bluuebunny/crossref_metadata_2025_split huggingface dataset:
Estrogen Replacement Therapy with Its Physiological Dose Does Not Eliminate the Aggravating Effect of Ovariectomy on Glomerular Injury in Hypercholesterolemic Female Imai Rats
Authors: Sakemi Takanobu , Tomiyoshi Yoshiyuki , Miyazono Motoaki , Ikeda Yuji 
Published: April 2003

Hypercholesterolemic Imai rats spontaneously develop proteinuria and glomerulosclerosis, especially in males. Estrogen administration attenuated glomerular injury in male Imai rats, and the aggravating effect of ovariectomy in female rats is found. To clarify whether this aggravating effect of ovariectomy is due to a lack of estrogen, we administered estrogen to ovariectomized female Imai rats. At 6 weeks of age, group 1 (control) was sham-operated and group 2 was ovariectomized. Groups 3 and 4 were ovariectomized and received estrogen replacement therapy (0.1 mg in group 3 and 0.2 mg in group 4 once a month subcutaneously). Body weight, urinary protein and serum constituents were investigated every month from 3 to 6 months of age. At 6 months of age, rats were studied morphologically. Estrogen replacement therapy increased serum estrogen to levels close to those of controls when 0.1 mg was used, or higher when 0.2 mg was used. Estrogen replacement therapy with 0.1 mg did not eliminate the aggravating effect of ovariectomy on glomerular injury and rather aggravated it, but conversely therapy with 0.2 mg attenuated glomerular injury and abolished the aggravating effect of ovariectomy. Estrogen replacement therapy markedly elevated serum GH levels dose-dependently. These results suggested that other hormones as well as estrogen may play a protective role of the ovary for the development of glomerular injury, and that estrogen seems to exert a dual effect on glomerular injury.
Quantitative Assessment of HCV Load in Chronic Hemodialysis Patients: A Cross-Sectional Survey
Authors: Fabrizi F. , Martin P. , Dixit V. , Brezina M. , Cole M.J. , Gerosa S. , Vinson S. , Mousa M. , Gitnick G. 
Published: April 2003

Recent evidence has been accumulated showing that chronic hemodialysis (HD) patients have a very high prevalence of antibodies to hepatitis C virus (HCV). In contrast, there is little information addressing the virological characteristics of HCV infection in this population. <b>Aim:</b> To measure HCV viral load and to correlate this with demographic, biochemical, and clinical features of a large cohort of HCV-infected patients on chronic HD. <b>Methods:</b> 394 chronic HD patients were tested by branched-DNA signal amplification assay, anti-HCV enzyme-linked immunosorbent assay 2.0, and on the basis of the aspartate aminotransferase/alanine aminotransferase (AST/ALT) activity. Multivariate analysis by ordinal logistic regression model was performed: age, gender, race, time on HD, allocation of the patients among the HD units, etiology of end-stage renal disease, HBsAg status, anti-HCV positivity, HCV genotype, and AST/ALT levels were independent factors, and viremic levels of HCV in serum were assumed as dependent variables. <b>Results:</b> 88 (22.3%) patients showed serological and/or virological signs of HCV infection. 59 (15%) out of 394 had detectable HCV RNA in serum, the mean HCV load was 19.4 × 10<sup>5</sup> (95% CI, 6.06 × 10<sup>7</sup> to 6.2 × 10<sup>4</sup>) Eq/ml. According to the criteria suggested by others [J Infect Dis 1994;169:1219–1225], there were 8 (13.5%) individuals with high-titer viremia (>1 × 10<sup>7</sup> Eq/ml) in the subset of viremic patients. A small subset (8/394 or 2%) of individuals was seronegative, but viremic; 29 (7%) out of 394 were seropositive without detectable HCV RNA in serum. Univariate analysis showed that the frequency of anti-HCV positivity was significantly higher in viremic patients as compared with individuals with no detectable HCV viremia: 51/59 (86%) vs. 29/335 (8.6%), p = 0.0001. Serum AST and ALT levels were significantly higher in viremic patients than in individuals with no detectable HCV RNA in serum: 23.8 (95% CI 60.8–9.3) vs. 17.1 (95% CI 50.4–5.8) U/l (p = 0.009) and 14.4 (95% CI 48.9–4.3) vs. 9.8 (95% CI, 37.3– 2.5) U/l (p = 0.008). Logistic regression analysis showed an association between HCV viremia and anti-HCV positivity (p = 0.00001) and ALT activity (p = 0.01). <b>Conclusions:</b> Hepatitis C virus infection is highly prevalent in the HD population; the viral load is relatively low, and it was associated with elevated hepatic enzyme levels and anti-HCV positivity. No other clinical characteristics were associated with HCV RNA levels. Seronegative but viremic patients were also found. Longitudinal studies with long follow-up periods are necessary to evaluate the course of HCV load over time in this population.
Renal Function in Cyanotic Congenital Heart Disease
Authors: Burlet Anne , Drukker Alfred , Guignard Jean-Pierre 
Published: April 2003

