bluuebunny/crossref_metadata_2025 huggingface dataset:
Neutral metalloproteinases in human urine from normal patients and renal disease patients
Authors: FUJIMOTO Shouichi , HAMAI Keiko , SATO Yuji , YAMAMOTO Yoshitaka , ETO Tanenao
Published: April 2007

Summary: We examined the activity and the characteristics of gelatinolytic enzymes in the urine from normal subjects and the patients with glomerulonephritis (GN). Gelatinolytic activity was assayed by using [3H]gelatin (heat‐denatured type I collagen) as a substrate. the activity found to be 2463 ± 204 U/day (mean ± SEM, n = 17) in the urine from the healthy individuals, but was negligible in plasma samples. In GN patients (n=24) urinary gelatinolytic activity (724± 149 U/day, P < 0.001) was significantly lower compared with the healthy individuals. Partial purification (anion exchange column chromatography followed by gel filtration) revealed that two active gelatinolytic enzymes (molecular weight [Mr]92 kDa; high molecular weight [HMW] gelatinase, Mr 40 kDa; low molecular weight [LMW] gelatinase) were present in the urine obtained from the healthy individuals. the activity of these enzymes was inhibited by EDTA, 1,10‐phenanthroline and α2‐macroglobulin, but not by inhibitors for serine, cystein and aspartic proteinase. As the optimum pH was in the neutral range (pH 6–9), these gelatinases were considered to be neutral endometalloproteinases. These enzymes could degrade acid soluble type IV collagen and native rat glomerular basement membrane (GBM) in addition to gelatin, but not type I collagen. Immunoblotting with antibodies against human metalloproteinases (MP) identified HMW gelatinase with matrix metalloproteinase (MMP)‐9 (gelatinase B) and LMW gelatinase with MMP‐2 (gelatinase A), respectively. As these enzymes are metalloproteinase (MP) capable of degrading GBM and its component, urinary MP may be a useful subject as a tool searching the metabolic alteration of glomerular extracellular matrix in renal diseases.
Oral 1,25‐dihydroxyvitamin D3 loading test in normal subjects and patients with chronic renal failure under haemodialysis
Authors: YUMITA Shigeru , SEKINO Hiroshi , YAMAUCHI Sshigeki , TAKEZAWA Junichi
Published: April 2007

Summary: The present study was designed to determine the criterion for 1,25‐dihydroxyvitamin D3 (1,25 (OH)2D3) loading test in normal subjects and haemodialysis patients. Fourteen normal subjects were administered 1.0 μg of 1,25(OH)2D3 per os and serum 1,25(OH)2D was monitored every hour up to 6 h afterwards under conditions of overnight fasting, and six haemodialysis patients were administered 2.0 μg of 1,25(OH)2D3 per os and serum 1,25(OH)2D was monitored every 2 h up to 12 h afterwards. Peak time of serum 1,25 (OH)2D varied between 2 and 5 h after administration in normal subjects. However, there was a good correlation between the maximum increment of 1,25(OH)2D (maxΔ1,25(OH)2D) and the increment at 4 h after administration (Δ1,25(OH)2D(4 h)). the peak time of Δ1,25(OH)2D in six haemodialysis patients was also at 4 h after administration. From these observations, Δ1,25(OH)2D(4 h) was evaluated in subsequent studies. Twenty‐six normal subjects and 24 haemodialysis patients were administered 0.5–2.0 μg of 1,25(OH)2D3 per os, according to their bodyweights, under conditions of overnight fasting. Blood samples were drawn for measuring 1,25(OH)2D prior to and 4 h after administration. Δ1,25(OH)2D(4 h) showed good correlation with the dose of 1, 25 (OH)2D3 adjusted by bodyweight (ng/kg bodyweight). the ratio of Δ1,25(OH)2D(4 h) and adjusted dose of 1,25(OH)2D3 was more than 2.0 in all normal subjects (range: 1.97−2.89, mean ± SD: 2.38 ± 0.287). Moreover, the ratio of Δ1,25(OH)2D(4 h) and adjusted dose of 1,25(OH)2D3 showed a good reproducibility (CV%= 5.7 Δ 0.32, n=5), and did not depend on the administered dose of 1,25(OH)2D3, suggesting that this ratio is a good parameter for the intestinal absorption of 1,25(OH)2D3. In haemodialysis patients, the mean ratio of Δ1,25 (OH)2D(4 h) and adjusted dose of 1,25(OH)2D3 was 2.14 Δ 0.489, which was not significantly different from the ratio in normal subjects, suggesting that, fundamentally, there was no impairment of intestinal absorption of 1,25(OH)2D3 in these patients. However, low ratios of Δ(4 h) and the dose of 1,25(OH)2D3 with low basal levels of 1,25(OH)2D were observed in some patients (less than 1.5 in four patients), suggesting that there exist haemodialysis patients with malabsorption of 1,25(OH)2D3. From these results, the criterion for normal response in 1,25(OH)2D loading test was proposed, namely, that the ratio of Δ1,25(OH)2D(4 h) and adjusted dose of 1,25(OH)2D3 be more than 2.0.
A study of erythropoiesis inhibitory factors in chronic renal failure sera
Authors: YAO Jian , ZHAO Jun , CHEN Hong , LOU Dingxiu , DONG Dechang
Published: April 2007

