Search PubMed⌕ Search

Biomedical subjects

C Y Lin

Publications and source records attributed to C Y Lin.

At least 145 records · Page 8Linked to original sources
PubMed1998

Identification of new renal scarring in repeated episodes of acute pyelonephritis using Tc-99m DMSA renal SPECT.

PURPOSE: This prospective study compared the value of Tc-99m DMSA renal planar scintigraphy with SPECT to detect new renal involvement in patients with repeated episodes of acute pyelonephritis (APN). MATERIALS AND METHODS: Children with suspected APN were transferred to our department for DMSA renal scans. Seventy-two children (ages 1 week to 15 years) had DMSA planar and SPECT imaging performed twice because of clinical or laboratory suspicion of repeated APN. In addition, radiographic voiding cystourethrography was also performed in all cases. The presence of vesicoureteral reflux (VUR) was graded on a scale of 0 to 5. RESULTS: New lesions were observed with SPECT in 56 kidneys and with planar scintigraphy in 38 kidneys. No patients had a negative result of Tc-99m DMSA renal SPECT who also had a positive Tc-99m DMSA planar result. The degree of VUR as related to APN was diagnosed better with SPECT than with planar scintigraphy (46 compared with 30 and 10 compared with 8, respectively). There is a significant difference (P < 0.05) between the diagnostic ability of these two methods to identify the increased tendency of repeated APN to occur with high-grade VUR compared with low-grade or no VUR. CONCLUSIONS: High-grade VUR is more commonly associated with renal injury than is low-grade or no VUR. If only Tc-99m DMSA renal planar scintigraphy is performed, renal scarring may be underestimated. Our results suggest that Tc-99m DMSA renal SPECT, rather than planar scintigraphy, should be used routinely in children with a clinical suspicion of APN, especially for those with scarred kidneys and high-grade VUR.

Acute Disease↗
PubMed1998

Cerebral cortex participation in the physiological mechanisms of acupuncture stimulation: a study by auditory endogenous potentials (P300).

Although acupuncture has traditionally used the acupoints formula to treat diseases, the physiological mechanisms involved and the effectiveness of therapy remain unclear. This study investigated the physiological mechanism(s) and response to acupuncture stimulation using the acupoints formula. Scalp-recorded potentials P300 were evoked by auditory stimulation of non-target and target in 13 normal adult volunteers. Latencies and amplitudes were measured. Three assessments were performed in each subject over a period of at least one week. Each assessment was divided into a control period with no acupuncture stimulation, followed by an acupuncture period and then a post-acupuncture period. Acupuncture needles were inserted into the body as follows: 1) non-acupoint: acupuncture needles were inserted 2 cm lateral to both Zusanli acupoints; 2) acupoint: acupuncture needles were inserted into both Zusanli acupoints; 3) acupoints formula: acupuncture needles were inserted into both Zusanli and Shousanli acupoints. Our results showed that both acupoint and acupoints formula assessments resulted in a significant decrease of P300 amplitudes during the acupuncture and post-acupuncture periods. However, there was significant difference in P300 amplitudes in the non-acupoint assessment during these periods. P300 changes in latencies and amplitudes were not significantly different between the acupoint assessment and the acupoints formula assessment. We concluded that acupuncture stimulation of both Zusanli acupoints resulted in a decrease of P300 amplitudes, suggesting the involvement of the cerebral cortex in sensory interaction when simultaneous sensations of the two types are received. No similar changes were observed in the non-acupoint assessment, which have been suggested to be related to so-called acupoint specificity. Results obtained using the acupoints formula were not significantly different from those using acupoints alone. These findings suggested that neuropsychological effects from stimulation of Zusanli acupoints and Shousanli acupoints are different.

Acoustic Stimulation↗
PubMed1998

Persistent transforming growth factor-beta 1 expression may predict peritoneal fibrosis in CAPD patients with frequent peritonitis occurrence.

