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Abstract

M.V. Pahl, C.C. Nast and S.G. Adler

¹Nephrology, University of California, Orange, CA, ²Pathology, Cedars-Sinai Medical Center, Los Angeles, CA, and ³Nephrology, Harbor UCLA, Torrance, CA, USA
Controversy exists regarding the level of proteinuria in patients with nephrosclerosis. Material and methods: We retrospectively examined the clinical parameters of 67 patients with the histologic diagnosis of nephrosclerosis defined as arteriolar hyalinization and/or arterial intimal fibrosis in the absence of other findings in an adequate renal biopsy. Biopsies were performed for clinical indications and were submitted to Cedars-Sinai Pathology Department from January 1994 to March 1999. Results: The mean age and blood pressure (± SD) was 60 ± 17 years, and 139 ± 19/80 ± 12 mmHg. Mean serum creatinine was 2.3 ± 1.3 mg/dl and 24-hour urinary protein excretion was 0.94 ± 0.73 g, 66% had £ 1 g/day, 25% had > 1 but £ 2 g/day, 6% had > 2 g but < 3 g/day and 1 patient had nephrotic range proteinuria. Twelve patients had no history of hypertension. They had a mean blood pressure of 121 ± 8/76 ± 8. Their mean serum creatinine was 1.5 ± 0.6 mg/dl and their mean 24-hour urinary protein excretion was 0.78 ± 0.43 g. Conclusions: Our data do not confirm that of Innes et al. [1993] who reported proteinuria > 1.5 g/day in 40% and nephrotic syndrome in 22% of patients with nephrosclerosis; systemic hypertension may not be a prerequisite for the development of nephrosclerosis.

Abstract

C. Nailescu¹, M. Castaneda², M. Del Rio¹ and J.T. Flynn¹

¹Division of Pediatric Nephrology, Children’s Hospital at Montefiore, Albert Einstein College of Medicine of Yeshiva University, Bronx, New York, USA, and ²Hospital Bloom – Children’s Hospital, San Salvador, El Salvador
Aims: Iron supplementation is necessary in children on hemodialysis, but the optimal protocol remains unknown. We studied the effects of changing our unit’s protocol from oral iron with periodic doses of parenteral iron dextran to routine administration of parenteral sodium ferric gluconate on anemia and iron parameters. Methods: We followed seven hemodialysis patients aged 15 – 20 years (mean 17 years). Hemoglobin, hematocrit, serum iron, transferrin saturation, ferritin, erythropoietin dose, total elemental iron dose and total iron cost for the six months prior to the protocol change were compared to the same variables during the six months following the change. Results: There was no statistically significant difference between the doses of parenteral iron between the two protocols; however, the total dose of elemental iron administered in the oral iron plus iron dextran protocol was greater than in the sodium ferric gluconate protocol (19.6 ± 13.1 (mean ± SD) mg/kg/week versus 1.1 ± 0.3 mg/kg/week; p = 0.03). Both protocols had equivalent efficacy with respect to hemoglobin, ferritin and other measures of iron stores. On the other hand, the costs of sodium ferric gluconate were significantly higher than those of oral iron plus intermittent iron dextran (157.75 ± 45.94 $/patient/month versus 52.08 ± 49.88 $/patient/month; p = 0.01). Conclusions: Routine administration of sodium ferric gluconate is equivalent if not superior to use of oral iron plus iron dextran for maintenance of iron stores in adolescents on hemodialysis, but more expensive.Correspondence to:
J.T. Flynn, M.D., M.S.
Division of Pediatric Nephrology
Children’s Hospital at Montefiore
111 East 210th Street
Bronx, NY 10467, USA
Email: [email protected]

Abstract

C. Nagl, W. Spangl und J. Schneider

Abteilung für Lufthygiene, Umweltbundesamt, Wien
Die Messung von Schwebestaub erfolgt nach EU-rechtlichen Vorgaben als PM₁₀ (particulate matter < 10 mm). Die Referenzmethode ist ein gravimetrisches Verfahren. Andere Methoden sind prinzipiell zulässig, allerdings ist die Äquivalenz zur Referenzmethode nachzuweisen. Vergleichsmessungen zeigen aber z.T. deutliche Unterschiede zwischen den Verfahren. Durchgeführt werden die Messungen an verschiedenen Standorten, zumeist an Belastungsschwerpunkten sowie im städtischen und ländlichen Hintergrund. Die Messungen zeigen Grenzwertüberschreitungen an zahlreichen Standorten, vor allem in Graz, im Nordosten, in größeren Städten und in Städten in Tal- und Beckenlagen. Verursacher im Zusammenspiel mit ungünstigen Ausbreitungsbedingungen sind Verkehr, Hausbrand, Industrie und Gewerbe; in manchen Regionen trägt auch Fernverfrachtung zur Belastung bei.Correspondence to:
Dr. C. Nagl
Abteilung für Lufthygiene
Umweltbundesamt
Spittelauer Lände
A-1090 Wien
Email: [email protected]