Summary: Three separate high molecular weight fractions, designated as FI, FII and FIII, were isolated from sera of chronic renal failure (CRF) patients by precipitate with ammonium sulfate of different concentrations and DEAE celluose. All fractions had obvious suppressive effect on red blood cell growth, both erythroid colony (CFU‐E) and BFU‐E in vitro, but the maximal inhibitory rate that may be found in Fl or in FII and FIII depends entirely on individuals. the study also showed that none of these fractions was a homogeneous substance in SDS‐PAGE electrophoresis. As well, a close correlationship between serum erythropoietin level and the inhibitory rate of the isolated fractions was observed. It is suggested that the inhibitory factors might exist in CRF sera and play a role in triggering the anaemia of CFR.
Arteriovenous access fistulae diminish cardiac reserve, anaerobic threshold and work capacity: A case for fistula closure in stable renal transplant recipients
Authors: AGAR John WM , JACKSON Trevor J , WEDEL Jason A STEIN , CORKE Charles F , APPELBE Alan F
Published: April 2007

Summary: A patent arteriovenous fistula (AVF) in stable renal transplant recipients may be viewed as ‘insurance’ against late graft failure and a return to haemodialysis. A patent AVF may, however, exert significant chronic demands on cardiac output (CO) which may in turn adversely affect the prognosis of patients already at risk of cardiac disease. Doppler echocardiography and anaerobic threshold (AT) assessment were used to measure the CO and the work capacity of nine stable renal transplant recipients > 15 months post transplantation who had patent AVF. Cardiac output fell from 6.9 ± 1.48L/min with the AVF open to 6.0 ± 0.97L/min with the AVF closed (P < 0.002). the AT rose from 14.1 ± 5.67 with the AVF open to 16.5 ± 6.72 with the AVF closed (P < 0.002). the work capacity to reach the AT improved from 68.7 ± 30.8 watts with the AVF open to 84.6 ± 38.0 watts with the AVF closed (P < 0.004). This study suggests that a significant and chronic increase in left ventricular work‐load accompanies a patent AVF resulting in a markedly reduced exercise efficiency. A patent AVF is ideal where graft survival is doubtful but, where long‐term graft function is expected, the adverse effects of AVF patency, a chronic elevation in CO and reduced exercise capacity make a strong case for considering AVF closure. the prognostic advantage for left ventricular function may outweigh AVF preservation in stable renal transplant recipients.
Mechanisms of decreased pressor response to infused angiotensin II in the pregnant rat
Authors: YANG Ye , MACDONALD Graham J , DUGGAN Karen A
Published: April 2007

Summary: This study sought to investigate two possible mechanisms underlying the decrease in the pressor response to infused angiotensin II (Ang II) in pregnancy. First, whether vascular Ang II receptors show parallel regulatory changes to their uterine counterparts during pregnancy and thus if a decrease in vascular angiotensin receptor number might explain this phenomenon. Second, we investigated the possibility that the rate of clearance of Ang II from the plasma was accelerated in pregnancy as a basis for this loss of pressor sensitivity. For receptor studies age‐matched female Wistar‐Kyoto rats were exposed to an appropriate breeding male and killed at days 7, 14 and 21 of gestation. Aortic, glomerular and uterine receptor binding was determined by saturation analysis using 125I(Sar1 Ileu8) Ang II. Binding site density and dissociation constants were derived using the iterative computer program LIGAND. Metabolic clearance studies were performed by the equilibrium infusion method in a separate group of rats on day 14 after exposure to the breeder. Uterine and vascular Ang II receptors showed different patterns of regulation during gestation. the uterine receptors increased in number at day 7 (P < 0.001), then decreased significantly (P < 0.05). Receptor affinity was unchanged at day 7 but decreased significantly at day 14 (P < 0.005). In contrast, in the aorta and glomeruli receptor affinity was unchanged throughout gestation, while receptor numbers were maximal at day 14. Although the total or uncorrected metabolic clearance rate was increased during gestation (P < 0.05) no significant difference was observed after correction for either bodyweight or glomerular filtration rate. We conclude that neither a decrease in vascular Ang II receptor number or affinity explains the loss of pressor sensitivity to infused Ang II. In addition, this phenomenon is not explained by an increase in the rate of removal of Ang II from the circulation.
Recurrent nephrotic syndrome in a renal allograft recipient with focal and segmental glomerulosclerosis: Efficacy of plasmapheresis
Authors: JAGOSE Jinni T , PEEBLES John E , BAILEY Ross R
Published: April 2007

Summary: We report a 29‐year‐old man with renal failure due to focal and segmental glomerulosclerosis (FSGS) who received a well‐matched cadaveric renal allograft and had the early appearance of the nephrotic syndrome and renal insufficiency. His condition responded dramatically to plasmapheresis. the pathogenesis of FSGS recurring in a renal allograft may involve a recently identified circulating factor. the possible efficacy of plasmapheresis in the treatment of recurrent FSGS may be attributable to the removal of this factor.
Effect of erythropoietin on lipid profile in haemodialysis patients
Authors: JAMIL Bilal , NAQVI Saj
Published: April 2007

Summary: Effect of recombinant human erythropoietin (rHuEPO) was determined on lipid levels (i.e. total cholesterol, triglycerides, high density lipoproteins [HDL], low density lipoproteins [LDL]) of 17 anaemic patients on maintenance haemodialysis. Estimations were done before initiating rHuEPO therapy and repeated 6 months later. There was an increase in haemoglobin (7.6 ± 1.09 to 10.9 ± 1.62 gm/dL, P < 0.001), and a significant decrease in total cholesterol (217 ± 22 to 196 ± 18 mg/dL, P < 0.001) and triglyceride levels (200 ± 20 to 186 ± 15 mg/dL, P < 0.001). There was no significant effect on HDL and LDL levels.
Cellular immunity in IgA nephropathy
Authors: SAKAI HIDETO , YAMAUCHI FUMIO , YANO NAOHIRO , ENDOH MASAYUKI , NOMOTO YASUO
Published: April 2007