The efficiency of continuous ambulatory peritoneal dialysis depends on the permeability of the peritoneal membrane. Peritoneal fibrosis (PF) causes loss of the dialytic function. Several studies have indicated that PF is closely related to the proliferation of peritoneal fibroblasts and the deposition of extracellular matrix. Transforming growth factor-beta 1 (TGF-beta1) plays a major role in stimulating extracellular matrix deposition. Frequent peritonitis occurrence may cause persistent TGF-beta1 mRNA expression. In an attempt to search for a factor related to PF, we designed a longitudinal study to measure TGF-beta1 levels in dialysate and TGF-beta1 mRNA expression in peritoneal mononuclear cells from peritoneal dialysate before onset, once a week during peritonitis, and after peritonitis in high and low peritonitis occurrence (HPO and LPO) patients. Fifteen patients with a LPO rate and 5 patients with a HPO rate were followed up longitudinally. Meanwhile, TGF-beta1 levels and TGF-beta1 mRNA expression were augmented in peritoneal dialysate effluents before, during, and after the episodes of peritonitis. The peritoneal permeability was evaluated by the peritoneal equilibration test. The results revealed that in the LPO group, TGF-beta1 and TGF-beta1 mRNA were detectable at early stages of peritonitis, but the levels decreased rapidly and were undetectable 2 weeks after peritonitis. On the other hand, in the HPO group, TGF-beta1 and TGF-beta1 mRNA persisted for a long time. We could detect TGF-beta1 and TGF-beta1 mRNA in dialysate effluents and peritoneal mononuclear cells even 2, 3, and 4 weeks after episodes of peritonitis. When compared with that of first or second episode of peritonitis, the peritoneal function evaluated with the peritoneal equilibration test was found to obviously deteriorate during the third episode of peritonitis. These findings were confirmed by an in situ hybridization technique to evaluate the relationship between TGF-beta1 mRNA expression and PF from biopsied peritoneal specimens. These findings suggest that the high TGF-beta1 levels in the dialysate are related to an increased expression of TGF-beta1 in the peritoneum. Thus, the persistent TGF-beta1 expression in the peritoneum may serve as a useful parameter in predicting PF in continuous ambulatory peritoneal dialysis patients with frequent peritonitis occurrence.

Adolescent↗
PubMed1998

Endogenous apoE expression modulates HDL3 binding to macrophages.

We have previously shown that expression of a human apoE cDNA in J774 macrophages enhances cholesterol efflux to HDL3. We have also shown that endogenous apoE expression produces a cell surface pool of apoE associated with proteoglycans. In this series of experiments, we first demonstrate the presence of a cell surface proteoglycan-associated apoE pool in human monocyte-derived macrophages. We then examine the hypothesis that endogenous expression of apoE modulates HDL3 binding to macrophages, thereby, accounting for enhanced cholesterol efflux to HDL3, specifically examining a role for the cell surface pool. Enhanced binding of apoE-free human HDL3 to apoE-expressing macrophages, compared to non-expressing macrophages, was observed at 37 degrees C and 4 degrees C. The enhanced binding was not due to apoE secreted into the medium, as determined by experiments utilizing conditioned medium from apoE-secreting cells. Removal of the cell surface pool of apoE, however, substantially reduced the incremental HDL3 binding produced by apoE expression. Cellular cholesterol mass measurements demonstrated that experimental conditions that reduced HDL3 binding to apoE-expressing macrophages, did not substantially reduce cholesterol efflux to HDL3. In summary, our results document a clear role for cell surface pool of apoE in modulating HDL3 interaction with macrophages. The enhanced binding, however, does not appear to be a major mechanism contributing to the increased cholesterol efflux to HDL3, which results from endogenous macrophage expression of apoE.

Apolipoproteins E↗
PubMed1997

Characterization of an ADP-ribosylation factor-like 1 protein in Saccharomyces cerevisiae.

ADP-ribosylation factors (ARFs) are highly conserved approximately 20-kDa guanine nucleotide-binding proteins that enhance the ADP-ribosyltransferase activity of cholera toxin and are believed to participate in vesicular transport in both exocytic and endocytic pathways. Several ARF-like proteins (ARLs) have been cloned from Drosophila, rat, and human; however, the biological functions of ARLs are unknown. We have identified a yeast gene (ARL1) encoding a protein that is structurally related (>60% identical) to human, rat, and Drosophila ARL1. Biochemical analyses of purified recombinant yeast ARL1 (yARL1) protein revealed properties similar to those ARF and ARL1 proteins, including the ability to bind and hydrolyze GTP. Like other ARLs, recombinant yARL1 protein did not stimulate cholera toxin-catalyzed auto-ADP-ribosylation. yARL1 was not recognized by antibodies against mammalian ARLs or yeast ARFs. Anti-yARL1 antibodies did not cross-react with yeast ARFs, but did react with human ARLs. On subcellular fractionation, yARL1, similar to yARF1, was localized to the soluble fraction. The amino terminus of yARL1, like that of ARF, was myristoylated. Unlike Drosophila Arl1, yeast ARL1 was not essential for cell viability. Like rat ARL1, yARL1 might be associated in part with the Golgi complex. However, yARL1 was not required for endoplasmic reticulum-to-Golgi protein transport, and it may offer an opportunity to define an ARL function in another kind of vesicular trafficking, such as the regulated secretory pathway.

