sclerosis

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Related to glomerular sclerosis: focal glomerular sclerosis, Diabetic nephropathy

sclerosis

1. Pathol a hardening or thickening of organs, tissues, or vessels from chronic inflammation, abnormal growth of fibrous tissue, or degeneration of the myelin sheath of nerve fibres, or (esp on the inner walls of arteries) deposition of fatty plaques
2. the hardening of a plant cell wall or tissue by the deposition of lignin

Sclerosis

 

the hardening of an organ or tissue in humans and animals caused by connective-tissue overgrowth. Functionally valuable elements of the parenchyma of a sclerosed organ are destroyed and replaced by mature and sometimes coarse-fibered connective tissue, which often contains deposits of amyloid, hyalin, and lime. New connective tissue is usually formed by the reproduction of fibroblasts (connective-tissue cells) and by the intensified formation of collagen molecules by the fibroblasts.

In cases of sclerosis, parenchymal elements may be destroyed by inflammatory processes that are usually chronic in nature, including tuberculosis, rheumatic fever, and syphilis, and by circulatory disturbances, including passive congestion. Parenchymal elements may also be destroyed by involutional changes, for example, the postpartum sclerosis of the corpus lutea, and by changes associated with age and by metabolic disturbances. Sclerosis may be focal or diffuse. The proliferated connective tissue may become corrugated, resulting in the deformation of the organ, or cirrhosis. During cirrhosis, the hardening and reduction of an organ are accompanied by surface changes, including alternating outpouchings and invaginations, such as in a granular kidney or nodular liver.

sclerosis

[sklə′rō·səs]
(pathology)
Hardening of a tissue, especially by proliferation of fibrous connective tissue.
References in periodicals archive ?
Our findings are relevant for the reversion of the damage observed by the facts that the elevated Pc and SNGFR are associated with progressive proteinuria and eventual glomerular sclerosis (Anderson et al.
The histomorphologic changes in a renal biopsy from a patient with systemic amyloidosis comprise a spectrum of glomerular, interstitial, and vascular amyloid deposition, with or without associated renal lesions, such as interstitial fibrosis, tubular atrophy, interstitial inflammation, global glomerular sclerosis, or proliferative glomerular lesions.
The most common diagnosis was diabetic nephropathy (n = 59; 33%) followed by primary and secondary forms of focal segmental glomerular sclerosis (n = 37; 21%), hypertensive and atherosclerotic renal disease (n = 30; 17%), membranous nephropathy (n = 19; 11%), primary chronic tubulointerstitial nephritis (n = 7; 4%), amyloidosis/monoclonal immunoglobulin deposition disease (n = 7; 4%), thin basement membrane nephropathy/Alport syndrome (n = 6; 3%), minimal change disease superimposed on nephrosclerosis (n = 4; 2%), fibrillary glomerulonephritis (n = 3; 2%), inactive membranoproliferative glomerulonephritis or idiopathic nodular glomerular sclerosis (n = 3; 2%), inactive lupus nephritis (n = 1; 1%), and fibronectin glomerulopathy (n = 1; 1%).
This agent has been in phase 1 clinical trials for idiopathic pulmonary fibrosis, focal segmental glomerular sclerosis (FSGS), and DKD microalbuminuric patients and is currently in a study involving macroalbuminuric patients.
The diagnoses of the patients included segmental glomerular sclerosis, membranous glomerulopathy, membranous lupus nephritis, necrosis, membranous nephropathy, interstitial fibrosis, and sclerosis of glomeruli.
This can be caused by a number of underlying diseases and disorders, including iMN, primary focal segmental glomerular sclerosis (FSGS) and other conditions.