bluuebunny/crossref_metadata_2025 huggingface dataset:
The value of PE‐10, a monoclonal antibody against pulmonary surfactant, in distinguishing primary and metastatic lung tumours
Authors: NICHOLSON A.G. , McCORMICK C.J. , SHIMOSATO Y. , BUTCHER D.N. , SHEPPARD M.N.
Published: April 2007

A new monoclonal antibody (PE‐10) raised against components of pulmonary surfactant has been assessed for its ability to distinguish primary from secondary carcinomas in the lung. We applied this antibody to a series of 107 primary lung carcinomas, 40 adenocarcinomas of other sites, and 26 cases of adenocarcinoma metastatic to lung and pleura. Of the primary lung carcinomas, all the non‐mucinous bronchiolo‐alveolar carcinomas were positive whereas all the mucinous cases were negative; 60% of other types of adenocarcinoma were positive and 10% of large cell undifferentiated carcinomas, 20% of small cell carcinomas and 40% of atypical carcinoids also showed focal positivity. Squamous cell carcinomas were all negative. Adenocarcinomas of the breast, kidney, large bowel and ovaries were all negative, as were all 26 cases of adenocarcinoma metastatic to the lung and pleura. We conclude that this antibody is highly specific and moderately sensitive for primary tumours of the lung.
Keratin expression in the normal anal canal
Authors: WILLIAMS G.R. , TALBOT I.C. , NORTHOVER J.M.A. , LEIGH I.M.
Published: April 2007

The pattern of epithelial keratin expression in the normal anal canal has not been extensively defined and is a necessary prerequisite to the interpretation of alterations in these intermediate filaments in pathological anal epithelial lesions. Thirty‐five frozen tissue specimens of resected haemorrhoids were investigated immunohistolo‐gically for expression of 14 individual keratins (K) using a panel of 17 monoclonal antibodies. Perianal skin showed basal expression of karatinocyte Ks 5, 14 and 17, and suprabasal expression of keratinocyte Ks 14, 10, 1 and 16. Anal squamous epithelium showed persistent basal K5 and 17, basal and suprabasal K4, 13 and 16 positivity, with sporadic expression of K1 and 10. The expression of simple epithelial keratins in squamous epithelium adjacent to the anal transitional zone varied with basal expression of K7, K8, K18 and K19 and sporadic suprabasal expression of K7 and K19. The anal transitional zone (ATZ) expressed K19, as found in transitional epithelia elsewhere. The full thickness of epithelium was positive for the simple epithelial Ks 7, 8 18 and 19. Marked heterogeneity of keratinocyte keratin expression was seen. Basal layers expressed Ks 4, 13, 14 and 17 and variably K16, while suprabasal layers expressed Ks4 and 13, 14 and 17 and variably K16, while suprabasal layers expressed Ks4 and 13 and variably K14, 16 and 17. This anomalous expression of keratinocyte K4 and 13 has also been documented in transitional epithelium of the bladder. The anal glands and ducts showed a keratin distribution similar to the transition zone. Rectal columnar epithelium expressed simple keratins 7, 8 18 and 19. In addition, low levels of keratinocyte keratins were found as indicated by heterogeneous staining for K4, 13, 14 and 16. The overall pattern, particularly in the region of the anal transitional zone and immediately adjacent squamous and columnar epithelia, is of a flexible epithelial cell population able to express a range of keratins unrestricted by a particular morphological phenotype. In the light of these results, analysis of changes in keratin distribution within anal carcinomas may assist classification by providing information on the state of differentiation and histogenesis of these tumours.
p53 immunoreactivity in hepatocellular adenoma, focal nodular hyperplasia, cirrhosis and hepatocellular carcinoma
Authors: OJANGUREN I. , ARIZA A. , CASTELLÀ E.M. , FERNÁNDEZ‐VASALO A. , MATE J.L. , VAS‐PALACIOS J.J. NA
Published: April 2007

The prolonged half‐life of mutant p53 makes feasible its immunocytochemical detection. In order to assess the pathogenetic role of mutant p53 in regenerative and neoplastc liver disease we studied its immunohistochemical expression in cases of hepatic cirrhosis, hepatocellular carcinoma (HCC), cirrhosis with areas of HCC, hepatocellular adenoma and focal nodular hyperplasia. The study included needle and wedge biopsies of 50 cirrhotic livers, 59 HCCs (36 of them with associated cirrhosis), six adenomas and two focal nodular hyperplasias. Sixty‐five HCC fineneedle cytology specimens were also included in the study. There was no immunohistochemical evidence of mutant p53 expression in any of the cases of cirrhotic liver (except for one instance associated with HCC) adenoma or focal nodular hyperplasia. In contrast p53 was detected in 8.5% of HCC cases in the biopsy series and 24% of HCC cases in the fine needle aspiration series. In addition, mutant p53 expression in HCC was positively correlated with tumour grade. According to grade, the distribution of p53 positive immunoreactivity among HCCs was as follows: Grade I‐II, 0% of cases in the biopsy series and 9% in the fine needle aspirates; Grade III, 18% in the biopsy series and 55% in the fine needle aspirates; and Grade IV, 40% in the biopsy series. Therefore, mutant p53 expression does not seem to be associated with benign liver lesions but seems to correlate with the progression of HCC through various grades of increasing malignancy.
Sensitivity of Botrytis cinerea from vegetable greenhouses to boscalid
Authors: Zhang C. Q. , Yuan S. K. , Sun H. Y. , Qi Z. Q. , Zhou M. G. , Zhu G. N.
Published: March 2007

