DOCSLIB.ORG

Electrolyte and Acid-Base

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Electrolyte and Acid-Base Special Feature American Society of Nephrology Quiz and Questionnaire 2013: Electrolyte and Acid-Base Biff F. Palmer,* Mark A. Perazella,† and Michael J. Choi‡ Abstract The Nephrology Quiz and Questionnaire (NQ&Q) remains an extremely popular session for attendees of the annual meeting of the American Society of Nephrology. As in past years, the conference hall was overflowing with interested audience members. Topics covered by expert discussants included electrolyte and acid-base disorders, *Department of Internal Medicine, glomerular disease, ESRD/dialysis, and transplantation. Complex cases representing each of these categories University of Texas along with single-best-answer questions were prepared by a panel of experts. Prior to the meeting, program Southwestern Medical directors of United States nephrology training programs answered questions through an Internet-based ques- Center, Dallas, Texas; † tionnaire. A new addition to the NQ&Q was participation in the questionnaire by nephrology fellows. To review Department of Internal Medicine, the process, members of the audience test their knowledge and judgment on a series of case-oriented questions Yale University School prepared and discussed by experts. Their answers are compared in real time using audience response devices with of Medicine, New the answers of nephrology fellows and training program directors. The correct and incorrect answers are then Haven, Connecticut; ‡ briefly discussed after the audience responses, and the results of the questionnaire are displayed. This article and Division of recapitulates the session and reproduces its educational value for the readers of CJASN. Enjoy the clinical cases Nephrology, Department of and expert discussions. Medicine, Johns Clin J Am Soc Nephrol 9: 1132–1137, 2014. doi: 10.2215/CJN.11731113 Hopkins University, Baltimore, Maryland Correspondence: Introduction: Mark A. Perazella and Michael complicated and challenging electrolyte/acid-base Dr. Biff F. Palmer, J. Choi (Comoderators) cases. Overall, an educational experience was had Department of For most American Society of Nephrology Kidney by all participants. We hope that this “distillate” Internal Medicine, Week attendees, case-based clinical nephrology talks CJASN University of Texas from Atlanta will serve the subscribers well Southwestern Medical are the most exciting venues of the meeting. The Ne- and provide some fresh insights into the complex- Center, 5323 Harry phrology Quiz and Questionnaire (NQ&Q) is the ity and vibrancy of clinical nephrology for those Hines Boulevard, essence of clinical nephrology and represents what who were unable to attend the meeting (Mark A. Dallas, TX 75390. drew many of us into the field of nephrology. The Email: biff.palmer@ Perazella, MD, Yale University, Comoderator, and utsouthwestern.edu 2013 NQ&Q in Atlanta, Georgia, with full-house at- Michael Choi, MD, Johns Hopkins University, tendance, was no exception. Each of the discussants Comoderator). prepared vignettes of puzzling cases, each illustrat- ing some topical, challenging, or controversial as- pect of the diagnosis or management of various Electrolyte Case 1: Biff F. Palmer (Discussant) areas of nephrology. These eight interesting cases A 19-year-old woman is transported to the emergency were presented and eloquently discussed by our department after being found on the floor of her four expert The American Society of Nephrology apartment unable to move. The patient states she was in (ASN) faculty. Subsequently, each discussant pre- her usual state of health up until 36 hours earlier, when pared a manuscript summarizing his or her discus- she noticed the onset of episodic but progressively sion of the cases, which serves as the main text of this worsening generalized weakness. There was no history of article. bladder or bowel incontinence or loss of consciousness. In this NQ&Q, Dr. Biff Palmer presents his two Medical history was unremarkable, and the patient challenging electrolyte/acid-base cases and elo- reported no ingestions; however, the roommate who quently synthesizes the available data to make the accompanies her says she has been acting “alittle correct diagnosis. The audience responses are re- crazy” recently. Vital signs on admission showed a tem- viewed along with the responses of training program perature of 37°C, BP of 110/60 mmHg, and pulse of directors and nephrology fellows obtained before the 95 beats/min. Physical examination is remarkable meeting. This review provides an interesting perspec- for erythematous discoloration around her lips and tive into the thought processes of nephrologists with nose and erythema of the oral and pharyngeal mucosa. varying levels of training and experience. Dr. Palmer Conjunctival injections are present. There is 2/6 reviews essential clinical and laboratory data avail- weakness in both upper and lower extremities and able in the cases and walks the reader through the generalized hyporeflexia. Laboratory data are given in diagnosis and appropriate management of these two Table 1. 