DOCSLIB.ORG

Nephrotic Syndrome

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Nephrotic Syndrome Nephrotic Syndrome GRANT GALLIMORE, MD, MAJ, USAF, MC NEPHROLOGY CHIEF, KEESLER MEDICAL CENTER Overview o History and terminology o Major causes of nephrotic syndrome and prevalence o Patient presentation, history and exam o Laboratory and imaging based on potential etiology o Selected pathology and microscopy o Complications and management History and Terminology o Nephrotic was coined in 1905 by Friedrich von Müller, a distinguished German Pathologist o The term nephrotic syndrome is attributed to Louis Leiter of the University of Chicago, using the term in a widely read review in 1930 o Percutaneous renal biopsy was introduced in 1951, resulting in description of many distinct disease entities Glassock RJ, Fervenza FC, Hebert L, Cameron JS. Nephrotic syndrome redux. Nephrology Dialysis Transplantation. 2014;30(1):12–7. History and Terminology o Berman and Schreiner 1958 biopsy series threshold of 3.5g/24h was determined o All patients had hypoalbuminemia and oval fat bodies in urine o Edema was absent in 27% and hyperlipidemia absent in 25% Glassock RJ, Fervenza FC, Hebert L, Cameron JS. Nephrotic syndrome redux. Nephrology Dialysis Transplantation. 2014;30(1):12–7. History and Terminology o Definition should be based on 24h urine excretion of protein rather than albumin, although 60-90% of proteinuria should be albumin o Many conditions can give rise to nephrotic range proteinuria but not to nephrotic syndrome o With preserved albumin, responsible lesions are likely to result from secondary processes like hyperfiltration, obesity, nephron loss o For example, the majority of African Americans with FSGS have nephrotic-range proteinuria but not nephrotic syndrome Glassock RJ, Fervenza FC, Hebert L, Cameron JS. Nephrotic syndrome redux. Nephrology Dialysis Transplantation. 2014;30(1):12–7. Glassock RJ, Fervenza FC, Hebert L, Cameron JS. Nephrotic syndrome redux. Nephrology Dialysis Transplantation. 2014;30(1):12–7. Floege J, Feehaly J. Introduction to Glomerular Disease. In: Feehally J, Floege Jürgen, Tonelli M, Johnson RJ. Comprehensive clinical nephrology. Edinburgh: Elsevier; 2019. p. 184-98 Sara Conti, Norberto Perico, et al. Early and late scanning electron microscopy findings in diabetic kidney disease. Scientific Reports 8, Article number: 4909 (2018) https://doi.org/10.1038/s41598-018-23244-2 Sara Conti, Norberto Perico, et al. Early and late scanning electron microscopy findings in diabetic kidney disease. Scientific Reports 8, Article number: 4909 (2018) https://doi.org/10.1038/s41598-018-23244-2 Figure 3 American Journal of Kidney Diseases 2015 66, 376-377DOI: (10.1053/j.ajkd.2015.04.006) Copyright © 2015 National Kidney Foundation, Inc. Terms and Conditions Patient History o Wide spectrum varying from asymptomatic to life-threatening disease o The following historical elements may be relevant: oSystemic disease o SLE, RA, Crohn’s, DM, HTN, obesity, nephron loss, frequent UTI o Family history o FSGS, complement disorders o Medications o NSAIDs, interferon, bisphosphonates o History of malignancy o Breast, lung, gastrointestinal, lymphoma o History of infection o HIV, Hepatitis B or C, syphilis, malaria Floege J, Feehaly J. Introduction to Glomerular Disease. In: Feehally J, Floege Jürgen, Tonelli M, Johnson RJ. Comprehensive clinical nephrology. Edinburgh: Elsevier; 2019. p. 184-98 Floege J, Feehaly J. Introduction to Glomerular Disease. In: Feehally J, Floege Jürgen, Tonelli M, Johnson RJ. Comprehensive clinical nephrology. Edinburgh: Elsevier; 2019. p. 184-98 Exam o Edema is often periorbital in the morning (no orthopnea) o This is in contrast to heart failure (pulmonary congestion producing orthopnea) and cirrhosis (diaphragmatic pressure from ascites) o Massive weight gain is common, with fluid