ADP-Ribosylation Factors↗
PubMed1997

Degradation of macrophage ApoE in a nonlysosomal compartment. Regulation by sterols.

Macrophage-derived apoE has been shown to play an important role in the susceptibility of the vessel wall to atherosclerosis. Previous studies have shown that macrophage sterol content modulates apoE synthesis and secretion, associated with a large transcriptional response of the apoE gene. The current studies were undertaken to evaluate the existence of additional post-transcriptional regulatory loci for the effect of sterols on apoE synthesis and secretion. Using a macrophage cell line transfected to constitutively express an apoE cDNA to facilitate detection of a post-transcriptional regulatory locus, we demonstrated that preincubations in 25-hydroxycholesterol and cholesterol lead to increased apoE secretion in pulse/chase experiments. Examination of cell lysates in these experiments showed that apoE not secreted by control cells was degraded and not detectable, suggesting that the preincubation in sterols increased secretion by decreasing degradation of newly synthesized apoE. The measurement of total protein and apoE degradation in cell fractions revealed an intermediate density fraction that degraded significant amounts of newly synthesized total protein and newly synthesized apoE. In this fraction, degradation of total protein and apoE was unaffected by chloroquine but was substantially reduced by N-acetyl-Leu-Leu-norleucinal plus N-acetyl-Leu-Leu-methioninal or by lactacystin, suggesting the involvement of proteasomes. Preincubation in sterol/oxysterol or acetylated low density lipoprotein did not modify total protein degradation by this fraction but inhibited apoE degradation. Similar results were obtained using intermediate density fractions isolated from human monocyte-derived macrophages. The results of our studies indicate that newly synthesized apoE in the macrophage can be degraded in an intermediate density nonlysosomal cellular compartment, which is sensitive to proteasomal inhibitors. Alteration of cellular lipid homeostasis by preincubation in sterol/oxysterol or acetylated low density lipoprotein inhibits apoE, but not total protein, degradation in this fraction. Inhibition of the degradation of apoE in this fraction likely contributes to the increased apoE secretion observed in sterol-enriched cells.

Apolipoproteins E↗
PubMed1997

Expression of a gene encoding a 16.9-kDa heat-shock protein, Oshsp16.9, in Escherichia coli enhances thermotolerance.

A gene encoding the rice 16.9-kDa class I low-molecular-mass (LMM) heat-shock protein (HSP), Oshsp16.9, was introduced into Escherichia coli using the pGEX-2T expression vector to analyze the possible function of this LMM HSP under heat stress. It is known that E. coli does not normally produce class I LMM HSPs. We compared the survivability of E. coli XL1-Blue cells transformed with a recombinant plasmid containing a glutathione S-transferase (GST)-Oshsp16.9 fusion protein (pGST-FL cells) with the control E. coli cells transformed with the pGEX-2T vector (pGST cells) under heat-shock (HS) after isopropyl beta-D-thiogalactopyranoside induction. The pGST-FL cells demonstrated thermotolerance at 47.5 degrees C, a treatment that was lethal to the pGST cells. When the cell lysates from these two E. coli transformants were heated at 55 degrees C, the amount of protein denatured in the pGST-FL cells was 50% less than that of the pGST cells. Similar results as pGST-FL cells were obtained in pGST-N78 cells (cells produced a fusion protein with only the N-terminal 78 aa in the Oshsp16.9 portion) but not in pGST-C108 cells (cells produced a fusion protein with C-terminal 108 aa in the Oshsp16.9 portion). The acquired thermotolerant pGST-FL cells synthesized three types of HSPs, including the 76-, 73-, and 64-kDa proteins according to their abundance at a lethal temperature of 47.5 degrees C. This finding indicates that a plant class I LMM HSP, when effectively expressed in transformed prokaryotic cells that do not normally synthesize this class of LMM HSPs, may directly or indirectly increase thermotolerance.

Cloning, Molecular↗
PubMed1997

Characterization of a novel, membrane-bound, 80-kDa matrix-degrading protease from human breast cancer cells. Monoclonal antibody production, isolation, and localization.