Summary: A comprehensive study on the role of various cytokines in the regulation of IgA synthesis and progression of glomerular damage in IgA nephropathy was attempted. Semi‐quantitative PCR for IL‐I, IL‐2, IL‐4, IL‐6, IL‐10, IL‐12, interferon (IFN)‐γ, transforming growth factor (TGF)‐β, tumour necrosis factor (TNF)‐α, platelet derived growth factor (PDGF) and monocyte chemoattractant protein‐1 (MCP‐1) was performed. In parallel studies, protein production of some cytokines was also determined. It was demonstrated that IL‐4, IFN‐γ and presumably IL‐12 expressed predominantly in peripheral blood mononuclear cells in patients with IgA nephropathy. Some positive correlations between the mRNA expression of these cytokines and the degree of tissue damage were observed. It was concluded that these cytokines may play some role in the alteration of cellular immunity in this disease.
Treatment of IgA nephropathy: an overview
Authors: WOO KENG‐THYE
Published: April 2007

Summary: Any form of therapy for IgA nephritis (IN) must be rational and practical. the least toxic agent should be chosen with a view to life‐long therapy for patients with poor prognostic indices. While we accept that there is no cure for the disease, we could still offer these patients therapeutic measures to retard the pro gression to end‐stage renal failure (ESRF). In IN there is a general defect in clearance of immune complexes. to limit the amount of mesangial deposits you can reduce antigen load, downregulate lymphokines and employ enzymes to remove glomerular deposits. the use of steroids in treatments have had varying results, some reporting reduction of proteinuria and stability of renal function. A short course of cyclosporine A can reduce proteinuria. Dual therapy with dipyridamole and low dose warfarin can retard progression to ESRF. Results of fish oil therapy are variable, except for two studies, most of the other studies have reported no bene ficial effects. Urokinase have been shown to decrease proteinuria and stabilize renal function. Angiotensin converting enzyme (ACE) inhibitors are proven to retard progression to ESRF by decreasing intraglomerular hypertension. Other therapeutic measures have included low protein and gluten‐free diet and, in some cases a tonsillectomy has blunted disease progression. the single most important factor in treatment is adequate control of systemic hypertension to retard progression of the disease. For patients with the nephrotic syndrome with selective proteinuria the response to prednisolone and cyclophosphamide is usually good. Future therapeutic strategies would include inhibition of mediators and cytokines (platelet‐derived growth factor [PDGF]) antagonist, tumour necrosis factor (TNF) inhibitor) and gene therapy.
The treatment of severe lupus nephritis
Authors: CAMERON J STEWART
Published: April 2007

Summary: The treatment of lupus nephritis involves two distinct phases of management: (i) induction therapy of acute severe disease; and (ii) maintenance treatment of chronic, sometimes relapsing disease. Since the introduction of effective immunosuppression, first with corticosteroids and then with cytotoxic agents in addition, the prognosis for lupus nephritis has improved greatly, especially that of more severe disease, whose prognosis now matches that of milder forms. There is now good evidence that the addition of a cytotoxic agent to corticosteroids improves both histological evolution and the development of renal failure, but both the choice of cytotoxic agent and the route of administrations remain controversial. Although the use of intravenous cyclophosphamide at intervals is popular, the long term outcome using azathioprine is as good and the drug is less toxic, particularly in relation to gonadal function and pregnancy. Therefore, we prefer to use induction with oral cyclophosphamide for 12 weeks, followed by azathiorpine therapy. the dose and route of corticosteroid in the acute phase is likewise controversial: high dose intravenous methylprednisolone perhaps has the advantage of lower side‐effects than high dose oral corticosteroids. Controlled trials of plasma exchange have so far failed to reveal any benefits in the acute phase of lupus. Newer forms of immunosuppression using biological reagents against the immune reaction show promise, but their use is still experimental.
The kidney in malaria: Renal and systemic haemodynamics
Authors: SITPRIJA VISITH , SUITHICHAIYAKUL TAWORN , MOOLLAOR PRACHAK
Published: April 2007

Summary: Renal and systemic haemodynamic alterations in malaria vary with the severity of infection. In mild malaria there is no change in renal and systemic haemodynamics. In moderate infection hypervolaemia, increased cardiac index and decreased, systemic vascular resistance are noted. the renal blood flow and glomerular filtration rate are decreased, accompanied by an increase in plasma arginine vasopressin, norepinephrine and renin activity. Yet in some patients only plasma arginine vasopressin and blood volume are increased while renal and systemic haemodynamics are normal. In severe infection blood volume is either normal or decreased; the cardiac index and systemic vascular resistance are normal, while the renal blood flow and glomerular filtration rate are markedly decreased, leading to renal failure.
How is plasma calcium concentration held constant?
Authors: KUROKAWA KIYOSHI
Published: April 2007

Summary: Extracellular or plasma calcium ion concentration is held constant at 5 mg/dL through the actions of parathyroid hormone (PTH), vitamin D and calcitonin, on their target organs, kidney and bone. the thresholds of renal tubular calcium reabsorption and bone resorption and formation are both set at 5 mg/dL. the set‐point of PTH secretion is also set at 5 mg/dL plasma calcium ion. Thus, the sensing system (parathyroid cell) and the effectors, kidney and bone, are all set to maintain plasma calcium at 5 mg/dL, and such setpoint in each organ may be determined by the membrane bound calcium sensor proteins. the effectiveness of this system depends upon the presence of bone remodelling, which allows a swift move of plasma calcium from and to bone in response to PTH and calcitonin, respectively. In this regard, directing haematopoiesis to bone marrow which provides bone resorbing osteoclasts is critical. It is likely that this shift of haematopoiesis occurs through evolution at the transition from the aquatic to the terrestrial life and this event is directed by expression of ‘homing molecule’ in bone marrow stromal cells. This brief review provides a factual and conceptual framework of the current understanding how plasms calcium is held constant at 5 mg/dL.
On‐line haemodiafiltration: Effective removal of high molecular weight toxins and improvement in clinical manifestations of chronic haemodialysis patients
Authors: KIM SUNG‐TEH , YAMAMOTO CHIEKO , ASABE HIROMI , SATO TAKASHI , TAKAMIYA TOMI
Published: April 2007

