Urinalysis and Kidney Disease: What You Need to Know
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Acute Kidney Injury: Challenges and Opportunities
Acute kidney injury: Challenges and opportunities Abstract: Community-acquired acute kidney injury (CA-AKI) can be a devastating diagnosis for any patient and can increase mortality during hospitalization. There can be long-term consequences for those who survive the initial insult. This article discusses CA-AKI and its implications for APRNs. By Nhan L.A. Dinh, MSN, CNP, AGACNP-BC, CCRN cute kidney injury (AKI) is a heterogeneous risk of CKD, but if clinicians do not recognize the kidney disorder that increases in-hospital diagnosis, they cannot follow up or intervene. An AKI A morbidity and mortality. In 2016 data, the diagnosis also increases the chance of another AKI incidence of AKI was 20% for Medicare patients with episode, with a 30% risk of a recurrent AKI episode both chronic kidney disease (CKD) and diabetes.1 Us- within 1 year.1 ing Veterans Affairs (VA) 2016 data, AKI occurred in Mortality is increased with an AKI episode. Medi- more than 25% of hospitalized veterans over age 22, care data from 2016 shows an in-hospital mortality of but less than 50% of those with lab-documented AKI 8.2% but this increases to over 13% when includ- were coded as such.1 The chief concern here is a missed ing patients who were discharged to hospice.1 The in- opportunity for intervention. AKI increases long-term hospital mortality for patients without AKI was only Keywords: acute kidney injury (AKI), Acute Kidney Injury Network (AKIN), chronic kidney disease (CKD), community-acquired acute kidney injury (CA-AKI), hospital-acquired acute kidney injury (HA-AKI), Kidney Disease Improving Global Outcomes (KDIGO), SvetaZi / Shutterstock Nephrotoxic Injury Negated by Just-in-time Action (NINJA), sick day rules 48 The Nurse Practitioner • Vol. -
Detection of Continuous Erythropoietin Receptor Activator in Blood And
Letters to the Editor 5 A Pugliese-Ciaccio, Catanzaro; Dipartimento di Oncologia, 1.0 Biologia e Genetica Università degli Studi di Genova, Italy. Funding: supported from Associazione Italiana Ricerca sul Cancro 0.8 (AIRC) (to FM and MF) and Fondazione ‘Amelia Scorza’ β2-mneg Onlus, Cosenza, Italy. 0.6 Acknowledgments: we would like to acknowledge Dr. Vincenzo not treated Callea, Prof Luca Baldini, Dr Ugo Consoli and Dr Serena Matis 0.4 for their contribution and useful suggestions.We thank Laura Veroni and Brigida Gulino for precious secretarial assistance. Proportion 0.2 p=0.002 pos β β2-m Key words: 2-microglobulin, CD38, IgVH mutational status, CLL, prognosis. 0.0 Correspondence: Fortunato Morabito, Unità Operativa Complessa di Ematologia, Dipartimento di Medicina Interna, 0 3 6 9 12 15 Azienda Ospedaliera di Cosenza, Viale della Repubblica, years 87100 Cosenza, Italy. Phone: international +39.0984.681329. B Fax: international +39.0984.791751. Univariate analysis E-mail: [email protected] Risk categories HR (95% C.I., p value) Citation: Gentile M, Cutrona G, Neri A, Molica S, Ferrarini M, No factor 1 and Morabito F. Predictive value of B2-microglobulin (B2-m) levels One factor 1,5 (0.7-3.4, p=ns) in chronic lymphocytic leukemia since Binet A stages. Two factor 5.0 (2.5-10.2, p<0.0001) Haematologica 2009; 94:887-888. Three factors 15.4 (7.3-32.5, p<0.0001) doi:10.3324/haematol.2009.005561 C 1.0 References 0.8 1. Rossi D, Zucchetto A, Rossi FM, Capello D, Cerri M, no factor Deambrogi C, et al. -
Inherited Renal Tubulopathies—Challenges and Controversies