1132 Copyright © 2014 by the American Society of Nephrology www.cjasn.org Vol 9 June, 2014 Clin J Am Soc Nephrol 9: 1132–1137, June, 2014 Quiz and Questionnaire 2013, Palmer 1133 choice C the correct answer (Figure 1). Signs of inhalant Table 1. Laboratory data for Case 1 abuse include drying and redness around the mouth and nose, spots or sores around the mouth, and red or runny Laboratory Test Value eyes or nose. Inhalant abuse now includes a broad range Serum creatinine (mg/dl) 1.8 of volatile solvents and gas products to include model BUN (mg/dl) 38 airplane glue, paint thinner, gasoline, and nail polish Serum electrolytes (mEq/L) remover. Na+ 136 Examination of the metabolic profile discloses evidence K+ 1.5 2 of a triple acid-base disturbance composed of anion gap Cl 105 metabolic acidosis, hyperchloremic normal gap metabolic HCO3 10 acidosis, and respiratory acidosis. One should systemati- Arterial blood gas on room air cally interpret serum chemistries in order to identify the pH 7.1 overt and, more important, the subtle abnormalities that pCO2 35 pO 110 may exist in a laboratory report (1). 2 fi Glucose (mg/dl) 132 In this regard, a useful starting point is to rst examine Albumin (g/dl) 4.2 the serum Na+ concentrationinordertodetermine Urine electrolytes (mEq/L) whether a disturbance in the plasma tonicity is present. Na+ 42 This patient’s serum Na+ is mildly reduced, suggesting a K+ 38 2 relative excess of free water. Despite the downward trend Cl 65 in Na+, the serum Cl2 concentration is increased. Changes in Urine pH 6.0 hydration status alone will cause the serum Cl2 to change in Urine urea (mg/dl) 38 parallel and to the same extent as the serum Na+ concentra- Urine osmolality (mOsm/kg) 610 tion. Whenever the serum Cl2 moves in a direction opposite or changes disproportionately to the change in serum Na+, an acid-base disorder is suggested. In this patient, the serum Question 1 Cl2 is increased with respect to the serum Na+, suggesting Which one of the following best describes the acid-base the presence of chronic respiratory alkalosis or normal anion findings in this case? gap metabolic acidosis (2). The next step is to calculate the serum anion gap. A. Proximal renal tubular acidosis Calculation of the anion gap should be a routine part of B. Renal tubular acidosis of renal insufficiency the examination of every set of electrolytes, no matter how C. Overproduction of an organic acid normal the individual values may appear. In this case, the D. Distal renal tubular acidosis anion gap is 21 mEq/L, thus identifying the presence of an anion gap metabolic acidosis as at least one of the Discussion of Case 1 acid-base disturbances in this case. This 19-year-old woman presents with severe weakness Given the anion gap metabolic acidosis, the next step is 2 in the setting of hypokalemia and metabolic acidosis to determine whether the measured serum HCO3 is equal 2 resulting from deliberate inhalation of toluene. As dis- to the predicted serum HCO3 . In general, the serum 2 cussed in more detail below, the mechanism by which the HCO3 concentration will fall by an amount equal to the acid-base disturbance develops in this setting can best be increase in anion gap. Assuming a normal value of 12, the described as overproduction of an organic acid, making anion gap has increased by 9 in this patient. One would Figure 1. | Question 1: Distribution of answers from fellows in training, training program directors (TPD), and audience members at the Kidney Week meeting. The correct answer is C. 1134 Clinical Journal of the American Society of Nephrology 2 predict the serum HCO3 should be approximately 15 of urinary ammonium by calculating the urinary anion mEq/L, assuming a normal value of 24 mEq/L (2429=15). gap (UAG): Because the measured value is 10 mEq/L, one can con- þ þ 2 clude that a normal gap hyperchloremic metabolic acido- UAG ¼ðUrine Na þ Urine K Þ 2 Urine Cl sis is also present, as suggested by the disproportionate rise in serum Cl2 concentration noted above. The expected Under normal circumstances the UAG is positive, with 2 respiratory compensation for a measured HCO3 of 10 values ranging from 30 to 50. A negative value for the UAG mEq/L in the setting of metabolic acidosis would be a suggests the presence of increased renal excretion of an + + pCO2 of approximately 25 mmHg. The measure value of unmeasured cation, a cation other than Na or K . One + 35 mmHg indicates insufficient respiratory compensation such cation is NH4 . Metabolic acidosis of extrarenal origin and confirms the presence of respiratory acidosis. The re- is associated with a marked increase in urinary ammonium mainder of the discussion will focus on the cause of each of excretion, and therefore a large negative value will be the acid-base disorders identified in this patient with tolu- obtained for the UAG.