Between 2004 and 2006, 228 isolates of Botrytis cinerea from two regions in China were characterized for baseline sensitivity to boscalid, a new active ingredient that interferes with succinate ubiquinone reductase in the electron transport chain. The isolates showed similar sensitivity in different years and regions. Baseline sensitivities were distributed as unimodal curves with mean EC50 values of 1·07 (± 0·11) and 0·42 (± 0·05) mg L−1 for inhibition of mycelial growth and conidial germination, respectively. Laboratory studies were conducted to evaluate the risk of development of resistance to boscalid. Boscalid‐resistant mutants were obtained by UV‐treatment at lower frequencies and with smaller resistance factors than pyrimethanil‐resistant mutants. All boscalid‐resistant mutants were also significantly more sensitive to Qo inhibitors than their wild‐type parents and showed reduced sporulation in vitro and pathogenicity on aubergine leaves. The results suggested that the risk of resistance developing for boscalid was lower than for pyrimethanil. However, as B. cinerea is a high‐risk pathogen, appropriate precautions against resistance development should be taken. Synergism between the activity of boscalid and that of kresoxim‐methyl was observed.
Acute febrile neutrophilic dermatosis (Sweet's syndrome): a study of 15 cases in Iran
Authors: Zamanian Abbas , Ameri Ahmad
Published: March 2007

Background Sweet's syndrome is well recognized by dermatologists and is not infrequently diagnosed in Iran; however, few case series have been reported.

Methods A clinicopathologic study was carried out on 15 cases of Sweet's syndrome in Hamedan, in the west of Iran, between 1994 and 2004.

Results The incidence of Sweet's syndrome was 3 per 10,000 amongst new dermatologic patients. All were women with a mean age of 58 years. All 15 cases were of the classic type, with no associated diseases. Fever was seen in only six (40%) patients.

Conclusions Sweet's syndrome has a broad spectrum of clinical and pathologic findings in various areas of the world. Further investigation is necessary to determine the etiology and effect of environmental factors in this disease.
Azelaic acid (15% gel) in the treatment of acne rosacea
Authors: Gupta Aditya K. , Gover Melissa D.
Published: March 2007

In December of 2002, the FDA approved azelaic acid 15% gel for the topical treatment of inflammatory papules and pustules of mild to moderate rosacea. Azelaic acid is a saturated dicarboxylic acid, which is naturally occurring and has been used in the treatment of rosacea, acne, and melasma. The 15% gel has a high efficacy and is generally well tolerated, with the local irritation (burning, stinging, itching, and scaling) being typically mild and transient. Azelaic acid 15% gel is considered effective and safe as a therapy for inflammatory papulo‐pustular rosacea and is suitable for use on all skin types.
Convergent evolution of eye ultrastructure and divergent evolution of vision‐mediated predatory behaviour in jumping spiders
Authors: SU K. F. , MEIER R. , JACKSON R. R. , HARLAND D. P. , LI D.
Published: March 2007

All jumping spiders have unique, complex eyes with exceptional spatial acuity and some of the most elaborate vision‐guided predatory strategies ever documented for any animal of their size. However, it is only recently that phylogenetic techniques have been used to reconstruct the relationships and key evolutionary events within the Salticidae. Here, we used data for 35 species and six genes (4.8 kb) for reconstructing the phylogenetic relationships between Spartaeinae, Lyssomaninae and Salticoida. We document a remarkable case of morphological convergence of eye ultrastructure in two clades with divergent predatory behaviour. We, furthermore, find evidence for a stepwise, gradual evolution of a complex predatory strategy. Divergent predatory behaviour ranges from cursorial hunting to building prey‐catching webs and araneophagy with web invasion and aggressive mimicry. Web invasion and aggressive mimicry evolved once from an ancestral spartaeine that was already araneophagic and had no difficulty entering webs due to glue immunity. Web invasion and aggressive mimicry was lost once, inParacyrba, which has replaced one highly specialized predation strategy with another (hunting mosquitoes). In contrast to the evolution of divergent behaviour, eyes with similarly high spatial acuity and ultrastructural design evolved convergently in the Salticoida and inPortia.
EGF and EGF‐receptor expression in rat anti‐Thy‐1 mesangial proliferative nephritis
Authors: NIKOLIC‐PATERSON David J , TESCH Gregory H , LAN Hui Y , NUKII Kiyotaka , FOTI Rita , ATKINS Robert C
Published: April 2007

Summary: Epidermal growth factor (EGF) is a potent mesangial cell and tubular epithelial cell mitogen. Based upon the novel finding that rat mesangial cells express EGF mRNA and protein in vitro, we investigated whether renal EGF production was involved in mesangial proliferation and concomitant tubular epithelial proliferation in rat anti‐Thy‐1 mesangial proliferative nephritis. During the period of mesangial proliferation in anti‐Thy‐1 nephritis (days 4–14) no EGF immunoreactive material was detected within the glomerulus. Epidermal growth factor‐receptor (EGF‐R) expression, which is strong on podocytes in normal glomeruli, was notably absent from focal areas of proliferating mesangial cells, suggesting that EGF available from the circulation was not involved in mesangial cell proliferation. Concomitant with the transient decline in creatinine clearance on day 8 of disease, there was mild tubular injury and a significant increase in cortical tubular proliferation as assessed by expression of the proliferating cell nuclear antigen (PCNA). Double immunohistochemistry staining found that the increased cortical tubular proliferation on day 8 occurred in EGF− tubules, but not EGF+ tubules. In contrast, there was an increase in proliferation of EGF+ tubules, but not EGF− tubules, on day 28. Renal EGF mRNA and protein expression was down‐regulated over days 1‐14, with a rebound in expression on day 28 which correlated with proliferation of EGF+ tubules. Tubular EGF‐R expression, which is most clearly seen on EGF+ tubules in normal rat kidney, was unchanged over the disease course. the potential role of EGF in tubular proliferation in normal and diseased states is discussed. In summary, this study finds no evidence to implicate EGF in mesangial cell proliferation in rat anti‐Thy‐1 nephritis, even though mesangial cells can express EGF in vitro, and suggests that EGF may regulate proliferation of tubular epithelial cells in different stages of disease.
In situ hybridization studies of stromelysin and tissue inhibitor of metalloproteinase 1 in IgA nephropathy
Authors: MIYAZAKI Masanobu , KOJI Takehiko , FURUSU Akira , ABE Katsushige , OZONO Yoshiyuki , HARADA Takashi , NAKA Raita , SUZUKI Daisuke , YAGAME Mitsunori , ENDOH Masayuki , NOMOTO Yasuo , HARA Kohei , NAKANE Paul K , SAKAI Hideto
Published: April 2007