Abstract

S. Teijeira¹, B. San Millán¹, J.M. Fernández², E. Rivas¹, I. Viéitez¹, S. Miranda¹, F. González³ and C. Navarro¹

¹Department of Pathology and Neuropathology, Complexo Hospitalario Universitario de Vigo (Meixoeiro), ²Department of Clinical Neurophysiology, Complexo Hospitalario Universitario de Vigo (Xeral-Cies) and ³Department of Laboratory Medicine, Complexo Hospitalario Universitario de Vigo (Meixoeiro), Vigo, Spain
Myoadenylate deaminase deficiency (MADD) is the most common metabolic muscle disorder. Here we report the largest study to date of MADD in Spanish patients, including clinical, histological, and molecular data. Most of the patients presented with moderate clinical symptoms of exercise intolerance, including myalgia, fatigability and cramps. In 70% of the patients, serum creatine kinase (CK) was elevated. Muscle biopsy showed mild, nonspecific alterations with absent histochemical reaction for MAD. Eight cases of MADD were coincidental with other associated diseases, and had more severe tissue alterations upon muscle biopsy. The mutation C34T in the MAD gene was present in a homozygous state in 26 of the 27 patients. One patient was a compound heterozygote for the C34T/G468T mutations. We conclude that MADD should be suspected in patients with exercise intolerance and with idiopathic hyperCKemia. Since symptoms may be subtle, we recommend routine histochemical analysis of MAD in all muscle biopsies, followed by molecular analysis in MAD-negative cases.Correspondence to:
C. Navarro, MD, PhD; Department of Pathology and Neuropathology, Complexo Hospitalario Universitario de Vigo (Meixoeiro), Meixoeiro, s/n, 36215 Vigo, Spain
Email: [email protected]

Abstract

C. Naito

Tokyo Teishin Hospital, Chiyoda-ku, Tokyo
The mainstays of the harmonized final document about ethnic factors in the acceptability of foreign clinical data include a complete clinical data package and a bridging study (for efficacy and/or for safety). A clinical data package that meets all of the regional regulatory requirements is defined as a complete clinical data package for submission and potential approval, irrespective of its geographic origin. The acceptability of the foreign clinical data component of the complete data package depends upon whether it can be extrapolated or employed as a bridge to the population of the new region. Ethnic factors can be defined as the intrinsic characteristics of recipients of a medicine, and extrinsic characteristics associated with the environment and culture in which the subjects reside. Based on retrospective studies, inter-ethnic differences in ADME seem to be not greater than intra-ethnic variations for most medicines, and extrinsic factors appear to be more important than intrinsic factors for the assessment of efficacy and safety of the drug across ethnicity. Medical practice may represent one of the biggest differences and may perhaps prove to be very difficult to provide a harmonization for these extrinsic factors. The bridging study concept has primarily been brought up to overcome the difficulties inherent to extrinsic factors caused by different ethnicity. In Japan, the clinical trials advice division of the organization for pharmaceutical safety and research (OPSR) has been dealing with consultations about bridging studies since February 1998. The contents of consultations can be classified into 5 types. The most common type involves the desire by industries to bridge or extrapolate the results of foreign, phase III, clinical studies by conducting the dose-response studies domestically in the form of bridging studies. Until we have more information and have collected experiences in the variations caused by the regional differences as a result of extrinsic as well as intrinsic ethnic factors, we hope and believe that this document will serve to help provide great advancements in the acceptance of foreign clinical data.Correspondence to:
Dr. C. Naito; Tokyo Teishin Hospital, The Organization for Pharmaceutical Safety and Research (OPSR), 2-14-23 Fujimi, Chiyoda-ku, Tokyo 102-8798, Japan

Abstract

Clinical Nephrology, Vol. 74 – No. 6/2010 (465-470)