Load more

Recommended publications
  • CURRENT Essentials of Nephrology & Hypertension
    a LANGE medical book CURRENT ESSENTIALS: NEPHROLOGY & HYPERTENSION Edited by Edgar V. Lerma, MD Clinical Associate Professor of Medicine Section of Nephrology Department of Internal Medicine University of Illinois at Chicago College of Medicine Associates in Nephrology, SC Chicago, Illinois Jeffrey S. Berns, MD Professor of Medicine and Pediatrics Associate Dean for Graduate Medical Education The Perelman School of Medicine at the University of Pennsylvania Philadelphia, Pennsylvania Allen R. Nissenson, MD Emeritus Professor of Medicine David Geffen School of Medicine at UCLA Los Angeles, California Chief Medical Offi cer DaVita Inc. El Segundo, California New York Chicago San Francisco Lisbon London Madrid Mexico City Milan New Delhi San Juan Seoul Singapore Sydney Toronto Lerma_FM_p00i-xvi.indd i 4/27/12 10:33 AM Copyright © 2012 by The McGraw-Hill Companies, Inc. All rights reserved. Except as permitted under the United States Copyright Act of 1976, no part of this publication may be reproduced or distributed in any form or by any means, or stored in a database or retrieval system, without the prior written permission of the publisher. ISBN: 978-0-07-180858-3 MHID: 0-07-180858-2 The material in this eBook also appears in the print version of this title: ISBN: 978-0-07-144903-8, MHID: 0-07-144903-5. All trademarks are trademarks of their respective owners. Rather than put a trademark symbol after every occurrence of a trademarked name, we use names in an editorial fashion only, and to the benefi t of the trademark owner, with no intention of infringement of the trademark.
