Uremic Toxins Affect Erythropoiesis During the Course of Chronic
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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. -
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. -
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. -
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. -
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. -
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. -
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. -
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. -
What Is Lupus Nephritis
What is lupus nephritis (LN)? Lupus nephritis (LN) is inflammation of the kidney that occurs as a common symptom of systemic lupus erythematosus (SLE), also known as lupus. Proteins in the immune system called antibodies damage important structures in the kidney. ⅱ Why are the kidneys important? To understand how lupus nephritis damages the kidney, it is important to understand how the kidneys work. The kidneys’ main function is to filter out excess waste and water from the blood through the urine. Kidneys also balance the salts and minerals circulating in the blood, help control blood pressure and make red blood cells. So, when the kidneys are damaged or fail, they can’t do their job as well. As a result, the kidneys are not able to filter out waste and water into the urine causing it to stay in the blood. What are the signs and symptoms of LN? Signs to ask the doctor about include blood in the urine or foamy urine which can mean that there is excess protein. Other signs to notice are swelling of legs, ankles, hands or tissue around the eyes as well as weight gain that can be caused by fluid the body isn’t getting rid of. ⅲ Symptoms of lupus nephritis also include high blood pressure, joint/muscle pain, high levels of waste (creatinine) in the blood, or impaired/failing kidney. ⅳ How common is LN? Lupus nephritis is the most common complication of lupus. Five out of 10 adults with lupus will have lupus nephritis, while eight out of 10 children with lupus will have kidney damage, which usually stems from lupus nephritis.