DOCSLIB.ORG

Pathophysiology of Experimental Glomerulonephritis Inrats

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Pathophysiology of Experimental Glomerulonephritis Inrats Pathophysiology of Experimental Glomerulonephritis in Rats MARJORIE E. M. ALLISON, CuRTIs B. WILSON, and CARL W. GOrrSCHALK, with the technical assistance of SARAH K. DAVIS From the Department of Medicine, University of North Carolina School of Medicine, Chapel Hill, North Carolina 27514 and the Department of Experimental Pathology, Scripps Clinic and Research Foundation, La Jolla, California 92037 A B S T R A C T Micropuncture, clearance, immunofluo- the more chronic AICN disease. Tubular damage was rescence and light microscopy techniques were used to more marked in AICN, and extraction of p-aminohip- study kidney structure and single nephron function in purate was reduced in this group. rats with autologous immune complex nephritis (AICN), a membranous glomerulonephritis develop- ing over 5 to 20 mo, in the more acute and prolifera- INTRODUCTION tive glomerular basement membrane (GBM) nephritis Since the classical description by Richard Bright in and in controls. Both models are known to have clinical 1827 of the clinical effects of chronic renal disease a counterparts in human disease. Kidney functional ab- multitude of detailed studies have been made of whole normalities correlated with the degree of architectural kidney function in such patients (1-5). The pains- derangement. In both AICN and anti-GBM nephritis taking microdissection studies of Oliver (6) have filtration fraction fell in direct proportion to the fall in shown that such kidneys are "a heterogeneous collec- glomerular filtration rate (GFR), renal plasma flow tion of various and disparate organs, the abnormal being unchanged. Fractional electrolyte excretion in- nephrons of chronic renal disease" (7). Impressive creased as the GFR fell. Despite marked heterogeneity overall functional renal adaptation accompanies these of single nephron filtration rate (SNGFR) (AICN, 5- marked structural changes (8-11 ). Information on 93 nl/min; anti-GBM, 0-50 nl/min) and of proximal the function of individual structurally altered nephrons, tubular hydrostatic pressure (4-48 mm Hg), each however, is sparse and apparently contradictory (12- nephron showed almost complete glomerulotubular bal- 17). ance, absolute reabsorption to the late proximal con- We have used micropuncture, clearance, immunofluo- volution varying directly with filtration rate. In addi- rescence and light microscopy techniques to study kid- tion SNGFR could be related both to proximal intra- ney structure and single nephron function in rats with tubular hydrostatic pressure and to calculated glomeru- two forms of immunologically induced glomerulone- lar capillary pressure (Pg), being lowest in those phritis. nephrons with the highest intratubular pressure. Ne- Firstly, autologous immune complex or Heymann's phrons with very high filtration rates did not appar- nephritis (AICN) 1 (18, 19) was chosen as a model ently reach filtration equilibrium. Mean SNGFR was resembling human membranous glomerulonephritis. significantly lower in the anti-GBM group, while cal- 1Abbreviations used in this paper: ADH, antidiuretic hor- culated Pg was the same in both. This probably re- mone; AICN, autologous immune complex nephritis; anti- flects the acute and diffuse involvement of the anti- GBM, antiglomerular basement membrane; BUN, blood GBM lesion with different filtration characteristics from urea nitrogen; C, clearance; CFA, complete Freund's ad- juvant; E, extraction; EFP, effective filtration pressure; Dr. Allison was a Career Investigator Fellow, American FF, filtration fraction; GBM, glomerular basement mem- Heart Association. Her present address is the Renal Unit, brane; GFR, glomerular filtration rate; PAH, p-aminohip- Glasgow Royal Infirmary, Glasgow, Scotland. purate; PAS, periodic acid-Schiff; PBS, 0.01 M phosphate- Dr. Gottschalk is a Career Investigator, American Heart buffered 0.15 M NaCl, pH 7.0; Pg, glomerular capillary Association. hydrostatic pressure; RPF, renal plasma flow; RTA, renal Received for publication 22 June 1973 and in revised tubular antigen; SNGRF, single nephron glomerular filtra- form 8 October 1973. tion rate; TBM, tubular basement membrane. 