A High-Powered View of the Filtration Barrier
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Calcium Phosphate Microcrystals in the Renal Tubular Fluid Accelerate Chronic Kidney Disease Progression
The Journal of Clinical Investigation RESEARCH ARTICLE Calcium phosphate microcrystals in the renal tubular fluid accelerate chronic kidney disease progression Kazuhiro Shiizaki,1,2 Asako Tsubouchi,3 Yutaka Miura,1 Kinya Seo,4 Takahiro Kuchimaru,5 Hirosaka Hayashi,1 Yoshitaka Iwazu,1,6,7 Marina Miura,1,6 Batpurev Battulga,8 Nobuhiko Ohno,8,9 Toru Hara,10 Rina Kunishige,3 Mamiko Masutani,11 Keita Negishi,12 Kazuomi Kario,12 Kazuhiko Kotani,7 Toshiyuki Yamada,7 Daisuke Nagata,6 Issei Komuro,13 Hiroshi Itoh,14 Hiroshi Kurosu,1 Masayuki Murata,3 and Makoto Kuro-o1 1Division of Anti-aging Medicine, Center for Molecular Medicine, Jichi Medical University, Shimotsuke, Japan. 2Yurina Medical Park, Shimotsuga, Japan. 3Graduate School of Arts and Sciences, University of Tokyo, Tokyo, Japan. 4Division of Cell and Molecular Medicine, 5Division of Cardiology and Metabolism, Center for Molecular Medicine, 6Division of Nephrology, Department of Internal Medicine, 7Department of Clinical Laboratory Medicine, and 8Division of Histology and Cell Biology, Department of Anatomy, Jichi Medical University, Shimotsuke, Japan. 9Division of Ultrastructural Research, National Institute for Physiological Sciences, Okazaki, Japan. 10Electron Microscopy Analysis Station, Research Network and Facility Service Division, National Institute for Materials Science, Tsukuba, Japan. 11Healthcare Business Unit, Nikon Corporation, Yokohama, Japan. 12Division of Cardiovascular Medicine, Department of Internal Medicine, Jichi Medical University, Shimotsuke, Japan. 13Department of Cardiovascular Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan. 14Division of Endocrinology, Metabolism and Nephrology, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan. The Western pattern diet is rich not only in fat and calories but also in phosphate. -
Nitric Oxide Synthase in Macula Densa Regulates Glomerular Capillary
Proc. Nati. Acad. Sci. USA Vol. 89, pp. 11993-11997, December 1992 Pharmacology Nitric oxide synthase in macula densa regulates glomerular capillary pressure (kidney/tubuloglomerular feedback response/glomerular ifitration rate/afferent arteriole) CHRISTOPHER S. WILCOX*t, WILLIAM J. WELCH*, FERID MURADf, STEVEN S. GROSS§, GRAHAM TAYLOR¶, ROBERTO LEVI§, AND HARALD H. H. W. SCHMIDTII** *Division of Nephrology, Hypertension and Transplantation Departments of Medicine, Pharmacology and Therapeutics, University of Florida College of Medicine and Department of Veterans Affairs Medical Center, Gainesville, FL 32608; I'Department of Pharmacology, Northwestern University School of Medicine, Chicago, IL; tAbbott Laboratories, Abbott Park, IL 60064-3500; iDepartment of Pharmacology, Cornell University Medical College, New York, NY 10021; and IDepartment of Clinical Pharmacology, The Royal Postgraduate Medical School, Hammersmith Hospital, London, England W12 OHS Communicated by Robert F. Furchgott, September 3, 1992 ABSTRACT Tubular-fluid reabsorption by specialized Previous studies have established that L-arginine-derived cells of the nephron at the junction of the ascending limb of the nitric oxide (NO) is produced by several cells within the loop of Henle and the distal convoluted tubule, termed the kidney, including isolated glomerular mesangial (6) and en- macula densa, releases compounds causing vasoconstriction of dothelial cells (7), and a renal epithelial cell line (8), but its the adjacent afferent arteriole. Activation of this tubuloglo- integrative role in the control ofrenal function is not yet clear merular feedback response reduces glomerular capillary pres- (9). In the vessel wall, the endothelium can mediate vasodi- sure of the nephron and, hence, the glomerular filtration rate. lator responses to agents such as acetylcholine (10) and can The tubuloglomerular feedback response functions in a nega- blunt the actions of certain vasoconstrictors (11). -
« Glomerulogenesis and Renal Tubular Differentiation : Role of Hnf1β »
