Proteinuria in Nephrotic Syndrome: Mechanistic and Clinical Considerations in Optimizing Management

Tumlin, James A.

doi:10.1159/000481632

Cited by 12 publications

(11 citation statements)

References 4 publications

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“…Those with minimal change disease were predominant. Many other workers have reported similar findings [16] . In our series, incidence of minimal change disease was highest with 44.08%.…”

Section: Acute Glomerulonephritissupporting

confidence: 64%

A clinico-pathological study of percutaneous renal biopsies in South-western region of Maharashtra

Bhosale¹,

Pande²,

Gavali³

2021

Int. J. Clin. Diagn. Pathol.

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Introduction: Renal biopsy is the corner stone of diagnostics modalities in renal parenchymal disease and offers vital prognostic information for nephrologists. The present study was undertaken with a view to become familiar with the histological patterns of different renal lesions and their correlation with clinical manifestations, hematological and biochemical changes. Methods: This study includes 129 renal biopsies received in the Department of Pathology, Prakash institute of medical sciences and research over a period 3 years January 2017 to December 2019. In all the cases, percutaneous renal biopsy was done under local anesthesia. The technique used was that of Kark and Muehrcke via Wilms Silverman needle with Franklin's modification. Results: The commonest lesion observed was minimal change disease (31.87%). This was followed by acute glomerulonephritis (26.36%). Maximum number of cases were observed in second and third decade of life, together comprising about 70% of cases. Overall male preponderance was observed. The commonest cause of nephrotic syndrome was observed to be minimal change disease. Conclusion: Nephrotic syndrome is common in adults also as against the general belief. Minimal change disease and acute glomerulonephritis are the commonly observed lesions causing nephrotic syndrome in most of the cases.

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“…Those with minimal change disease were predominant. Many other workers have reported similar findings [16] . In our series, incidence of minimal change disease was highest with 44.08%.…”

Section: Acute Glomerulonephritissupporting

confidence: 64%

A clinico-pathological study of percutaneous renal biopsies in South-western region of Maharashtra

Bhosale¹,

Pande²,

Gavali³

2021

Int. J. Clin. Diagn. Pathol.

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“…Here, we provide an overview of podocyte biology, highlighting some recent developments and identifying areas for future study. It is the first of a series of articles summarizing presentations and discussions from a roundtable discussion focused on the management of proteinuria in nephrotic syndrome [2].…”

Section: Introductionmentioning

confidence: 99%

A Review of Podocyte Biology

Garg¹

2018

Am J Nephrol

214

169

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Background: Podocyte biology is a developing science that promises to help improve understanding of the mechanistic nature of multiple diseases associated with proteinuria. Proteinuria in nephrotic syndrome has been linked to mechanistic dysfunctions in the renal glomerulus involving the function of podocyte epithelial cells, including podocyte foot process effacement. Summary: Developments in imaging technology are improving knowledge of the detailed structure of the human renal glomerulus and cortex. Podocyte foot processes attach themselves to the glomerular capillaries at the glomerular basement membrane (GBM) forming intercellular junctions that form slit diaphragm filtration barriers that help maintain normal renal function. Damage in this area has been implicated in glomerular disease. Injured podocytes undergo effacement whereby they lose their structure and spread out, leading to a reduction in filtration barrier function. Effacement is typically associated with the presence of proteinuria in focal segmental glomerulosclerosis, minimal change disease, and diabetes. It is thought to be due to a breakdown in the actin cytoskeleton of the foot processes, complex contractile apparatuses that allow podocytes to dynamically reorganize according to changes in filtration requirements. The process of podocyte depletion correlates with the development of glomerular sclerosis and chronic kidney disease. Focal adhesion complexes that interact with the underlying GBM bind the podocytes within the glomerular structure and prevent their detachment. Key Messages: Knowledge of glomerular podocyte biology is helping to advance our understanding of the science and mechanics of the glomerular filtering process, opening the way to a variety of new potential applications for clinical targeting.

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“…This review focuses on damage to the podocyte and the consequences of this injury in patients with FSGS, the genetics of FSGS, and approaches to treatment of this disorder. It is one of a series of articles published in this supplement that summarize the presentations and discussions from a roundtable discussion focused on management of proteinuria in nephrotic syndrome [14] (see Introduction for details).…”

Section: Introductionmentioning

confidence: 99%

Protecting Podocytes: A Key Target for Therapy of Focal Segmental Glomerulosclerosis

Tumlin

2018

Am J Nephrol

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Background: Focal segmental glomerulosclerosis (FSGS) is a histologic pattern of injury demonstrated by renal biopsy that can arise from a diverse range of causes and mechanisms. It has an estimated incidence of 7 per 1 million and is the most common primary glomerular disorder leading to end-stage renal disease in the United States. This review focuses on damage to the podocyte and the consequences of this injury in patients with FSGS, the genetics of FSGS, and approaches to treatment with a focus on the effects on podocytes. Summary: The podocyte is central to the glomerular filtration barrier and is particularly vulnerable because of its highly differentiated post-mitotic phenotype. The progressive structural changes involved in the pathology of FSGS include podocyte foot process effacement, death of podocytes and exposure of the glomerular basement membrane, filtration of nonspecific plasma proteins, expansion of capillaries, misdirected filtration at points of synechiae, and mesangial matrix proliferation. Although damage to and death of podocytes can result from single-gene disorders, evidence also suggests a role for soluble factors, such as soluble urokinase-type plasminogen activator receptor, cardiotrophin-like cytokine-1, and anti-CD40 antibodies, that promote FSGS recurrence post transplant. Several classes of medications, including corticosteroids, calcineurin inhibitors, endothelin receptor antagonists, adrenocorticotropic hormone, and rituximab, have been shown to be effective for the treatment of FSGS and have been demonstrated to have significant protective effects on podocytes. Key Messages: Greater understanding of podocyte biology is essential to the identification of new treatment targets and medications for the management of patients with FSGS.

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Proteinuria in Nephrotic Syndrome: Mechanistic and Clinical Considerations in Optimizing Management

Cited by 12 publications

References 4 publications

A clinico-pathological study of percutaneous renal biopsies in South-western region of Maharashtra

A clinico-pathological study of percutaneous renal biopsies in South-western region of Maharashtra

A Review of Podocyte Biology

Protecting Podocytes: A Key Target for Therapy of Focal Segmental Glomerulosclerosis

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