A major, apparently novel extracellular matrix-degrading protease was previously identified and partially isolated from hormone-dependent but not from hormone-independent human breast cancer cells (Shi, Y. E., Torri, J., Yieh, L., Wellstein, A., Lippman, M. E., and Dickson, R. B. (1993) Cancer Res. 53, 1409-1415). Although initially the 80-kDa protease was identified from breast cancer cell-conditioned medium, immunofluorescence staining of breast cancer cells with anti-80-kDa protease monoclonal antibody 21-9 showed that in addition to its detection in intracellular compartments, the protease was uniformly localized around periphery of the cells with more intensive staining on the pseudopodia and membrane ruffles. A surface biotinylation technique confirmed the plasma membrane localization of the protease. In addition, the 80-kDa protease could not be washed from the membrane fraction of homogenized breast cancer cells with high concentrations of salts or with EDTA. The 80-kDa protease may noncovalently associate with other protein(s) to form complexes, the 95- and 110-kDa proteases. Both complexes showed gelatinolytic activity and bore the epitopes recognized by monoclonal antibody 21-9. Furthermore, both complexes could be converted to 80-kDa forms by boiling in SDS in the absence of reducing agents. Expression of this novel, integral membrane gelatinase could allow breast cancer cells an alternative to other previously described matrix-degrading enzymes for degradation of the extracellular matrix in close proximity to their surfaces.

Antibodies, Monoclonal↗
PubMed1997

Regional perfusion abnormalities with phenylephrine during normothermic bypass.

BACKGROUND: Hypotension and vasopressors during cardiopulmonary bypass may contribute to splanchnic ischemia. The effect of restoring aortic pressure on visceral organ, brain, and femoral muscle perfusion during cardiopulmonary bypass by increasing pump flow or infusing phenylephrine was examined. METHODS: Twelve anesthetized swine were stabilized on normothermic cardiopulmonary bypass. After baseline measurements, including regional blood flow (radioactive microspheres), aortic pressure was reduced to 40 mm Hg by decreasing the pump flow. Next, aortic pressure was restored to 65 mm Hg either by increasing the pump flow or by titrating phenylephrine. The animals had both interventions in random order. RESULTS: At 40 mm Hg aortic pressure, perfusion to all visceral organs and femoral muscle, but not to the brain, was significantly reduced. Increasing pump flow improved perfusion to the pancreas, colon, and kidneys. In contrast, infusing phenylephrine (2.4 +/- 0.6 micrograms.kg-1.min-1) increased aortic pressure but failed to improve splanchnic perfusion, so that significant perfusion differences existed between the pump flow and phenylephrine intervals. CONCLUSIONS: Increasing systemic pressure during cardiopulmonary bypass with phenylephrine causes significantly lower values of splanchnic blood flow than does increasing the pump flow. Administering vasoconstrictors during normothermic cardiopulmonary bypass may mask substantial hypoperfusion of splanchnic organs despite restoration of perfusion pressure.

Animals↗
PubMed1997

Measurement of synovial tumor necrosis factor-alpha in diagnosing emergency patients with bacterial arthritis.

Because of the high morbidity and mortality in patients with bacterial arthritis, rapidly and correctly diagnosing this critical condition is a challenge to emergency clinicians. Synovial fluid samples were obtained from 75 patients with arthritis disorders who presented to an emergency service, and levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), and interleukin-6 (IL-6) were measured. Twenty patients with culture-proven bacterial arthritis had higher levels of synovial TNF-alpha than patients with osteoarthritis or with inflammatory arthritis, including gouty arthritis, rheumatoid arthritis, reactive arthritis, and lupus arthritis. There was a good sensitivity for synovial TNF-alpha level in diagnosing patients with bacterial arthritis. Nearly 100% of patients with bacterial arthritis had elevated synovial TNF-alpha levels. However, synovial IL-1 beta and IL-6 levels failed to discriminate bacterial arthritis from other inflammatory arthritis. Measurement of synovial TNF-alpha level may be useful as a diagnostic aid in emergency patients with bacterial arthritis disorders.

Adult↗
PubMed1997

Functional activity of sporamin from sweet potato (Ipomoea batatas Lam.): a tuber storage protein with trypsin inhibitory activity.