Enhanced degradation of tryptophan in patients on hemodialysis

P. Koenig¹, C. Nagl², G. Neurauter², H. Schennach⁴, G. Brandacher³ and D. Fuchs²

¹Department of Internal Medicine, ²Division of Biological Chemistry, Biocenter, ³Department of Surgery, Innsbruck Medical University, and ⁴Central Institute of Blood Transfusion and Immunology, University Clinics, Innsbruck, Austria
Background: Hemodialysis patients often present with increased concentrations of tryptophan catabolites perhaps related to an enhanced activity of tryptophan-degrading enzyme indoleamine 2,3-dioxygenase (IDO) that is inducible by pro-inflammatory stimuli. The often chronic inflammation and immune activation status in dialysis patients may accelerate tryptophan degradation, which could influence patients’ psychological performance. Patients and methods: In this study, plasma concentrations of kynurenine and tryptophan were determined by HPLC in 75 dialysis patients, aged 65.3 ± 15.0 years. Forty patients were female, 35 male; 21 (28%) had diabetes mellitus Type 1 or 2 and 32 (43%) suffered from sleep disturbances and/or depression. Their dialysis vintage was 4.26 ± 4.72 years. HPLC results were compared to concentrations obtained from 40 healthy blood donors, to immune activation marker neopterin, and to psychological test results based on INTERMED scores. Results: Compared to those in healthy controls, tryptophan concentrations were decreased in patients. Neopterin, kynurenine and the kynurenine to tryptophan ratio (kyn/trp, an index of tryptophan degradation) were increased in patients (all p < 0.01). Kyn/trp correlated with neopterin concentrations (rs = 0.393, p < 0.01). INTERMED scores were 21.0 + 8.4 and slightly higher in females (U = –1.831, p < 0.07); they correlated with tryptophan concentrations (rs = –0.227, p < 0.05) but with no other parameter studied. Data point to a possible relationship between tryptophan metabolic disturbances and psychologic presentation of patients, although only a rather weak relationship was found. Conclusion: We conclude that tryptophan degradation is increased in dialysis patients. The association with increased neopterin concentrations indicates activated IDO.Correspondence to:
Dr. D. Fuchs
Division of Biological Chemistry Biocenter, Innsbruck Medical University
Fritz Pregl Straße 3, 6020 Innsbruck, Austria
Email: [email protected]

Abstract

Clinical Neuropathology, Vol. 33 – No. 3/2014 (179-185)

Gender difference in limb-girdle muscular dystrophy: a muscle fiber morphometric study in 101 patients

Marina Fanin¹, Anna C. Nascimbeni¹, and Corrado Angelini²

¹Department of Neurosciences, University of Padova, and ²IRCCS Fondazione San Camillo Hospital, Lido Venice, Italy
Aims: Limb girdle muscular dystrophies (LGMD), a genetically and clinically heterogeneous group of neuromuscular disorders, may show gender differences in the disease severity. We aimed to measure the extent of muscle fiber atrophy and evaluate possible gender differences at fiber level. Methods: We conducted a thorough morphometric analysis of muscle fiber size and fiber area in 101 muscles from patients with various forms of LGMD (43 LGMD2A, 30 LGMD2B, 21 LGMD2C-2D-2E, 7 LGMD1C) and 12 normal controls. Results: Reduced fiber size (atrophy) was pronounced in LGMD2A and LGMD2B, while LGMD1C showed a significant fiber hypertrophy. When we compared LGMD patients and controls of the same gender, males with LGMD2A and LGMD2B showed significantly higher fiber atrophy than control males, whereas female LGMD patients had similar values to female controls, suggesting a gender difference in muscle fiber atrophy. Discussion: Less recovery to disuse atrophy in men than in women has been attributed to the possibility that in women a smaller initial muscle size associated to endocrine factors could attenuate gender-specific muscle loss. The possibility that males with LGMD may be clinically more severely affected than females has been explored, but the mechanism remains elusive.Correspondence to:
Dr. Marina Fanin
Department of Neurosciences
University of Padova, Biomedical Campus “Pietro d’Abano”
via Giuseppe Orus 2B, 35129 Padova, Italy
Email: [email protected]

