Electrolyte and Acid-Base
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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. -
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 -
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. -
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 . -
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. -
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 -
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. -
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 -
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. -
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. -
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). -
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.