G C A T T A C G G C A T genes Review Inherited Renal Tubulopathies—Challenges and Controversies Daniela Iancu 1,* and Emma Ashton 2 1 UCL-Centre for Nephrology, Royal Free Campus, University College London, Rowland Hill Street, London NW3 2PF, UK 2 Rare & Inherited Disease Laboratory, London North Genomic Laboratory Hub, Great Ormond Street Hospital for Children National Health Service Foundation Trust, Levels 4-6 Barclay House 37, Queen Square, London WC1N 3BH, UK; [email protected] * Correspondence: [email protected]; Tel.: +44-2381204172; Fax: +44-020-74726476 Received: 11 February 2020; Accepted: 29 February 2020; Published: 5 March 2020 Abstract: Electrolyte homeostasis is maintained by the kidney through a complex transport function mostly performed by specialized proteins distributed along the renal tubules. Pathogenic variants in the genes encoding these proteins impair this function and have consequences on the whole organism. Establishing a genetic diagnosis in patients with renal tubular dysfunction is a challenging task given the genetic and phenotypic heterogeneity, functional characteristics of the genes involved and the number of yet unknown causes. Part of these difficulties can be overcome by gathering large patient cohorts and applying high-throughput sequencing techniques combined with experimental work to prove functional impact. This approach has led to the identification of a number of genes but also generated controversies about proper interpretation of variants. In this article, we will highlight these challenges and controversies. Keywords: inherited tubulopathies; next generation sequencing; genetic heterogeneity; variant classification. 1. Introduction Mutations in genes that encode transporter proteins in the renal tubule alter kidney capacity to maintain homeostasis and cause diseases recognized under the generic name of inherited tubulopathies. -
Hypertensive Kidney Disease Hypertensive Kidney
JAMA PATIENT PAGE The Journal of the American Medical Association KIDNEY DISEASE Hypertensive Kidney Disease ypertension (high blood pressure) causes problems for many organs in the body, including the kidneys. Kidney problems Hcaused by high blood pressure (hypertensive kidney disease) occur often in persons who have undetected, untreated, or poorly controlled hypertension. Kidney problems are also called renal dysfunction or renal failure. Certain groups of people, including African Americans and Native Americans, are more at risk for having hypertensive kidney disease. High blood pressure is the second leading cause of kidney failure, surpassed only by diabetes. African Americans are 6 times more likely than whites to have chronic renal failure related to high blood pressure. The November 20, 2002, issue of JAMA includes an article about high blood pressure and its effect on the kidneys. WHY IS HIGH BLOOD PRESSURE DANGEROUS? FOR MORE INFORMATION High blood pressure makes the heart work harder and can also damage the small blood • American Heart Association vessels in the body. These vessels are in all organs of the body, including the kidneys, the 800/242-8721 heart, and the brain. Damage to the arteries (blood vessels that carry blood to organs) www.americanheart.org results in insufficient blood flow to those organs and organ damage. In the kidney, this • National Institute of Diabetes & organ damage is called nephrosclerosis. The kidneys lose their ability to filter blood, Digestive & Kidney Diseases allowing buildup of substances that can be toxic to the body. Eventually the kidneys fail, www.niddk.nih.gov/health/kidney and dialysis (filtration of blood by a special machine) or a kidney transplant becomes /pubs/highblood/highblood.htm necessary to preserve the person’s life. -
Aldosterone Resistance; a Rare Differential Diagnosis for Persistent Hyperkalemia
MOJ Women’s Health Case Report Open Access Aldosterone resistance; a rare differential diagnosis for persistent hyperkalemia Abstract Volume 5 Issue 5 - 2017 In the human body, Aldosterone is an important hormone for sodium conservation in the kidneys, salivary glands, sweat glands and colon. Aldosterone is synthesized Muhammad Umair, Afsoon Razavi, Zehra exclusively in the zona glomerulosa of the adrenal gland. Significance of aldosterone Tekin, Issac Sachmechi production along with its appropriate action on the receptors is undeniable as far as Department of Medicine, Icahn School of Medicine, USA hemostasis of intracellular and extracellular electrolytes