THESE DE DOCTORAT DE L’UNIVERSITE PARIS DESCARTES Ecole doctorale « Bio Sorbonne Paris Cité », ED 562 Département Développement, Génétique, Reproduction, Neurobiologie et Vieillissement (DGRNV) Spécialité : Développement Présentée pour obtenir le titre de DOCTEUR de l’Université Paris Descartes « Glomerulogenesis and renal tubular differentiation : Role of HNF1 β » Par Mlle Arianna FIORENTINO Soutenance le 13 décembre 2016 Composition du jury : Mme. Evelyne Fischer Directrice de thèse M. Marco Pontoglio Examinateur M. Jean-Jacques Boffa Rapporteur M. Yves Allory Rapporteur M Rémi Salomon Examinateur M Jean-Claude Dussaule Examinateur Equipe "Expression Génique, Développement et Maladies" (EGDM) INSERM U1016/ CNRS UMR 8104 / Université Paris-Descartes Institut Cochin, Dpt. Développement, Reproduction et Cancer 24, Rue du Faubourg Saint Jacques, 75014 Paris, France A. Fiorentino HNF1beta in kidney development “Connaître ce n'est pas démontrer, ni expliquer. C'est accéder à la vision.” (Le Petit Prince- Antoine de Saint-Exupéry) 2 A. Fiorentino HNF1beta in kidney development Aknowledgments - Remerciements – Ringraziamenti During this long adventure of the PhD, I was surrounded by many people that I will try to thank to in these pages. In first place, I would like to thank the members of the jury that have kindly accepted to evaluate my work: Jean-Jacques Boffa, Yves Allory, Jean-Claude Dussaule and Rémi Salomon. For the supervision and the precious advices, I would like to thank Evelyne Fischer and Marco Pontoglio that overviewed all my work. I thank Evelyne, my thesis director, for the scientific exchanges of ideas, for the guidance to complete my project and for her help in difficult moments. I thank Marco for the discussions, even for the heated ones, because the pressure in the environment not only helped me to work harder on science but more importantly on my character, to face the problems and solve them. -
Basic Histology (23 Questions): Oral Histology (16 Questions
Board Question Breakdown (Anatomic Sciences section) The Anatomic Sciences portion of part I of the Dental Board exams consists of 100 test items. They are broken up into the following distribution: Gross Anatomy (50 questions): Head - 28 questions broken down in this fashion: - Oral cavity - 6 questions - Extraoral structures - 12 questions - Osteology - 6 questions - TMJ and muscles of mastication - 4 questions Neck - 5 questions Upper Limb - 3 questions Thoracic cavity - 5 questions Abdominopelvic cavity - 2 questions Neuroanatomy (CNS, ANS +) - 7 questions Basic Histology (23 questions): Ultrastructure (cell organelles) - 4 questions Basic tissues - 4 questions Bone, cartilage & joints - 3 questions Lymphatic & circulatory systems - 3 questions Endocrine system - 2 questions Respiratory system - 1 question Gastrointestinal system - 3 questions Genitouirinary systems - (reproductive & urinary) 2 questions Integument - 1 question Oral Histology (16 questions): Tooth & supporting structures - 9 questions Soft oral tissues (including dentin) - 5 questions Temporomandibular joint - 2 questions Developmental Biology (11 questions): Osteogenesis (bone formation) - 2 questions Tooth development, eruption & movement - 4 questions General embryology - 2 questions 2 National Board Part 1: Review questions for histology/oral histology (Answers follow at the end) 1. Normally most of the circulating white blood cells are a. basophilic leukocytes b. monocytes c. lymphocytes d. eosinophilic leukocytes e. neutrophilic leukocytes 2. Blood platelets are products of a. osteoclasts b. basophils c. red blood cells d. plasma cells e. megakaryocytes 3. Bacteria are frequently ingested by a. neutrophilic leukocytes b. basophilic leukocytes c. mast cells d. small lymphocytes e. fibrocytes 4. It is believed that worn out red cells are normally destroyed in the spleen by a. neutrophils b. -
Renal Corpuscle Renal System > Histology > Histology
Renal Corpuscle Renal System > Histology > Histology Key Points: • The renal corpuscles lie within the renal cortex; • They comprise the glomerular, aka, Bowman's capsule and capillaries The capsule is a double-layer sac of epithelium: — The outer parietal layer folds upon itself to form the visceral layer. — The inner visceral layer envelops the glomerular capillaries. • As blood passes through the glomerular capillaries, aka, glomerulus, specific components, including water and wastes, are filtered to create ultrafiltrate. • The filtration barrier, which determines ultrafiltrate composition, comprises glomerular capillary endothelia, a basement membrane, and the visceral layer of the glomerular capsule. • Nephron tubules modify the ultrafiltrate to form urine. Overview Diagram: • Tuft of glomerular capillaries; blood enters the capillaries via