Letters| April 28 1999 The Serum Cystatin C Concentration Measured by Particle-Enhanced Immunonephelometry Is Well Correlated with Inulin Clearance in Patients with Various Types of Glomerulonephritis Subject Area: Nephrology Tetsuo Hayashi; Tetsuo Hayashi Department of Medicine, Kidney Center, Tokyo Women's Medical University, Tokyo, Japan Search for other works by this author on: This Site PubMed Google Scholar Kosaku Nitta; Kosaku Nitta Department of Medicine, Kidney Center, Tokyo Women's Medical University, Tokyo, Japan Search for other works by this author on: This Site PubMed Google Scholar Michiyasu Hatano; Michiyasu Hatano Department of Medicine, Kidney Center, Tokyo Women's Medical University, Tokyo, Japan Search for other works by this author on: This Site PubMed Google Scholar Miyuki Nakauchi; Miyuki Nakauchi Department of Medicine, Kidney Center, Tokyo Women's Medical University, Tokyo, Japan Search for other works by this author on: This Site PubMed Google Scholar Hiroshi Nihei Hiroshi Nihei Department of Medicine, Kidney Center, Tokyo Women's Medical University, Tokyo, Japan Search for other works by this author on: This Site PubMed Google Scholar Nephron (1999) 82 (1): 90–92. https://doi.org/10.1159/000045380 Article history Published Online: April 28 1999 Content Tools Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Tools Icon Tools Get Permissions Cite Icon Cite Search Site Citation Tetsuo Hayashi, Kosaku Nitta, Michiyasu Hatano, Miyuki Nakauchi, Hiroshi Nihei; The Serum Cystatin C Concentration Measured by Particle-Enhanced Immunonephelometry Is Well Correlated with Inulin Clearance in Patients with Various Types of Glomerulonephritis. Nephron 1 May 1999; 82 (1): 90–92. https://doi.org/10.1159/000045380 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsNephron Search Advanced Search Article PDF first page preview Close Modal 1999Copyright / Drug Dosage / DisclaimerCopyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements. You do not currently have access to this content.

Retrobulbar optic neuritis associated with trigeminal herpes zoster is very rare [1,2]. In most published cases, this condition was treated with steroids and acyclovir, but the efficacy of these treatments is controversial [3-7]. We report a woman with retrobulbar optic neuritis caused by varicella-zoster virus in whom loss of visual acuity was markedly improved by stellate ganglion block (SGB) and minimally improved by aggressive administration of steroids. Case Report A 50-yr-old woman developed herpes zoster in the first division of the left trigeminal nerve, including the nasociliary nerve. The skin lesions and pain gradually resolved with intravenous (IV) administration of acyclovir 750 mg/day for 5 days, followed by 250 mg/day for 3 days. Six weeks after the onset of herpes zoster, the patient noticed a gradual decrease in visual acuity in her left eye and severe itching of her left forehead. She developed complete loss of visual acuity in her left eye over a 24-h period and was admitted to the hospital. Her left eye had no light perception; the visual acuity of her right eye was normal. The mobility of her eyes was unaffected. The left pupil was slightly larger than the right one, with left eye reaction almost absent to direct light and normal to indirect light. Slit lamp examination and ophthalmoscopy disclosed no abnormal signs. Intraocular pressure was within the normal range in both eyes. General physical and neurologic examinations were normal. Brain computed tomography and magnetic resonance imaging revealed no abnormalities. The serum complement fixation titer of varicella-zoster virus was 1:128 (normal range less than 1:4). Retrobulbar optic neuritis due to varicella-zoster virus was suspected, and treatment was initiated with IV methylprednisolone 1000 mg/day for 3 days, followed by oral prednisolone 30 mg, which was tapered 10 mg/wk. She received a second course of IV methylprednisolone 1000 mg/day for 3 days from the 15th hospital day, when visual acuity gradually improved to finger counting at 30 cm. Visual field testing at that time revealed a central scotoma in her left eye. Left eye visual acuity remained 20/330 on the 29th hospital day. On the 30th hospital day, she was referred to the pain clinic for treatment of left visual disturbance and severe itching. We performed left SGB using 6 mL of 1% mepivacaine daily for 2 wk. Within 30 min after the first SGB, she noticed marked improvement of vision, and this improvement lasted until the following day, when her left eye visual acuity was 20/220. Visual acuity then improved to 20/70 after the third SGB and to 20/33 after the seventh SGB. Her severe itching eased slightly through the series of SGBs. Eight months after the onset of optic neuritis, left eye visual acuity remained at 20/33, and color perception was impaired. Ophthalmoscopic examination revealed temporal pallor of the disc, and brain computed tomography revealed left optic nerve atrophy. Discussion Optic neuritis after trigeminal herpes zoster appears weeks to months after the onset of skin lesions, and loss of visual acuity varies from severe bilateral impairment to moderate unilateral impairment. Because pathologic examination of the optic nerve cannot be performed, the definitive confirmation of the link between varicella-zoster virus and optic neuritis depends on clinical findings and the exclusion of other etiologies. In the present case, a diagnosis of retrobulbar optic neuritis associated with herpes zoster was made based on the history of herpes zoster infection, profound loss of vision, and absence of other abnormal findings. Optic neuritis after herpes zoster is usually treated with steroids but often has a fulminant course unresponsive to steroids [3-5]. In our patient, loss of visual acuity was markedly improved by SGB, and only minimally improved by aggressive administration of steroids. In some cases, steroids improved visual acuity disturbed by optic neuritis after herpes zoster [6,7], but these improvements were more gradual and slighter than the marked improvement in our patient with SGB. The process by which herpes zoster leads to subsequent optic neuritis is not well understood, but it may be related to multiple mechanisms, including viral spread, ischemic vasculitis, demyelination, and host-immune response to infection [8-10]. The mechanism by which SGB improves the visual acuity is equally unclear. SGB may relieve optic nerve ischemia, because sympathetic blockade by SGB increases central retinal blood flow [11]. Further clinical study is required to determine whether SGB should be used with steroid therapy for the treatment of optic neuritis after herpes zoster. In summary, we treated a patient with retrobulbar optic neuritis after herpes zoster. SGB performed 30 days after the onset of visual disturbance was more effective than steroid therapy. Early initiation of SGB may have the potential to improve visual acuity decreased by optic neuritis after herpes zoster.