    [Show full text]
  • A Lady with Renal Stones
    A lady with renal stones Dr KC Lo, Dr KY Lo, Dr SK Mak KWH History 53/F NSND, NKDA Good past health Complained of bilateral loin pain for few years No urinary symptoms/UTIs No haematuria Not on regular medications/vitamins No significant family history History Attended private practitioner in Feb, 2006: Blood test : Na/K 143/3.9 Ur/Cr 7.3/101 LFT N Urine test : RBC numerous/HPF WBC 5-8/HPF CXR unremarkable Given analgesics History Still on-and-off bilateral loin and lower chest pain Seek advice from Private Hospital: Blood test: WBC 3.2 Hb 12.9 Plt 139 Na/K 146/ 3.0 Ur/Cr 6.3/108 Ca2+/PO4 2.11/1.39 LFT unremarkable Urine test : RBC 6-8/HPF, WBC 0-1/HPF no cast KUB: bilateral renal stones (as told by patient) History ESWL done to right renal stone in 5/06, planned to have ESWL to left stone later But she then defaulted FU History This time admitted to our surgical ward complaining of similar bilateral lower chest wall pain (for six months) Had vomiting of undigested food 8 times per day for 1 day, no diarrhoea No fever Recent intake of herbs one week ago Physical exam BP 156/77 P 68 afebrile Hydration normal Chest, CVS unremarkable Local tenderness over bilateral lower chest wall Abdomen soft, mild epigastric tenderness, no rebound and guarding KUB Multiple tiny calcific densities projecting in bilateral renal areas with apparent distribution of the renal medulla bilateral medullary nephrocalcinosis CT Scan 1 yr ago in private CT Scan 1 yr ago in private Investigations WBC 3.1 HB 13.1 Plt 137 Na
    [Show full text]
  • Cerebral Salt Wasting Syndrome and Systemic Lupus Erythematosus: Case Report
    Elmer ress Case Report J Med Cases. 2016;7(9):399-402 Cerebral Salt Wasting Syndrome and Systemic Lupus Erythematosus: Case Report Filipe Martinsa, c, Carolina Ouriquea, Jose Faria da Costaa, Joao Nuakb, Vitor Braza, Edite Pereiraa, Antonio Sarmentob, Jorge Almeidaa Abstract disorders, that results in hyponatremia and a decrease in ex- tracellular fluid volume. It is characterized by a hypotonic hy- Cerebral salt wasting (CSW) is a rare cause of hypoosmolar hypona- ponatremia with inappropriately elevated urine sodium con- tremia usually associated with acute intracranial disease character- centration in the setting of a normal kidney function [1-3]. ized by extracellular volume depletion due to inappropriate sodium The onset of this disorder is typically seen within the first wasting in the urine. We report a case of a 46-year-old male with 10 days following a neurological insult and usually lasts no recently diagnosed systemic lupus erythematosus (SLE) initially pre- more than 1 week [1, 2]. Pathophysiology is not completely senting with neurological involvement and an antiphospholipid syn- understood but the major mechanism might be the inappropri- drome (APS) who was admitted because of chronic asymptomatic ate and excessive release of natriuretic peptides which would hyponatremia previously assumed as secondary to syndrome of inap- result in natriuresis and volume depletion. A secondary neu- propriate antidiuretic hormone secretion (SIADH). Initial evaluation rohormonal response would result in an increase in the renin- revealed a hypoosmolar hyponatremia with high urine osmolality angiotensin system and consequently in antidiuretic hormone and elevated urinary sodium concentration. Clinically, the patient’s (ADH) production. Since the volume stimulus is more potent extracellular volume status was difficult to define accurately.
    [Show full text]
  • Parenteral Nutrition Primer: Balance Acid-Base, Fluid and Electrolytes
    Parenteral Nutrition Primer: Balancing Acid-Base, Fluids and Electrolytes Phil Ayers, PharmD, BCNSP, FASHP Todd W. Canada, PharmD, BCNSP, FASHP, FTSHP Michael Kraft, PharmD, BCNSP Gordon S. Sacks, Pharm.D., BCNSP, FCCP Disclosure . The program chair and presenters for this continuing education activity have reported no relevant financial relationships, except: . Phil Ayers - ASPEN: Board Member/Advisory Panel; B Braun: Consultant; Baxter: Consultant; Fresenius Kabi: Consultant; Janssen: Consultant; Mallinckrodt: Consultant . Todd Canada - Fresenius Kabi: Board Member/Advisory Panel, Consultant, Speaker's Bureau • Michael Kraft - Rockwell Medical: Consultant; Fresenius Kabi: Advisory Board; B. Braun: Advisory Board; Takeda Pharmaceuticals: Speaker’s Bureau (spouse) . Gordon Sacks - Grant Support: Fresenius Kabi Sodium Disorders and Fluid Balance Gordon S. Sacks, Pharm.D., BCNSP Professor and Department Head Department of Pharmacy Practice Harrison School of Pharmacy Auburn University Learning Objectives Upon completion of this session, the learner will be able to: 1. Differentiate between hypovolemic, euvolemic, and hypervolemic hyponatremia 2. Recommend appropriate changes in nutrition support formulations when hyponatremia occurs 3. Identify drug-induced causes of hypo- and hypernatremia No sodium for you! Presentation Outline . Overview of sodium and water . Dehydration vs. Volume Depletion . Water requirements & Equations . Hyponatremia • Hypotonic o Hypovolemic o Euvolemic o Hypervolemic . Hypernatremia • Hypovolemic • Euvolemic • Hypervolemic Sodium and Fluid Balance . Helpful hint: total body sodium determines volume status, not sodium status . Examples of this concept • Hypervolemic – too much volume • Hypovolemic – too little volume • Euvolemic – normal volume Water Distribution . Total body water content varies from 50-70% of body weight • Dependent on lean body mass: fat ratio o Fat water content is ~10% compared to ~75% for muscle mass .