Summary: Accumulation of the extracellular matrix (ECM) in IgA nephropathy (IgAN) is thought to cause deterioration of glomerular function. Stromelysin and tissue inhibitor of matrix proteinase 1 (TIMP1) may play an important role in the turnover of the glomerular ECM. However, the expression of these enzymes in human renal tissues remains undefined. In the present study, non‐radioactive in situ mRNA hybridization, which permitted the analysis at a cellular level, was performed to localize stromelysin and TIMP1 in renal tissue of IgAN. We also determined the percentage of cells positive for stromelysin or TIMP1 mRNA among intraglomerular cells. A total of 16 patients with IgAN were examined, including eight patients with severe histopathological changes and eight with mild changes. Three patients without glomerular disease were also studied. Stromelysin and TIMP1 mRNA were weakly expressed in the mesangium of normal kidneys and IgAN renal tissues with mild damage. However, the expression of both mRNA was significantly increased in the area of mesangial proliferation, in glomerular epithelial cells and in Bowman's capsule of advanced lesions. Several cells in the area of mesangial proliferation were double positive for stromelysin and TIMP1 mRNA, while certain cells positive for stromelysin mRNA did not express TIMP1 mRNA. In the interstitium, epithelial cells of certain tubules and some mononuclear cells were positively stained for these mRNA, especially in advanced lesions. Our results indicated that stromelysin and TIMP1 genes were expressed in glomerular resident cells, tubular epithelial cells and infiltrated mononuclear cells in IgAN, and their expression was enhanced in advanced tissue damage. the demonstration of a co‐expression and discordant expression of the genes indicates that each gene expression may be regulated in a cell type‐specific manner and that it could also be altered by cellular environmental factors.
Pre‐eclampsia: Recognition, prevention and management
Authors: BROWN Mark A
Published: April 2007

Summary: Pre‐eclampsia is the most common medical disorder of pregnancy and has a large variety of clinical presentations. It is a multisystem disorder affecting maternal kidneys, coagulation system, liver, brain and the placenta. Hypertension is an important but secondary phenomenon.

Methods of measuring blood pressure (BP) in hypertensive pregnant women need to be standardized. There is presently a shift towards using the 5th Korotkoff sound to record diastolic BP but this has not been adopted universally. No test or set of tests reliably predicts which pregnant women will develop pre‐eclampsia and no therapy reliably prevents pre‐eclampsia although in some populations supplemental calcium appears to be a promising treatment. Low‐dose aspirin appears to have a role only in highly selected subgroups of pregnant women.

Management of ‘gestational hypertension’(mild pre‐eclampsia) requires continued monitoring to detect transformation from this relatively mild disorder to the more severe disorder of pre‐eclampsia. Such monitoring requires measurement of platelet count, proteinuria, liver function, serum creatinine and careful clinical examination (particularly reflexes, clonus and epigastric tenderness) and fetal assessment. Blood tests are generally required only twice weekly though in severe cases more frequent testing is necessary, perhaps even daily when, for example, thrombocytopenia is progressive.

Conservative management is adopted initially in most cases, invoving monitoring, careful use of antihypertensives and, in selected cases, anticonvulsant therapy and/or volume expander therapy. the latter is best employed to prevent sudden hypotension following epidural anaesthesia or parenteral antihypertensive therapy. Delivery is mandatory when monitoring indicates progressive disease despite conservative treatment.
Up‐regulation of ICAM‐1 and VCAM‐1 expression during macrophage recruitment in lipid induced glomerular injury in ExHC rats
Authors: HATTORI Motoshi , NIKOLIC‐PATERSON David J , LAN Hui Y , KAWAGUCHI Hiroshi , ITO Katsumi , ATKINS Robert C.
Published: April 2007

