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Fibrosis in the kidney: is a problem shared a problem halved?

Hewitson TD - Fibrogenesis Tissue Repair (2012)

Bottom Line: No better example of this exists than the progressive fibrosis that accompanies all chronic renal disease.Although it manifests itself histologically as an increase in extracellular matrix, we know that the histological appearance can be caused by a de novo synthesis of matrix (primarily collagen), or a disproportionate loss of renal parenchyma.In both cases the process depends on a resident mesenchymal cell, the so-called myofibroblast, and is independent of disease etiology.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Nephrology, Royal Melbourne Hospital & Department of Medicine, University of Melbourne, Melbourne, Australia.

ABSTRACT
Fibrotic disorders are commonplace, take many forms and can be life-threatening. No better example of this exists than the progressive fibrosis that accompanies all chronic renal disease. Renal fibrosis is a direct consequence of the kidney's limited capacity to regenerate after injury. Renal scarring results in a progressive loss of renal function, ultimately leading to end-stage renal failure and a requirement for dialysis or kidney transplantation. Although it manifests itself histologically as an increase in extracellular matrix, we know that the histological appearance can be caused by a de novo synthesis of matrix (primarily collagen), or a disproportionate loss of renal parenchyma. In both cases the process depends on a resident mesenchymal cell, the so-called myofibroblast, and is independent of disease etiology. Potentially we can ameliorate fibrosis, either indirectly by modifying the environment the kidney functions in, or more directly by interfering with activation and function of myofibroblasts. However, while renal fibrosis shares many features in common with the wound healing response in other organs, we also recognise that the consequences can be highly kidney specific. This review highlights the similarities and differences between this process in the kidney and other organs, and considers the therapeutic implications.

No MeSH data available.


Related in: MedlinePlus

Histology of end-stage kidney disease consists of tubulointerstitial fibrosis (middle), glomerulosclerosis (bottom left) and vascular sclerosis (top right). Silver methenamine/Masson trichrome stain. Scale bar = 50 μm.
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Figure 1: Histology of end-stage kidney disease consists of tubulointerstitial fibrosis (middle), glomerulosclerosis (bottom left) and vascular sclerosis (top right). Silver methenamine/Masson trichrome stain. Scale bar = 50 μm.

Mentions: Kidney disease consists of a diverse range of etiologies, including immunological, mechanical, metabolic and toxic insults amongst others. These variously affect the three functional compartments of the kidney; the vasculature, glomerulus and tubulointerstitium. It is these compartments that are collectively responsible for the delivery of blood, plasma filtration and modification of the glomerular filtrate respectively. Regardless of etiology, all patients with chronic kidney disease show a decline in renal function with time [2]. The process is irreversible, inevitably leading to end-stage renal failure, a condition that requires life-long dialysis or renal transplantation. Histologically end-stage kidney disease manifests itself as fibrotic lesions affecting each compartment; glomerulosclerosis, vascular sclerosis and tubulointerstitial fibrosis (Figure 1). Even though matrix synthesis is of course part of the normal repair process that occurs after injury, excessive synthesis of extracellular matrix is itself destructive, further exacerbating injury in a vicious cycle.


Fibrosis in the kidney: is a problem shared a problem halved?

Hewitson TD - Fibrogenesis Tissue Repair (2012)

Histology of end-stage kidney disease consists of tubulointerstitial fibrosis (middle), glomerulosclerosis (bottom left) and vascular sclerosis (top right). Silver methenamine/Masson trichrome stain. Scale bar = 50 μm.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3368763&req=5

Figure 1: Histology of end-stage kidney disease consists of tubulointerstitial fibrosis (middle), glomerulosclerosis (bottom left) and vascular sclerosis (top right). Silver methenamine/Masson trichrome stain. Scale bar = 50 μm.
Mentions: Kidney disease consists of a diverse range of etiologies, including immunological, mechanical, metabolic and toxic insults amongst others. These variously affect the three functional compartments of the kidney; the vasculature, glomerulus and tubulointerstitium. It is these compartments that are collectively responsible for the delivery of blood, plasma filtration and modification of the glomerular filtrate respectively. Regardless of etiology, all patients with chronic kidney disease show a decline in renal function with time [2]. The process is irreversible, inevitably leading to end-stage renal failure, a condition that requires life-long dialysis or renal transplantation. Histologically end-stage kidney disease manifests itself as fibrotic lesions affecting each compartment; glomerulosclerosis, vascular sclerosis and tubulointerstitial fibrosis (Figure 1). Even though matrix synthesis is of course part of the normal repair process that occurs after injury, excessive synthesis of extracellular matrix is itself destructive, further exacerbating injury in a vicious cycle.

Bottom Line: No better example of this exists than the progressive fibrosis that accompanies all chronic renal disease.Although it manifests itself histologically as an increase in extracellular matrix, we know that the histological appearance can be caused by a de novo synthesis of matrix (primarily collagen), or a disproportionate loss of renal parenchyma.In both cases the process depends on a resident mesenchymal cell, the so-called myofibroblast, and is independent of disease etiology.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Nephrology, Royal Melbourne Hospital & Department of Medicine, University of Melbourne, Melbourne, Australia.

ABSTRACT
Fibrotic disorders are commonplace, take many forms and can be life-threatening. No better example of this exists than the progressive fibrosis that accompanies all chronic renal disease. Renal fibrosis is a direct consequence of the kidney's limited capacity to regenerate after injury. Renal scarring results in a progressive loss of renal function, ultimately leading to end-stage renal failure and a requirement for dialysis or kidney transplantation. Although it manifests itself histologically as an increase in extracellular matrix, we know that the histological appearance can be caused by a de novo synthesis of matrix (primarily collagen), or a disproportionate loss of renal parenchyma. In both cases the process depends on a resident mesenchymal cell, the so-called myofibroblast, and is independent of disease etiology. Potentially we can ameliorate fibrosis, either indirectly by modifying the environment the kidney functions in, or more directly by interfering with activation and function of myofibroblasts. However, while renal fibrosis shares many features in common with the wound healing response in other organs, we also recognise that the consequences can be highly kidney specific. This review highlights the similarities and differences between this process in the kidney and other organs, and considers the therapeutic implications.

No MeSH data available.


Related in: MedlinePlus