overload including ascites, pleural effusions, abdominal and genital edema o Muehrcke lines and xanthelasma may be seen o Palpable purpura in vasculitis, SLE, cyroglobulinemia Floege J, Feehaly J. Introduction to Glomerular Disease. In: Feehally J, Floege Jürgen, Tonelli M, Johnson RJ. Comprehensive clinical nephrology. Edinburgh: Elsevier; 2019. p. 184-98 Floege J, Feehaly J. Introduction to Glomerular Disease. In: Feehally J, Floege Jürgen, Tonelli M, Johnson RJ. Comprehensive clinical nephrology. Edinburgh: Elsevier; 2019. p. 184-98 Floege J, Feehaly J. Introduction to Glomerular Disease. In: Feehally J, Floege Jürgen, Tonelli M, Johnson RJ. Comprehensive clinical nephrology. Edinburgh: Elsevier; 2019. p. 184-98 Floege J, Feehaly J. Introduction to Glomerular Disease. In: Feehally J, Floege Jürgen, Tonelli M, Johnson RJ. Comprehensive clinical nephrology. Edinburgh: Elsevier; 2019. p. 184-98 Parvovirus Metabolic, Autoimmune, Infectious, Neoplastic, Drugs Floege J, Feehaly J. Introduction to Glomerular Disease. In: Feehally J, Floege Jürgen, Tonelli M, Johnson RJ. Comprehensive clinical nephrology. Edinburgh: Elsevier; 2019. p. 184-98 Laboratory o Consider serology for Hepatitis B (MN) and C (MPGN), HIV (FSGS) o Low C3/C4 may be seen in SLE, MPGN, infection-associated, dense deposit disease, HUS o ANA to screen SLE as a cause of membranous o RF may be positive due to RA (MN, amyloid) or cryoglobulinemia o SPEP and serum free light chains may reveal paraprotein-associated disease whether myeloma, amyloidosis, or others Floege J, Feehaly J. Introduction to Glomerular Disease. In: Feehally J, Floege Jürgen, Tonelli M, Johnson RJ. Comprehensive clinical nephrology. Edinburgh: Elsevier; 2019. p. 184-98 Imaging o Ultrasound scanning to ensure 2 kidneys, rule out obstruction or anatomic abnormalities o Large kidneys (>14cm) may suggest diabetic nephropathy, amyloid disease, HIV, acute severe GN, or AIN o Small kidneys (<9cm) and/or cortical thinning should limit enthusiasm for biopsy or aggressive immunosuppression Floege J, Feehaly J. Introduction to Glomerular Disease. In: Feehally J, Floege Jürgen, Tonelli M, Johnson RJ. Comprehensive clinical nephrology. Edinburgh: Elsevier; 2019. p. 184-98 Figure 2 American Journal of Kidney Diseases 2015 66, 376-377DOI: (10.1053/j.ajkd.2015.04.006) Copyright © 2015 National Kidney Foundation, Inc. Terms and Conditions Couser WG. Primary Membranous Nephropathy. CJASN June 2017, 12 (6) 983-997; DOI: https://doi.org/10.2215/CJN.1176111 Membranous Nephropathy Beck LH et al. N Engl J Med 2009; 361: 11-21. FSGS light microscopy patterns Focal Segmental Glomerulsclerosis [Internet]. [cited 2019 Jul 5]. Available from https://unckidneycenter.org/kidneyhealthlibrary/glomerular-disease/focal-segmental-glomerulosclerosis-fsgs/ Complications and Management Floege J, Feehaly J. Introduction to Glomerular Disease. In: Feehally J, Floege Jürgen, Tonelli M, Johnson RJ. Comprehensive clinical nephrology. Edinburgh: Elsevier; 2019. p. 184-98 Edema formation o Overfill is actually much more common than underfill o This seems to be related to activation of the epithelial sodium channel (ENaC) by proteolytic enzymes in tubular lumen o Leads to increased blood volume, RAAS suppression, tendency to hypertension o Increased blood volume with low oncotic pressure leads to transudation of fluid into interstitium Floege J, Feehaly J. Introduction to Glomerular Disease. In: Feehally J, Floege Jürgen, Tonelli M, Johnson RJ. Comprehensive clinical nephrology. Edinburgh: Elsevier; 2019. p. 184-98 Edema formation o The argument for overfill theory o Individuals lacking serum albumin often do not have sodium retention o During recovery, natriuresis occurs prior to improvement in hypoalbuminemia o IV albumin does not consistently improve natriuresis o Studies with radioactive albumin have demonstrated low plasma and