Summary: The aim of this study was to validate the purity of the injection fluid in an on‐line haemodiafiltration (HDF) system, and to investigate whether the aggressive removal of high molecular weight toxins achieved by the on‐line HDF will reduce symptoms such as shoulder pain and pruritus. the dialysate for substitution use contained no endotoxin, β‐D‐glucan, or peptidoglycan, suggesting that contamination with gram‐negative/positive bacteria and fungi are kept clear or at extremely low levels. No deleterious complications occurred during the on‐line HDF treatments. the improvement in shoulder pain and pruritus indicated by a decrease in patients' self‐rating scores, was more apparent with treatment that removed both β2‐microglobulin (β2‐m) and α1‐microglobulin (α‐m) than with treatment removing either β2‐m or α1‐m alone. On‐line HDF is much easier to operate and less costly than conventional HDF, and it may become one of the standard therapies for chronic renal failure patients.
Lupus nephritis in children
Authors: LIN CHING‐YUANG
Published: April 2007

Summary: Relatively few studies of children with lupus nephritis have been published. the prognosis of children with lupus nephritis is ominous for those with diffuse proliferative glomerulonephritis and active interstitial inflammation. to evaluate the clinical course, histopathology and prognosis of lupus nephritis in children, to identify the risk factors for renal failure and mortality, and to share our experience in managing lupus nephritis in children, 167 children under 18 years of age with lupus nephritis at Veterans General Hospital‐Taipei, Taiwan from 1979 to 1991 were retrospectively studied. All patients received a renal biopsy and follow‐up biopsies were performed on 36 children. the clinical and serologic parameters at the time of renal biopsy were recorded. There were 55 (33%) patients with class II, 30 (18%) with class III, 69 (41.3%) with class IV and 13 (7.8%) with class V nephritis based on initial biopsy. the mean follow‐up time was 59 months. Follow‐up biopsies were histologically stationary in 29 patients, progressive in five and improved in two. the results revealed that those with persistent hypertension, anaemia, increased serum creatinine concentration, and decreased creatinine clearance at initial biopsy were more prone to develop renal failure. Low titre of CH50 haemolytic assay appeared to be a poor prognostic indicator. the overall renal and patient 5 year survival rates were 93.1% (135/145) and 91.08% (143/157), respectively. They were 87.7% (50/57) and 82% (55/67), respectively, in patients with class IV proliferative glomerulonephritis. the prognosis of children with class IV nephritis in this study was better than that reported previously. All children surviving without renal failure were maintaining their normal lives with little organ dysfunction. the improved results may be due to earlier renal biopsy for precise histopathologic definition, better supportive care, and selective use of aggressive therapy, including methylprednisolone pulse therapy, intravenous cyclophosphamide, intravenous prostaglandin E1 therapy, high‐dose intravenous gammaglobulin therapy, and cyclosporine A for those with high risk factors.
Renal rehabilitation: Effecting improvement through the team approach
Authors: PORTER George A
Published: April 2007

Summary: Renal rehabilitation involves a team effort. Assessment is critical to provide a comprehensive treatment plan. the treatment plan should include the five ‘E's’of renal rehabilitation.
Hypertensive renal damage: Modulation expression of smooth muscle myosin heavy chain isoforms
Authors: SUZUKI Naoe , KIMURA Kenjiro , NAGAI Ryozo , OHBA Shigeyoshi , MISE Naobumi , HIROI Junko , TOJO Akihiro , HIRATA Yasunobu , NAGAOKA Akinobu , GOTO Atsuo , OMATA Masao
Published: April 2007

Summary: The aim of this study was to determine the phenotypic modulation in preglomerular vascular smooth muscles and glomerular cells in hypertension. Eight‐week‐old stroke‐prone spontaneously hypertensive rats (SHRSP) fed high sodium pellets (3%) were untreated or treated with a calcium antagonist, manidipine HCI (2 mg/kg per day), for 8 weeks. the expression of myosin heavy chain isoforms (MHC), SM2 (muscletype) and SMemb (non‐muscle‐type) or α‐actin was examined by the immunohistochemical technique. In normotensive Wistar‐Kyoto rats, both SM2 and α‐actin were expressed equally in the smooth muscles of preglomerular vessels, and SMemb was expressed slightly in the glomerular epithelial cells. In the SHRSP, however, the expression of SM2 and α‐actin was significantly decreased or disappeared in the afferent arterioles, depending on the degree of vascular damage. In damaged glomeruli, SMemb and α‐actin were newly expressed in mesangial cells. Manidipine HCI attenuated the renal damage and restored the expression of α‐actin in the afferent arterioles. There was a significant correlation between the glomerular damage and the attenuation of SM2 expression (r=0.87). In conclusion, phenotypic modulation of vascular smooth muscles occurred in hypertensive renal damage and was correlated with the glomerular damage, where the phenotypic modulation also took place in the mesangial cells. These results indicate that the phenotypic modulations revealed by the expression of myosin isoforms might play an important role in the development of hypertensive renal damage.
Intraperitoneal penetration of pefloxacin in patients on continuous ambulatory peritoneal dialysis
Authors: NGEOW Yun F , TAN Hee W , CHUA Chin T
Published: April 2007

