RESUMO
BACKGROUND: The renal system has a specific pleural effusion associated with it in the form of "urothorax", a condition where obstructive uropathy or occlusion of the lymphatic ducts leads to extravasated fluids (urine or lymph) crossing the diaphragm via innate perforations or lymphatic channels. As a rare disorder that may cause pleural effusion, renal lymphangiectasia is a congenital or acquired abnormality of the lymphatic system of the kidneys. As vaguely mentioned in a report from the American Journal of Kidney Diseases, this disorder can be caused by extrinsic compression of the kidney secondary to hemorrhage. CASE SUMMARY: A 54-year-old man with biopsy-proven acute tubulointerstitial nephropathy experienced bleeding 3 d post hoc, which, upon clinical detection, manifested as a massive perirenal hematoma on computed tomography (CT) scan without concurrent pleural effusion. His situation was eventually stabilized by expeditious management, including selective renal arterial embolization. Despite good hemodialysis adequacy and stringent volume control, a CT scan 1 mo later found further enlargement of the perirenal hematoma with heterogeneous hypodense fluid, left side pleural effusion and a small amount of ascites. These fluid collections showed a CT density of 3 Hounsfield units, and drained fluid of the pleural effusion revealed a dubiously light-colored transudate with lymphocytic predominance (> 80%). Similar results were found 3 mo later, during which time the patient was free of pulmonary infection, cardiac dysfunction and overt hypoalbuminemia. After careful consideration and exclusion of other possible causative etiologies, we believed that the pleural effusion was due to the occlusion of renal lymphatic ducts by the compression of kidney parenchyma and, in the absence of typical dilation of the related ducts, considered our case as extrarenal lymphangiectasia in a broad sense. CONCLUSION: As such, our case highlighted a morbific passage between the kidney and thorax under an extraordinarily rare condition. Given the paucity of pertinent knowledge, it may further broaden our understanding of this rare disorder.
RESUMO
OBJECTIVE: To investigate the effect and mechanism of Erigeron Injection (EI) on renal interstitial fibrosis in rats. METHODS: Unilateral ureteral obstruction (UUO) model rats were taken as the subject of study. Thirty-six Sprague-Dawley rats were randomly divided into the control group (A), the UUO model group (B) and the treatment group (C) treated with intraperitoneal injection of EI 5 mL/kg per day from 24 h before to 9 days after the operation. On the 10th day of UUO, rats were killed and their kidneys were processed to paraffin sections with HE, PAS and picro-sirius-red staining. The pathological change of renal tubular interstitial tissue and relative cortical/interstitial volume (C/I) as well as the relative content of collagen (RC) were observed by light microscope. The expression of transforming growth factor beta1 (TGF-beta1), alpha-smooth muscle actin (alpha-SMA) and collagen I in the renal mesenchyma were examined by immunohistochemistry. RESULTS: Marked renal interstitial fibrosis changes were found in Group B and C, but the changes were milder in Group C. C/I and RC were higher in Groups B and C as compared with those in Group A (P < 0.01), but they were much lower in Group C than in Group B (P < 0.01). The expression of TGF-beta1, alpha-SMA and collagen I were higher in Group B and C than those in Group A (P < 0.05), but they were lower in Group C than in Group B (P < 0.05). CONCLUSION: EI could ameliorate renal interstitial fibrosis in rats, which might be partially realized by down-regulating the expression of TGF-beta1 to prevent the renal epithelial cell differentiation and reducing the synthesis of collagen I.
