investigate the involvement of innate immunity in INS pathogenesis by examining the expressions of toll-like receptors (TLRs). Method Kidney tissue samples from two INS patients were collected at two points of time: the first biopsy was performed during nephrosis and the second during remission. Total RNA was extracted from the kidney tissue samples, and RNA-sequencing was performed to investigate RNA expression profiles. The differences between RNA expression profiles of TLRs and molecules related to TLR pathways in the tissue samples collected during nephrosis and remission were analyzed. Results There was a significant decrease in RNA expression of TLR9 and TLR10 during remission compared to nephrosis: fold change in each patient was -2.12 and -2.12 for TLR9, and -2.51 and -2.09 for TLR10. RNA expression of TLR8 also decreased: fold change in each patient was -1.19 and -1.75. There were no significant changes in the RNA expression profiles of TLR1, 2, 3, 4, 5, 6, and 7. In addition, there were no differences in the RNA expression profiles of MYD88, IRAK family, and TRAF family molecules that are associated with TLR pathways. However, RNA expressions of IL6, IL1B, IL12B, and TNF, as well as the cytokines controlled by TLR8 and TLR9 pathways, which were activated during nephrosis, disappeared or decreased during remission. Conclusion The involvement of the innate immune system in the pathogenesis of nephrotic syndrome has been suggested in some reports. Based on the fact that the onset or recurrence of nephrosis is triggered by non-specific viral infection, it is highly possible that innate immunity is involved in the pathogenesis of nephrotic syndrome. TLRs play a key role in innate immunity as they elicit the innate immune system after detecting pathogens, induce inflammatory cytokine production, and trigger signaling pathways that activate lymphocytes via maturation of dendritic cells. Specifically, TLR8, 9, and 10 mediate pathways of the first immune response to viral infections. Our study reveals that TLRs play a pivotal role in innate immunity associated with renal tissue during the onset of nephrosis.

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The Nephrotic Syndrome in Adults with ‘Minimal Change’ Glomerular Lesions

QJM ◽

10.1093/oxfordjournals.qjmed.a067400 ◽

1974 ◽

Keyword(s):

Nephrotic Syndrome ◽

Minimal Change ◽

Glomerular Lesions

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Urinary N-acetyl-beta-D-glucosaminidase isoenzyme activity as measured by fast protein liquid chromatography in patients with nephrotic syndrome

Clinical Chemistry ◽

10.1093/clinchem/36.1.102 ◽

1990 ◽

Vol 36 (1) ◽

pp. 102-103 ◽

Cited By ~ 7

Author(s):

T Shibasaki ◽

H Gomi ◽

F Ishimoto ◽

T Miyahara

Keyword(s):

Nephrotic Syndrome ◽

Liquid Chromatography ◽

Column Chromatography ◽

Healthy Subjects ◽

Deae Cellulose ◽

Proximal Tubules ◽

Fast Protein Liquid Chromatography ◽

Healthy Controls ◽

Glomerular Lesions

Abstract Exactly why N-acetyl-beta-D-glucosaminidase (NAG) excretion is increased in patients with nephrotic syndrome with glomerular lesions is poorly understood. Glomeruli contain less NAG than do proximal tubules. In this study, we have tried to measure the NAG isoenzymes automatically by use of the recently developed fast protein liquid chromatography (FPLC) system, followed by column chromatography on DEAE cellulose (Mono Q). Three isoenzyme peaks--B, I + II, and A--were observed for urine from both healthy subjects and nephrotic patients. The B isoenzyme usually constituted about 10% of the total NAG in healthy controls, 30% in nephrotic patients. In contrast, the proportion of the A isoenzyme was inversely related to that of the B isoenzyme when healthy controls and nephrotic patients were compared. Our system for measuring NAG isoenzymes is reproducible and fast, and it should be useful in further studies.

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P0488IG A NEPHROPATHY: ANALYSIS OF 501 BIOPSY

Nephrology Dialysis Transplantation ◽

10.1093/ndt/gfaa142.p0488 ◽

2020 ◽

Vol 35 (Supplement_3) ◽

Author(s):

Marwa Omrane ◽

Raja Aoudia ◽

Mondher Ounissi ◽

Soumaya Chargui ◽

Mouna Jerbi ◽

...