blood volumes in as few as 2% of cases o Adrenalectomized rats with nephrotic syndrome have sodium retention o Proteases such as plasminogen have been shown to activate ENAC Ray, E. C., Rondon-Berrios, H., Boyd, C. R., & Kleyman, T. R. (2015). Sodium Retention and Volume Expansion in Nephrotic Syndrome: Implications for Hypertension. Advances in Chronic Kidney Disease, 22(3), 179-184. doi:10.1053/j.ackd.2014.11.006 Treatment of edema o Diuretic efficacy is likely to be impaired o Transport from peritubular capillaries requires protein binding o Increased protein binding in tubular lumen limits access to transporters o Gastrointestinal absorption may be limited o Ways to overcome diuretic resistance o Use of IV therapy o Use of thiazide in addition to loop diuretic with close monitoring o Addition of amiloride (ENaC highly relevant to pathophysiology) o Consideration of IV albumin Floege J, Feehaly J. Introduction to Glomerular Disease. In: Feehally J, Floege Jürgen, Tonelli M, Johnson RJ. Comprehensive clinical nephrology. Edinburgh: Elsevier; 2019. p. 184-98 Addition of thiazide Addition of amiloride Use of IV therapy Use of albumin Floege J, Feehaly J. Introduction to Glomerular Disease. In: Feehally J, Floege Jürgen, Tonelli M, Johnson RJ. Comprehensive clinical nephrology. Edinburgh: Elsevier; 2019. p. 184-98 Response to hypoalbuminemia o Increased protein synthesis is not discriminating, as the synthesis of many proteins other than albumin is upregulated o This includes large molecular weight proteins that are not filtered and may actually increase in concentration o This has implications for both hyperlipidemia and hypercoagulability Floege J, Feehaly J. Introduction to Glomerular Disease. In: Feehally J, Floege Jürgen, Tonelli M, Johnson RJ. Comprehensive clinical nephrology. Edinburgh: Elsevier; 2019. p. 184-98 Floege J, Feehaly J. Introduction to Glomerular Disease. In: Feehally J, Floege Jürgen,
Load more

Recommended publications
  • Study Guide Medical Terminology by Thea Liza Batan About the Author
    Study Guide Medical Terminology By Thea Liza Batan About the Author Thea Liza Batan earned a Master of Science in Nursing Administration in 2007 from Xavier University in Cincinnati, Ohio. She has worked as a staff nurse, nurse instructor, and level department head. She currently works as a simulation coordinator and a free- lance writer specializing in nursing and healthcare. All terms mentioned in this text that are known to be trademarks or service marks have been appropriately capitalized. Use of a term in this text shouldn’t be regarded as affecting the validity of any trademark or service mark. Copyright © 2017 by Penn Foster, Inc. All rights reserved. No part of the material protected by this copyright may be reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, or by any information storage and retrieval system, without permission in writing from the copyright owner. Requests for permission to make copies of any part of the work should be mailed to Copyright Permissions, Penn Foster, 925 Oak Street, Scranton, Pennsylvania 18515. Printed in the United States of America CONTENTS INSTRUCTIONS 1 READING ASSIGNMENTS 3 LESSON 1: THE FUNDAMENTALS OF MEDICAL TERMINOLOGY 5 LESSON 2: DIAGNOSIS, INTERVENTION, AND HUMAN BODY TERMS 28 LESSON 3: MUSCULOSKELETAL, CIRCULATORY, AND RESPIRATORY SYSTEM TERMS 44 LESSON 4: DIGESTIVE, URINARY, AND REPRODUCTIVE SYSTEM TERMS 69 LESSON 5: INTEGUMENTARY, NERVOUS, AND ENDOCRINE S YSTEM TERMS 96 SELF-CHECK ANSWERS 134 © PENN FOSTER, INC. 2017 MEDICAL TERMINOLOGY PAGE III Contents INSTRUCTIONS INTRODUCTION Welcome to your course on medical terminology. You’re taking this course because you’re most likely interested in pursuing a health and science career, which entails ­proficiency­in­communicating­with­healthcare­professionals­such­as­physicians,­nurses,­ or dentists.