    [Show full text]
  • Guidelines for Approach to a Child with Metabolic Acidosis (Including RTA)
    Guidelines for approach to a child with Metabolic acidosis (including RTA) Children’s Kidney Centre University Hospital of Wales Cardiff CF14 4XW DISCLAIMER: These guidelines were produced in good faith by the authors reviewing available evidence/opinion. They were designed for use by paediatric nephrologists at the University Hospital of Wales, Cardiff for children under their care. They are neither policies nor protocols but are intended to serve only as guidelines. They are not intended to replace clinical judgment or dictate care of individual patients. Responsibility and decision-making (including checking drug doses) for a specific patient lie with the physician and staff caring for that particular patient. Version 1, S. Hegde/Sept 2007 Metabolic acidosis ormal acid base balance Maintaining normal PH is essential for cellular enzymatic and other metabolic functions and normal growth and development. Although it is the intracellular PH that matter for cell function, we measure extra cellular PH as 1. It is easier to measure 2. It parallels changes in intracellular PH 3. Subject to more variation because of lesser number of buffers extra cellularly. Normal PH is maintained by intra and extra cellular buffers, lungs and kidneys. Buffers attenuate changes in PH when acid or alkali is added to the body and they act by either accepting or donating Hydrogen ions. Buffers function as base when acid is added or as acid when base is added to body. Main buffers include either bicarbonate or non-bicarbonate (proteins, phosphates and bone). Source of acid load: 1. CO2- Weak acid produced from normal metabolism, dealt with by lungs pretty rapidly(within hours) 2.
    [Show full text]
  • ACP NATIONAL ABSTRACTS COMPETITIONS MEDICAL STUDENTS 2019 Table of Contents
    ACP NATIONAL ABSTRACTS COMPETITIONS MEDICAL STUDENTS 2019 Table of Contents MEDICAL STUDENT RESEARCH PODIUM PRESENTATIONS ...................................................................... 8 COLOMBIA RESEARCH PODIUM PRESENTATION - Andrey Sanko ........................................................ 9 Clinical Factors Associated with High Glycemic Variability Defined by the Variation Coefficient in Patients with Type 2 Diabetes .......................................................................................................... 9 MARYLAND RESEARCH PODIUM PRESENTATION - Asmi Panigrahi ................................................... 11 Influence of Individual-Level Neighborhood Factors on Health Promoting and Risk Behaviors in the Hispanic Community Health Study/Study of Latinos (HCHS/SOL) ........................................... 11 NEW YORK RESEARCH PODIUM PRESENTATION - Kathryn M Linder ................................................ 13 Implementation of a Medical Student-Led Emergency Absentee Ballot Voting Initiative at an Urban Tertiary Care University Hospital ......................................................................................... 13 OREGON RESEARCH PODIUM PRESENTATION - Sherry Liang ............................................................ 15 A Novel Student-Led Improvement Science Curriculum for Pre-Clinical Medical Students .......... 15 TENNESSEE RESEARCH PODIUM PRESENTATION - Zara Latif ............................................................. 17 Impaired Brain Cells Response in Obesity
    [Show full text]
  • Severe Hyponatremia in a COVID-19 Patient