We performed renal function tests in 18 young patients, 1.8–14.6 years of age, with cyanotic congenital heart disease (CCHD). Glomerular filtration rate was normal (116 ± 4.5 ml/min/1.73 m<sup>2</sup>), and renal plasma flow was decreased (410 ± 25 ml/min/1.73 m<sup>2</sup>) with a rise in the filtration fraction (29 ± 1.1%). The suggested pathophysiologic explanation of these findings is that the blood hyperviscosity seen in patients with CCHD causes an overall increase in renal vascular resistance with a rise in intraglomerular blood pressure. Despite a sluggish flow of blood in the glomerular capillary bed, the effective filtration pressure was adjusted to conserve the glomerular filtration rate. In addition to these renal hemodynamic parameters, we also studied renal acidification and tubular sodium and water handling during a forced water diuresis. Our data indicate that children with CCHD have a mild to moderate normal ion gap metabolic acidosis due to a low proximal tubular threshold for bicarbonate. Proximal tubular sodium and water reabsorption under these conditions were somewhat increased, though not significantly, probably due to intrarenal hydrostatic forces, in particular the rise in the oncotic pressure in the postglomerular capillaries in patients with high hematocrit values. The distal tubular functions such as sodium handling and acidification were not affected.
<i>Phyllanthus niruri</i> Inhibits Calcium Oxalate Endocytosis by Renal Tubular Cells: Its Role in Urolithiasis
Authors: Campos Alexandre H. , Schor Nestor 
Published: April 2003

We investigated the in vitro effect of an aqueous extract of Phyllanthus niruri L. on a model of CaOx crystal endocytosis by Madin-Darby canine kidney cells. The extract exhibited a potent and effective non-concentration-dependent inhibitory effect on the CaOx crystal internalization. This response was present even at very high (pathologic) CaOx concentrations and no P. niruri L.-induced toxic effect could be detected. Biochemical analysis of culture media containing P. niruri L. did not provide any clues for the elucidation of the cellular pathways affected by this natural product. Although further studies are necessary for a better understanding of the role of P. niruri L. in urolithiasis, our findings show that this natural product could be an attractive alternative for the treatment of urinary stones.
Pentanucleotide Repeat and Size Polymorphisms in the Apolipoprotein(a) Gene Are Associated with the Lipoprotein(a) Concentration in Chronic Hemodialysis Patients
Authors: Tanaka Mari , Yanagi Hisako , Ando Ryoichi , Kurihara Satoshi , Hirano Chiaki , Kobayashi Kimiko , Kikuchi Shuichi , Hamaguchi Hideo , Tsuchiya Shigeru , Tomura Shigeo 
Published: April 2003