Summary: Six patients with continuous ambulatory peritoneal dialysis (CAPD) associated peritonitis were treated with oral pefloxacin 400 mg twice a day. the concentration of pefloxacin was assayed in 20 sets of serum and peritoneal dialysate samples taken from these patients. With a mean starting serum level of 7.6 mg/L, pefloxacin was detected in all peritoneal dialysates within 15 min and attained a mean concentration of 4.2 mg/L within 2 h. the percentage penetration of pefloxacin into peritoneal fluid was 72.9% (SD 19.4%). the results showed that the administration of oral pefloxacin 400 mg b.d. could result in peritoneal drug levels that should be adequate for the treatment of peritonitis caused by common pathogens like Enterobacteriaceae species and Staphylococcus aureus. However, it may be necessary to give the drug parenterally on the first day of treatment before steady‐state plasma concentrations are achieved and, in empirical therapy, combination antibiotics may be required when infection by more resistant pathogens is suspected.
Calcium channel blocker therapy and retarding the progression of chronic renal disease
Authors: IBELS Lloyd S
Published: April 2007

Summary: Calcium channel blockers are a heterogeneous group of agents that interfere with transmembrane calcium influx, and are effective and widely used as antihypertensive agents. At the level of the renal microcirculation they reverse the afferent arteriolar vasoconstriction induced by diverse agonists, and therefore should theoretically counteract the maladaptive haemodynamic changes that initiate and modulate the progression of kidney disease. In addition to achieving good control of systemic and thus intraglomerular blood pressures, calcium channel blockers have specific renoprotective effects. Their use has been associated, in experimental animals and in man, with retarding the progression of both chronic renal disease and diabetic renal disease. Combined therapy with an ACE inhibitor appears to offer additional protection to the kidney and allows for the use of lower doses of both agents and thus a lower side‐effect profile. From a practical point of view, in patients with chronic renal disease it is often difficult to achieve control of blood pressure with one antihypertensive medication alone, and therapy with two agents offering renoprotective potential is a preferred strategy. In view of the preferential dilatation of afferent arterioles by calcium channel blockers, it is important to achieve tight control of systemic blood pressure and to use long‐acting agents to protect the glomeruli from the deleterious effects of raised intraglomerular pressures. Calcium channel blockers should be used in patients with potentially progressive renal disease in an endeavour to help slow this progression.
Significance of tubulointerstitial fibrosis in paediatric IgM nephropathy
Authors: JUNGTHIRAPANICH Jaakchai , SINGKHWA Vararat , WATANA Dhevy , FUTRAKUL Prasit , SENSIRIVATANA Rachanee , YENRUDI Saowanee
Published: April 2007

Summary: The significance of tubulointerstitial fibrosis in paediatric patients with primary diffuse mesangial proliferative glomerulonephritis and IgM deposition (IgM nephropathy) has not been well documented. the clinical course, therapeutic response and final outcome of 35 patients in whom renal biopsies showed IgM nephropathy are reported. They have been subdivided into two groups according to the absence (19 patients: group I) or presence (16 patients: group II) of superimposed lesion of tubulointerstitial fibrosis. Clinical presentation was similar in both groups but the patients in group I were male predominant (2.8:1 vs 1: 1). 6/19 (31.6%) of the patients in group I and 1/16 (6.3%) in group II responded to corticosteroid, 11/19 (57.9%) in group I and 8/16 (50.0%) in group II had steroid dependent, whereas 2/19 (10.5%) in group I and 7/16 (43.7%) in group II had steroid resistant. About 42% of the patients in group I and 94% in group II required cyclophosphamide therapy by which similar response in both groups (approximately 75%) were observed. the steroid non‐responders and cyclophosphosphamide therapy among patients in group II were significantly higher (P<0.05) than the group I. At the latest assessment, 5/16 (31.3%) in group I and 7/14 (50%) in group II had impaired renal function. the follow‐up period in both groups were 3.1 ± 2.8 and 3.4 ± 2.9 years, respectively. In conclusion, the finding of tubulointerstitial fibrosis in a paediatric IgM nephropathy indicates an unfavourable therapeutic response.
Increased release of myeloperoxidase in vitro from neutrophils of patients with myeloperoxidase‐specific anti‐neutrophil cytoplasmic antibody (MPO‐ANCA) related glomerulonephritis
Authors: MINOSHIMA Shinobu , ARIMURA Yoshihiro , NAKABAYASHI Kimimasa , KITAMOTO Kiyoshi , NAGASAWA Toshihiko , ISHIDA‐OKAWARA Akiko , SUZUKI Kazuo
Published: April 2007

Summary: In order to elucidate the role of neutrophils in the pathogenesis of MPO‐specific anti‐neutrophil cytoplasmic antibody (MPO‐ANCA) related glomerulonephritis (GN), MPO release, beta‐glucuronidase (BGL) release, superoxide anion (O2−) production from the neutrophils of patients with MPO‐ANCA related GN were measured. the effect of plasma on MPO release from neutrophils was also studied in patients with MPO‐ANCA related GN. Neutrophils and plasma were obtained from patients with MPO‐ANCA related GN, GN unrelated to MPO‐ANCA and healthy controls. MPO release from the neutrophils of patients with MPO‐ANCA related GN was higher than that of controls significantly. This was also higher than that in patients with GN unrelated to MPG‐ANCA, but this was not statistically significant. Superoxide anion production from neutrophils of patients with MPO‐ANCA related GN was significantly higher than that in patients with GN unrelated MPO‐ANCA, However, BGL release was not significantly different among three groups. Furthermore, MPO release and O2− production increased in parallel with clinical activity of MPO‐ANCA related GN. Neutrophils of patients with MPO‐ANCA related GN showed to be significantly more sensitive to FMLP on MPO release than those in the other two groups. However, plasma from MPO‐ANCA related GN increased the sensitivity to FMLP on MPO release, but not BGL release, in neutrophils obtained from healthy controls, whereas it suppressed MPO release from neutrophils with MPO‐ANCA related GN. This suggests that in patients with MPO‐ANCA related GN MPO can be highly released from activated neutrophils and that the plasma of patients with MPO‐ANCA contains factor(s) which modulate reactivity of neutrophils.
Prostacyclin and prostaglandin E2 inhibit proinflammatory cytokine‐induced macrophage colony‐stimulating factor production in cultured human glomerular mesangial cells
Authors: KITAHARA Masashi , MORI Tetsuo
Published: April 2007