the afferent arteriole, and exits via efferent arteriole. • The visceral layer of the glomerular capsule envelops the capillaries, then folds outwards to become the parietal layer. • The capsular space lies between the parietal and visceral layers; this space fills with ultrafiltrate. • Vascular pole = where the arterioles pass through the capsule • Urinary pole = where the nephron tubule begins • Distal tubule passes by the afferent arteriole. Details of Capillary and Visceral Layer: • Fenestrated glomerular capillary; fenestrations are small openings, aka, pores, in the endothelium that confer permeability. • Thick basement membrane overlies capillaries • Visceral layer comprises podocytes: — Cell bodies — Cytoplasmic extensions, called primary processes, give rise to secondary foot processes, aka, pedicles. • The pedicles interdigitate to form filtration slits; molecules pass through these slits to form the ultrafiltrate in the 1 / 3 capsular space. • Subpodocyte space; healthy podocytes do not adhere to the basement membrane. Clinical Correlation: • Podocyte injury causes dramatic changes in shape, and, therefore, their ability to filter substances from the blood. -
Urinary System
OUTLINE 27.1 General Structure and Functions of the Urinary System 818 27.2 Kidneys 820 27 27.2a Gross and Sectional Anatomy of the Kidney 820 27.2b Blood Supply to the Kidney 821 27.2c Nephrons 824 27.2d How Tubular Fluid Becomes Urine 828 27.2e Juxtaglomerular Apparatus 828 Urinary 27.2f Innervation of the Kidney 828 27.3 Urinary Tract 829 27.3a Ureters 829 27.3b Urinary Bladder 830 System 27.3c Urethra 833 27.4 Aging and the Urinary System 834 27.5 Development of the Urinary System 835 27.5a Kidney and Ureter Development 835 27.5b Urinary Bladder and Urethra Development 835 MODULE 13: URINARY SYSTEM mck78097_ch27_817-841.indd 817 2/25/11 2:24 PM 818 Chapter Twenty-Seven Urinary System n the course of carrying out their specific functions, the cells Besides removing waste products from the bloodstream, the uri- I of all body systems produce waste products, and these waste nary system performs many other functions, including the following: products end up in the bloodstream. In this case, the bloodstream is ■ Storage of urine. Urine is produced continuously, but analogous to a river that supplies drinking water to a nearby town. it would be quite inconvenient if we were constantly The river water may become polluted with sediment, animal waste, excreting urine. The urinary bladder is an expandable, and motorboat fuel—but the town has a water treatment plant that muscular sac that can store as much as 1 liter of urine. removes these waste products and makes the water safe to drink. -
L8-Urine Conc. [PDF]
The loop of Henle is referred to as countercurrent multiplier and vasa recta as countercurrent exchange systems in concentrating and diluting urine. Explain what happens to osmolarity of tubular fluid in the various segments of the loop of Henle when concentrated urine is being produced. Explain the factors that determine the ability of loop of Henle to make a concentrated medullary gradient. Differentiate between water diuresis and osmotic diuresis. Appreciate clinical correlates of diabetes mellitus and diabetes insipidus. Fluid intake The total body water Antidiuretic hormone is controled by : Renal excretion of water Hyperosmolar medullary Changes in the osmolarity of tubular fluid : interstitium 1 2 3 Low osmolarity The osmolarity High osmolarity because of active decrease as it goes up because of the transport of Na+ and because of the reabsorbation of water co-transport of K+ and reabsorption of NaCl Cl- 4 5 Low osmolarity because of High osmolarity because of reabsorption of NaCl , also reabsorption of water in reabsorption of water in present of ADH , present of ADH reabsorption of urea Mechanisms responsible for creation of hyperosmolar medulla: Active Co- Facilitated diffusion transport : transport : diffusion : of : Na+ ions out of the Only of small thick portion of the K+ , Cl- and other amounts of water ascending limb of ions out of the thick from the medullary the loop of henle portion of the Of urea from the tubules into the into the medullary ascending limb of inner medullary medullary interstitium the loop of henle collecting -
Juxtaglomerular Apparatus Debajyoti Bhattacharya the Juxtaglomerular