The elevation of serum or plasma lipoprotein(a) [Lp(a)] levels is regarded as an independent risk factor for cardiovascular disease, and many previous reports demonstrated that Lp(a) levels in hemodialysis patients were significantly higher than in controls. The purpose of this study was to investigate the effect of a pentanucleotide repeat polymorphism [(TTTTA)n] in the 5′-flanking region of the apolipoprotein(a) [apo(a)] gene and of a size polymorphism of apo(a) for elevated Lp(a) concentrations observed in chronic hemodialysis patients. We studied 172 patients on chronic hemodialysis and 199 healthy adults. For analysis of the pentanucleotide repeat polymorphism, polymerase chain reaction products were loaded on polyacrylamide gel for electrophoresis. apo(a) size phenotyping was performed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoblotting. The median level of Lp(a) in the patients was 14.2 mg/dl which was significantly higher than that in controls (12.0 mg/dl; p < 0.05). In the genotype of (TTTTA)8/8, the median Lp(a) level in the patients (15.9 mg/dl) was significantly higher than that in controls (13.0 mg/dl; p < 0.05). In the genotype of (TTTTA)8/8 with large-sized apo(a) isoforms (A16–A25), the patients had significantly higher Lp(a) levels than the controls (p < 0.05). In conclusion, increased Lp(a) levels in chronic hemodialysis patients were mainly attributed to the combination of eight repeats of the pentanucleotide polymorphism and large-sized isoforms of apo(a).
Decrease of Apoptosis Rate in Patients with Renal Transplantation Treated with Mycophenolate Mofetil
Authors: Pardo-Mindán F.J. , Errasti P. , Panizo A. , Sola I. , de Alava E. , Lozano M.D. 
Published: April 2003

<i>Background/Aims:</i> Mycophenolate mofetil (MMF) is a powerful immunosuppressant that inhibits the proliferation of lymphocytes by blocking the enzyme inosine monophosphate dehydrogenase. MMF prevents acute graft rejection in organ transplants. The aim of this investigation is to study whether MMF has any influence on apoptosis and proliferation rates of cells other than lymphocytes. <i>Methods:</i> We conducted a retrospective study of renal allograft biopsies taken during the 1st week after transplantation in 25 patients receiving triple therapy with prednisone, ciclosporin and azathioprine 75 mg/day and in 25 patients treated with MMF at a dose of 2 g/day instead of azathioprine, in order to investigate the differences in the proliferation and apoptosis rates of the glomerular, tubular, interstitial and endothelial cells of the kidney. Twelve normal kidneys were used as controls. Conventional histopathological techniques were applied as usual for pathological diagnosis. Proliferative activity was assessed by use of MIB-1 antibody. Sections of formalin-fixed, paraffin-embedded tissue blocks were stained for the presence of apoptotic cells by TUNEL assay. Evaluation of proliferative or apoptotic rates was made by counting the number of positive cells in 10 glomeruli and in 10 transversely cut tubuli in each biopsy. The positive cells in the interstitium were counted in ten high-power fields. Positive cells in the endothelium were scored semiquantitatively from 0 to 3: 0 = none, 1 = isolated cells, 2 = small groups of cells, 3 = most endothelial cells. Mann-Whitney U and chi-square tests were used for intergroup comparisons. <i>Results:</i> All biopsies were normal or had borderline (Banff classification) acute rejection. MIB–1 rates were similar in both groups, without statistical differences (p > 0.05) between them. Significantly lower apoptotic rates were found in the group treated with MMF in tubular epithelium (23.41 ± 8.86 vs. 57.4 ± 13.42; p = 0.021), in glomerular (1.25 ± 0.78 vs. 5.3 ± 1.66; p = 0.027), and interstitial cells (1.58 ± 0.6 vs. 5.8 ± 1.54; p = 0.043). Apoptosis in endothelial cells (p > 0.05) was similar in both groups. <i>Conclusion:</i> We conclude that treatment with MMF of kidney transplant patients does not affect the proliferative rate of cells of the allograft, but decreases the number of apoptotic cells in tubular epithelium.
Association of a Novel 3-Amino Acid Deletion Mutation of Apolipoprotein E (Apo E Tokyo) with Lipoprotein Glomerulopathy
Authors: Konishi Konosuke , Saruta Takao , Kuramochi Shigeru , Oikawa Shinichi , Saito Takao , Han Hua , Matsunaga Akira , Sasaki Jun 
Published: April 2003