Sporamin accounts for about 60% to 80% of total soluble protein in sweet potato tubers, and the predicted protein sequence of sporamin shares significant amino acid sequence identity with some Kunitz-type trypsin inhibitors. We constructed three recombinant plasmids with cDNAs that encode preprosporamin, prosporamin, and sporamin, and these three were expressed in Escherichia coli cells as fusion proteins. All three forms of sporamin expressed in E. coli were shown to have strong inhibitory activity to trypsin in vitro, suggesting that post-translational modifications are not essential for trypsin inhibitory activity. Northern blot analysis showed that sporamin transcripts could be systemically induced in leaf tissue of sweet potato by wounding. Therefore, sporamin may have a defense role as a protease inhibitor, in addition to its role as a storage protein.

Amino Acid Sequence↗
PubMed1997

Cyclosporin pharmacokinetics following administration of capsules and Neoral in paediatric patients with lupus nephritis.

AIMS: Neoral is a new microemulsion form of cyclosporin. Pharmacokinetic reports in children are scarce. Therefore, we performed a pharmacokinetic study between Cyclosporin A (CsA) capsules and Neoral in paediatric patients with lupus nephritis. METHODS: A single 5 mg kg(-1) dose orally of either CsA capsules or Neoral was given to 10 paediatric patients (serum creatinine < 1.5 mg dl(-1)). CsA whole blood levels were measured for 24 h post-dose by h.p.l.c. RESULTS: Neoral had a higher C(max) and AUC(C(max): 943 +/- 176 ng ml(-1); AUC: 4612 +/- 785 ng ml(-1) h) than those of the CsA capsules (C(max): 697 +/- 187 ng ml(-1); AUC: 3483 +/- 873 ng ml(-1) h; P < 0.05). There was no difference in t(max) and t(1/2,z) between the two groups. CONCLUSIONS: CsA Neoral had improved absorption and bioavailability, which is similar to what is reported in adults. However, interpatient variability still existed. Careful drug monitoring and dose adjustment should be performed during treatment to avoid nephrotoxicity, especially in lupus nephritis.

Adolescent↗
PubMed1997

Anti-GAD65 autoantibody in Taiwanese patients with insulin-dependent diabetes mellitus: effect of HLA on anti-GAD65 positivity and clinical characteristics.

OBJECTIVE: Anti-GAD65 antibody has been studied widely in patients with insulin-dependent diabetes mellitus (IDDM) in many different populations. However, the prevalence of GAD65 autoantibody has not been assessed in Taiwanese patients with IDDM. We therefore characterized GAD65 antibody and investigated the effect of HLA-DR phenotypes on GAD65 autoimmunity and other clinical characteristics in Taiwanese subjects with IDDM. SUBJECTS AND MEASUREMENTS: Two hundred and twenty-five patients (male 102, female 123) with IDDM were recruited. The diagnostic criteria for IDDM were age of onset before 30 years, presence of diabetic ketoacidosis, and insulin-dependency within 3 years of onset. We employed a radioligand method to detect GAD65 antibody. HLA-DR typing was performed by the PCR-SSO techniques. Plasma C-peptide and anti-thyroid microsomal antibody were also measured. RESULTS: The prevalence of GAD65 antibody according to duration of disease were 50/91 (54.9%), 37/95 (38.9%), 8/24 (33%), and 3/15 (20%) among the groups of duration < or = 5, 6-10, 11-15, and > 15 years, respectively (p = 0.0011). There were no significant differences between GAD(+) and GAD(-) patients in age of onset (11.5 +/- 6.5 and 11.6 +/- 13.4 years, respectively), gender distribution (male:female 39:59 and 58:69, respectively) and percentage with residual beta cell function (38.8% and 29.1%, respectively). Multiple regression analysis revealed that duration of IDDM correlated inversely with residual beta cell function. Earlier onset of IDDM correlated with a loss of beta cell function and a HLA-DR phenotype containing DR3/4, DR3/3 or DR3/9. CONCLUSIONS: Prevalence of GAD65 autoantibody among Taiwanese subjects with IDDM was negatively correlated with duration of disease. Different determinants in the HLA-DR locus contributed to the clinical onset of IDDM but not to GAD autoimmunity.

Adolescent↗
PubMed1997

Photochemical inactivation of viruses and bacteria in platelet concentrates by use of a novel psoralen and long-wavelength ultraviolet light.