    http://crim.sciedupress.com Case Reports in Internal Medicine 2020, Vol. 7, No. 3 CASE REPORTS Severe hyponatremia in a COVID-19 patient Waqar Haider Gaba∗1, Sara Al Hebsi2, Rania Abu Rahma3 1Consultant Physician Internal Medicine, Sheikh Khalifa Medical, Abu Dhabi, United Arab Emirates 2Medical Resident Internal Medicine, Sheikh Khalifa Medical, Abu Dhabi, United Arab Emirates 3Nephrology Specialist, Sheikh Khalifa Medical, Abu Dhabi, United Arab Emirates Received: August 13, 2020 Accepted: August 31, 2020 Online Published: September 23, 2020 DOI: 10.5430/crim.v7n3p15 URL: https://doi.org/10.5430/crim.v7n3p15 ABSTRACT Hyponatremia is one of the most common electrolyte abnormalities found in hospitalized patients. The diagnosis of the underlying cause of hyponatremia could be challenging. However, common causes include the syndrome of inappropriate anti-diuretic hormone (SIADH), diuretic use, polydipsia, adrenal insufficiency, hypovolemia, heart failure, and liver cirrhosis. The ongoing pandemic of coronavirus disease 2019 (COVID-19) can present with severe hyponatremia. The association of hyponatremia and COVID-19 infection has been described, though pathophysiology is not clear. Here we describe a case of a 61-year-old male who presented with severe hyponatremia (Na+ 100 mmol/L) thought to be secondary to SIADH associated with COVID-19 pneumonia. Key Words: Hyponatremia, COVID-19, Syndrome of Inappropriate Antidiuretic Hormone (SIADH) 1.I NTRODUCTION sense RNA virus. It causes mild respiratory symptoms simi- lar to a common cold. Around 50% of COVID-19 positive Hyponatremia is defined as a serum sodium concentration patients were found to have hyponatremia on admission.[2] < 135 mEq/L. Clinical presentation could vary from mild to severe or life-threatening.
    [Show full text]
  • Hypercalcemia and Hyponatremia
    Hypercalcemia and Hyponatremia Santosh Reddy MD FACP Assistant Professor Scott & White/Texas A&M Etiology of Hypercalcemia Hypercalcemia results when the entry of calcium into the circulation exceeds the excretion of calcium into the urine or deposition in bone. Sources of calcium are most commonly the bone or the gastrointestinal tract Etiology Hypercalcemia is a relatively common clinical problem. Elevation in the physiologically important ionized (or free) calcium concentration. However, 40 to 45 percent of the calcium in serum is bound to protein, principally albumin; , increased protein binding causes elevation in the serum total calcium. Increased bone resorption Primary and secondary hyperparathyroidism Malignancy Hyperthyroidism Other - Paget's disease, estrogens or antiestrogens in metastatic breast cancer, hypervitaminosis A, retinoic acid Increased intestinal calcium absorption Increased calcium intake Renal failure (often with vitamin D supplementation) Milk-alkali syndrome Hypervitaminosis D Enhanced intake of vitamin D or metabolites Chronic granulomatous diseases (eg, sarcoidosis) Malignant lymphoma Acromegaly Pseudocalcemia Hyperalbuminemia 1) severe dehydration 2) multiple myeloma who have a calcium- binding paraprotein. This phenomenon is called pseudohypercalcemia (or factitious hypercalcemia) Other causes Familial hypocalciuric hypercalcemia Chronic lithium intake Thiazide diuretics Pheochromocytoma Adrenal insufficiency Rhabdomyolysis and acute renal failure Theophylline toxicity Immobilization
    [Show full text]
  • Pathophysiology of Water Electrolyte Metabolism