Lipoprotein glomerulopathy (LPG) is a newly recognized renal disease characterized by abnormal lipoprotein deposition in the glomeruli, dysbetalipoproteinemia, and a high level of plasma apolipoprotein (apo) E. We identified a novel apo E mutation in a 56-year-old Japanese male with LPG. Although the plasma cholesterol and triglyceride levels were normal, the levels of intermediate-density lipoprotein cholesterol and apo E were elevated to 13 mg/dl (0.336 mmol/l; 4.2±2.9 mg/dl, mean ± SD, in 12 normolipidemic controls) and 9.2 mg/dl, respectively. Biochemical analysis revealed an unusual apo E phenotype (E1/3). Apo E genotyping using DNA digested by a restriction enzyme (<i>Hha</i>I) identified a 66-bp fragment which was not seen with any of the common alleles. Sequence analysis of the amplified genomic DNA fragments showed a 9-bp deletion in exon 4 of the apo E gene resulting in a 3-amino acid deletion (residues 141–143). This novel mutation involves the region of the apo E molecule known to be critically involved in binding to its receptor, and this may well transform the apo E molecule, an inefficient ligand, to its receptor(s). How this mutations causes glomerular damage remains to be determined.
Renal Findings and Glomerular Pathology in Diabetic Subjects
Authors: Wirta Ole , Helin Heikki , Mustonen Jukka , Kuittinen Elina , Savela Tero , Pasternack Amos 
Published: April 2003

<i>Background:</i> To describe the relationship between proteinuria, hematuria, and renal insufficiency, on one hand, and glomerular pathology, on the other hand, in a consecutive biopsy series of diabetic patients. <i>Subjects and Methods:</i> All diabetic subjects (n = 200) biopsied from 1979 to 1995 at Tampere University Hospital were identified in retrospect. The clinician-based indication (any unexplained renal finding) for renal biopsy was consistent during the years and was: proteinuria alone in 68%; combined with hematuria in 10%; with renal insufficiency in 10%; with both in 9%, and with isolated hematuria or renal failure in 3%. One third of the subjects had proteinuria of ≧3 g/24 h and 16% a serum creatinine level of ≧200 µ<i>M</i>. Glomerulopathy was found in 171 specimens and defined as nodular diabetic (group A), diffuse diabetic (group B) and primary (group C). The 24-hour urinary protein excretion rate [mean (range)] was 3.5 (1.6–6.9), 1.0 (0.5–3.5), and 3.6 (1.1–6.6) g in groups A, B and C, respectively (ANOVA p = 0.001). The corresponding serum creatinine values [mean (SD)] were 175 (115), 105 (142) and 169 (138) µ<i>M</i> (p = 0.001). <i>Results:</i> Nodular diabetic glomerulopathy was found in 40%, diffuse diabetic glomerulopathy in 42% and primary glomerulopathy in 18%. A primary glomerulopathy was found in any indication and in both types of diabetes (prevalence range 14–26%). The best multivariate logistic regression model obtained (χ<sup>2</sup> = 13.5, p = 0.008) in predicting the presence of diabetic glomerulosclerosis (group A + B) in contrast to a primary glomerulopathy (group C) included retinopathy (p = 0.04), renal insufficiency (p = 0.03), hematuria (p = 0.12) and type of diabetes (p = 0.10). <i>Conclusion:</i> In this series of diabetic subjects, biopsied due to proteinuria, hematuria and not severe renal insufficiency, 18% had evidence of a primary glomerulopathy.
Effects of Potassium Citrate/Citric Acid Intake in a Mouse Model of Polycystic Kidney Disease
Authors: Tanner George A. , Vijayalakshmi Kodi , Tanner Judith A. 
Published: April 2003