Summary: Monocyte/macrophages within the mesangium plays some important roles in the progression of renal glomerular injury in which prostanoids exert a broad range of actions. We have examined the production of macrophage colony‐stimulating factor (M‐CSF), a monocyte‐specific cytokine, by human glomerular mesangial cells (MC) and its regulation by prostacyclin and prostaglandin E2 (PGE2). the MCSF production by MC under non‐stimulatory conditions was below detectable levels by ELISA, and was also at a trace level in the steady‐state M‐CSF mRNA expression. Proinflammatory cytokines, interleukin‐1β (IL‐1β) or tumour necrosis factor‐α (TNF‐α) induced the M‐CSF production in the protein and mRNA levels. Both beraprost, a stable analogue of prostacyclin, and PGE2 attenuated the IL‐1β‐ or TNF‐α‐driven M‐CSF production. Indomethacin, a non‐selective cyclooxygenase inhibitor, enhanced the IL‐1β‐ or TNF at‐induced M‐CSF production. Beraprost and PGE2 showed similar inhibitory effects in the presence of indomethacin. Forskolin, a direct activator of adenylate cyclase, and dibutyryl cAMP decreased the M‐CSF production. These results indicate that: (i) human MC have capacity to produce M‐CSF; (ii) exogenous prostacyclin and PGE2 downregulate the IL‐1β‐ or TNF‐α‐driven M‐CSF production possibly by an increase of intracellular cAMP; and (iii) endogenous prostanoids can exert on the M‐CSF production.
Bacterial colonization and peripheral bacteraemia associated with central venous haemodialysis catheters: A cross‐sectional study
Authors: DITTMER Ian D , SHARP Dot , McNULTY Cliodna AM , WILLIAMS Anthony J , BANKS Richard A
Published: April 2007

Summary: Septicaemia related to internal luminal colonization of central venous catheters has been described in many clinical settings including haemodialysis. the prevalence and consequence of intraluminal colonization of central venous haemodialysis catheters is unknown. A cross‐sectional study of asymptomatic patients receiving haemodialysis through central venous catheters was performed. Differential (central line and peripheral) quantitative blood cultures were taken on three occasions. Twenty‐one patients were studied and 20 had colonized central venous catheters. the organisms isolated were Coagulase negative Staphylococci (16 cases), Bacillus species (three), Corynebacterium (three), Pseudomonas species (three), and others (three). Fifteen patients also had significant peripheral bacteraemia associated with the same organism that was cultured from their central line. Seven patients had septic episodes associated with these same organisms. Swabs taken of the internal catheter surfaces also cultured these organisms. the vast majority (95%) of central venous haemodialysis catheters are colonized by bacteria. Seventy‐six per cent have associated peripheral bacteraemia, which can lead to systemic infection.
The influence of erythropoietin on cytokines in haemodialysis patients
Authors: RUTKOWSKI Boleslaw , SZOLKIEWICZ Marek , MANITIUS Jacek , MYLAWSKA Jolanta , BRYL Ewa , MYSALIWSKI Andrzej
Published: April 2007

Summary: In this study, the administration of erythropoietin to haemodialysis patients revealed its immunomodulating properties. to dissociate the immunological effects of erythropoietin action from its haematological effects the patients in our study were administered recombinant human erythropoietin (rhEpo) at the doses that would not affect erythropoiesis. After baseline data had been obtained, six haemodialysis patients were given rhEpo (Eprex‐Cilag) at the dose 7‐10 U/kg bodyweight/s.c., three times a week, for 12 weeks. All patients maintained a stable haemoglobin concentration; no blood transfusions were required. Serum levels of tumour necrosis factor (TNF), IL‐2 and IL‐6 levels of the study patients and the four control patients, not receiving rhEpo, were monitored every 2 weeks. the levels of IL‐6 and TNF remained unchanged; however, a low serum level of IL‐2, recorded before therapy, increased gradually for 10 weeks until it reached the values observed in normal healthy humans (P<0.01). After that it dropped to the initial values. During the study the red blood cell numbers did not change. This study supports the thesis that erythropoietin administered to haemodialysis patients not only corrects anaemia but also independently modulates immunological response.
Expression of TGF‐α, EGF and their common receptor in human fetal kidney
Authors: YASUI Masato , TANAKA Hiroyuki , ITO Toshiyuki , SEINO Yoshiki
Published: April 2007