    PATHOPHYSIOLOGY OF WATER ELECTROLYTE METABOLISM. PATHOPHYSIOLOGY OF MINERAL METABOLISM. I. PLAN OF STUDY OF THE TOPIC. 1. Changes in water distribution and water volume. 2. Types of dehydration, causes and mechanisms of development. 3. Effect of dehydration on the body. 4. Edema and dropsy: definition, classification. 5. Mechanisms of edema development: pathogenic factors and pathogenesis of different types of edema. 6. Significance of edema for organism. 7. Etiological and pathogenetic principles of edema and dehydration treatment. 8. Disturbance of trace elements metabolism. 9. Disturbance of macronutrients metabolism. II. QUATIONS FOR SELFCONTROL. 1. Types of water balance disturbances. 2. Extracellular water sector. 3. Basic mechanisms of volume water sectors changes. 4. Types of dehydration according to mechanisms of development. 5. Mechanisms of dehydration caused by primary absolute lack of water. 6. Types of dehydration according to speed of water losing. 7. Types of dehydration according to degree of water or electrolyte lack. 8. Pathological conditions when develops " water deficiency due to of limited water supply." 9. Manifestations of intracellular dehydration. 10. Main mechanisms of dehydration from due to a lack of electrolytes. 11. Main causes of hyperosmolar dehydration in the loss of electrolytes through the gastrointestinal tract. 12. Phenomena arising from the violation of the blood supply to the nervous tissue during dehydration. 13. Definition of edema. 14. Classification of edema according to prevalence. 15. Classification of edema according to speed of development. 16. Classification of edema according to pathogenesis. 17. Classification of edema according to etiology. 18. Definition of dropsy. 19. Types of dropsy. 20. Types of lymphatic insufficiency. 21.
    [Show full text]
  • The Journey of Kidney Disease
    2/8/2021 THE JOURNEY OF KIDNEY DISEASE • BY LORETTA DICAMILLO DNP, MSN,RN • RENAL SPECIALISTS • FEBRUARY 6, 2021 FUNCTIONS OF THE KIDNEY The most Vascular organ of the body… Maintenance of body fluids Excretion of wastes Regulation of blood pressure Production of hormones 1 2/8/2021 STATISTICS U.S Department of Health and Human Services More than 726 thousand Americans in 2016 were on dialysis or living with a kidney transplant. Each day over 240 individuals on dialysis pass away. Chronic kidney disease (CKD) is more common in people age 65 and older. 40% of hospitalizations for acute kidney injury (AKI) were among persons with diabetes. The total number of hospitalizations have increased from 900 thousand in the year 2000 to over 3 million in the year 2014. RISKS OF AKI NON-MODIFIABLE MODIFIABLE CHRONIC LIVER DISEASE ANEMIA, HYPERTENSION CONGESTIVE HEART HYPONATREMIA FAILURE, DIABETES HYPOALBUMINEMIA > 65 YEARS OF AGE DRUG USAGE, SEPSIS PERIPHERICAL VASCULAR RHABDOMYOLYSIS DISEASE RENAL ARTERIAL STENOSIS 2 2/8/2021 STAGES OF AKI KDIGO GUIDELINES STAGE 1 STAGE 2 STAGE 3 CREATININE X 1.5 CREATININE X2 CREATININE X 3 BASELINE BASELINE BASELINE OR AN INCREASE TO > 4.0 >0.3 MG/DL URINE OUTPUT < 0.5 MG/DL OLIGURIA < 0.5 MG/KG/HR. FOR > 12 MG/KG/HR. X 6-12 HRS. HRS. ANURIA FOR >12 HRS. BY STAGE THREE PROBABLY NEED RENAL REPLACEMENT THERAPY (RRT) ETIOLOGIES OF AKI PRERENAL – 25% INTRINSIC - 65% PRE-RENAL INTRINSIC POST- ATI- 45% RENAL AKI ON CKD -13% Etiology Hypoperfusion True Kidney Obstruction GN OR VASCULITIS -4% Injury ATHEROEMBOLIC - 1% POSTRENAL – 10% FENa 1% 3.4% Low Yield 3 2/8/2021 PATHOPHYSIOLOGY COMMON ENDPOINT IN ALL TYPES OF ATI IS CELLULAR INSULT SECONDARY TO ISCHEMIA OR DIRECT TOXINS, EFFACEMENT OF THE BRUSH BORDER AND EVENTUALLY CELL DEATH, WHICH SHUTS DOWN THE FUNCTION OF TUBULAR CELLS.