Summary: A number of studies have demonstrated an important role for macrophages (Mo) in lipid induced glomerular injury; however, little is known of the mechanisms which facilitate Mo infiltration in this disease. the present study examined the expression of adhesion molecules, intercellular adhesion molecule‐1 (ICAM‐1) and vascular cell adhesion molecule‐1 (VCAM‐1) during the development of glomerular Mo infiltration in ExHC rats; a strain which is susceptible to lipid induced glomerular injury. Twenty‐five male 6 week old ExHC rats were placed on a normal diet supplemented with 3% cholesterol, 0.6% sodium cholate and 15% olive oil (high‐cholesterol diet, HCD). Groups of five rats were killed prior to the beginning of the HCD or after 3 days, 1, 2 and 6 weeks on a HCD. A group of five matched ExHC rats on a normal diet served as a control. ExHC rats fed a HCD showed marked hypercholesterolaemia in the absence of any increase in plasma triglyceride levels from day 3 (190 ± 14 vs 42 ± 2 mg/dL in control; mean ± s.e.m., P<0.01), and developed mild proteinuria (21.9 ± 2.7 vs 5.2 ± 0.5 mg/24 h in control; P<0.01) and segmental glomerular lesions at week 6. Immunoperoxidase staining identified a significant increase in glomerular ED1+Mo at week 1 (2.0 ± 0.2 vs 1.0 ± 0.1 ED1+Mo/glomerular cross‐section in control, P<0.01) which was further increased at week 6 (6.9 ± 0.4 ED1+Mo/gcs). There was also a significant increase in glomerular cells expressing the adhesion molecule ligands lymphocyte function‐associated antigen‐1 (LFA‐1) and very late antigen‐4 (VLA‐4). Coincident with Mo infiltration, there was an increase in the intensity of glomerular ICAM‐1 protein expression as shown by antibody staining. In addition, northern blot analysis of cortical RNA and in situ hybridization demonstrated an increase in glomerular ICAM‐1 and VCAM‐1 mRNA expression from day 3 onwards. In conclusion, these results suggest that both ICAM‐1/LFA‐1 and VCAM‐1/VLA‐4 interactions play an important role in Mo recruitment and accumulation during the development of lipid induced glomerular injury.
No linkage to the COL4A3 gene locus in Japanese thin basement membrane disease families
Authors: YAMAZAKI Hajime , NAKAGAWA Yoichi , SAITO Akihiko , NISHI Shinichi , SAKATSUME Shiminoru , TAKEDA Tetsuro , MARUYAMA Yuichiro , OGINO Sojiro , MARUYAMA Shiro , MOCHIZUKI Toshio , REEDERS Stephen T , ARAKAWA Masaaki
Published: April 2007

Summary: Patients with thin basement membrane disease (TBMD) exhibit persistent haematuria with a diffuse thinning of the glomerular basement membrane (GBM), especially of the lamina densa. It appears to be an autosomal dominant trait. It has been reported that the Goodpasture epitope, which is located in the non‐collagenous domain of type IV collagen α 3 chain, may be reduced in patients with TBMD. We speculated that the candidate gene for TBMD could be the type IV collagen α 3 chain gene (COL4A3), which is present closely to type IV collagen α 4 chain gene (COL4A4) on chromosome 2q35–37. We conducted a linkage analysis to investigate the relationship between familial TBMD and COL4A3 gene, using COL4A3 cDNA polymorphism and a (CA)n microsatellite marker located in the COL4A3 gene. We examined 32 individuals from four Japanese families with TBMD. There were no associations between the patients with haematuria and certain alleles of the two markers in the pedigrees of three families. It has been reported that type IV collagen α 1 chain gene (COL4A1) and α 2 chain gene (COL4A2) are not involved in TBMD, and that α 5 chain gene (COL4A5) and a 6 chain gene (COL4A6) map to chromosome X. In conclusion, our findings suggested that familial TBMD is not caused by the genetic abnormalities of type IV collagen genes isolated thus far.
Mechanisms causing muscle wasting in uraemia: From cultured cells to patients
Authors: MITCH William E
Published: April 2007

Summary: Loss of muscle mass is a common problem in patients with acute or chronic renal failure. the mechanisms causing this problem involve blocking the metabolic responses that must be activated to maintain protein balance whenever protein intake is reduced (e.g. by anorexia or for other reasons). In uraemia, the ability to reduce degradation of essential amino acids or protein is blocked and muscle protein is lost; the signal is metabolic acidosis. In cultured myocytes, isolated muscles and patients, acidification increases the degradation of branched‐chain amino acids and protein. This response requires glucocorticoids and involves stimulation of the activity of specific enzymes, branched‐chain ketoacid dehydrogenase and components of the ATP‐ubiquitin‐proteasome dependent proteolytic pathway. the response also involves increased transcription of genes encoding these enzymes. Understanding regulation of these pathways could improve therapy of uraemia and other catabolic illnesses because the same pathways are activated in cancer, sepsis, burns, starvation and muscle denervation.
Immunolocalization of fibroblast growth factor‐1 and ‐2 in the embryonic rat kidney
Authors: CANCILLA Belinda , CAUCHI Jennifer , KEY Brian , NURCOMBE Victor , ALCORN Daine , BERTRAM John
Published: April 2007

Summary: Fibroblast growth factors (FGF) regulate cell proliferation, migration, differentiation and angiogenesis during morphogenesis in many different tissues. Recent evidence indicates that exogenous FGF‐2 stimulates mesenchymal condensation in cultured rat metanephroi, a crucial epithelial‐mesenchymal induction event in the developing nephron. the aim of the present investigation was to determine the in vivo distribution of FGF‐1 and FGF‐2 in developing rat metanephroi at embryonic days 14, 15, 16, 18 and 20. Avidin‐biotin enhanced indirect immunohistochemistry was used to demonstrate that both FGF‐1 and FGF‐2 were co‐localized in metanephroi at all ages studied. High levels of FGF‐1 and FGF‐2 were present in ureteric bud branches and in developing distal tubules. Fibroblast growth factor‐1 and FGF‐2 were colocalized in developing nephron elements, from vesicles to S‐shaped bodies, and in the mesangium of capillary loop and maturing stage glomeruli. Both growth factors were present in the mesenchyme of the nephrogenic zone and in the interstitium of the developing cortex. However, immunostaining for FGF was not evident in mesenchymal condensates, endothelial cells, medullary interstitial cells, or in the thin undifferentiated epithelium of the immature loop of Henle. These findings indicate that the expression of both FGF‐1 and FGF‐2 is tightly regulated in the embryonic kidney and suggest a role for these molecules in kidney development.
Comparison of the rehabilitation status of continuous ambulatory peritoneal dialysis and in‐centre haemodialysis in Chinese patients
Authors: LAW MC , HUI YH , CHEUNG Amy LC , LAM YH , POON MY , LEUNG KP , CHAN Amy LK , LI Philip KT
Published: April 2007