1402 The Journal of Clinical Investigation Volume 53 May 1974-1402-1423 Secondly, antiglomerular basement membrane (Anti- Blood pressure was recorded continuously from the carotid GBM) nephritis (20) was studied as a more acute, artery by using a Statham P23Db transducer (Statham In- struments, Inc., Oxnard, Calif.) and a Beckman Dynograph proliferative model of human glomerular injury. recorder (Beckman Instruments, Inc., Fullerton, Calif.). All rats were studied during hydropenia, modified Ring- METHODS er's solution (NaCl, 0.85 g/100 ml; KCl, 0.042 g/100 ml; CaCl2, 0.025 g/100 ml; NaHCO3, 0.02 g/100 ml) being AICN. 50 100 g male Wistar rats (Research Animals given i.v. at the rate of 0.4 ml/100 g body wt/h, together Inc., Braddock, Pa.) were given rear foot pad injections with d-aldosterone (Ciba Pharmaceutical Company, Sum- totalling 12.5 mg of partially purified rat renal tubular an- mit, N. J.), vasopressin (Parke, Davis & Co., Detroit, tigen (RTA) in 0.25 ml complete Freund's adjuvant Mich), ['H]methoxy inulin (International Chemical and (CFA) containing 2.5 mg of Mycobacterium butyricum Nuclear Corporation, Burbank, Calif.) and in most in- (Difco Laboratories, Detroit, Mich.). Intraperitoneal in- stances ['C]p-aminohippurate (PAH) (New England Nu- jections (18) were not used because we wished to avoid clear Corp., Boston, Mass.). In those rats in which intra- granulomatous peritonitis with subsequent micropuncture renal pressure measurements were made a priming dose difficulties. RTA was prepared by a slight modification of of 3 Ag of d-aldosterone, 60 ,uCi ['H] inulin, and 2 GCi that described by Edgington, Glassock, and Dixon (21). [CIC]PAH was followed by infusion of d-aldosterone, 2.4 A suspension of Wistar and Sprague Dawley rat renal ,ug/h; antidiuretic hormone (ADH), 0.03 ,g/h; ['C] PAH, cortex (Pel-Freez Biologicals, Inc., Rogers, Ark.) was 5-7 ,Ci/h; and ['H]inulin at a rate of 20 ,Ci/100 g body prepared by passing cortical fragments through a 150 mesh wt/h. When proximal tubular F/P inulin levels were to stainless steel screen. Basement membrane and cellular be measured this infusion was increased to 40-80 ,uCi [3H]- fragments were removed by low speed centrifugation (150 inulin/100 g body wt/h. g). The supernate was then centrifuged at 78,000 g for 30 Three consecutive timed urine collections, each lasting min and the resultant sediment washed two times in PBS approximately 45-0 min, were made from both kidneys. (0.01 M phosphate buffered, 0.15 M NaCl, pH 7.0) and Blood (<30 ,ul) was obtained from the carotid artery and lyophilized. (L) renal vein at approximately 45-min intervals for In 15 rats a second dose of 12.5 mg of RTA in CFA measurement of hematocrit, ['H] inulin, and ["C] PAH was given intradermally 51 days (five rats), 93 days (three levels. Clearances were determined as previously described rats), and 187 days (seven rats) later. In 28 rats, two addi- (27). Glomerular filtration rate (GFR) was calculated tional 12.5-mg doses were given 51 and 106 days (19 rats) separately for the left and right kidneys, renal plasma flow and 93 and 187 days (nine rats) after the initial injection. (RPF) for the left kidney only. 24-h urinary protein excretion rates were used to follow In those rats not given ["C] PAH the left RPF was the onset of overt glomerulonephritis. Determination of calculated as follows: urine protein concentration was made by using either the Biuret technique or salicylsulphonic acid. Clearance and micropuncture studies were done 5-20 mo after the first RPF = V(U-R) injection. Anti-GBM glomerulonephritis. Rabbit anti-rat GBM where V = urine flow rate and U, A, and R= inulin con- antibody was induced by biweekly injections (foot pads and centration in urine, arterial