    [Show full text]
  • Neurologic Complications of Electrolyte Disturbances and Acid–Base Balance
    Handbook of Clinical Neurology, Vol. 119 (3rd series) Neurologic Aspects of Systemic Disease Part I Jose Biller and Jose M. Ferro, Editors © 2014 Elsevier B.V. All rights reserved Chapter 23 Neurologic complications of electrolyte disturbances and acid–base balance ALBERTO J. ESPAY* James J. and Joan A. Gardner Center for Parkinson’s Disease and Movement Disorders, Department of Neurology, UC Neuroscience Institute, University of Cincinnati, Cincinnati, OH, USA INTRODUCTION hyperglycemia or mannitol intake, when plasma osmolal- ity is high (hypertonic) due to the presence of either of The complex interplay between respiratory and renal these osmotically active substances (Weisberg, 1989; function is at the center of the electrolytic and acid-based Lippi and Aloe, 2010). True or hypotonic hyponatremia environment in which the central and peripheral nervous is always due to a relative excess of water compared to systems function. Neurological manifestations are sodium, and can occur in the setting of hypovolemia, accompaniments of all electrolytic and acid–base distur- euvolemia, and hypervolemia (Table 23.2), invariably bances once certain thresholds are reached (Riggs, reflecting an abnormal relationship between water and 2002). This chapter reviews the major changes resulting sodium, whereby the former is retained at a rate faster alterations in the plasma concentration of sodium, from than the latter (Milionis et al., 2002). Homeostatic mech- potassium, calcium, magnesium, and phosphorus as well anisms protecting against changes in volume and sodium as from acidemia and alkalemia (Table 23.1). concentration include sympathetic activity, the renin– angiotensin–aldosterone system, which cause resorption HYPONATREMIA of sodium by the kidneys, and the hypothalamic arginine vasopressin, also known as antidiuretic hormone (ADH), History and terminology which prompts resorption of water (Eiskjaer et al., 1991).
    [Show full text]
  • Clinical Features, Genetic Background, and Outcome in Infants with Urinary Tract Infection and Type IV Renal Tubular Acidosis
    www.nature.com/pr CLINICAL RESEARCH ARTICLE Clinical features, genetic background, and outcome in infants with urinary tract infection and type IV renal tubular acidosis Min-Hua Tseng1, Jing-Long Huang2, Shih-Ming Huang3, Jeng-Daw Tsai4,5,6,7, Tai-Wei Wu8, Wen-Lang Fan9, Jhao-Jhuang Ding1,10 and Shih-Hua Lin11 BACKGROUND: Type IV renal tubular acidosis (RTA) is a severe complication of urinary tract infection (UTI) in infants. A detailed clinical and molecular analysis is still lacking. METHODS: Infants with UTI who exhibited features of type IV RTA were prospectively enrolled. Clinical, laboratory, and image characteristics and sequencing of genes responsible for phenotype were determined with follow-up. RESULTS: The study cohort included 12 infants (9 males, age 1–8 months). All exhibited typical type IV RTA such as hyperkalemia with low transtubular potassium gradient, hyperchloremic metabolic acidosis with positive urine anion gap, hypovolemic hyponatremia with renal salt wasting, and high plasma renin and aldosterone levels. Seven had hyperkalemia-related arrhythmia and two of them developed life-threatening ventricular tachycardia. With prompt therapy, all clinical and biochemical abnormalities resolved within 1 week. Five had normal urinary tract anatomy, and three of them carried genetic variants on NR3C2. Three variants, c.1645T>G (S549A), c.538G>A (V180I), and c.1-2C>G, on NR3C2 were identified in four patients. During follow-up, none of them had recurrent type IV RTA, but four developed renal scaring. CONCLUSIONS: Genetic mutation on NR3C2 may contribute to the development of type IV RTA as a complication of UTI in infants fi 1234567890();,: without identi able risk factors, such as urinary tract anomalies.
    [Show full text]