Summary: In Hong Kong, dialysis treatment has become more accessible in recent years. Due to a shortage of kidney donors patients are required to stay on dialysis for longer periods. the rehabilitation status of 181 end‐stage renal failure (ESRF) patients on dialysis, 34 on in‐centre haemodialysis (ICHD) and 147 on continuous ambulatory peritoneal dialysis (CAPD), at the Prince of Wales Hospital was studied. There was no statistically significant difference in physical functioning due to treatment type; however, CAPD patients were shown to be more socially active and had a better family life than ICHD patients (P < 0.01). There were no statistically significant correlations between physical functioning, social life or family life and the duration of dialysis in both ICHD and CAPD patients. In both groups of patients 52.9% of ICHD and 52.4% of CAPD patients had decreased employment status. All the patients were assessed by doctors‐in‐charge on their physical fitness for employment, 85.7% (n= 6) of the unemployed ICHD patients and 71% (n= 44) of the unemployed CAPD patients were considered to be physically fit to work. Due to the ageing of the general population and greater availability of dialysis treatment and higher survival rate of the chronically ill have led to an increase in the number of elderly patients on dialysis (aged 60 years and over). the proportion of elderly dialysis patients in our renal centre increased from 7–23% in the past 5 years. Continuous ambulatory peritoneal dialysis patients aged less than 60 years were found to be significantly more physically active and socially active than CAPD patients aged over 60 years (P < 0.01). In the aspect of a better family life for these patients, no statistically significant difference was found between the two groups. Rehabilitation of ESRF patients can be achieved by renal replacement therapy. It is concluded that CAPD patients have better adaptation in social life and family life than ICHD patients.
Acute renal failure prior to the onset of hepatic encephalopathy in fulminant hepatitis
Authors: URIU Kohei , KAIZU Kazo , MATUO Norio , SOEJIMA Masanori , HASHIMOTO Osamu , KOMINE Norikuni , IKEDA Masanori , IWASAKI Tetumi , OTUKI Makoto , YAMADA Sinwa , ETO Sumiya , SUGITA Atuo
Published: April 2007

Summary: We investigated the clinical characteristics of eight patients with fulminant hepatitis who developed acute renal failure (ARF). They were divided into two groups according to the time point when ARF occurred in the course of the disease: (i) group 1 (n=4), ARF occurred prior to the onset of hepatic encephalopathy; and (ii) group 2 (n=4), ARF occurred after the onset of hepatic encephalopathy. All cases in group 1 had an acute type of fulminant hepatitis, whereas a subacute type was present in the patients in group 2. All cases in group 1 and two cases in group 2 were given non‐steroidal antiinflammatory drugs before the onset of ARF. Urinary findings and/or renal biopsy findings suggested that acute tubular necrosis was the cause of ARF in group 1. Three patients in group 1 and none in group 2 recovered from both ARF and fulminant hepatitis. Although it is well‐known that a patient with fulminant hepatic failure complicated by ARF has a poor prognosis, our findings suggest that ARF that occurs prior to the onset of hepatic encephalopathy in acute type of viral fulminant hepatitis is not a determinant of the poor prognosis, and that the prognosis will be improved by intensive care.
Cellular and sub‐cellular location of kallikrein gene products induced in outer medullary tubules by furosemide treatment
Authors: PENSCHOW Jennifer D , COGHLAN John P
Published: April 2007

Summary: Renal kallikrein is normally synthesized and secreted by connecting tubule cells of the renal cortex. Treatment of mice with furosemide induces an expansion of the kallikrein synthesizing tubule cell population from the cortex to the inner stripe of the outer medulla. There is no induction of kallikrein gene expression in the medulla in sodium restricted mice or in untreated controls. We used hybridization histochemistry on semi‐thin plastic sections to identify the medullary segment recruited to express the renal kallikrein gene after furosemide treatment. In the outer medulla, the thick ascending limb (TAL) was the only tubule segment in which kallikrein gene expression was identified. Immunogold cytochemistry revealed that kallikrein is in granules located in the cytoplasm of medullary TAL cells from furosemide‐treated mice, confirming that furosemide‐induced kallikrein mRNA is translated in these cells. There was no immunoreactive kallikrein found in other tubule segments of the outer medulla, nor in TAL cells from sodium or untreated mice. Granules containing immunoreactive kallikrein were secreted from both poles of the cells into the tubule lumen from the apical surface and into the interstitial space from the basolateral surface. Secretion of kallikrein from the basolateral pole of TAL cells into the interstitial space enables kinins to be generated in close apposition to the vasculature underlying renal tubules, promoting local vasodilatation. the expansion of kallikrein synthesis and secretion to the medulla after furosemide treatment may contribute to the vasodilatation which follows furosemide‐induced diuresis.
Uncomplicated acute pyelonephritis in young men
Authors: BAILEY Ross R
Published: April 2007