The kidney function in a model of autosomal dominant polycystic kidney disease (PKD), the Han:SPRD rat, is dramatically improved by chronic ingestion of a solution of potassium citrate and citric acid (KCitr). This study investigated whether this treatment would also be beneficial in the pcy/pcy mouse, a model of autosomal recessive PKD. Starting at 1 month of age, male CD-1 pcy/pcy and normal CD-1 mice were provided with a solution of 55 m<i>M</i> K<sub>3</sub> citrate/67 m<i>M</i> citric acid or tap water to drink. The pcy/pcy mice on the KCitr solution failed to grow normally and showed elevated plasma urea levels when compared to water-drinking littermates. Growth of normal CD-1 mice was not affected by KCitr intake. The pcy/pcy mice were then provided with a more dilute solution of KCitr to drink: this resulted in greater kidney wet and dry weights and a higher kidney weight/body weight ratio, but no beneficial effects. We conclude that pcy/pcy mice cannot tolerate a high level of KCitr intake and that a lower level is of no benefit. Whether KCitr therapy would be helpful in patients with PKD is still an open question.
Cytomegalovirus Infection in a Seroendemic Renal Transplant Population: A Longitudinal Study of Virological Markers
Authors: Rao M. , Finny G.J. , Abraham P. , Juneja R. , Thomas P.P. , Jacob C.K. , Sridharan G. 
Published: April 2003

<i>Background/Aims: </i>The detection of viremia by polymerase chain reaction (PCR) in cytomegalovirus (CMV) infection in renal allograft recipients has been shown to have a predictive value for disease. However, its diagnostic utility in a population with high background seropositivity has not been defined. This prospective study was undertaken to assess the relationship of CMV DNAemia, and/or IgM seropositivity to CMV disease in a seroendemic transplant population. <i>Methods:</i> Consecutive patients undergoing renal transplantation between August 1997 and February 1998 were enrolled. Blood was sampled before transplantation from the donors and recipients for CMV serology and nested PCR for CMV DNA, and after transplantation from the recipients only at monthly intervals until 6 months. Patients were observed for the development of any CMV-like illness during follow-up. CMV DNA was quantitated using limiting dilution PCR on samples obtained from symptomatic patients at the time of illness and from asymptomatic patients at the end of their 6-month follow-up. <i>Results: </i>A total of 57 recipient-donor pairs were recruited. Immunosuppression was cyclosporine-based in 55 of 57 (95.6%). The CMV serologic status was D+R+ in 55 of 57 and D+R– in 2 of 57 pairs. PCR positivity indicating viremia increased from 5% before transplantation to 95% at 6 months after transplantation. Similarly IgM positivity reached 80% at 3 months and thereafter; positivity for any marker was 100% by 6 months. Viremia was sustained in over half the patients. The incidence of CMV-attributable disease peaked at 3 months, and was predominantly mild and self-limiting. Tissue-invasive disease appeared later in 4 patients (7%). Asymptomatic viremia was seen in 60–70% of patients at each sampling point. The positive predictive value (PPV) of PCR positivity for disease was 35–40%, and the negative predictive value (NPV), 90–100%. However, the high NPV was of use only in the early post-transplant period, negativity for markers declining rapidly with time. Quantitative assay showed significantly higher levels of CMV DNA in symptomatic patients (p = 0.01). A cutoff of 0.001 µg had a specificity of 95% and a PPV of 92.3% for symptomatic CMV disease. <i>Conclusion: </i>Qualitative tests to detect CMV DNAemia and IgM, although useful markers of viremia and active infection, have limited utility for the diagnosis of disease in a seroendemic transplant population. Quantitation of CMV DNAemia may play an important role in diagnosis in such a setting.
Kidney Disease and Silicosis
Authors: Rosenman K.D. , Moore-Fuller M. , Reilly M.J. 
Published: April 2003