plasma, and renal venous intradermally) of 10-30 mg of rat GBM (22) in CFA. plasma, respectively. Antibody production was quantitated by the paired-label In those rats given ["C]PAH the RPF was calculated as isotope technique (23, 24). Male Wistar rats (100-150 g) were given 1.75-2.25 ml CPAH (five rats) and 1.5-2.2 ml (five rats) rabbit anti-rat GBM EPAH antibody containing 113 and 130 ,ug of kidney fixing anti- body per ml, respectively, and were studied 10-38 days later. where C = clearance and E = extraction. Intensified glomerular lesions were produced by enhancing Two groups of micropuncture experiments were carried the recipients immune response to the heterologous anti- out In the first series (six AICN, five anti-GBM, and GBM antibody by administering 1.8 mg of rabbit IgG in three control rats) the kidney was bathed with mineral oil incomplete Freund's adjuvant 3 days before receipt of anti- heated to 36+1'C. Sharpened siliconized glass pipettes, ex- GBM antibody (25). ternal tip diameter 4-6 ,sm, filled with isotonic saline colored Controls. 17 male Wistar rats, of a similar age to the with lissamine green (K and K Laboratories, Inc., Plain- AICN animals, were used as controls. In eight that were view, N. Y.) were used to puncture a superficial proximal 4-wk old, CFA alone was injected intradermally in the convolution, and the free flow hydrostatic pressure was proportions given above, and injections were repeated 93 measured by using the "Landis" technique (26). Simul- days later in four of them. The remaining nine rats re- taneously the last loop of the proximal tubule visible on ceived no injections. the surface of the kidney was identified by following the Clearance and micropuncture studies. Clearance and, in passage of the lissamine green colored saline. This last most instances, micropuncture studies were made in 24 rats convolution was later punctured with a sharpened silicon- with AICN, in all 10 rats with anti-GBM nephritis, and ized glass pipette, external tip diameter 11-12 Am, and a in 12 control rats.
Load more

Recommended publications
  • Albumin in Health and Disease: Protein Metabolism and Function*
    Article #2 CE An In-Depth Look: ALBUMIN IN HEALTH AND DISEASE Albumin in Health and Disease: Protein Metabolism and Function* Juliene L. Throop, VMD Marie E. Kerl, DVM, DACVIM (Small Animal Internal Medicine), DACVECC Leah A. Cohn, DVM, PhD, DACVIM (Small Animal Internal Medicine) University of Missouri-Columbia ABSTRACT: Albumin is a highly charged, 69,000 D protein with a similar amino acid sequence among many veterinary species. Albumin is the major contributor to colloid oncotic pressure and also serves as an important carrier protein. Its ability to modulate coagulation by preventing pathologic platelet aggrega- tion and augmenting antithrombin III is important in diseases that result in moderately to severely decreased serum albumin levels. Synthesis is primar- ily influenced by oncotic pressure, but inflammation, hormone status, and nutrition impact the synthetic rate as well. Albumin degradation is a poorly understood process that does not appear to be selective for older mole- cules.The clinical consequences of hypoalbuminemia reflect the varied func- tions of the ubiquitous albumin protein molecule. he albumin molecule has several characteristics that make it a unique protein. Most veterinarians are aware of the importance of this molecule in maintain- Ting colloid oncotic pressure, but albumin has many other less commonly recog- nized functions as well. The clinical consequences of hypoalbuminemia are reflections of the many functions albumin fulfills. Understanding the functions, synthesis, and *A companion article on degradation of the albumin molecule can improve understanding of the causes, conse- causes and treatment of quences, and treatment of hypoalbuminemia. hypoalbuminemia appears on page 940. STRUCTURE Email comments/questions to Albumin has a molecular weight of approximately 69,000 D, with minor variations [email protected], among species.