Summary: It is widely believed that symptomatic urinary tract infections (UTI) are very uncommon in males, except in infancy and the ‘prostatic’ age group. Most men with a UTI have been considered to have a functional or anatomical abnormality of the urinary tract. Recent reports have suggested that there is an increasing number of otherwise healthy young men presenting with uncomplicated acute pyelonephritis with similar clinical features as those affecting sexually active young women. From 1 January 1988 to 31 July 1995 a total of 42 men were admitted with acute pyelonephritis (fever >37.8°C, loin pain or tenderness and infected urine). of the total of 42 men, 23 (55%) were under the age of 40 years. Five of these 23 young men were known to have a serious underlying urinary tract abnormality and had required frequent admission for a symptomatic UTI. of the other 18 young men with an isolated episode of acute pyelonephritis, 14 were infected with Escherichia coli, 2 with Proteus mirabilis and 1 each with Enterococcus faecadis and Staphylococcus saprophyticus. All 18 had normal imaging of the urinary tract, and all were cured (sterile urine 7–10 days later) with a 5‐day course of treatment. In summary, more than half of the males admitted with acute pyelonephritis were under the age of 40 years. Men with an isolated episode of acute pyelonephritis should be treated in the same way as for women in a similar age group. Not all require extensive urinary tract investigations.
Role of intravenous cyclophosphamide in lupus nephritis patients with renal impairment
Authors: KHER V , ARORA P , KRISHNANI N , PANDEY RK , GUPTA Amit
Published: April 2007

Summary: Twenty‐three patients with lupus nephritis (21 diffuse proliferative glomerulonephritis and two with focal proliferative glomerulonephritis) with impaired renal functions were evaluated for their response to pulse cyclophosphamide. Diagnosis of lupus nephritis was based on American rheumatism association criteria or on the basis of renal manifestations with high anti dsDNA antibody titres. Cyclophosphamide was given in dosage of 900mg/m2 as infusion in 500 mL of 5% dextrose (reduced by 25% if serum creatinine was more than 6 mg/dL) once every month for 6 months then 3 monthly for a minimum of 3 years. Response was defined by 24h protein excretion less than 500mg and serum creatinine less than 1.4mg/dL. Nine patients (group I) had normal function (serum creatinine 1.16 ± 0.21mg/dL) and 14 patients (group II) had impaired renal function at presentation (serum creatinine 3.72 ± 4.06 mg/dL). Both groups were compared for response to therapy. All patients in group I were in complete remission at last follow up of 44.6 ± 8.3 months (serum creatinine 1.14 ± 0.2mg/dL, 24h proteinuria 0.3 ± 0.3g). While in group 2, 13 patients showed improvement. Two patients were in complete remission, seven in partial remission, one patient died and four patients had mild renal failure at last follow up of 40.2 ± 10.4 months (serum creatinine 1.81 ± 0.74, 24h proteinuria 2.19 ± 2.54g). the side effects of therapy included infection, transient leucopenia and vomiting. We conclude that intravenous (I.V) cyclophosphamide is an effective therapy in severe lupus nephntis with renal impairment.
Conformational dependence of the fractional clearance of dextran and Ficoll
Authors: SMIT Madonna F , PRATT Lynette M , COMPER Wayne D
Published: April 2007

Summary: This study demonstrates that there is only small conformational dependence for the fractional clearance, as studied in the isolated perfused kidney, of random coil dextran as compared to the spherical Ficoll when these probes are standardized on the basis of effective hydrodynamic radii by gel exclusion chrotography. This is particularly for molecules with the same effective hydrodynamic radii of 3.6 nm as albumin. the influence of osmotic stress exerted by plasma concentrations of albumin is shown to be minor for dextran. These studies demonstrate that there must be some other factor apart from conformation that accounts for the relatively low fractional clearance of albumin compared with dextran of equivalent hydrodynamic radius.
Phosphate removal in haemodialysis: Effect of two different dialysis membranes
Authors: MITSUHASHI Miwako , KERR Peter G
Published: April 2007

Summary: Phosphate removal with two different dialysis membranes (a standard cellulose acetate membrane and a high performance cellulose diacetate membrane) were studied in ten haemodialysis patients. All patients were dialysed sequentially with two membranes (surface area was 1.5 m2) against bicarbonate buffered dialysis for 4 hours three times a week. With the diacetate membrane, the instantaneous clearances of urea and phosphate after 1 hour of haemodialysis were significantly higher than with the cellulose membrane. Also, the weekly total amount of urea and phosphate removal were significantly increased with the diacetate membrane (a 15% increase in urea and a 16% increase of phosphate). Although there was a significant increase in urea reduction ratio and significantly lower post dialytic plasma urea concentration with the diacetate membrane, these for phosphate did not reach statistical significance. These data suggest that the use of the diacetate membrane potentially offer clinical benefit. However, whether 16% of phosphate removal could improve clinical control of serum phosphate levels will need further investigation.
Neutrophils in IgA nephropathy
Authors: LAI KAR NENG
Published: April 2007