    [Show full text]
  • PDI Appendix G Intermediate-Risk Immunocompromised State Ef Ec2
    AHRQ QI™ ICD‐10‐CM/PCS Specification Enhanced Version 5.0 1 of 6 Pediatric Quality Indicators Appendices www.qualityindicators.ahrq.gov Pediatric Quality Indicators Appendices APPENDIX G: Intermediate-Risk Immunocompromised State Diagnosis Codes Intermediate-risk immunocompromised state diagnosis codes: (IMMUITD) ICD-9-CM Description ICD-10-CM Description 07022 VIRAL HEPATITIS B W HEPATIC COMA, CHRONIC WO B180 Chronic viral hepatitis B with delta‐agent MENTION OF HEPATITIS DELTA 07023 VIRAL HEPATITIS B W HEPACTIC COMA, CHRONIC W B181 Chronic viral hepatitis B without delta‐agent HEPATITIS DELTA 07044 CHRONIC HEPATITIS C WITH HEPACTIC COMMA B182 Chronic viral hepatitis C 2894 HYPERSPLENISM B520 Plasmodium malariae malaria with nephropathy 28950 DISEASE OF SPLEEN NOS D5702 Hb‐SS disease with splenic sequestration 28951 CHRONIC DIGESTIVE SPLENOMEGALY D57212 Sickle‐cell/Hb‐C disease with splenic sequestration 28952 SPLENIC SEQUESTRATION D57412 Sickle‐cell thalassemia with splenic sequestration 28959 OTHER DISEASE OF SPLEEN, OTHER D57812 Other sickle‐cell disorders with splenic sequestration 4560 ESOPHAGEAL VARICES W BLEEDING D730 Hyposplenism 4561 ESOPHAGEAL VARICES WO MENTION OF BLEEDING D731 Hypersplenism 45620 ESOPHAGEAL VARICES IN DISEASE CLASSIFIED D732 Chronic congestive splenomegaly ELSEWHERE, W BLEEDING 45621 ESOPHAGEAL VARICES IN DISEASE CLASSIFIED D733 Abscess of spleen ELSEWHERE, WO MENTION OF BLEEDING 5723 PORTAL HYPERTENSION D735 Infarction of spleen 5728 OTHER SEQUELAE OF CHRONIC LIVER DISEASE D7389 Other diseases of spleen 5735
    [Show full text]
  • Extrarenal Complications of the Nephrotic Syndrome
    Kidney International, Vol. 33 (/988), pp. 1184—1202 NEPHROLOGY FORUM Extrarenal complications of the nephrotic syndrome Principal discussant: DAVID B. BERNARD The University Hospital and Boston University Sc/zoo!ofMedicine, Boston, Massachusetts present and equal. The temperature was 100°F. The blood pressure was 110/70 mm Hg in the right arm with the patient supine and standing. The Editors patient had no skin rashes, peteehiae, clubbing, or jaundice. Examina- JORDANJ. COHEN tion of the head and neck revealed intact cranial nerves and normal fundi. Ears, nose, and throat were normal. The jugular venous pressure Jot-IN T. HARRtNOTON was not increased. No lymph glands were palpable in the neck or JEROME P. KASSIRER axillae, and the trachea was midline, cardiac examination was normal. NICOLA05 E. MAmAs Examination of the lungs revealed coarse rales at the right base but no other abnormalities. Abdominal examination revealed aseites, but no Editor abdominal guarding, tenderness, or rigidity. The liver and spleen were Managing not palpable and no masses were present. The urine contained 4± CHERYL J. ZUSMAN protein; microscopic examination revealed free fat droplets, many oval fat bodies, and numerous fatty casts. Five to 10 red blood cells were seen per high-power field, but no red blood cell casts were present. A Universityof'Chicago Pritzker School of Medicine 24-hr urine collection contained 8 g of protein. The BUN was 22 mg/dl; creatinine, 2.0 mg/dl; and electrolytes were and normal. Serum total calcium was 7.8 mg/dl, and the phosphorus was 4.0 Taf is University School of' Medicine mg/dl.