    [Show full text]
  • Renal Sodium Handling in Minimal Change Nephrotic Syndrome
    Arch Dis Child: first published as 10.1136/adc.59.9.825 on 1 September 1984. Downloaded from Archives of Disease in Childhood, 1984, 59, 825-830 Renal sodium handling in minimal change nephrotic syndrome A-B BOHLIN AND U BERG Department of Paediatrics, Karolinska Institute, Huddinge Hospital, Stockholm, Sweden SUMMARY Renal sodium handling was studied in 23 children at three different stages of the minimal change nephrotic syndrome-the oedema forming state, proteinuric steady state, and remission. Clearances of inulin and para-aminohippuric acid and urinary sodium excretion were determined basally, after intravenous infusion of isotonic saline and hyperoncotic albumin, and after furosemide injection. Absolute and fractional basal sodium excretion were significantly lower in oedema forming patients than in proteinuric patients in steady state, and non-proteinuric patients. In contrast to proteinuric patients in steady state and non-proteinuric patients, the oedema forming patients failed to respond to isotonic saline infusion with increased sodium excretion. After diuretic blockade with furosemide, the fractional sodium excretion of the oedema forming patients increased to values no different from those of the non-proteinuric patients, whereas the fractional sodium excretion of the steady state patients increased to significantly higher values. The plasma aldosterone concentration was within normal limits in 11 of 14 proteinuric patients, and did not correlate with the basal sodium excretion. Thus, sodium copyright. retention in the minimal change nephrotic syndrome was found only in oedema forming patients, and since this is not related to the plasma aldosterone concentration it may be caused by an intrarenal mechanism, probably sited in distal parts of the nephron.
    [Show full text]
  • 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.
    [Show full text]
  • « 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.
    [Show full text]
  • Determinants of Glomerular Filtration in Experimental Glomerulonephritis in the Rat
    Determinants of glomerular filtration in experimental glomerulonephritis in the rat. D A Maddox, … , T M Daugharty, B M Brenner J Clin Invest. 1975;55(2):305-318. https://doi.org/10.1172/JCI107934. Research Article Pressures and flows were measured in surface glomerular capillaries, efferent arterioles, and proximal tubules of 22 Wistar rats in the early autologous phase of nephrotoxic serum nephritis (NSN). Linear deposits of rabbit and rat IgG and C3 component of complement were demonstrated in glomerular capillary walls by immunofluorescence microscopy. Light microscopy revealed diffuse proliferative glomerulonephritis, and proteinuria was present. Although whole kidney and single nephron glomerular filtration rate (GFR) in NSN (0.8 plus or minus 0.04 SE2 ml/min and 2 plus or minus 2 nl/min, respectively) remained unchanged from values in 16 weight-matched NORMAL HYDROPENIC control rats (0.8 plus or minus 0.08 and 28 plus or minus 2), important alterations in glomerular dynamics were noted. Mean transcapillary hydraulic pressure difference (deltaP) averaged 41 plus or minus 1 mm Hg in NSN versus 32 plus or minus 1 in controls (P LESS THAN 0.005). Oncotic pressures at the afferent (piA) end of the glomerular capillary were similar in both groups ( 16 mm /g) but increased much less by the efferent end (piE) in NSN (to 29 plus or minus 1 mm Hg) than in controls (33 plus or minus 1, P less than 0.025). Hence, equality between deltaP and piE, denoting filtration pressure equilibrium, obtained in control but not in NSN rats. While glomerular plasma flow rate was slightly higher […] Find the latest version: https://jci.me/107934/pdf Determinants of Glomerular Filtration in Experimental Glomerulonephritis in the Rat D.
    [Show full text]
  • Glomerulonephritis Management in General Practice
    Renal disease • THEME Glomerulonephritis Management in general practice Nicole M Isbel MBBS, FRACP, is Consultant Nephrologist, Princess Alexandra lomerular disease remains an important cause Hospital, Brisbane, BACKGROUND Glomerulonephritis (GN) is an G and Senior Lecturer in important cause of both acute and chronic kidney of renal impairment (and is the commonest cause Medicine, University disease, however the diagnosis can be difficult of end stage kidney disease [ESKD] in Australia).1 of Queensland. nikky_ due to the variability of presenting features. Early diagnosis is essential as intervention can make [email protected] a significant impact on improving patient outcomes. OBJECTIVE This article aims to develop However, presentation can be variable – from indolent a structured approach to the investigation of patients with markers of kidney disease, and and asymptomatic to explosive with rapid loss of kidney promote the recognition of patients who need function. Pathology may be localised to the kidney or further assessment. Consideration is given to the part of a systemic illness. Therefore diagnosis involves importance of general measures required in the a systematic approach using a combination of clinical care of patients with GN. features, directed laboratory and radiological testing, DISCUSSION Glomerulonephritis is not an and in many (but not all) cases, a kidney biopsy to everyday presentation, however recognition establish the histological diagnosis. Management of and appropriate management is important to glomerulonephritis (GN) involves specific therapies prevent loss of kidney function. Disease specific directed at the underlying, often immunological cause treatment of GN may require specialist care, of the disease and more general strategies aimed at however much of the management involves delaying progression of kidney impairment.