Summary: Neutrophil participation is prominent in proliferative forms of glomerulonephritis. They are recruited by antibody‐mediated chemoattractant complement fragments. Monocyte and endothelial derived cytokines or adhesion molecules may also recruit these cells. In most situations of inflammation, neutrophils induce injury by the release of reactive oxygen radicals and their production of lysosomal proteolytic enzymes. the clinical importance of neutrophils in mediating glomerular injury in IgA nephropathy (IgAN) has often been downplayed, although it has been recognized that IgA is involved in the initiation of intracellular oxidative metabolism in normal neutrophils. That disordered neutrophil activation could be relevant to the pathogenesis of IgAN seems likely from their prominent infiltration in glomerular capillaries in the acute phase of primary IgAN, increased expression of complement 3 receptors on neutrophils from patients with IgAN, and increased oxidative metabolism of neutrophils in these patients. Furthermore, recent data revealed heat‐aggregated forms of IgA prepared from patients with IgAN exert an up‐regulatory effect on calcium mobilization, inositol triphosphate production, and oxidative metabolism in human neutrophils. Interestingly, the plasma level of E‐selectin, mainly derived from activated vascular endothelial cells upon interaction with neutrophil, was elevated following synpharyngitic macrohaematuria in patients with IgAN. There was also a significant stepwise increase in circulating E‐selectin associated with increased histopathologic severity in these patients. These data tend to support the notion that neutrophils could be activated in IgAN despite lack of acute clinical exacerbation and may potentially be participating in the inflammatory process of glomerular and interstitial injury.
Identification of the novel calcium mediated cellular events in the pathogenesis of hypoxia‐induced proximal tubular injury
Authors: YAQOOB MUHAMMAD , EDELSTEIN CHARLES L , SCHRIER ROBERT W
Published: April 2007

Summary: Acute renal failure (ARF) is a clinical syndrome that is frequently present in hospitalized patients and is associated with high mortality. the duration of the clinical course of ARF correlates with a mortality that remains high despite the availability of dialysis treatment. the virtual complete recovery of renal function in those patients who survive ARF, as well as the minimal renal histological abnormalities, suggest that there are reversible components in the pathophysiology of ARF. A better understanding of the pathogenesis of ARF is therefore needed to allow interventions that would prevent the need for haemodialysis and improve survival. A role of cytoplasmic free calcium [Ca2+]i in hypoxia‐induced proximal tubule damage has been proposed. to further investigate the role of [Ca2+]i, in mediating hypoxic proximal tubular injury, a video imaging technique has been developed in which [Ca2+]i can be measured simultaneously with propidium iodide (PI) staining of nuclei as an index of hypoxia‐induced membrane damage. Hypoxia in rat proximal tubules is associated with a significant rise in [Ca2+]i, which precedes evidence of membrane damage as assessed by PI staining. This rise in [Ca2+]i activates calpain, a Ca2+‐dependent cysteine protease and constitutive nitric oxide synthase (NOS), the Ca2+ dependent form of NOS. Inhibition of calpain with mechanistically and chemically dissimilar inhibitors provides marked cytoprotection against hypoxic and ionomycin induced proximal tubular injury. Similarly, inhibition of NOS with L‐NAME, acidosis, tetra hydrobiopterin depletion and low extracellular calcium is associated with marked cytoprotection against hypoxic cellular injury. These observations are consistent with the early rise in [Ca2+]i initiating hypoxic injury by activating NOS and calpain.
Complement, adipocytes and the kiney
Authors: MATHIESON PETER W , PETERS D KEITH
Published: April 2007

Summary: The complement system has traditionally been thought of as a group of circulating proteins predominantly produced in the liver, with functions in both afferent and efferent arms of the immune response, primarily concerned with host defence. In recent years, it has become apparent that many tissues synthesize and secrete complement components and that the complement cascade may have previously unsuspected local actions in these tissues in health and disease. Perhaps one of the most surprising organs in this respect is adipose tissue. the adipocyte is capable of producing all the key components of the alternative pathway, and produces particularly abundant quantities of factor D, previously thought to be mainly produced by cells of the monocyte/macrophage lineage. Adipose tissue is probably the main source of factor D in vivo: factor D expression is decreased in various experimental models of obesity, and is increased in fasting or catabolic states, suggesting that factor D (and hence the alternative pathway) may play a role in physiological regulation of adipose tissue. Another link between adipocytes and the complement pathway is illustrated by the recent demonstration that the complement cleavage product C3a has potent activity as an acylation stimulating protein, promoting the esterification of fatty acids into triglyceride. the production of factor D by adipocytes probably underlies the association between complement activation by the autoantibody nephritic factor (NeF) and adipose tissue loss in partial lipodystrophy (PLD): in vitro data indicate that serum containing NeF causes complement‐mediated lysis of adipocytes. There is preliminary evidence of a regional variation in factor D gene expression with higher levels of expression in the regions affected by adipocyte loss in PLD. This illustrates a novel toncept in immunopathology: by expression of factor D the adipocyte contributes to its own destruction when the normal regulation of the alternative pathway is subverted by the presence of NeF. In relation to the nephritis associated with NeF, we postulate that a similar mechanism may operate. Intrinsic renal cells are known to produce complement components, and NeF may lead to injury to these cells, aggravated perhaps by cytokines which are known to up‐regulate complement protein expression in renal cells. Other situations by which dysregulation of the alternative pathway occurs may lead to nephritis by a similar mechanism. For example, in rare human cases with factor H deficiency, and in a recently described variety of Yorkshire pig with factor H deficiency, nephritis is common and is histologically similar to the nephritis associated with NeF. Thus, recent advances in adipocyte biology have led to novel ideas about actions of complement, and similar principles may apply to physiology and pathology in the kidney.
Nephropathy in Type II diabetes
Authors: RITZ EBERHARD
Published: April 2007