    [Show full text]
  • 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.
    [Show full text]
  • Management of Anemia in Non-Dialysis Chronic Kidney Disease: Current Recommendations, Real-World Practice, and Patient Perspectives
    Kidney360 Publish Ahead of Print, published on July 1, 2020 as doi:10.34067/KID.0001442020 Management of Anemia in Non-Dialysis Chronic Kidney Disease: Current recommendations, real-world practice, and patient perspectives Murilo Guedes1,2, Bruce M. Robinson1,3, Gregorio Obrador4, Allison Tong5,6, Ronald L. Pisoni1, Roberto Pecoits-Filho1,2 1Arbor Research Collaborative for Health, Ann Arbor, MI, USA 2School of Medicine, Pontifícia Universidade Católica do Paraná, Curitiba, Brazil 3University of Michigan, Department of Internal Medicine, Ann Arbor, MI, USA 4Universidad Panamericana - Campus México, DF, MX, Mexico 5 Sydney School of Public Health, University of Sydney, Sydney, Australia 6 Centre for Kidney Research, The Children’s Hospital at Westmead, Sydney, Australia Corresponding Author Roberto Pecoits-Filho Arbor Research Collaborative for Health 3700 Earhart Road Ann Arbor, MI 48105 [email protected] 1 Copyright 2020 by American Society of Nephrology. Abstract In non-dialysis chronic kidney disease (ND-CKD), anemia is a multi-factorial and complex condition in which several dysfunctions dynamically contribute to a reduction in circulating hemoglobin (Hb) levels in red blood cells. Anemia is common in CKD, and represents an important and modifiable risk factor for poor clinical outcomes. Importantly, symptoms related to anemia, including reduced physical functioning and fatigue, have been identified as high priorities by patients with CKD. The current management of anemia in ND-CKD, i.e., parameters to initiate treatment, Hb and iron indexes targets, choice of therapies, and impact of treatment on clinical and patient-reported outcomes, remains controversial. In this review article, we explore the epidemiology of anemia in NDD-CKD, and revise current recommendations and controversies in its management.
