Blood Clots and Chronic Kidney Disease
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Deep Vein Thrombosis in Behcet's Disease
BRIEF PAPER Clinical and Experimental Rheumatology 2001; 19 (Suppl. 24): S48-S50. Deep vein thrombosis ABSTRACT stitute the most frequent vascular mani- Objective festation seen in 6.2 to 33 % cases of in Behcet’s disease We aimed to describe the epidemiologi - BD (1, 2). We carried out this study to cal and clinical aspects of deep vein d e t e rmine the fre q u e n cy, the cl i n i c a l M.H. Houman1 thrombosis (DVT) in Behçet’s disease characteristics and course of deep vein 1 (BD) and to determine the patients at thrombosis (DVT) in BD patients and I. Ben Ghorbel high risk for this complication. to define a subgroup of patients at high I. Khiari Ben Salah1 Methods risk for this complication. M. Lamloum1 Among 113 patients with BD according 2 to the international criteria for classifi - Patients and methods M. Ben Ahmed cation of BD, those with DVT were ret - The medical records of one hundred M. Miled1 rospectively studied.The diagnosis of and thirteen patients with BD were re- DVT was made in all cases using con - viewed in order to investigate the pa- 1Department of Internal Medicine. La ventional venous angiography, venous tient’s medical history, the clinical ma- Rabta Hospital, 2Department of Immuno- ultrasonography and/or thoracic or ab - nifestations and outcome of the disease logy, Institute Pasteur. Tunis, Tunisia. dominal computed tomograp hy. Pa - as well as the treatment prescribed.The Houman M Habib, MD; Ben Ghorbel tients were divided in two subgroups diagnosis of BD was made based on the Imed, MD; Khiari Ben Salah Imen; a c c o rding to the occurrence of DV T criteria established by the international Lamloum Mounir, MD; Ben Ahmed other than cereb ral thromboses. -
Peripheral Vascular Disease (PVD) Fact Sheet
FACT SHEET FOR PATIENTS AND FAMILIES Peripheral Vascular Disease (PVD) What is peripheral vascular disease? Vascular disease is disease of the blood vessels (arteries and veins). Peripheral vascular disease (PVD) affects The heart receives blood, the areas that are “peripheral,” or outside your heart. sends it to The most common types of PVD are: the lungs to get oxygen, • Carotid artery disease affects the arteries and pumps that carry blood to your brain. It occurs when it back out. one or more arteries are narrowed or blocked by plaque, a fatty substance that builds up inside artery walls. Carotid artery disease can increase Veins carry Arteries carry your risk of stroke. It can also cause transient blood to your oxygen-rich [TRANZ-ee-ent] ischemic [iss-KEE-mik] attacks (TIAs). heart to pick blood from up oxygen. your heart TIAs are temporary changes in brain function to the rest of that are sometimes called “mini-strokes.” your body. • Peripheral arterial disease (PAD) often affects the arteries to your legs and feet. It is also caused by Healthy blood vessels provide oxygen plaque buildup, and can for every part of your body. cause pain that feels like a dull cramp or heavy tiredness in your hips or legs when • Venous insufficiency affects the veins, usually you exercise or climb stairs. in your legs or feet. Your veins have valves that This pain is sometimes Damaged Healthy keepvalve blood fromvalve flowing backward as it moves called claudication. If PAD toward your heart. If the valves stop working, blood worsens, it can cause cold Plaque can build backs up in your body, usually in your legs. -
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. -
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 -
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. -
What Is Dvt? Deep Vein Thrombosis (DVT) Occurs When an Abnormal Blood Clot Forms in a Large Vein
What is DVt? Deep vein thrombosis (DVT) occurs when an abnormal blood clot forms in a large vein. These clots usually develop in the lower leg, thigh, or pelvis, but can also occur in other large veins in the body. If you develop DVT and it is diagnosed correctly and quickly, it can be treated. However, many people do not know if they are at risk, don’t know the symptoms, and delay seeing a healthcare professional if they do have symptoms. CAn DVt hAppen to me? Anyone may be at risk for DVT but the more risk factors you have, the greater your chances are of developing DVT. Knowing your risk factors can help you prevent DVt: n Hospitalization for a medical illness n Recent major surgery or injury n Personal history of a clotting disorder or previous DVT n Increasing age this is serious n Cancer and cancer treatments n Pregnancy and the first 6 weeks after delivery n Hormone replacement therapy or birth control products n Family history of DVT n Extended bed rest n Obesity n Smoking n Prolonged sitting when traveling (longer than 6 to 8 hours) DVt symptoms AnD signs: the following are the most common and usually occur in the affected limb: n Recent swelling of the limb n Unexplained pain or tenderness n Skin that may be warm to the touch n Redness of the skin Since the symptoms of DVT can be similar to other conditions, like a pulled muscle, this often leads to a delay in diagnosis. Some people with DVT may have no symptoms at all. -
A Comprehensive Study on Incidence and Risk Factors of Deep Vein Thrombosis in Asymptomatic Patient After Prolonged Surgery
D. Princess Beulah, T. Avvai. A comprehensive study on incidence and risk factors of deep vein thrombosis in asymptomatic patient after prolonged surgery. IAIM, 2019; 6(3): 237-242. Original Research Article A comprehensive study on incidence and risk factors of deep vein thrombosis in asymptomatic patient after prolonged surgery D. Princess Beulah1, T. Avvai2* 1Assistant Professor, Department of General Surgery, Govt. Stanley Medical College, Tamil Nadu, India 2Associate Professor, Department of General Surgery, Govt. Omandurar Medical College and Hospital, Tamil Nadu, India *Corresponding author email: [email protected] International Archives of Integrated Medicine, Vol. 6, Issue 3, March, 2019. Copy right © 2019, IAIM, All Rights Reserved. Available online at http://iaimjournal.com/ ISSN: 2394-0026 (P) ISSN: 2394-0034 (O) Received on: 28-02-2019 Accepted on: 04-03-2019 Source of support: Nil Conflict of interest: None declared. How to cite this article: D. Princess Beulah, T. Avvai. A comprehensive study on incidence and risk factors of deep vein thrombosis in asymptomatic patient after prolonged surgery. IAIM, 2019; 6(3): 237-242. Abstract Background: Deep vein thrombosis (DVT) is one of the most dreaded complications in postoperative patients as it is associated with considerable morbidity and mortality. The prevalence of Deep Vein Thrombosis (DVT) in various series involving Western population ranges from 15% to 40% among patients undergoing major general surgical procedures. The aim of the study: To identify risk factors of deep vein thrombosis in asymptotic patients after prolonged surgery Age, Gender, Diabetes, Hypertension, COPD, Hyperlipidemia, Renal disorder, liver disorder, duration of surgery, blood transfusion, nature of surgery elective or emergency, type of surgery. -
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. -
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.