Keyword(s):

Renal Biopsy ◽

Iga Nephropathy ◽

Vascular Lesions ◽

Macroscopic Hematuria ◽

Systematic Screening ◽

Female Ratio ◽

Male Predominance ◽

Glomerular Lesions ◽

Stage Renal Disease ◽

End Stage

Abstract Background and Aims Mesangial deposits Ig A was described the first time in 1968 by Berger and Hinglais. It remains the most common primary glomerulonephritis worldwide. It is often idiopathic but can also be secondary. The aim of our study is to describe the epidemiologic characteristics, the incidence and the anatomopathological features of 501 IgA nephropathy (IgA N) patients. Method It is a retrospective mono-centric study including patients having IgA N in the renal biopsy done in our department among a period of 17 years. Results We analyzed data of 8427 patients who underwent renal biopsy. 81% had glomerular nephropathy with 7.3% (501) IgA N. A male-to-female ratio of 2.27. The average age was 28.7 years. IgA N was primary in 80.2% cases and secondary in 17.8% cases. The most frequent secondary IgA N was rheumatoid purpura (74.8%). There was a male predominance in Berger‘s disease as well as in rheumatoid purpura. Berger’s disease was more common in adults, whereas rheumatoid purpura was more common in children. The main indication of renal biopsy was proteinuria with hematuria in 23.2% of cases and nephrotic syndrome in 23.8%. The association of non-nephrotic proteinuria, hematuria, arterial hypertension and renal injury was found in 9.3% whereas isolated macroscopic hematuria only in 6.4% of cases. According to HAAS classification, HAAS 3 was the most frequent. OXFORD classification used only from 2010, and M1, S1, E0, T0 and M1, S1, E0, T2 were the most frequent. Glomerular lesions were associated to tubulo interstitial and vascular lesions in 48.2% of cases. Conclusion IgA nephropathy is the most common glomerular disease and a frequent cause of end stage renal disease. Because of a clear increase of it’s incidence in our country and the delay in the diagnosis, a systematic screening of urines is needed in our country as it’s done in Singapore and Japan.

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Relationship between the morphologic alterations of vocal cords from adult autopsies and the cause of death

Revista do Hospital das Clínicas ◽

10.1590/s0041-87812004000200003 ◽

2004 ◽

Vol 59 (2) ◽

pp. 63-66 ◽

Cited By ~ 4

Author(s):

Ana Karina Marques Salge ◽

Eumenia Costa da Cunha Castro ◽

Mara Lúcia Fonseca Ferraz ◽

Marlene Antônia dos Reis ◽

Vicente de Paula Antunes Teixeira

Keyword(s):

Vocal Cord ◽

Cause Of Death ◽

Respiratory Diseases ◽

Periodic Acid ◽

Basal Membrane ◽

Vocal Cords ◽

Periodic Acid Schiff ◽

White Ethnicity ◽

Staining Methods ◽

Hematoxylin Eosin

PURPOSE: The purpose of this study was to identify the possible alteration in the thickness of the epithelium basal membrane of the vocal cords and correlate it with the cause of death. METHOD: Larynxes collected from adult autopsies during the period of 1993 to 2001 were utilized. We used the hematoxylin-eosin and periodic acid-Schiff staining methods for the morphological and morphometric analysis. RESULTS: Sixty-six vocal cords were analysed; increased thickness was identified in 14 cases (21.2%), with equal proportions between the genders. Increased vocal-cord thickness was more frequent in patients of the white ethnicity (12 cases, 85.7%). Respiratory alterations were found in 10 (71.4%) of the cases with increased vocal-cord thickness. Of the patients that were maintained with mechanical ventilation before death, 7 (18.4%) had thickening of the basal membrane. Among the smokers, 9 (19.63%) had basal membrane thickening. CONCLUSION: No statistically significant differences were found between the cases in which the cause of death was related to respiratory diseases as compared to non-respiratory diseases and the thickening of the basal membrane of the vocal cords. However, new studies are needed in order to verify the etiopathogenesis of this thickening.

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