Serum from patients with membranoproliferative glomerulonephritis (MPGN) and acute poststreptococcal glomerulonephritis (APSGN) accelerated the decay of the cell bound C4b2a (C42) and C4b hemolytic activity relative to pooled normal human serum (pNHS) after 5 min incubation at 30 degrees C in EDTA-GVB. The accelerated decay of the C42 hemolytic activity was heat stable (56 degrees C 30 min) and was inhibited by monoclonal antibody against human C4 binding protein (MoAb:C4BP) or C4 binding protein (C4BP) depleted serum. C4 nephritic factor (C4NeF) was employed to stabilize the labile classical pathway C3 convertase C42 complex. Serum from patients with MPGN and APSGN reduced the C4NeF stabilizing activity. Sera from 32 of 46 patients with MPGN and all of 7 patients with APSGN reduced the C42 hemolytic activity relative to 50 normal human serum (NHS) after 5 min incubation at 30 degrees C in EDTA-GVB, and there was no relationship with the serum concentration of C4BP. In vivo, accelerated decay of C42 convertase might interfere with the clearing and processing mechanism of circulating immune complexes (IC) by reducing deposition of C3b on the IC lattice.

To evaluate the contribution of l arginine as a precursor of the endothelium-derived relaxing factor (EDRF) on vascular cyclic GMP formation, we examined the effects of lNG-monomethyl arginine (lNMMA), and analog of larginine, on basal and acetylcholine (ACh)-, sodium nitroprusside (SNP)- and atrial natriuretic peptide (ANP)-induced cyclic GMP formations in rat mesenteric arteries. The mesenteric arteries were perfused with Krebs-Henseleit solution containing 0.2 mM isobutyl methyl xanthine. The effluents from the arteries were collected before and after infusions of graded doses of ACh, SNP or ANP in the absence or presence of 100 µM lNMMA, and the levels of cyclic GMP were measured. Basal and ACh-induced cyclic GMP formations in the mesenteric arteries were significantly inhibited in the presence of lNMMA, whereas a concomitant infusion of 300 µM larginine restored the inhibition of basal as well as ACh-induced cyclic GMP formations. lNMMA did not affect SNP- and ANP-stimulated cyclic GMP formations, respectively. These results suggest that larginine is necessary for not only the stimulated cyclic GMP formation but also the basal cyclic GMP formation in the mesenteric arteries, whereas the SNP- and ANP-stimulated cyclic GMP formations in the arteries are independent of larginine.