Abstract

CDAllergologie, Jahrgang 39, Nr. 3/2016, S. 109–115

CD4+-CD25+-TReg-Zellen bei Patienten mit allergischer Rhinitis

Y. Shaoqing¹, C. Yinjian², Y. Zhiqiang³, Z. Ruxin⁴, C. Na¹ und G. Rongming¹

¹Department of Otolaryngology, Tongji Hospital, Tongji University, Shanghai, ²Department of Laboratory Medicine, Jinan General Hospital of PLA, Shandong, ³Department of Otolaryngology, Xuzhou ⁹⁷th Hospital of PLA, Jiangsu, ⁴Department of Otolaryngology, Huadong Hospital, Fudan University, Shanghai, China
Hintergrund: Es ist bereits bekannt, dass regulatorische T-Zellen vom Typ CD4⁺- CD25⁺ (CD4⁺-CD25⁺-T_Reg) an allergischen Erkrankungen beteiligt sind. Unbekannt ist jedoch, ob auch eine Beteiligung an der allergischen Rhinitis (AR) vorliegt. Methoden: Im frischen Vollblut von 20 Patienten mit AR und 16 gesunden Spendern wurde die Häufigkeit von CD4⁺CD25⁺- und CD4⁺CD25^hi-T_Reg-Zellen mittels Durchflusszytometrie untersucht. Zudem wurde die Gesamt-IgEKonzentration im Serum (IU/ml) mittels Enzyme-Linked Immunosorbent Assay (ELISA) gemessen. Ergebnisse: Bei den ARPatienten war die Konzentration von CD4⁺- CD25⁺-T_Reg-Zellen (2,80 ± 1,36% vs. 3,94 ± 0,97%, p < 0,01) und der CD4⁺-CD25^hi-T_Reg (1,53 ± 0,62% vs. 2,00 ± 0,52%, p < 0,05) niedriger als bei den Kontrollpersonen. Die Anzahl der CD4⁺-CD25⁺-T_Reg-Zellen und der CD4⁺-CD25^hi-T_Reg-Zellen war negativ mit der Gesamt-IgE-Konzentration korreliert (r = -0,79, p < 0,01 bzw. r = -0,61, p < 0,01). Schlussfolgerung: Ein Mangel an regulatorischen T-Zellen könnte bei der Entstehung der AR eine Rolle spielen.Correspondence to:
Yu Shaoqing
Department of Otolaryngology
Tongji Hospital
389 Xincun road, Putuo District
Shanghai city 200065, China
Email: [email protected]

Abstract

Allergologie, Jahrgang 24, Nr. 9/2001, S. 408–418

Die mögliche Bedeutung der Neurotrophine in der Pathogenese des allergischen Asthmas

C. Nassenstein¹, S. Mayer¹, A. Braun², M. Lommatzsch¹, H. Renz³, W. Luttmann¹ und J.C. Virchow jr.¹

¹Abteilung Pneumologie, Universitätsklinikum Freiburg, ²Fraunhofer-Institut für Toxikologie und Aerosolforschung, Hannover, ³Abteilung Klinische Chemie, Universitätsklinikum Marburg
Asthma bronchiale ist eine entzündliche Erkrankung, die mit einer bronchialen Hyperreagibilität (BHR) einhergeht. Obwohl sowohl die Anzahl verschiedener Immunzellen, die die Bronchialschleimhaut infiltrieren, als auch die Konzentration der freigesetzten Mediatoren in einigen Studien mit dem Grad der BHR korreliert werden konnten, ist es bisher nicht gelungen, den pathophysiologisch zugrunde liegenden Mechanismus, der die allergisch bedingte Atemwegsentzündung und die BHR verbindet, aufzudecken. Neurotrophine, beim Asthma in erhöhten Konzentrationen nachweisbar, induzieren die Synthese von Neuropeptiden sensorischer Neurone und können dadurch, wie im Tiermodell gezeigt, an der Pathogenese der BHR beteiligt sein. Da verschiedene Immunzellen, die an der asthmatischen Entzündung mitwirken, Neurotrophine bilden, scheint die Entzündung wichtige Voraussetzung für eine Augmentation der Neurotrophinbildung zu sein. Diese Immunzellen exprimieren darüber hinaus Neurotrophin-Rezeptoren, über die möglicherweise durch auto- bzw. parakrine Mechanismen eine lokale Entzündung aufrechterhalten werden kann. Neurotrophine könnten also sowohl an der BHR als auch an der Chronifizierung der Atemwegsentzündung beteiligt sein, wodurch ihnen eine zentrale Rolle in der Pathogenese des allergischen Asthmas zukommen würde. Correspondence to:
PD Dr. med. J.C. Virchow jr.
Abteilung Pneumologie
Universitätsklinikum Freiburg
Hugstetter Straße 55
D-79106 Freiburg