Juxtaglomerular Apparatus Debajyoti Bhattacharya FNTA SEM II The juxtaglomerular apparatus (also known as the juxtaglomerular complex) is a structure in the kidney that regulates the function of each nephron, the functional units of the kidney. The juxtaglomerular apparatus is named because it is next to (juxta-[1]) the glomerulus. The juxtaglomerular apparatus is a specialized structure formed by the distal convoluted tubule and the glomerular afferent arteriole. It is located near the vascular pole of the glomerulus and its main function is to regulate blood pressure and the filtration rate of the glomerulus. The Macula densa is a collection of specialized epithelial cells in the distal convoluted tubule that detect sodium concentration of the fluid in the tubule. In response to elevated sodium, the macula densa cells trigger contraction of the afferent arteriole, reducing flow of blood to the glomerulus and the glomerular filtration rate. The juxtaglomerular cells, derived from smooth muscle cells, of the afferent arteriole secrete Renin when blood pressure in the arteriole falls. Renin increases blood pressure via the Renin-angiotensin-aldosterone system. Lacis cells, also called extraglomerular mesangial cells, are flat and elongated cells located near the macula densa. Their function remains unclear. The juxtaglomerular apparatus consists of three types of cells: 1. The macula densa, a part of the distal convoluted tubule of the same nephron 2. Juxtaglomerular cells, (also known as granular cells) which secrete Renin 3. Extraglomerular mesangial cells Structure: The juxtaglomerular apparatus comprises afferent and efferent arterioles, complemented by granular, Renin-secreting cells, the macula densa, a specialized group of distal tubular cells and Lacis cells (Goormaghtigh cells or Polkissen cells, polar cushion, extraglomerular mesangial cells). -
An in Vitro Approach to the Study of Macula Densa-Mediated Glomerular Hemodynamics
Kidney International, Vol. 38 (1990), pp. 1206—1210 TECHNICAL NOTE An in vitro approach to the study of macula densa-mediated glomerular hemodynamics SADAYOSHI ITO and OSCAR A. CARRETERO Hypertension Research Division, Heart and Vascular Institute, Hen,y Ford Hospital, Detroit, Michigan, USA Tubuloglomerular feedback (TGF), which operates between arm (500 U). The aorta was catheterized below the renal the tubule and the parent glomerulus, is important to renalarteries and clamped with a hemostat above the kidneys. The autoregulation and homeostasis of body fluid and electrolyteskidneys were perfused with cold medium 199 (Gibco Laborato- [1, 2]. Since the juxtaglomerular apparatus (JGA) displays anries, Grand Island, New York, USA) containing 5% bovine intimate anatomical relationship between the specialized tubu-serum albumin (BSA), then removed and sliced along the lar epithelial cells (macula densa) and the vasculature (afferentcorticomedullary axis. Slices were placed in ice-cold medium and efferent arterioles), it has long been suggested as the199 containing 5% BSA (medium 199-5% BSA) and microdis- anatomical site of TGF [3]. However, attempts to obtain directsected under a stereomicroscope (SZH; Olympus, Overland evidence to support this have been hindered by the anatomicalPark, Kansas, USA) at magnifications up to bOx, using thin complexity of the JGA. Since the JGA is located beneath thesteel needles and sharpened forceps (No. 5, Dumont; Fine tubular layer at some distance from the surface of the kidney,Science Tools, Inc., Belmont, California, USA). the macula densa is not accessible to direct micropuncture in An interlobular artery was removed from the remainder of vivo, nor is direct observation of the vascular pole possible. -
A Study of the Effect of Protein in Tubular Fluid in Proximal Tubular Reabsorption Robert Lee Mitchell Yale University
Yale University EliScholar – A Digital Platform for Scholarly Publishing at Yale Yale Medicine Thesis Digital Library School of Medicine 1964 A study of the effect of protein in tubular fluid in proximal tubular reabsorption Robert Lee Mitchell Yale University Follow this and additional works at: http://elischolar.library.yale.edu/ymtdl Recommended Citation Mitchell, Robert Lee, "A study of the effect of protein in tubular fluid in proximal tubular reabsorption" (1964). Yale Medicine Thesis Digital Library. 