    [Show full text]
  • The Links Between Microbiome and Uremic Toxins in Acute Kidney Injury: Beyond Gut Feeling—A Systematic Review
    toxins Article The Links between Microbiome and Uremic Toxins in Acute Kidney Injury: Beyond Gut Feeling—A Systematic Review Alicja Rydzewska-Rosołowska 1,* , Natalia Sroka 1, Katarzyna Kakareko 1, Mariusz Rosołowski 2 , Edyta Zbroch 1 and Tomasz Hryszko 1 1 2nd Department of Nephrology and Hypertension with Dialysis Unit, Medical University of Białystok, 15-276 Białystok, Poland; [email protected] (N.S.); [email protected] (K.K.); [email protected] (E.Z.); [email protected] (T.H.) 2 Department of Gastroenterology and Internal Medicine, Medical University of Białystok, 15-276 Białystok, Poland; [email protected] * Correspondence: [email protected] Received: 30 October 2020; Accepted: 9 December 2020; Published: 11 December 2020 Abstract: The last years have brought an abundance of data on the existence of a gut-kidney axis and the importance of microbiome in kidney injury. Data on kidney-gut crosstalk suggest the possibility that microbiota alter renal inflammation; we therefore aimed to answer questions about the role of microbiome and gut-derived toxins in acute kidney injury. PubMed and Cochrane Library were searched from inception to October 10, 2020 for relevant studies with an additional search performed on ClinicalTrials.gov. We identified 33 eligible articles and one ongoing trial (21 original studies and 12 reviews/commentaries), which were included in this systematic review. Experimental studies prove the existence of a kidney-gut axis, focusing on the role of gut-derived uremic toxins and providing concepts that modification of the microbiota composition may result in better AKI outcomes. Small interventional studies in animal models and in humans show promising results, therefore, microbiome-targeted therapy for AKI treatment might be a promising possibility.
    [Show full text]
  • Full Text (PDF)
    www.jasn.org EDITORIALS 5. Grimm PR, Coleman R, Delpire E, Welling PA: Constitutively active Cachexia with muscle wasting is prevalent and closely associated SPAK causes hyperkalemia by activating NCC and remodeling distal with mortality and morbidity in patients with CKD.1 The patho- – tubules. JAmSocNephrol28: 2597 2606, 2017 physiology of muscle wasting in CKD is complex. Inadequate 6. Moriguchi T, Urushiyama S, Hisamoto N, Iemura S, Uchida S, Natsume T, Matsumoto K, Shibuya H: WNK1 regulates phosphorylation of cation- nutritional intake, physical inactivity from muscle weakness, sys- chloride-coupled cotransporters via the STE20-related kinases, SPAK temic inflammation and aberrant signaling of neuropeptides have and OSR1. J Biol Chem 280: 42685–42693, 2005 been implicated.2 To date, there is no effective therapy. Exercise 7. YangSS,MorimotoT,RaiT,ChigaM,SoharaE,OhnoM,UchidaK,LinSH, training has well documented health benefits, including mainte- Moriguchi T, Shibuya H, Kondo Y, SasakiS,UchidaS:Molecularpatho- nance of muscle mass as well as increased physical performance genesis of pseudohypoaldosteronism type II: Generation and analysis of a fi Wnk4(D561A/1) knockin mouse model. Cell Metab 5: 331–344, 2007 resulting from changes in muscle ber phenotype leading to in- 8. Lalioti MD, Zhang J, Volkman HM, Kahle KT, Hoffmann KE, Toka HR, Nelson- creased mitochondrial biogenesis. The molecular signaling mech- Williams C, Ellison DH, Flavell R, Booth CJ, Lu Y, Geller DS, Lifton RP: Wnk4 anism underlying adaptations to increased physical activity in controls blood pressure and potassium homeostasis via regulation of mass CKD-associated muscle wasting is not well understood. – and activity of the distal convoluted tubule.
    [Show full text]
  • Mineralocorticoid-Resistant Renal Hyperkalemia Without Salt Wasting
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Kidney International, Vol. 19 (1981), pp. 716—727 Mineralocorticoid-resistant renal hyperkalemia without sal wasting (type II pseudohypoaldosteronism): Role of increased renal chloride reabsorption MORRIS SCHAMBELAN, ANTHONY SEBASTIAN, and FLOYD C. RECTOR, JR. Medical Service and Clinical Study Center, San Francisco General Hospital Medical Center, and the Department of Medicine, Cardiovascular Research Institute, and the General Clinical Research Center, University of California, San Francisco, California Mineralocorticoid-resistant renal hyperkalemia without salt Hyperkaliemie rénale resistant aux minéralocorticoides sans wasting (type II pseudohypoaldosteronism): Role of increased perte de sel (pseudohypoaldostéronisme de type II): Role de l'aug- renal chloride reabsorption. A rare syndrome has been described mentation iie Ia reabsorption de chlore. Un syndrome rare a été in which mineralocorticoid-resistant hyperkalemia of renal origin décrit dans lequel une hyperkaliemie d'origine rénale resistant occurs in the absence of glomerular insufficiency and renal aux minéralocorticoides survient en l'absence de diminution du sodium wasting and in which hyperchioremic acidosis, hyperten- debit de filtration glomerulaire et de perte rénale de sodium et sion, and hyporeninemia coexist. The primary abnormality has dans lequel une acidose hyperchioremique, une hypertension et been postulated to be a defect of the potassium secretory une hyporéninémie coexistent. L'anomalie primaire qui a été mechanism of the distal nephron. The present studies were postulée est un deficit du mécanisme de secretion de potassium carried out to investigate the mechanism of impaired renal du nephron distal. Ce travail a etC entrepris pour étudier le potassium secretion in a patient with this syndrome.
