Hematuria Is a Risk Factor Towards End-Stage Renal
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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. -
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. -
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. -
Urinalysis and Kidney Disease: What You Need to Know
URINALYSIS AND KIDNEY DISEASE What You Need To Know 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. What is a urinalysis (also called a “urine test”)? A urinalysis is a simple test that looks at a small sample of your urine. It can help find conditions that may need treatment, including infections or kidney problems. It can also help find serious diseases in the early stages, like chronic kidney disease, diabetes, or liver disease. -
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. -
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, -
Role of Urinalysis in the Diagnosis of Chronic Kidney Disease (CKD)
Research and Reviews Role of Urinalysis in the Diagnosis of Chronic Kidney Disease (CKD) JMAJ 54(1): 27–30, 2011 Kunitoshi ISEKI*1 Abstract As of the end of Year 2008, 1 out of 450 people was a dialysis patient in Japan, and patients with chronic kidney disease (CKD) at stages 3 and 4 accounted for nearly 10% of the total population. An epidemiological study in Okinawa that used the introduction of dialysis treatment as the outcome revealed that the 10-year cumulative incident rate of end-stage renal disease (ESRD) was about 3% of the participants who were positive (Ն 1ϩ) for both proteinuria and hematuria, while there was hardly any difference between those who were positive for hematuria alone and those who were negative for both proteinuria and hematuria. When the incidence of ESRD (dialysis introduction) was examined in relation to the severity of proteinuria (5 grades ranging from [Ϫ] to [Ն 3ϩ]) as determined by dipstick, the cumulative incidence rate during the 17-year observation period was 16% for proteinuria (Ն 3ϩ) and about 7% for proteinuria (2ϩ). In contrast, among participants who were negative for proteinuria, the rate of dialysis introduction in 10 years is about 1 out of 1 million. The CKD Practice Guide of the Japanese Society of Nephrology recommends referral to a nephrologist when a case meets any of the following 3 criteria: 1) 0.5g/g creatinine or higher, or proteinuria (Ն 2ϩ), 2) an estimated glomerular filtration rate of less than 50ml/min/1.73m2, or 3) positive results (Ն 1ϩ) for both proteinuria and hematuria tests. -
Chronic Kidney Disease (Ckd)
CHRONIC KIDNEY DISEASE ISSUE BRIEF prevent and control progressiveawareness obesity untreated end-stage renal disease kidney failure heart disease high blood pressure lifestyle changes stages complications family history damage to kidneys diabetes CKD few signs or symptoms PROGRESSION OF CHRONIC KIDNEY DISEASE (CKD) RISK FACTORS FOR CKD MAY INCLUDE ■ Heart Disease ■ Lupus ■ Diabetes ■ Family History of CKD ■ High Blood Pressure ■ Age ■ Obesity ■ High Cholesterol REDUCED INCREASED KIDNEY KIDNEY NORMAL KIDNEY RISK DAMAGE FUNCTION FAILURE Preventing CKD and its complications is possible by managing risk factors and treating the disease to slow its progression and reduce the risk of complications PROGRESSION OF CHRONIC KIDNEY DISEASE (CKD) What Is Chronic Kidney Disease? Fast Fact: Kidney diseases are the 9th leading cause of death in the United States. ■ Chronic kidney disease (CKD) is a condition in which a person has damaged kidneys or reduced kidney function for more than 3 months. During this time, the kidneys cannot properly filter waste out of the blood. If not detected and treated early, CKD can cause many health problems and even lead to kidney failure and early death. ■ CKD can start at any age, but the chances of developing it increase as people get older. It is most common among adults aged 70 years or older. ■ Once a person has CKD, it usually gets worse over time and lasts for the rest of the person’s life. Kidney failure—also called end-stage renal disease—is the final stage of CKD, when the kidneys stop working completely. How Big Is the CKD Problem and Who Is at Risk? Fast Fact: CDC estimates that more 6% than 20 million US adults aged 20 Unknown years or older have CKD—or more than 10% of the US adult population. -
Hematuria in the Child
Hematuria and Proteinuria in the Pediatric Patient Laurie Fouser, MD Pediatric Nephrology Swedish Pediatric Specialty Care Hematuria in the Child • Definition • ³ 1+ on dipstick on three urines over three weeks • 5 RBCs/hpf on three fresh urines over three weeks • Prevalence • 4-6% for microscopic hematuria on a single specimen in school age children • 0.3-0.5% on repeated specimens Sources of Hematuria • Glomerular or “Upper Tract” – Dysmorphic RBCs and RBC casts – Tea or cola colored urine – Proteinuria, WBC casts, renal tubular cells • Non-Glomerular or “Lower Tract” – RBCs have normal morphology – Clots/ Bright red or pink urine The Glomerular Capillary Wall The Glomerular Capillary Wall Glomerular Causes of Hematuria • Benign or self-limiting – Benign Familial Hematuria – Exercise-Induced Hematuria – Fever-Induced Hematuria Glomerular Causes of Hematuria • Acute Glomerular Disease – Poststreptococcal/ Postinfectious – Henoch-Schönlein Purpura – Sickle Cell Disease – Hemolytic Uremic Syndrome Glomerular Causes of Hematuria • Chronic Glomerular Disease – IgA Nephropathy – Henoch-Schönlein Purpura or other Vasculitis – Alport Syndrome – SLE or other Collagen Vascular Disease – Proliferative Glomerulonephritis Non-Glomerular Hematuria • Extra-Renal • UTI • Benign urethralgia +/- meatal stenosis • Calculus • Vesicoureteral Reflux, Hydronephrosis • Foreign body • Rhabdomyosarcoma • AV M • Coagulation disorder Non-Glomerular Hematuria • Intra-Renal • Hypercalciuria • Polycystic Kidney Disease • Reflux Nephropathy with Renal Dysplasia • -
Chronic Kidney Disease: an Inherent Risk Factor for Acute Kidney Injury?
Mini-Review Chronic Kidney Disease: An Inherent Risk Factor for Acute Kidney Injury? Prabhleen Singh, Dena E. Rifkin, and Roland C. Blantz Division of Nephrology-Hypertension, Department of Medicine, School of Medicine, University of California, San Diego, San Diego, California; and the Veterans Affairs San Diego Healthcare System, San Diego, California Epidemiologic evidence suggests that chronic kidney disease (CKD) is a risk factor for acute kidney injury (AKI) due to the prevalence of CKD in patients who have episodes of AKI. However, the high burden of comorbidities such as age, diabetes, peripheral vascular, cardiovascular, and liver disease accompanying CKD, and the difficulties of defining AKI in the setting of CKD make these observations difficult to interpret. These comorbidities not only could alter the course of AKI but also may be the driving force behind the epidemiologic association between CKD and AKI because of systemic changes and/or increased exposure to potential nephrotoxic risks. Here, we contend that studies suggesting that CKD is a risk factor for AKI may suffer from residual confounding and reflect an overall susceptibility to illness rather than biologic susceptibility of the kidney parenchyma to injury. In support of our argument, we discuss the clinical evidence from epidemiologic studies, and the knowledge obtained from animal models on the pathophysiology of AKI and CKD, demonstrating a preconditioning influence of the previously impaired kidneys against subsequent injury. We conclude that, under careful analysis, factors apart from the inherent pathophysiology of the diseased kidney may be responsible for the increased frequency of AKI in CKD patients, and the impact of CKD on the risk and severity of AKI needs further investigation. -
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