    [Show full text]
  • Glomerular Filtration I DR.CHARUSHILA RUKADIKAR Assistant Professor Physiology GFR 1
    Glomerular filtration I DR.CHARUSHILA RUKADIKAR Assistant Professor Physiology GFR 1. Definition 2. Normal value 3. Variation 4. Calculation (different pressures acting on glomerular membrane) 5. Factors affecting GFR 6. Regulation of GFR 7. Measurement of GFR QUESTIONS LONG QUESTION 1. GFR 2. RENIN ANGIOTENSIN SYSTEM SHORT NOTE 1. DYNAMICS OF GFR 2. FILTRATION FRACTION 3. ANGIOTENSIN II 4. FACTORS AFFECTING GLOMERULAR FILTRATION RATE 5. REGULATION OF GFR 6. RENAL CLEARANCE TEST 7. MEASUREMENT OF GFR Collecting duct epithelium P Cells – Tall, predominant, have few organelles, Na reabsorption & vasopressin stimulated water reabsorption I cells- CT and DCT, less, having more cell organelles, Acid secretion and HCO3 transport CHARACTERISTICS OF RENAL BLOOD FLOW 600-1200 ml/min (high) AV O2 difference low (1.5 mL/dL) During exercise increases 1.5 times Low basal tone, not altered in denervated / innervated kidney VO2 in kidneys is directly proportional to RBF, Na reabsorption & GFR Not homogenous flow, cortex more & medulla less Vasa recta hairpin bend like structure, hyperosmolarity inner medulla Transplanted kidney- cortical blood flow show autoregulation & medullary blood flow don’t show autoregulation, so no TGF mechanism Neurogenic vasodilation not exist 20% of resting cardiac output, while the two kidneys make < 0.5% of total body weight. Excretory function rather than its metabolic requirement. Remarkable constancy due to autoregulation. Processes concerned with urine formation. 1. Glomerular filtration, 2. Tubular reabsorption and 3. Tubular secretion. • Filtration Fluid is squeezed out of glomerular capillary bed • Reabsorption Most nutrients, water and essential ions are returned to blood of peritubular capillaries • Secretion Moves additional undesirable molecules into tubule from blood of peritubular capillaries Glomerular filtration Glomerular filtration refers to process of ultrafiltration of plasma from glomerular capillaries into the Bowman’s capsule.
    [Show full text]
  • 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.
    [Show full text]
  • Significance of Protein in Edema Fluids I C
    i Significance of Protein in Edema Fluids I C. L. Witte, M. H. "f itte, A. E. Dumont Departments of Surgery, University of Arizona College of Medicine, Tucson, Arizona and "'ewYorkl.Jniversity_School of Medicine, New York, N. Y. Lymphology 4 (1971), 29-31 The partition of extracellular fluid between plasma and tissues is largely regulated by the balance of hydrostatic an~ colloid osmotic (oncotic) pressure gradients across capillary membranes. Normally ~ small excess of tissue fluid forms, enters lymphatics and returns to the bloodstream. When an imbalance develops between the rate of lymph production and the rate of its return to the systemic venous circulation, edema.or effusion appear. Accumulation of edema, however, is not uniform in amount and composition throughout the body and depend, on the forces governing capillary filtration, regional differences in capillary permeabiFty, lymph flow and the specific factor tending to per­ petuate the edema. Obstruction td lymph return or disruption of capillary integrity (e.g. I infiltrating cancer or inflammation) promote effusion or edema high in protein content (so-called "exudate"). On the other hand, increased hydrostatic pressure in semiperme­ able capillaries promotes excess lymph and ultimately edema or effusion low in protein content (so-called "transudate"). iThe hepatic sinusoid is unique in its free permeability to plasma protein. Hepatic venous outflow obstruction, accordingly, produces excess hepatic and thoracic duct lymphi and eventually ascitic fluid, high in protein. In his monograph on The Fluids of the Body (1), Starling reasoned that increased capillary hydrostatic pressure Jas initially off set by a fall in tissue oncotic pressure. As the gradient in hydrostatic pressure rises in semipermeable capillary beds a progres­ sively more dilute capillary filtrate forms in tissues.