BACKGROUND: A photochemical treatment process has been developed for the inactivation of viruses and bacteria in platelet concentrates. This process is based on the photochemical reaction of a novel psoralen, S-59, with nucleic acids upon illumination with long-wavelength ultraviolet light (UVA, 320-400 nm). STUDY DESIGN AND METHODS: High levels of pathogens were added to single-donor platelet concentrates containing 3 to 5 x 10(11) platelets in 300 mL of 35-percent autologous plasma and 65-percent platelet additive solution. After treatment with S-59 (150 microM) and UVA (0-3 J/cm2), the infectivity of each pathogen was measured with established biologic assays. In vitro platelet function after photochemical treatment was evaluated during 7 days of storage by using a panel of 14 assays. The in vivo recovery and life span of photochemically treated platelets were evaluated after 24 hours of storage in a primate transfusion model. RESULTS: The following levels of pathogen inactivation were achieved: >10(6.7) plaque-forming units (PFU) per mL of cell-free human immunodeficiency virus (HIV), >10(6.6) PFU per mL of cell-associated HIV, >10(6.8) infectious dose (ID50) per mL of duck hepatitis B virus (a model for hepatitis B virus), >10(6.5) PFU per mL of bovine viral diarrhea virus (a model for hepatitis C virus), >10(6.6) colony-forming units of Staphylococcus epidermidis, and >10(5.6) colony-forming units of Klebsiella pneumoniae. Expression of integrated HIV was inhibited by 0.1 microM S-59 and 1 J per cm2 of UVA. In vitro and in vivo platelet function were adequately maintained after antiviral and antibacterial treatment. CONCLUSION: Photochemical treatment of platelet concentrates offers the potential for reducing transfusion-related viral and bacterial diseases.

Animals↗
PubMed1997

Phase II study of megestrol acetate in the treatment of hepatocellular carcinoma.

This is a report of a phase II study of megestrol acetate (160 mg/day, orally) in the treatment of hepatocellular carcinoma (HCC). Forty-six patients with advanced HCC were studied and tumour response, changes in appetite, bodyweight, a feeling of well-being, survival and toxicity were evaluated. Thirty-two patients were able to be evaluated for response; there were no complete responders or partial responders. Twelve patients (38%) had stable disease and seven of these patients had a minor response with a median size reduction in the tumour of 18%. Twenty patients (62%) had progressive disease. Five of 24 (21%) patients had a median reduction in alpha-fetoprotein levels of 59 ng/mL. The overall median survival was 4 months (range 1 week to 27 months). Twenty of 32 (62%) patients had an increased appetite and feeling of well-being. Fourteen of 22 (64%) patients had a median lean bodyweight gain of 5 kg (range 1-14 kg). Toxicities were minimal. Tests for glucocorticoid receptors were performed in 10 patients. Four of five patients who were positive for glucocorticoid receptors in the tumour had a stable disease and all five patients who were negative for glucocorticoid receptors had progressive disease. Megestrol acetate had no significant effect on the tumour in HCC patients. However, megestrol acetate is useful in the palliative management of HCC patients, with improvements in appetite, bodyweight and a feeling of well-being with minimal side effects. Some patients had stable disease, a minor reduction of tumour size and a prolonged survival after megestrol acetate treatment and this response may be related to the presence of glucocorticoid receptors in the HCC tumour.

Aged↗
PubMed1997

IgA nephropathy: to treat or not to treat?

IgA nephropathy (Berger's disease) is thought to be the most common primary glomerulonephritis in the world. Characteristically, it presents with intermittent macroscopic hematuria in association with upper respiratory infections. The diagnosis is established by demonstrating predominant IgA deposits in the glomerular mesangium. One third of the cases progress slowly over 25 years to glomerulosclerosis and end-stage renal disease. This rate of disease progression has not been altered by any known treatment, including the use of corticosteroids or cyclosporine. The pathogenesis of this disease is unknown; however, recent data implicated oxygen free radicals in the development of IgA nephropathy. The recent controlled, double-blind, 2-year study from the Mayo Clinic showed that fish oil slowed the progression of IgA nephropathy. This contrasts with the previous studies where the use of fish oil either accelerated the rate of deterioration of renal function in patients with IgA nephropathy or showed no change compared to untreated subjects. Furthermore, in experimental uremia, marked renal functional deterioration with fish oil administration has been reported. Experimental models of IgA nephropathy have been developed in the past few years. In addition, molecular biology offers an unique opportunity to study kidney tissue obtained from patients and animals with IgA nephropathy. These advances will enable the identification of the critical sequence of events that result in renal injury and provide new insight into the pathogenesis and progression of IgA nephropathy. This will help clarify the role of free oxygen radical release on disease progression, and an understanding on the mechanisms of antioxidants, such as vitamin E, in preventing such renal injury.

Animals↗