is concerned. Destruction or dysfunction of the adrenal gland in conditions such as primary adrenal insufficiency, Correspondence: Muhammad Umair, Department of congenital adrenal hypoplasia, isolated mineralocorticoid deficiency, acquired Medicine, Icahn School of Medicine at Mount Sinai/NYC Health secondary aldosterone deficiency (hyporeninemic hypoaldosteronism), acquired + Hospital/Queens Jamaica, Diabetes center, 4th floor, Suit primary aldosterone deficiency and inherited enzymatic defects in aldosterone P-432, pavilion building, Queens hospital center, 82-68 164th street, Jamaica, New York, USA, Tel +15163436454, biosynthesis cause clinical symptoms and laboratory characteristics owing to Email [email protected] aldosterone deficiency. Pseudohypoaldosteronism is an aldosterone resistance syndrome i.e. a condition due to insensitivity of target tissues to aldosterone resulting Received: July 25, 2017 | Published: August 09, 2017 in hyponatremia, hyperkalemia and metabolic acidosis. For a proper diagnosis of Aldosterone resistance; serum Sodium levels, serum Potassium levels, ACTH levels, plasma Renin and Aldosterone activity along with serum Cortisol levels play key roles. High doses of Fludrocortisone therapy helps in overcoming aldosterone resistance and assist in maintaining electrolyte balance in the body. -
GFR (Glomerular Filtration Rate) a Key to Understanding How Well Your Kidneys Are Working
GFR (Glomerular Filtration Rate) A Key to Understanding How Well Your Kidneys Are Working www.kidney.org About the Information in this Booklet Did you know that the National Kidney Foundation (NKF) offers guidelines and commentaries that help your healthcare provider make decisions about your medical treatment? The information in this booklet is based on those recommended guidelines. Stages of Kidney Disease There are five stages of kidney disease. They are shown in the table below. Your healthcare provider determines your stage of kidney disease, based on the presence of kidney damage and your glomerular filtration rate (GFR), which is a measure of your kidney function. Your treatment is based on your stage of kidney disease. Speak to your healthcare provider if you have any questions about your stage of kidney disease or your treatment. STAGES OF KIDNEY DISEASE Glomerular Stage Description Filtration Rate (GFR)* Kidney damage (e.g., protein 1 90 or above in the urine) with normal GFR Kidney damage with mild 2 60 to 89 decrease in GFR 3 Moderate decrease in GFR 30 to 59 4 Severe reduction in GFR 15 to 29 5 Kidney failure Less than 15 *Your GFR number tells your healthcare provider how much kidney function you have. As chronic kidney disease progresses, your GFR number decreases. 2 NATIONAL KIDNEY FOUNDATION Why is GFR Important? Most people are aware that their blood pressure and cholesterol numbers are important in knowing their risk for heart and blood vessel disease. Yet few know about glomerular filtration rate (GFR), one of the numbers that tells them about the health of their kidneys. -
Uremic Toxins Affect Erythropoiesis During the Course of Chronic
cells Review Uremic Toxins Affect Erythropoiesis during the Course of Chronic Kidney Disease: A Review Eya Hamza 1, Laurent Metzinger 1,* and Valérie Metzinger-Le Meuth 1,2 1 HEMATIM UR 4666, C.U.R.S, Université de Picardie Jules Verne, CEDEX 1, 80025 Amiens, France; [email protected] (E.H.); [email protected] (V.M.-L.M.) 2 INSERM UMRS 1148, Laboratory for Vascular Translational Science (LVTS), UFR SMBH, Université Sorbonne Paris Nord, CEDEX, 93017 Bobigny, France * Correspondence: [email protected]; Tel.: +33-2282-5356 Received: 17 July 2020; Accepted: 4 September 2020; Published: 6 September 2020 Abstract: Chronic kidney disease (CKD) is a global health problem characterized by progressive kidney failure due to uremic toxicity and the complications that arise from it. Anemia consecutive to CKD is one of its most common complications affecting nearly all patients with end-stage renal disease. Anemia is a potential