    [Show full text]
  • 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
    [Show full text]
  • 13-CAPILLARY CIRCULATIOJN.Pdf
    Very important Extra information * Guyton corners, anything that is colored with grey is EXTRA explanation Capillary Circulation Objectives : • Describe the structure of capillary wall: endothelial cells, basement membrane, intercellular clefts, vesicles, pores. • Blood brain barrier to water soluble agents. • Describe structure of liver and renal capillaries. • Compare and contrast diffusion and filtration. • State the Starling forces acting on the capillary wall: capillary blood pressure, interstitial fluid pressure, plasma protein colloid osmotic pressure, interstitial fluid colloid osmotic pressure. • Describe net loss of fluid from capillaries and discuss role of lymphatics. • Discuss importance of filtration giving clinical situations. • Define odema, state its causes and discuss its mechanisms. * We recommend studying Histology of Capillaries before this lecture 2 Contact us : [email protected] Functions of the circulation Serve the requirements of the tissues: 1- Transport nutrients & remove waste products. 2- Transport hormones, enzymes, body heat, electrolytes …etc. 3- Maintain normal homeostasis for optimal survival &function of cells. 3 Functional Parts of the circulation It is divided to : 1. Aorta : (Elastic recoil) 2. Arteries : Transport blood Rapidly under high pressure to the tissues (muscular, low resistance vessels) (Thick) 3. Arterioles : Can close the arteriole completely or dilate it several folds they alter blood flow to the capillaries in Response to needs(Thick). -Arterioles & small arteries are called (Resistance vessels) (high resistance vessels). 4. Capillaries: Have numerous Capillary pores and very large surface area (exchange blood vessels) for exchange of gases, nutrients, waste products etc. (Very thin wall with unicellular layer of endothelial cells and very small internal diameter). -Blood flow is intermittent (discontinuous) , turn on and off every few seconds or minutes (vasomotion), determined by oxygen demand.
    [Show full text]
  • 4 Edema in Childhood
    Kidney International, Vol. 51, Suppl. 59 (1997). pp. S-100-S-104 (1) Red Hypo Ne] Liv Edema in childhood Ma Pre Sev SATOSHI HISANO, SEUNGHOON HAHN, NANCY B. KUEMMERLE, JAMES CM. CHAN, (2) Incr. and NATALE G. DESANTO Cardi He: h Pediatric Nephrology Division, Virginia Commonwealth University's Medical College of Virginia, Richmond, Virginia, USA, and Divisione di Nefrologia Art dell' Adulto e del Bambino, Seconda Universita'degli Studi di Napoli, Naples, Italy Renal Act ACt Idiops Fan Edema in childhood. There are two types of edema: localized edema sympathetic nervous system (SNS) activity; and (3) antidiuretic Nor and generalized edema. The causes ofgeneralized edema in childhoodare hormone (ADH) release [4-6]. These forces and perhaps as yet diverse. Formation of generalizededema involves retention of sodium and Prej unidentified factors give rise to the consequential water and water in the kidney. The treatment of generalized edema depends on the (3) Incre primary etiology. Supportive nutritional and medicaltherapies are needed sodium retention, which promotes the development of edema, Allerg to prevent further edema. These and related features of edema in The sodium and water retention leads to further decreased Vascu childhood are discussed in this review. den plasma oncotic pressure, setting up a vicious cycle perpetuating dise the edema formation. The movement of water from intracellular space to interstitial space by itself also contributes to the devel­ opment of edema formation [1, 3]. Edema can be defined as the presence of excess fluid in the In contrast, the mechanism of "overfilling edema" is expanded interstitial space of the body. Edema is divided into two types, extracellular volume that results from primary renal sodium localized edema and generalized edema.
    [Show full text]