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Chun-Fu Lai

Publications and source records attributed to Chun-Fu Lai.

7 recordsLinked to original sources
PubMed2006

Early activation of bradykinin B2 receptor aggravates reactive oxygen species generation and renal damage in ischemia/reperfusion injury.

The kallikrein/kinin system is beneficial in ischemia/reperfusion injury in heart, controversial in brain, but detrimental in lung, liver, and intestine. We examined the role of the kallikrein/kinin system in acute ischemia/reperfusion renal injury induced by 40 min occlusion of the renal artery followed by reperfusion. Rats were infused with tissue kallikrein protein 5 days before (pretreated group) or after (treated group) ischemia. Two days later, the pretreated group exhibited the worst renal dysfunction, followed by the treated group, then the control group. Kallikrein increased tubular necrosis and inflammatory cell infiltration with generation of more tumor necrosis factor-alpha and monocyte chemoattractant protein-1. Reactive oxygen species (ROS), malondialdehyde, and reduced/oxidized glutathione measurement revealed that the oxidative stress was augmented by kallikrein administration in both ischemic and reperfusion phases. The groups with more ROS generation also had more apoptotic renal cells. The deleterious effects of kallikrein on ischemia/reperfusion injury were reversed by cotreatment with bradykinin B2 receptor (B2R) antagonist, but not B1 receptor antagonist, and were not associated with hemodynamic changes. We conclude that early activation of B2R augmented ROS generation in ischemia/reperfusion renal injury, resulting in subsequent apoptosis, inflammation, and tissue damage. This finding suggests the potential application of B2R antagonists in acute ischemic renal disease associated with bradykinin activation.

Animals↗
PubMed2006

Human immunodeficiency virus-associated nephropathy.

Human immunodeficiency virus-associated nephropathy (HIVAN) is characterized by high-grade proteinuria and rapid progression to end-stage renal disease (ESRD). Despite the large numbers of HIV-infected cases in Asian countries, data on HIVAN in this area are limited. We report a 54-year-old Taiwanese man with HIVAN who presented with cytomegalovirus retinitis, renal insufficiency (serum creatinine, 3.8 mg/dL) and nephrotic range proteinuria with a daily protein loss of 10.8 g. Despite highly active antiretroviral therapy (HAART) for 31 months, renal failure developed requiring maintenance hemodialysis. Renal biopsy showed collapsing focal segmental glomerular sclerosis, podocyte proliferation and tubulointerstitial nephritis with mononuclear cell infiltration. These features were compatible with HIVAN. Although hemodialysis was instituted, he died 2 months later due to nosocomial pneumonia complicated with multiple organ failure. In summary, this case of HIVAN in a Taiwanese patient shows that the condition may progress to ESRD despite successful viral suppression with HAART.

AIDS-Associated Nephropathy↗
PubMed2006

Quantitative comparison of skin colors in patients with ESRD undergoing different dialysis modalities.

BACKGROUND: Little is known about the alterations in skin pigmentation in patients with end-stage renal disease (ESRD) in the modern dialysis era. Aims of this study are to quantitatively investigate the skin color of patients with ESRD undergoing different dialysis modalities and determine factors associated with skin color changes. METHODS: One hundred twenty-four patients with ESRD undergoing either hemodialysis (HD; n = 51) or peritoneal dialysis (PD; n = 73) were enrolled, and 59 subjects with normal renal function served as controls. Skin colors of the abdomen (non-sun-exposed site) and forearm (sun-exposed site) were measured by using a reflected-light colorimeter and recorded by using the Commission Internationale de l'Eclairage recommended L*a*b* system, in which a higher L* value represents brighter skin. RESULTS: For sun-exposed skin, brightness was not different between patients with ESRD and controls. However, patients with ESRD had a lower L* value in the non-sun-exposed skin area (P < 0.001). HD and PD patients had similar L* values in both sun-exposed and non-sun-exposed skin areas. PD patients with adequate weekly creatinine clearance or residual urine greater than 100 mL/d had brighter skin in the non-sun-exposed area (P = 0.001 and P = 0.035, respectively). CONCLUSION: Patients with ESRD in Taiwan have significantly darker skin in the non-sun-exposed area, but not the sun-exposed area, than subjects with normal renal function. However, there is no difference in skin darkness between HD and PD patients. Efforts to increase weekly creatinine clearance and preserve residual urine may alleviate hyperpigmentation in PD patients.