<i>Aim:</i> To determine the prevalence of kidney disease in a cohort of individuals with silicosis. <i>Methods:</i> Review of medical records and questionnaires from patients reported to a state surveillance system for silicosis. Reporting of individuals with silicosis is required by state law. All individuals with silicosis reported as required by law to the State of Michigan. Individuals included in this article were reported from 1987 to 1995. Cases were reported by hospitals, physicians, the state workers’ compensation bureau, or from death certificates. Only individuals who met the criteria for silicosis developed by the National Institute for Occupational Safety and Health (NIOSH) were included. <i>Results:</i> Medical records were reviewed of 583 individuals with confirmed silicosis. This was mainly a population of elderly men. Ten percent of the 583 silicotics were found to have some mention of chronic kidney disease, and 33% of the 283 silicotics who we had laboratory tests on had a serum creatinine level >1.5 mg/dl. An association between kidney disease and age and between kidney disease and race was found among this cohort of 583 silicotics. Individuals with silicosis were more likely to have a serum creatinine level >1.5 mg/dl than age- and race-matched controls. However, no relationship between duration of exposure to silica or profusion of scarring on chest X-ray and prevalence of kidney disease or elevated creatinine levels was found. <i>Conclusions:</i> This study confirms previous case reports and epidemiologic studies of end-stage renal disease that found an association between kidney disease and exposure to silica. The epidemiologic data are conflicting on the mechanism by which silica causes kidney disease and are compatible with silica being able to cause kidney disease by both an autoimmune and direct nephrotoxic effect. Chronic kidney disease should be considered as a complication of silicosis.
Hemodialysis-Induced Degranulation of Polymorphonuclear Cells: No Correlation between Membrane Markers and Degranulation Products
Authors: Grooteman M.P.C. , van Tellingen A. , van Houte A.J. , Bos J.C. , Schoorl M. , van Limbeek J. , Nubé M.J. 
Published: April 2003

<i>Background/Aims: </i>Degranulation of polymorphonuclear leukocytes (PMN) during hemodialysis (HD) is usually assessed by measuring degranulation products. However, this process might also be estimated by the assessment of cell surface markers. In this study, the relationship between the expression of PMN degranulation markers (CD63 and CD66b) and the release of degranulation products [myeloperoxidase (MPO) and lactoferrin (LF)] was investigated during clinical HD in order to evaluate cell surface markers as a useful index of PMN degranulation. <i>Methods: </i>The expression of CD63 and CD66b on PMN and the release of MPO and LF were investigated in 10 chronic HD patients, during both heparin (HD<sub>hep</sub>) and trisodium citrate anticoagulation (HD<sub>cit</sub>), in a randomized order. Samples were drawn from both the efferent and afferent lines of the dialyzer at 0, 7.5, and 180 min. <i>Results: </i>During HD<sub>hep</sub> at first passage, a major increase in MPO (from 158 ± 32 to 448 ± 177 µg/l, p = 0.001) and LF (from 134 ± 52 to 260 ± 120 µg/l, p = 0.01) was found across the dialyzer, whereas marked changes were not observed during HD<sub>cit</sub>. The expression of CD63 and CD66b increased across the dialyzer during both anticoagulation modalities, but was only significant in the case of HD<sub>hep</sub> (CD63: mean fluorescence intensity from 247 ± 61 to 331 ± 118, p < 0.01; CD66b: mean fluorescence intensity from 340 ± 76 to 434 ± 103, p = 0.01). During HD<sub>hep</sub> a correlation was noted between the degranulation products and markers of both azurophilic and specific granules (MPO and CD63: r = 0.35; p < 0.01; LF and CD66b: r = 0.39, p < 0.01). Significant differences in the expression of CD63 and CD66b between HD<sub>hep</sub> and HD<sub>cit</sub> were not observed. When analyzing the combined data for both HD<sub>hep</sub> and HD<sub>cit</sub>, no correlation was observed between degranulation products and markers. <i>Conclusion: </i>Our data suggest that the measurements of cell surface markers may not be a reliable indicator of the degree of HD-induced PMN degranulation.