    [Show full text]
  • Supplemental Guide: Nephrology
    Supplemental Guide for Nephrology Supplemental Guide: Nephrology March 2020 1 Supplemental Guide for Nephrology TABLE OF CONTENTS INTRODUCTION ............................................................................................................................. 3 PATIENT CARE .............................................................................................................................. 4 Acute Kidney Injury ...................................................................................................................... 4 Chronic Dialysis Therapy ............................................................................................................. 6 Chronic Kidney Disease ............................................................................................................... 8 Transplant .................................................................................................................................. 10 Fluid and Electrolytes ................................................................................................................. 12 Hypertension .............................................................................................................................. 13 Competence in Procedures ........................................................................................................ 15 MEDICAL KNOWLEDGE .............................................................................................................. 17 Physiology and Pathophysiology ..............................................................................................
    [Show full text]
  • Urinary System Diseases and Disorders
    URINARY SYSTEM DISEASES AND DISORDERS BERRYHILL & CASHION HS1 2017-2018 - CYSTITIS INFLAMMATION OF THE BLADDER CAUSE=PATHOGENS ENTERING THE URINARY MEATUS CYSTITIS • MORE COMMON IN FEMALES DUE TO SHORT URETHRA • SYMPTOMS=FREQUENT URINATION, HEMATURIA, LOWER BACK PAIN, BLADDER SPASM, FEVER • TREATMENT=ANTIBIOTICS, INCREASE FLUID INTAKE GLOMERULONEPHRITIS • AKA NEPHRITIS • INFLAMMATION OF THE GLOMERULUS • CAN BE ACUTE OR CHRONIC ACUTE GLOMERULONEPHRITIS • USUALLY FOLLOWS A STREPTOCOCCAL INFECTION LIKE STREP THROAT, SCARLET FEVER, RHEUMATIC FEVER • SYMPTOMS=CHILLS, FEVER, FATIGUE, EDEMA, OLIGURIA, HEMATURIA, ALBUMINURIA ACUTE GLOMERULONEPHRITIS • TREATMENT=REST, SALT RESTRICTION, MAINTAIN FLUID & ELECTROLYTE BALANCE, ANTIPYRETICS, DIURETICS, ANTIBIOTICS • WITH TREATMENT, KIDNEY FUNCTION IS USUALLY RESTORED, & PROGNOSIS IS GOOD CHRONIC GLOMERULONEPHRITIS • REPEATED CASES OF ACUTE NEPHRITIS CAN CAUSE CHRONIC NEPHRITIS • PROGRESSIVE, CAUSES SCARRING & SCLEROSING OF GLOMERULI • EARLY SYMPTOMS=HEMATURIA, ALBUMINURIA, HTN • WITH DISEASE PROGRESSION MORE GLOMERULI ARE DESTROYED CHRONIC GLOMERULONEPHRITIS • LATER SYMPTOMS=EDEMA, FATIGUE, ANEMIA, HTN, ANOREXIA, WEIGHT LOSS, CHF, PYURIA, RENAL FAILURE, DEATH • TREATMENT=LOW NA DIET, ANTIHYPERTENSIVE MEDS, MAINTAIN FLUIDS & ELECTROLYTES, HEMODIALYSIS, KIDNEY TRANSPLANT WHEN BOTH KIDNEYS ARE SEVERELY DAMAGED PYELONEPHRITIS • INFLAMMATION OF THE KIDNEY & RENAL PELVIS • CAUSE=PYOGENIC (PUS-FORMING) BACTERIA • SYMPTOMS=CHILLS, FEVER, BACK PAIN, FATIGUE, DYSURIA, HEMATURIA, PYURIA • TREATMENT=ANTIBIOTICS,
    [Show full text]
  • 2012 CKD Guideline