cause of cardiovascular disease, faster deterioration of renal failure and mortality. Erythropoietin (produced by the kidney) and iron (provided from recycled senescent red cells) deficiencies are the main reasons that contribute to CKD-associated anemia. Indeed, accumulation of uremic toxins in blood impairs erythropoietin synthesis, compromising the growth and differentiation of red blood cells in the bone marrow, leading to a subsequent impairment of erythropoiesis. In this review, we mainly focus on the most representative uremic toxins and their effects on the molecular mechanisms underlying anemia of CKD that have been studied so far. Understanding molecular mechanisms leading to anemia due to uremic toxins could lead to the development of new treatments that will specifically target the pathophysiologic processes of anemia consecutive to CKD, such as the newly marketed erythropoiesis-stimulating agents. -
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. -
Renal Effects of Atrial Natriuretic Peptide Infusion in Young and Adult ~Ats'
003 1-3998/88/2403-0333$02.00/0 PEDIATRIC RESEARCH Vol. 24, No. 3, 1988 Copyright O 1988 International Pediatric Research Foundation, Inc. Printed in U.S.A. Renal Effects of Atrial Natriuretic Peptide Infusion in Young and Adult ~ats' ROBERT L. CHEVALIER, R. ARIEL GOMEZ, ROBERT M. CAREY, MICHAEL J. PEACH, AND JOEL M. LINDEN WITH THE TECHNICAL ASSISTANCE OF CATHERINE E. JONES, NANCY V. RAGSDALE, AND BARBARA THORNHILL Departments of Pediatrics [R.L.C., A.R.G., C.E.J., B. T.], Internal Medicine [R.M.C., J.M. L., N. V.R.], Pharmacology [M.J.P.], and Physiology [J.M.L.], University of Virginia, School of Medicine, Charlottesville, Virginia 22908 ABSTRAm. The immature kidney appears to be less GFR, glomerular filtration rate responsive to atrial natriuretic peptide (ANP) than the MAP, mean arterial pressure mature kidney. It has been proposed that this difference UeC~pV,urinary cGMP excretion accounts for the limited ability of the young animal to UN,V, urinary sodium excretion excrete a sodium load. To delineate the effects of age on the renal response to exogenous ANP, Sprague-Dawley rats were anesthetized for study at 31-32 days of age, 35- 41 days of age, and adulthod. Synthetic rat A* was infused intravenously for 20 min at increasing doses rang- By comparison to the adult kidney, the immature kidney ing from 0.1 to 0.8 pg/kg/min, and mean arterial pressure, responds to volume expansion with a more limited diuresis and glomerular filtration rate, plasma ANP concentration, natriuresis (I). A number of factors have been implicated to urine flow rate, and urine sodium excretion were measured explain this phenomenon in the neonatal kidney, including a at each dose. -
Pyelonephritis (Kidney Infection)
Pyelonephritis (Kidney Infection) Cathy E. Langston, DVM, DACVIM (Small Animal) BASIC INFORMATION urine collected from the bladder to be negative despite infection in the Description kidney. Abdominal x-rays and an ultrasound may be recommended. Bacterial infection of the kidney is termed pyelonephritis . Infection Although culture of a piece of kidney tissue obtained by biopsy may occur within kidney tissue or in the renal pelvis, the area of increases the chance of finding the infection, the invasiveness of the kidney where urine collects before being transported to the the procedure makes it too risky for general use (the biopsy would bladder. need to be taken from deeper within the kidney than the average Causes kidney biopsy). Contrast x-ray studies, such as an excretory uro- In most cases, a urinary tract infection starts in the bladder and gram (intravenous pyelogram), are sometimes helpful. An excre- the bacteria travel upstream to the kidney. Anything that decreases tory urogram involves taking a series of x-rays after a dye (that the free flow of urine, such as obstruction of the urethra (tube shows up white on x-rays) is given intravenously. Other tests may that carries urine from the bladder to the outside), bladder, ureter be recommended to rule out diseases that cause similar clinical (tube that carries urine from the kidney to the bladder), or kid- signs and other causes of kidney disease. ney, increases the risk that the infection will spread to the kid- ney. The presence of stones and growths in the bladder and kidney TREATMENT AND FOLLOW-UP also increases the risk. -
