Introduction
Tubular atrophy is a broad term that illustrates many patterns of chronic tubular injury with thickened basement membranes and clinically manifests as chronic kidney disease with decreased glomerular filtration rate. Interstitial fibrosis is stated as a condition in which there is a collection of collagen and related molecules. Tubular atrophy and interstitial fibrosis in combination show a poor prognosis. In tubular atrophy, extensive tubular epithelial changes can be observed. It is also defined as a condition with several chronic tubular injury patterns and thickened basement membranes.
Clinically, tubular atrophy is a chronic kidney disease with decreased glomerular filtration rate. Thick redundant basement membranes or reduction of more than fifty percent of atrophic tubules compared to surrounding non-atrophic tubules is present in tubular atrophy. Tubular atrophy is also a typical pathological feature of kidney fibrosis. Despite the fact that fibroblasts predominantly take part in tissue fibrosis, the role of fibroblasts in the repair of tubular epithelia in tubular atrophy is not clear. Focal adhesion kinase (FAK) mediated intratubular epithelial-mesenchymal transition (EMT) plays an important role in the pathogenesis of tubular atrophy after severe ischemia-reperfusion injury (IRI). Tubular atrophy is generally found in end-stage kidney disease (ESKD). It is the classic sign of chronic kidney disease (CKD)
What Is Atrophy?
The condition in which the mass is diminished or decreased in size is known as atrophy. Wasting or weakening of the body organ or any tissue can be seen in the trophic state. Before the diminution, the size of the atrophic organ, tissue, or cell was normal. The reduction can be seen in the normal size of that organ. Due to various underlying chronic conditions, the body's organs, cells, or tissues may shrink by suffering atrophy. The number of cells of the component organ can also be lowered in number, size, or both. Many organs go through atrophy at a certain age or because of any physiologic conditions, and several organs turn atrophic at the time of birth; for example, the adrenal glands get reduced in size soon after birth as an inner layer of the cortex shrinks. Thymus and lymphoid tissue go through atrophic changes in adolescence. Arteriosclerosis is also an example of atrophy, where the thickening and hardening of the arteries occur.
Variations of nutrition and blood supply that occur in human life are universal during active life. Muscle atrophy is the weakening or thinning of the muscle mass. The patient may also feel changes in the facial skin, such as pale, lifeless, and weak skin. The atrophied muscles around the face and the throat makes it unable to swallow food or speak normally. There are many types of atrophy, such as glandular atrophy, vaginal atrophy, skeletal muscle atrophy(further divided into disuse and neurogenic atrophy), spinal muscular atrophy, and multiple system atrophy. Cellular changes, reabsorption, breakdown of tissue, and increased protein degradation are some of the functional features of atrophy.
What Is Tubular Atrophy?
Tubular atrophy is a common histological anomaly of kidneys in which an inflated interstitial space replaces normal cortical structures. Tubular atrophy was included in the term chronic allograft nephropathy, along with another anomaly named interstitial fibrosis.
What Methods Are Needed to Diagnose Tubular Atrophy?
Tubular atrophy can be diagnosed and studied by the following methods:
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Animal experiments.
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Histological preparation of the tissue.
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By siRNA.
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Cell culture.
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Collagen cell contraction assay.
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Immunofluorescence analysis.
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RNA extraction.
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Western blot analysis, etc.
Diagnosis and extensive study are crucial to know more about tubular atrophy.
What Are the Mechanisms That Occur in Tubular Atrophy?
Several studies showed in both human and animal biopsiesthat in the case of progressive kidney diseases, the renal tubular epithelial cells underwent apoptosis (type of cell death). Recently, the most accepted debate was that apoptosis is the reason behind tubular atrophy. Because in some mice, it was observed that proximal tubule apoptosis happens before tubular atrophy, so it was concluded that proximal tubular atrophy is the reason for tubular atrophy. Cell senescence which also means cells getting old is an example where acute kidney disease (AKI) proceeds to chronic kidney disease (CKD). Cell senescence is a vital part of the mechanism of tubular atrophy. Pertubular refraction and altered blood flow result in tubular hypoxia and tubular epithelial cell death. The process associated with hypoxia or inflammation has been involved in tubular atrophy. These processes involve a few other factors of the mechanism of tubular atrophy, such as oxidative stress, epithelial-to-mesenchymal transition (EMT), inflammation, and lipotoxicity.
What Is the Pathology of Tubular Atrophy?
Chronic injury to the tissue of the glomerular, tubular, interstitial, and vascular origin leads to atrophic tubules. The renal artery and its branches undergo stenosis for the indoctrination patterns of tubular atrophy. Tubular atrophy was described by tubular epithelial thinning, pyknotic nuclei, or tubular dilation, with or without protein casts. The association of tubular atrophy with glomerular filtration rate (GFR) was stated in a case series from the United Kingdom, where fifty patients with biopsy-proven primary glomerulonephritis (GN) were included. Here, tubular atrophy was especially correlated with serum creatinine, creatinine clearance, and the capability to concentrate and acidify the urine. It was observed that there is a relationship between glomerular pathology and serum creatinine, creatinine clearance, and urine concentration. This juncture was followed by other scientists from the United States of America after two years; that study had 70 biopsies from patients ages 8 to 75. After 25 years, Bohle et al. examined the relationship between GFR and quantitative histomorphometric glomerular and tubulointerstitial pathology analyses, which was more evident and definite. Tubular atrophy correlates transplanted kidneys and renal dysfunction. Also, it was explained primarily that focal adhesion kinase (FAK) gets triggered in proximal tubules after an acute kidney injury (AKI).
Conclusion
Tubular atrophy is a potential sign of chronic kidney disease (CKD). Also, it explains that it is superior to glomerular pathology as a predecessor of glomerular filtration rate decline in chronic kidney disease. There are few definitive studies for tubular atrophy, which is why fewer therapeutic targets are known. If the pathophysiology of tubular atrophy and interstitial fibrosis gets known descriptively, it would be possible to bring in more therapeutic strategies.