    OFFICIAL JOURNAL OF THE INTERNATIONAL SOCIETY OF NEPHROLOGY KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease VOLUME 3 | ISSUE 1 | JANUARY 2013 http://www.kidney-international.org KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease KDIGO gratefully acknowledges the following consortium of sponsors that make our initiatives possible: Abbott, Amgen, Bayer Schering Pharma, Belo Foundation, Bristol-Myers Squibb, Chugai Pharmaceutical, Coca-Cola Company, Dole Food Company, Fresenius Medical Care, Genzyme, Hoffmann-LaRoche, JC Penney, Kyowa Hakko Kirin, NATCO—The Organization for Transplant Professionals, NKF-Board of Directors, Novartis, Pharmacosmos, PUMC Pharmaceutical, Robert and Jane Cizik Foundation, Shire, Takeda Pharmaceutical, Transwestern Commercial Services, Vifor Pharma, and Wyeth. Sponsorship Statement: KDIGO is supported by a consortium of sponsors and no funding is accepted for the development of specific guidelines. http://www.kidney-international.org contents & 2013 KDIGO VOL 3 | ISSUE 1 | JANUARY (1) 2013 KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease v Tables and Figures vii KDIGO Board Members viii Reference Keys x CKD Nomenclature xi Conversion Factors & HbA1c Conversion xii Abbreviations and Acronyms 1 Notice 2 Foreword 3 Work Group Membership 4 Abstract 5 Summary of Recommendation Statements 15 Introduction: The case for updating and context 19 Chapter 1: Definition, and classification
    [Show full text]
  • Chapter 10: Radiation Nephropathy
    Chapter 10: Radiation Nephropathy † Amaka Edeani, MBBS,* and Eric P. Cohen, MD *Kidney Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland; and †Nephrology Division, Department of Medicine, University of Maryland School of Medicine, and Baltimore Veterans Affairs Medical Center, Baltimore, Maryland INTRODUCTION Classical radiation nephropathy occurred after external beam radiation for treatment of solid The occurrence of renal dysfunction as a consequence cancers such as seminomas (6); the incidence has of ionizing radiation has been known for more than declined with the advent of more effective chemo- 100 years (1,2). Initial reports termed this condition therapy. In recent years, radiation nephropathy has “radiation nephritis,” but that is a misnomer, because occurred due to TBI used as part of chemo-irradiation it is not an inflammatory condition. Renal radiation conditioning just before hematopoietic stem cell injury may be avoided by the exclusion of an ade- transplantation (HSCT) and also from targeted ra- quate volume of kidney exposure during radiation dionuclide therapy used for instance in the treatment therapy, but the kidneys’ central location can make of neuroendocrine malignancies. TBI may be myelo- this difficult to impossible when tumors of the abdo- ablative or nonmyeloablative, with myeloablative men or retroperitoneum are treated, or during total regimens using radiation doses of 10–12 Gy to de- body irradiation (TBI) (3). stroy or suppress the recipient’s bone marrow. These doses are given in a single fraction or in nine fractions over 3 days (4). In addition, TBI for bone marrow BACKGROUND/CLINICAL SIGNIFICANCE transplantation (BMT) is preceded or accompanied by cytotoxic chemotherapy, which potentiates the Radiation nephropathy is renal injury and loss of effects of ionizing radiation (7).
    [Show full text]