Summary: Transforming growth factor‐α (TGF‐α) and epidermal growth factor (EGF) are structurally related mitogenic polypeptides. They share the same receptor; EGF receptor. the EGF receptor is widely expressed in human fetal tissues including the kidney, but little is known about the role of TGF‐α/EGF/EGF receptor system in human fetal kidney. the expression of TGF‐α, EGF and their common receptor was investigated immunohistochemically in the human fetal kidneys. In the cortex, immunoreactivity for TGF‐α was found in the differentiating proximal tubules. In contrast, immunoreactivity for EGF was present in the thick ascending limbs of the Henle's loop (TAL) and medullary collecting duct cells (CD). Immunoreactivity for their common receptor was present mainly in the TAL and medullary CD. These data support the assumption that the system of TGF‐α, EGF and its receptor has an important role in the proliferation and differentiation of the TAL and medullary CD. the different localization of TGF‐α and its receptor may indicate that TGF‐α acts through a paracrine mechanism. the co‐localization of EGF and its receptor in the TAL and medullary CD suggests that EGF may act as an autocrine growth factor.
Twelve years experience of acute renal failure in Taiwan
Authors: HUNG Kuan‐yu , SHYU Ren‐shi , CHEN Wan‐yu
Published: April 2007

Summary: A retrospective analysis of the records of 287 patients diagnosed with acute renal failure (ARF) who were admitted between 1 January 1983 and 30 November 1994 to the emergency Service Department of the National Taiwan University Hospital, Taiwan was conducted. A total of 176 men (61.3%) and 111 women (38.7%) were surveyed. the classification of ARF by year revealed a progressive increase in case numbers. the majority (57.5%) of the patients were elderly, particularly in the years 1987‐88 and 1993‐94, the differences (aged compared with the young) being statistically significant. There were 176 patients (61.3%) in the pre‐renal group (with evident intravascular volume depletion, haemodynamic instability or sepsis, with a urine excretion of sodium (FENa<1%), 43 (15%) in the renal group (urine analysis revealing protenuria, granular casts or/and tubular epithelial casts and without response to treatment of volume repletion), and 27 (9.4%) in the postrenal group (diagnosed when there were supporting image studies). Overall mortality was 63% and the pre‐renal ARF patients had the poorest survival rate (25.6%). the classification of mortality rates by diagnostic category and year revealed a persistently high mortality rate. We conclude that: there are increasing patients with ARF each year; aged patients comprise the majority of cases; and the mortality rate remains high because of the high mortality rate of the pre‐renal group, which was due to the presence of complicating underlying diseases and concomitant organ failure. the effects of having an ageing population were also apparent.
Renal failure in a patient with profound hypothyroidism
Authors: BALLAL SH , DHANRAJ P , MADRIGAL L SALINAS , BASTANI B
Published: April 2007

Summary: A young man presented with a 4 week history of easy fatiguability, loss of appetite, and puffiness of face and lower extremities, and was found to have a serum creatinine of 2.0 mg/dL with a normal urinalysis, negative serology for autoimmune disorders, but moderately elevated serum creatine phosphokinase (CPK). A renal biopsy revealed normal glomeruli with no evidence of any pathology except for the presence of brownish pigmented casts in some of the proximal and distal tubules suggestive of myoglobinuria. He was subsequently found to be profoundly hypothyroid with a thyroid stimulating hormone (TSH) level of >100 μU/mL. He had marked symptomatic improvement after institution of thyroid replacement therapy with a decline in serum creatinine to 1.3 mg/dL at 6 weeks follow up.
Vegetarian diet: Relevance in renal disease
Authors: SEGASOTHY Murugasu , BENNETT William M
Published: April 2007

Summary: Dietary habits are increasingly linked to health and disease. Vegetarian diets have stimulated medical and public interest because vegetarians typically maintain excellent health. In general, their diets are lower in energy, percentage of energy from fat and cholesterol, they have lower bodyweight, blood pressure and plasma lipid levels than omnivores. the vegetarian diet contains sufficient essential amino acids, minerals, and trace elements for optimal nutrition, being deficient only in vitamin B12. the medical possibilities for using vegetable protein as therapy in renal disease are diverse, ranging from treating hyperlipidaemia to protecting the kidney against experimental immune and ablation injury. A vegetarian diet, especially a vegetarian soy diet, has been shown to significantly reduce proteinuria disease progression in diabetic and non‐diabetic nephrotic patients. This review summarizes current information about vegetarian and other low protein diets in renal disease which, in the viewpoint of the authors, strongly supports their beneficial role in disease management.
A randomized prospective comparison of oral versus intraperitoneal ofloxacin as the primary treatment of CAPD peritonitis
Authors: CHENG Ignatius KP , LUI SL , FANG GX , CHAU PY , CHENG SW , CHIU Frances H , CHAN TM , LO WK , CHOY BY , LO CY
Published: April 2007

Summary: Oral ofloxacin has been successfully used in our centres for the primary treatment of peritonitis complicating continous ambulatory peritoneal dialysis (CAPD). In view of the progressive rise in the resistance rate to ofloxacin among peritoneal bacterial isolates, a study was conducted to determine if oral ofloxacin remains a viable first line treatment for CAPD peritonitis in our centres and if the result can be improved by changing from an oral to an intraperitoneal (i.p.) route. In patients on three 2 L daily CAPD exchanges, ofloxacin given at the i.p. dosage of 200 mg loading followed by 25 mg/L of peritoneal dialysate achieved overnight trough peritoneal levels which are at least four times the minimal 90% inhibitory concentration (MIC90) of most bacterial pathogens without significant accumulation in the systemic circulation. This i.p. dosage was therefore chosen for the clinical study and the result was compared to that using ofloxacin given in the oral dosage of 400 mg loading followed by 300 mg once daily as maintenance. of all the recruited episodes, 35 were eligible for analysis. the overall primary cure rate including primary failures and relapses was 55.6% (10/18) in the oral treatment group and 70.6% (12/17) in the i.p. treatment group. the corresponding figures for gram positive bacterial (g +) infections were 36.4% and 50%, for gram negative bacterial (g ‐) infections were 66.7 and 80% and for culture negative infections were 75 and 80%. In culture positive cases, all treatment failures were due to resistant infections which were observed in 42.3% of all bacterial isolates, 47.1% of g + isolates and 33.3% of g ‐ isolates. Due to the high background level of bacterial resistance among our CAPD population, ofloxacin monotherapy given either by the oral or the i.p. route can no longer be recommended for the primary treatment of CAPD peritonitis.
Disposition of fusidic acid during peritoneal dialysis
Authors: COLLINS John , MOULTRIE Samantha , PAXTON James , FINDON Glenne , DITTMER Ian , MILLER Thomas
Published: April 2007