Summary: The incidence and prevalence of end‐stage renal failure due to renal involvement in patients with type II diabetes has increased in the Western world and in Asia. Interesting differences of prevalence of this disease are found between nations. the reasons for the increase in the frequency of nephropathy in type II diabetes include: (i) an increasing prevalence of type II diabetes; (ii) ageing of the population; and (iii) improved survival of patients with type II diabetes. Today patients frequently live long enough to develop diabetic nephropathy. In contrast with previous opinion, no major differences in renal involvement is found between type I and type II diabetes. This applies to renal haemodynamics as well as renal histology, although non‐specific changes, presumably of an ischaemic nature are more frequently found in patients with type II diabetes. the renal risk appears to be similar in type II diabetes (i.e. cumulative prevalence of proteinuria and rate of progression to renal failure).
Matrix accumulation in diabetic nephropathy: Studies by confocal microscopy
Authors: BECKER G , BIRCHALL I , CHEN YP , GROSS J
Published: April 2007

Summary: Confocal scanning laser microscopy (CSLM) has the potential to provide new insights into matrix deposition in renal pathology. For example laser stimulated light emission from Kimmelstiel Wilson (KW) nodules emphasizes a difference between peripheral and central nodule contents, an observation matching immunoperoxidase studies, which fails to demonstrate high density of renal matrix proteins in the core.
Evaluation and treatment of renovascular hypertension and ischaemic renal disease
Authors: BAILEY ROSS R , YOUNG ANTHONY T
Published: April 2007

Summary: Hypertension in the presence of renal artery stenosis may not necessarily be renovascular hypertension. the two conditions may simply co‐exist. Some features of renovascular hypertension include: a worse prognosis than essential hypertension, less amenable to drug treatment, a greater risk of dose‐dependent side effects, a higher risk of progression to accelerated hypertension and it may result in irreversible ischaemic failure of the affected kidney. Renovascular hypertension is usually symptomless, while hypertension that is difficult to control with antihypertensive therapy is probably the best indication as to whether further diagnostic evaluation is indicated. A clue is a rise in the plasma creatinine concentration following the introduction of an angiotensin converting enzyme inhibitor (ACEI). Renal artery stenosis may be present in up to 30% of drug resistant hypertensive patients. Arteriosclerotic renovascular disease is an increasingly important cause of renal failure. In this institution from 1 January 1988 to 31 December 1993,491 patients were referred with a plasma creatinine of ≥0.30 mmol/L. Hypertension/nephrosclerosis/renal artery stenosis was the diagnosis in 75 of 372 (20%) of those patients who had chronic renal failure. of the last 427 patients entering our renal replacement programme, 23 were due to hypertensive nephrosclerosis and an additional five due to renal artery stenosis (6.6% of the total). Functional diagnostic tests for renovascular hypertension such as rapid sequence intravenous urography have now been superseded by the captopril challenge test and in particular scintigraphy following captopril provocation. Tests of prediction as to whether correction of a demonstrated renal artery stenosis will lead to an improvement in the blood pressure include renal vein renin estimations and scintigraphy. the key diagnostic procedure is renal angiography. the approaches to management primarily include appropriate antihypertensive therapy, while there is an increasing place for percutaneous transluminal angioplasty, with or without stenting of an occluding lesion. There is still a small place for corrective surgery. Renal ischaemia due to atherosclerotic renovascular disease is becoming an increasing problem in nephrology. Treatment should be directed at preserving or even restoring renal function.
Clinical features, pathogenesis and treatment of hepatitis B virus‐associated membranous nephropathy in children
Authors: LIN CHING‐YUANG
Published: April 2007

Summary: Membranous nephropathy (MN) is the commonest named lesion associated with hepatitis B virus (HBV) infection in Taiwanese children. This review focuses on the clinical features, the pathogenesis and immune abnormality and possible treatment of HBV‐MN.
Haemorrhagic fever with renal syndrome: an emerging disease
Authors: LEE HO WANG
Published: April 2007

Summary: Worldwide about 150 000 people are hospitalized with haemorrhagic fever with renal syndrome (HRFS; 3–15% fatality) each year. the aetiologic agents of hantavirus infections are Hantaan, Belgrade, Seoul, Puumala and Sin Nombre virus of the genus Hantavirus, family Bunyaviridae. A severe form of HFRS caused by Hantaan and Belgrade virus occurs in Asian and Balcan countries. A new clinical form with 70% fatality, Hantavirus pulmonary syndrome, caused by novel hantaviruses occurs in Americas. A moderate form caused by Seoul virus occurs in Asia and in Europe and a mild form caused by Puumala virus occurs in Europe. Recently, Puumala virus infections in man and field mice were found in Siberia, in Korea and in Japan. the reservoirs of hantaviruses are rodents and other small mammals including bats and birds and mode of transmission is aerosol. Serologic and PCR studies of 72 hantaviruses isolated from patients and from animals throughout the world indicated that there are eight or more serotypes. Many hantavirus patients have been misdiagnosed as influenza, interstitial nephritis, leptospirosis, scrub typhus, dengue, hepatitis and pneumonia. Recently, we developed simple serologic differential diagnostic kits (HDPA test) for Hantaan, Seoul and Puumala virus infections. an inactivated Hantaan virus vaccine against HFRS is available. In the 1990s, it is highly possible to identify new hantavirus illness in parts of the world where the disease is not known because of the availability of diagnostic tools.
Molecular approach to the study of inherited kidney diseases: A way to understand the mechanisms of disease
Authors: GRÜNFELD JEAN‐PIERRE
Published: April 2007

Summary: Recent progress in molecular genetics has provided understanding of the molecular mechanisms of inherited disorders (and also of more general mechanisms). This progress is first based on good clinical observations, as was recently demonstrated in the identification of the PKD1 gene in a family with a chromosomal translocation. These advances are also of value for better classification of hereditary diseases and for better genetic counselling of the affected families, as shown in Alport's syndrome.