2943. http://elischolar.library.yale.edu/ymtdl/2943 This Open Access Thesis is brought to you for free and open access by the School of Medicine at EliScholar – A Digital Platform for Scholarly Publishing at Yale. It has been accepted for inclusion in Yale Medicine Thesis Digital Library by an authorized administrator of EliScholar – A Digital Platform for Scholarly Publishing at Yale. For more information, please contact [email protected]. YALE UNIVERSITY LIBRARY 3 9002 06679 0909 A STUDY OF THE EFFECT OF PROTEIN IN TUBULAR FLUID IN OXIMAL TUBULAR REABSORPTION ROBERT L. MITCHELL 19 6 4 YALE MEDICAL LIBRARY Digitized by the Internet Archive in 2017 with funding from The National Endowment for the Humanities and the Arcadia Fund https://archive.org/details/studyofeffectofpOOmitc A STUDY OF THE EFFECT OF PROTEIN IN TUBULAR FLUID IN PROXIMAL TUBULAR REABSORPTION by Robert L, Mitchell (B.A. DePauw I960) A Thesis Presented to the Faculty of the Yale University School of Medicine in Partial Fulfillment of the Requirements for the Degree of Doctor of Medicine Yale University School of Medicine 196U ACKNOWLEDGMENT With sincere appreciation* I wish to express my gratitude to Dr. -
Possible Role of Adenosine in the Macula Densa Mechanism of Renin Release in Rabbits
Possible role of adenosine in the macula densa mechanism of renin release in rabbits. S Itoh, … , O A Carretero, R D Murray J Clin Invest. 1985;76(4):1412-1417. https://doi.org/10.1172/JCI112118. Research Article This study was designed to examine: (a) the effects of adenosine and its analogues on renin release in the absence of tubules, glomeruli, and macula densa, and (b) whether adenosine may be involved in a macula densa-mediated renin release mechanism. Rabbit afferent arterioles (Af) alone and afferent arterioles with macula densa attached (Af + MD) were microdissected and incubated for two consecutive 30-min periods. Hourly renin release rate from a single arteriole (or an arteriole with macula densa) was calculated and expressed as ng AI X h-1 X Af-1 (or Af + MD-1)/h (where AI is angiotensin I). Basal renin release rate from Af was 0.69 +/- 0.09 ng AI X h-1 X Af-1/h (means +/- SEM, n = 16) and remained stable for 60 min. Basal renin release rate from Af + MD was 0.20 +/- 0.04 ng AI X h-1 X Af + MD-1/h (n = 6), which was significantly lower (P less than 0.0025) than that from Af. When adenosine (0.1 microM) was added to Af, renin release decreased from 0.72 +/- 0.16 to 0.24 +/- 0.04 ng AI X h-1 X Af-1/h (P less than 0.025; n = 9). However, when adenosine was added to Af + MD, no significant change in renin release was observed. -
Macula Densa SGLT1-NOS1-Tubuloglomerular Feedback Pathway, a New Mechanism for Glomerular Hyperfiltration During Hyperglycemia
BASIC RESEARCH www.jasn.org Macula Densa SGLT1-NOS1-Tubuloglomerular Feedback Pathway, a New Mechanism for Glomerular Hyperfiltration during Hyperglycemia Jie Zhang,1 Jin Wei,1 Shan Jiang,1 Lan Xu,2 Lei Wang,1 Feng Cheng,3 Jacentha Buggs,4 Hermann Koepsell,5 Volker Vallon,6 and Ruisheng Liu1 1Department of Molecular Pharmacology and Physiology, College of Medicine, 2Department of Biostatistics, College of Public Health, and 3Department of Pharmaceutical Science, College of Pharmacy, University of South Florida, Tampa, Florida; 4Advanced Organ Disease & Transplantation Institute, Tampa General Hospital, Tampa, Florida; 5Institute of Anatomy and Cell Biology, University of Würzburg, Würzburg, Germany; and 6Division of Nephrology and Hypertension, Department of Medicine, University of California, San Diego, La Jolla, California ABSTRACT Background Glomerular hyperfiltration is common in early diabetes and is considered a risk factor for later diabetic nephropathy. We propose that sodium-glucose cotransporter 1 (SGLT1) senses increases in luminal glucose at the macula densa, enhancing generation of neuronal nitric oxide synthase 1 (NOS1)– dependent nitric oxide (NO) in the macula densa and blunting the tubuloglomerular feedback (TGF) response, thereby promoting the rise in GFR. Methods We used microperfusion, micropuncture, and renal clearance of FITC–inulin to examine the effects of tubular glucose on NO generation at the macula densa, TGF, and GFR in wild-type and macula densa–specificNOS1knockoutmice. Results Acute intravenous injection of glucose induced hyperglycemia and glucosuria with increased GFR in mice. We found that tubular glucose blunts the TGF response in vivo and in vitro and stimulates NO generation at the macula densa. We also showed that SGLT1 is expressed at the macula densa; in the presence of tubular glucose, SGLT1 inhibits TGF and NO generation, but this action is blocked when the SGLT1 inhibitor KGA-2727 is present.