scholarly journals Rare Case of Reversible Acute Symmetrical Lesions of the Bilateral Basal Ganglia Associated with Diabetic Nephropathy and Chronic Renal Failure

2014 ◽  
Vol 4 ◽  
pp. 29 ◽  
Author(s):  
Parag Suresh Mahajan ◽  
Mohamed Amin El Esnawi ◽  
Sheik Akbar Hussein ◽  
Nasser Jassim Al Maslamani
Keyword(s):  
Renal Failure ◽  
Diabetic Nephropathy ◽  
Chronic Renal Failure ◽  
Asian Indian ◽  
Far East ◽  
Acute Onset ◽  
Imaging Features ◽  
Indian Patient ◽  
Asian Patients ◽  
The Far East

Reversible acute symmetrical basal ganglial lesion on magnetic resonance imaging and/or computed tomography in cases of diabetic nephropathy and chronic renal failure exhibiting acute onset of movement abnormalities like chorea is a very rare entity. It has characteristic clinical and imaging features. Only 29 cases are described in the literature, including the current one. These cases are predominantly Asian patients from the Far East and only one Asian Indian patient has been described. We report the second Asian Indian case of this condition and describe its various clinical and imaging features. Our aim is to educate the clinicians and radiologists about this condition, so that more such cases can be detected.

scholarly journals Evaluation of cardiac function during hemodialysis in patients with chronic renal failure due to diabetic nephropathy

1985 ◽  
Vol 18 (2) ◽  
pp. 149-154
Author(s):  
Tsuneo Murasawa ◽  
Makoto Taguchi ◽  
Tohri Suzuki ◽  
Yoshiki Hirofuji ◽  
Yusuke Fujii ◽  
...  
Keyword(s):  
Renal Failure ◽  
Diabetic Nephropathy ◽  
Chronic Renal Failure ◽  
Cardiac Function

Growth factor ultrafiltration in experimental diabetic nephropathy contributes to interstitial fibrosis

2000 ◽  
Vol 278 (4) ◽  
pp. F554-F560 ◽  
Author(s):  
Shi-Nong Wang ◽  
Raimund Hirschberg
Keyword(s):  
Renal Failure ◽  
Diabetic Nephropathy ◽  
Chronic Renal Failure ◽  
Growth Factor ◽  
Collagen Type ◽  
Interstitial Fibrosis ◽  
Collagen Type Iii ◽  
Renal Interstitial Fibrosis ◽  
Tubular Cells ◽  
Ecm Proteins

Glomerular proteinuria is a risk factor for progression of chronic renal failure and contributes to renal interstitial fibrosis. In experimental diabetic glomerular sclerosis, there is translocation of high-molecular-weight growth factors, namely, hepatocyte growth factor (HGF) and transforming growth factor (TGF)-β, from plasma into tubular fluid, both of which act on tubular cells through apical membrane receptors. In the present studies, the hypothesis is examined that ultrafiltered HGF and TGF-β induce increased expression of extracellular matrix (ECM) proteins directly in tubular cells, or induce increased expression of cytokines that may act on interstitial myofibroblasts. Incubation of cultured tubular cells with recombinant human (rh) TGF-β modestly raises expression of collagen type III, but rhHGF dose dependently blocks expression of this ECM protein. Both growth factors raise fibronectin expression up to fourfold and increase expression of platelet-derived growth factor (PDGF)-BB up to sixfold, but not of fibroblast growth factor-2. Pooled, diluted glomerular ultrafiltrate that had been collected by nephron micropuncture from rats with diabetic nephropathy (24–30 wk) also raises expression of fibronectin as well as PDGF-BB in proximal tubular cells. In the presence of neutralizing antibodies that block actions of HGF and TGF-β, diabetic rat glomerular ultrafiltrate fails to increase tubular cell PDGF-BB expression. In NRK-49F renal interstitial myofibroblasts, rhPDGF-BB, in turn, raises the expression of collagen type III but not type I or fibronectin. The findings provide evidence for ultrafiltered HGF and TGF-β to contribute to interstitial accumulation of ECM proteins by direct effects on tubular cells as well as indirect mechanisms, via PDGF-BB and its action on myofibroblasts. These events may be important mechanisms of proteinuria-induced renal interstitial fibrosis and accelerated progression of chronic renal failure in diabetic nephropathy and perhaps other proteinuric glomerular diseases.

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