1. Urine Diversion
1. Urine diversion – hygienic risks and microbial guidelines for reuse © Caroline Schönning Department of Parasitology, Mycology and Environmental Microbiology Swedish Institute for Infectious Disease Control (SMI) SE-171 82 Solna Sweden [email protected] This chapter is based on the doctoral thesis published by the author in February 2001: Höglund, C. (2001). Evaluation of microbial health risks associated with the reuse of source separated human urine. PhD thesis, Department of Biotechnology, Royal Institute of Technology, Stockholm, Sweden. ISBN 91-7283-039-5. The full thesis (87 pages, without published papers) can be downloaded from: http://www.lib.kth.se/Sammanfattningar/hoglund010223.pdf Dr Håkan Jönsson, Swedish University for Agricultural Sciences is acknowledged for compiling Section 3, and Dr Jan-Olof Drangert, Linköping University is acknowledged for compiling Section 9. TABLE OF CONTENTS TABLE OF CONTENTS 1 1. INTRODUCTION 2 1.1 History 2 1.2 Nutrient content and volume of domestic wastewater 3 2. URINE DIVERSION 3 2.1 Urine diversion in Sweden 4 2.2 Source-separation of urine in other parts of the world 6 2.3 Ecological Sanitation 6 3. URINE AS A FERTILISER IN AGRICULTURE 7 3.1 Characteristics of diverted human urine 7 3.2 Collection and storage of the urine – developing countries 7 3.3 Urine as a fertiliser 8 3.4 Crops to fertilise 9 3.5 Dosage 9 3.6 Fertilising experiments 10 3.7 Acceptance 11 4. PATHOGENIC MICROORGANISMS IN URINE 11 5. FAECAL CONTAMINATION 13 5.1 Analysis of indicator bacteria to determine faecal contamination 14 5.2 Analysis of faecal sterols to determine faecal contamination 15 5.3 Discussion 16 6. -
High Blood Pressure and Chronic Kidney Disease: for People
HIGH BLOOD PRESSURE AND CHRONIC KIDNEY DISEASE For People with CKD Stages 1–4 www.kidney.org National Kidney Foundation's Kidney Disease Outcomes Quality Initiative Did you know that the National Kidney Foundation's Kidney Disease Outcomes Quality Initiative (NKF-KDOQI™) has guidelines and commentaries that help your doctor and healthcare team make important decisions about your medical treatment? The information in this booklet is based on the NKF- KDOQI recommended guidelines and commentaries. What is your stage of kidney disease? There are five stages of kidney disease. They are shown in the table below. Your doctor determines your stage of kidney disease based on the presence of kidney damage and your glomerular filtration rate (GFR), which is a measure of your level of kidney function. Your treatment is based on your stage of kidney disease. Speak to your doctor if you have any questions about your stage of kidney disease or your treatment. STAGES of KidNEY DISEASE AGES of KidNEY DISEASE STAGES OF KIDNEY DISEASE Stage Description Glomerular Filtration Rate (GFR)* Kidney damage (e.g., protein 1 90 or above in the urine) with normal GFR Kidney damage with mild 2 60 to 89 decrease in GFR 3 Moderate decrease in GFR 30 to 59 4 Severe reduction in GFR 15 to 29 5 Kidney failure Less than 15 *Your GFR number tells your doctor how much kidney function you have. As chronic kidney disease progresses, your GFR number decreases. 2 NATIONAL KIDNEY FOUNDATION TABLE of ConTEntS Did you know? ...............................4 What is chronic kidney disease? ................5 What is high blood pressure? ...................6 How are high blood pressure and kidney disease related? ..............................6 How do I know if my blood pressure is too high? ..................................7 How is blood pressure measured? How often should it be checked? ...............8 I have high blood pressure but am not sure if I have CKD.