TGF-beta1 is a key mediator that regulates, in a dose-dependent fashion, transdifferentiation of tubular epithelial cells into alpha-SMA+ myofibroblasts. This transdifferentiation is markedly enhanced by growth on collagen type I. These findings have identified a novel pathway that may contribute to renal fibrosis associated with overexpression of TGF-beta1 within the diseased kidney.

This study provides phenotypic and morphological evidence to support the hypothesis that TEC are pro-fibrogenitor cells capable of tubular epithelial-myofibroblast transdifferentiation in progressive renal fibrosis. In addition, we postulate that disruption of the TBM, which facilitates epithelial cell contact with the interstitial matrix, promotes this process of transdifferentiation.

TGF-beta/Smad7 signaling plays a critical role in the resolution of renal inflammation in rat remnant kidney model. Inhibition of NFkappaB activation is a key mechanism by which Smad7 suppresses renal inflammation, which suggests a crosstalk pathway between NFkappaB and Smad7. The ability of Smad7 to inhibit renal inflammation indicates that ultrasound-microbubble-mediated Smad7 gene therapy may represents a new therapeutic strategy for glomerulonephritis.

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Background/Aims: Pentoxifylline (PTX) has been shown to inhibit renal inflammation in a rat model of crescentic glomerulonephritis. The present study investigated the role of PTX in renal fibrosis in rats with crescentic glomerulonephritis. Methods: A rat model of accelerated anti-glomerular basement membrane glomerulonephritis was induced and treated with PTX or vehicle control for 3, 7, 14 and 28 days. The therapeutic effect and mechanism of PTX on renal fibrosis were examined by Northern blot and immunohistochemistry. Results: Diseased rats treated with vehicle control developed a severe crescentic glomerulonephritis with progressive renal fibrosis identified by a marked accumulation of α-SMA+ myofibroblasts and collagen matrix. This was associated with tubular epithelial-myofibroblast transition as evident by de novo expression of α-SMA and a loss of E-cadherin on damaged tubular epithelial cells. Further studies revealed that severe renal fibrosis was associated with upregulation of renal TGF-β1 and activation of TGF-β/Smad signaling, which was blocked by treatment with PTX. Conclusions: PTX may be an anti-fibrosis agent capable of inhibiting renal fibrosis in a rat model of crescentic glomerulonephritis. Blockade of TGF-β1 expression and Smad2/3 activation may be a mechanism by which PTX inhibits renal fibrosis.

Xanthogranulomatous pyelonephritis is an uncommon form of chronic bacterial pyelonephritis characterized by the destruction of renal parenchyma and the presence of granulomas, abscesses, and collections of lipid-laden macrophages (foam cells) replacing the renal parenchyma. This case report illustrates the clinical course of bilateral diffuse xanthogranulomatous pyelonephritis with a subtle manifestation in contrast to those typically presenting with fever, flank pain or urinary tract infection. The patient therefore received supportive treatment for 18 months without hemodialysis, instead of the curative treatment, bilateral nephrectomy, which would have caused immediate loss of residual renal function and dependence on hemodialysis.

The underlying diseases of our patients were consistent with the major disease categories that have been frequently linked to secondary MN. The HP group was more akin to undefined groups regarding their pathological and clinical profiles. Since the MN in the undefined group might be the only renal manifestation antedating other clinical presentations of the corresponding underlying disease, a long-term follow-up and meticulous search for aetiological factors are required to validate this assumption.

Although cold syrup containing dextromethorpan bromide is widely administered, the bromism due to cold syrup has not been reported. We report a patient who had negative anion gap with hyperchloremia and conscious loss because of daily intake of cold complex syrup (containing dextromethorphan bromide 0.4 mg/ml, acetaminophen 8.33 mg/ml) for headache for 4-5 years. The bromide content in cold complex syrup resulted in serum levels of bromide that interfered with the automated analyzers for chloride content. When conscious change is due to bromism, hemodialysis instead of forced hydration and diuresis should be performed immediately. Therefore, patients with a markedly negative anion gap with hyperchloremia should be considered as having halide intoxication.