Adult↗
PubMed2005

Pentoxifylline attenuates tubulointerstitial fibrosis by blocking Smad3/4-activated transcription and profibrogenic effects of connective tissue growth factor.

Pentoxifylline (PTX) is a potent inhibitor of connective tissue growth factor (CTGF), but its underlying mechanism is poorly understood. Here, it was demonstrated that PTX inhibited not only TGF-beta1-induced CTGF expression but also CTGF-induced collagen I (alpha1) [Col I (alpha1)] expression in normal rat kidney fibroblasts (NRK-49F) and alpha-smooth muscle actin expression in normal rat kidney proximal tubular epithelial cells (NRK-52E). Furthermore, PTX attenuated tubulointerstitial fibrosis, myofibroblasts accumulation, and expression of CTGF and Col I (alpha1) in unilateral ureteral obstruction kidneys. The mechanism by which PTX reduced CTGF in NRK-49F and NRK-52E was investigated. Activation of Smad3/4 was essential for TGF-beta1-induced CTGF transcription, but PTX did not interfere with TGF-beta1 signaling to Smad2/3 activation and association with Smad4 and their nuclear translocation. However, PTX was capable of blocking activation of TGF-beta1-induced Smad3/4-dependent reporter as well as CTGF promoter, suggesting that PTX affects a factor that acts cooperatively with Smad3/4 to execute transcriptional activation. It was found that PTX increased intracellular cAMP and caused cAMP response element binding protein phosphorylation. The protein kinase A antagonist H89 abolished the inhibitory effect of PTX on Smad3/4-dependent CTGF transcription, whereas dibutyryl cAMP and forskolin recapitulated the inhibitory effect. In conclusion, these results indicate that PTX inhibits CTGF expression by interfering with Smad3/4-dependent CTGF transcription through protein kinase A and blocks the profibrogenic effects of CTGF on renal cells. Because of the dual blockade, PTX potently attenuates the tubulointerstitial fibrosis in unilateral ureteral obstruction kidneys.

Actins↗
PubMed2005

Pneumatosis intestinalis and hepatic portal venous gas after CPR.

Pneumatosis intestinalis and hepatic portal venous gas are usually associated with severe intra-abdominal pathologies. As diagnostic technologies advanced, a number of variant etiologies have been identified. We report 2 cases in which pneumatosis intestinalis and hepatic portal venous gas developed after prolonged cardiopulmonary resuscitation (CPR). The pathogenic mechanism was most probably bowel infarction caused by poor mesenteric perfusion during and after CPR. Limited cardiac output during prolonged resuscitation and severe vasoconstriction after large doses of epinephrine and vasopressors might both contribute to the compromised mesenteric perfusion. The risk seems especially high for old patients with severe atherosclerosis. Once it happens, the prognosis is extremely poor. In patients of cardiac arrests receiving prolonged CPR, catastrophic complications like this should be considered in the postresuscitation phase, especially those with multiple risk factors like old age, severe atherosclerosis, and use of large doses of vasoconstrictors.

Aged↗
PubMed2005

The renoprotective potential of pentoxifylline in chronic kidney disease.

Current interventions with proven efficacy, such as glycemic and blood pressure control, dietary protein restriction, and angiotensin II blockade, slow the progression of chronic kidney disease (CKD); however, whether long-term cessation of CKD progression is possible remains unclear. Because of the pathogenetic complexity of this condition, multidrug interventions with the least adverse effects should be investigated as the next step in attempts to stop CKD progression. Pentoxifylline, a non-selective phosphodiesterase inhibitor with indiscernible toxicity, exerts potent inhibitory effects against cell proliferation, inflammation, and extracellular matrix accumulation, all of which play important roles in CKD progression. Pentoxifylline monotherapy markedly reduces proteinuria in patients with membranous nephropathy. Moreover, limited human studies have proven pentoxifylline efficacy in reducing proteinuria in patients with diabetes receiving angiotensin-converting enzyme inhibitors, and in patients with nephrotic syndrome secondary to lupus nephritis despite immunosuppressive therapy. Further clinical trials are necessary to examine whether pentoxifylline can improve renal outcomes in patients receiving interventions of proven efficacy.

Cell Proliferation↗