Biosynthesis of tropane alkaloids is thought to proceed by way of the diamine putrescine, followed by its methylation by putrescine N-methyltransferase (PMT; EC 2.1.1.53). High PMT activities were found in branch roots and/or cultured roots of several solanaceous plants. PMT was partially purified and characterized from cultured roots of Hyoscyamus albus that contain hyoscyamine as the main alkaloid. Initial velocity studies and product inhibition patterns of PMT are consistent with an ordered bi-bi mechanism, in which the K(m) values for putrescine and S-adenosyl-l-methionine are 277 and 203 mum, respectively, and the K(i) value for S-adenosyl-l-homocysteine is 110 mum. PMT efficiently N-methylated amines that have at least two amino groups separated by three or four methylene groups. Monoamines were good competitive inhibitors of PMT, among which n-butylamine, cyclohexylamine, and exo-2-aminonorbornane were most inhibitory, with respective K(i) values of 11.0, 9.1, and 10.0 mum. When n-butylamine was fed to root cultures of H. albus, the alkamine intermediates (tropinone, tropine, and pseudotropine) drastically decreased at 1 mm of the exogenous monoamine, and the hyoscyamine content decreased by 52% at 6 mm, whereas the contents of 6beta-hydroxyhyoscyamine and scopolamine did not change. Free and conjugated forms of polyamines were also measured. The n-butylamine treatment caused a large increase in the putrescine content (especially in the conjugated pool), and the spermine content also increased slightly, whereas the spermidine content decreased slightly. The increase in the putrescine pool size (approximately 40 nmol/mg dry weight) was large enough to account for the decrease in the total alkaloid pool size. Similar results were also obtained in root cultures of Datura stramonium. These studies further support the role of PMT as the first committed enzyme specific to alkaloid biosynthesis.

Low doses (10(-16)-10(-10) M) of endothelin-3 (ET-3) elicited continuous vasodilations of mesenteric arteries preconstricted with norepinephrine (NE) but not with KCl. In arteries perfused with Ca2+ free solution, ET-3 did not affect the perfusion pressure. In endothelium-denuded arteries preconstricted with NE, ET-3 significantly elevated the perfusion pressure in a dose-related manner. The levels of cyclic GMP and cyclic AMP from the intact arteries were significantly elevated by ET-3; the cyclic GMP elevasion disappeared with methylene blue. Following endothelium-denudation, cyclic GMP elevation was abolished, but cyclic AMP elevation was unaffected. Levels of 6-Keto-PGF1 alpha in the arteries were not changed appreciably by ET-3. These data indicate that the vasodilating effects of ET-3 depend on the presence of extracellular Ca2+ and the existence of endothelium. They are accompanied by elevations of cyclic nucleotides and the elevation of cyclic GMP depends on the endothelium. It is possible that the vasodilating effects of low doses of ET-3 are associated with endothelium-derived relaxing factor.

A sudden coronary thrombus formation was documented by chance during cardiac catheterization in a patient with postinfarction angina. The thrombus was successfully treated with intravenous urokinase and heparin infusions, and there after, coronary angioplasty was performed without any complication.

Interleukin-1 (IL-1) is a pleiotropic factor, eliciting a broad set of immunologic and inflammatory events. We have previously shown that IL-1 is present in inflamed glomeruli. To evaluate factors that might regulate of IL-1 production, we tested the effects of substances accessible to mesangial cells (MC): immune complexes (IC) are known to modulate MC function. We have attempted to assess the ability of soluble IC derived from rat glomerular basement membrane to induce the production of IL-1. When isolated MC were incubated with the soluble IC, substantial amount of IL-1 could be detected in the supernatants as measured by the mouse thymocyte assay. To block the effect of prostaglandins on the IL-1 assay, we cultured the MC with the addition of indomethacin and assayed IL-1 activity in the culture supernatants. The use of indomethacin resulted in a further increase in IL-1 production. These biological activities were neutralized by a specific antibody to IL-1. In the present report, we show that IC represent important sources of stimulation of MC for the production of IL-1. We speculate that IC could augment local inflammatory responses in the kidney partly due to their capacity to induce the production of IL-1.