Abstract

Allergologie select, Volume 2, No. 1/2018 (144-150)

The levels of CD4+CD25+ regulatory T cells in patients with allergic rhinitis

Y. Shaoqing¹, C. Yinjian², Y. Zhiqiang³, Z. Ruxin⁴, C. Na¹ and G. Rongming¹

¹Department of Otolaryngology, Tongji Hospital, Tongji University, Shanghai, ²Department of Laboratory Medicine, Jinan General Hospital of PLA, Shandong, ³Department of Otolaryngology, Xuzhou ⁹⁷th Hospital of PLA, Jiangsu, ⁴Department of Otolaryngology, Huadong Hospital, Fudan University, Shanghai, China
Background: The involvement of CD4⁺CD25⁺ regulatory T cells (CD4⁺CD25⁺ T_Regs) in allergic diseases was reported previously. However, it remains unclear whether CD4⁺CD25⁺ T_Regs are involved in allergic rhinitis (AR).
Methods: Fresh whole blood from 20 patients with AR and 16 healthy donors was used to investigate the frequency of CD4⁺CD25⁺ and CD4⁺CD25^hi T_Reg cells using flow cytometry. In addition, serum total IgE (IU/mL) levels were determined using enzyme-linked immunosorbent assays.
Results: Patients with AR had fewer CD4⁺CD25⁺ T_Reg cells (2.80 ± 1.36% vs. 3.94 ± 0.97%, P < 0.01) and CD4⁺CD25^hi T_Regs (1.53 ± 0·62% vs. 2.00 ± 0.52%, P < 0.05) than control subjects. The number of CD4⁺CD25⁺ and CD4⁺CD25^hi T_Regs was correlated negatively with total immunoglobulin E levels (r = -0.79, P < 0.01 and r = -0.61, P < 0.01, respectively).
Conclusion: Deficient regulatory T cells might play a role in the development of AR.

German version published in Allergologie, Vol. 39, No. 3/2016, p. 109-115Correspondence to:
Yu Shaoqing
Department of Otolaryngology
Tongji Hospital
389 Xincun road, Putuo District
Shanghai city 200065, China
Email: [email protected]

Abstract

Clinical Nephrology – Case Studies, Vol. 8/2020 (17-24)

Multiple morphological phenotypes of monoclonal immunoglobulin disease on renal biopsy: Significance of treatment

Sreedhar Adapa¹, Venu Madhav Konala², Srikanth Naramala³, and Cynthia C. Nast⁴

¹Division of Nephrology, The Nephrology Group, Fresno, CA, ²Department of Internal Medicine, Division of Medical Oncology, Ashland Bellefonte Cancer Center, Ashland, KY, ³Division of Rheumatology, Adventist Medical Center, Hanford, and ⁴Department of Pathology, Cedars-Sinai Medical Center, Los Angeles, CA, USA
Plasma cell dyscrasias frequently involve the kidney causing renal dysfunction. Multiple morphologic manifestations of κ light chain disease occurring simultaneously in the same kidney biopsy are uncommon and suggest local microenvironment effects in addition to structural properties of the light chain. A 61-year-old female presented with new onset renal failure and proteinuria. Serological workup revealed monoclonal gammopathy with elevated κ : λ ratio of 1,371. Renal biopsy revealed several paraprotein manifestations including κ light chain deposition disease, monoclonal fibrillary glomerulonephritis, cryocrystalglobulenemia and fibrillar/microtubular cast nephropathy. There was also incidental leukocyte chemotactic factor 2 amyloidosis (ALECT 2), negative for κ light chain and confirmed by immunohistochemistry (IHC). Bone marrow biopsy revealed 10 – 20% κ restricted plasma cells. The patient received 10 cycles of CyBorD (cyclophosphamide, bortezomib, and dexamethasone) chemotherapy. Renal function improved with decreased κ : λ ratio. Repeat bone marrow biopsy showed no evidence of abnormal plasma cells by IHC. The renal recovery demonstrates there may be response to chemotherapy irrespective of the morphologic manifestations of light chain-related injury. Additionally, if amyloid is not demonstrated to be of light chain origin, other amyloid types should be considered.Correspondence to:
Sreedhar Adapa, MD, The Nephrology Group, 568 East Herndon Avenue #201, Fresno, CA 93720, USA
Email: [email protected]

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