Summary: Fusidic acid has characteristics that suggest it might be a useful agent in the management of staphylococcal peritonitis in patients undergoing peritoneal dialysis. the present investigation was undertaken to establish the relationship between serum and peritoneal dialysis effluent concentrations of fusidic acid and to determine whether therapeutic levels of fusidic acid could be achieved in the dialysate following oral administration of the agent. Concentrations of fusidic acid up to 80 times the MIC for staphylococci were found after repeated oral doses. the results have provided basic data needed to initiate clinical studies of the role of fusidic acid as an adjunctive agent in the management of staphylococcal peritonitis.
Metalloproteinase activity is present in rat urine and derived from the renal cortex
Authors: SATO Yuji , FUJIMOTO Shouichi , HAMAI Keiko , ETO Tanenao
Published: April 2007

Summary: Matrix metalloproteinases (MP) are important candidates for the degradation of extracellular matrix, but the role of MP in the diseased kidney remains poorly understood. to examine the significance of urinary MP, we first investigated the characteristics of MP in normal rat urine and renal cortex, and then evaluated the urinary MP activity in anti‐thymocyte induced glomerulonephritis (Thy.1 GN). Metalloproteinase activity was measured as the EDTA‐inhibitable degradation of [3H] gelatin. the enzyme was purified from urine and the renal cortex homogenate in normal Wistar rats by using several chromatographic and gel filtration methods. Both materials contained the identical molecular weight (Mr 126 kDa by gel permeation method) of gelatin‐degrading enzymes, the activity of which was inhibited by metal chelating agents and reactivated by ZnC12 but not by other proteinase inhibitors. Thy.1 GN was induced by intravenous injection of rabbit anti‐thymocyte serum into rats, and daily urine was collected at sequential time points. Urinary MP activity was markedly reduced soon after the serum injection, and returned to the control level in 9 weeks. Conversely, urinary MP‐inhibitor activity (Mr 30 kDa), determined as inhibiting activity against MP derived from renal cortex, showed serial changes strikingly reflected as urinary MP activity. These findings suggested that rat urine contained the MP which seemed to be derived from the renal cortex, and the urinary MP activity was decreased in Thy.1 GN model, probably due to the presence of MP‐inhibitor. As urinary MP is likely to reflect intra‐renal MP, the evaluation of urinary MP may be useful to search metabolic alteration of extracellular matrix in the diseased kidney.
Molecular mechanisms of experimental glomerulonephritis: an overview
Authors: COUSER William G , NANGAKU Masaomi , SHANKLAND Stuart J , JOHNSON Richard J
Published: April 2007

Summary: Most glomerular diseases are autoimmune in nature with injury occurring as a consequence of antibody reacting with antigens on glomerular cell membranes or in glomerular matrix, or immune complex formation occurring on or near glomerular cell membrnes. Many of the structural and functional consequences of these events result from the response of resident glomerular cells to the injury, or may be induced by inflammatory effector cells derived from the circulation. In terms of glomerular cells, injury to the glomerular epithelial cell (GEC) may be induced by: (i) non‐complement fixing antibodies which mimic the glomerular lesions of minimal change nephrotic syndrome/focal glomerular sclerosis; or (ii) by antibodies which fix complement leading to GEC attack by C5b‐9 resulting in a lesion analogous to membranous nephropathy. C5b‐9 also mediates antibody induced injury to the mesangial cell resulting in a mesangioproliferative glomerulonephritis (IgA nephropathy, systemic lupus erythematosus; SLE) as well as to the glomerular endothelial cell (thrombotic microangiopathy, haemolytic uraemic syndrome). the effects of C5b‐9 may be lytic (mesangial cell, glomerular endothelial cell; GEN) or sublytic (GEC) resulting in stimulation of local oxident and protease production. Both lytic and sublytic effects are substantially modulated by cell‐bound complement regulatory proteins such as CD59 and Crry. When fixed or planted antigens are present in larger quantities and accessible to the circulation, complement activation generates chemotactic factors leading to neutrophil infiltration and producing injury through the myeloperoxidase (MPO)‐H2‐O2‐halide system, a mechanism substantially augmented by platelet‐neutrophil interaction (post‐infectious glomerulonephritis [GN], SLE). Macrophages may also be localized in glomeruli by either immune adherence mechanisms or as a consequence of cell mediated immune reactions in the glomerulus. Macrophages differ from neutrophils in producing large amounts of transforming growth factor‐β (TGF‐β) and procoagulants which contribute to crescent formation rapidly progressive glomerulonephritis (RPGN).
Cell proliferation and regulation of apoptosis in human glomerulonephritis
Authors: YOSHIOKA Kazuo
Published: April 2007

Summary: We examined the expression of the protein products and mRNA of protooncogenes associated with cell proliferation and inhibition of apoptosis (bcl‐2, c‐fos, c‐myc, and p53) in normal renal tissues and biopsy specimens from patients with glomerulonephritis. Bcl‐2 was up‐regulated in the glomeruli of several forms of human glomerulonephritis. Bcl‐2 expression was significantly correlated with mesangial hypercellularity and proteinuria, c‐myc and c‐fos expression is associated with mesangial proliferation and matrix expasion in human glomerulonephritis and may predict subsequent progression.