RENAL CASE 6.1 Nephrotic Syndrome
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Edema II, Clinical Significance
EDEMA II CLINICAL SIGNIFICANCE F. A. LeFEVRE, M.D., R. H. McDONALD, M.D., AND A. C. CORCORAN, M.D. It is the purpose of this paper to outline the clinical syndromes in which edema significantly appears, to discuss their differentiation, and to comment on the changes to which edema itself may give rise. The frequency with which edema occurs indicates the variety of its origins. Its physiologic bases have been reviewed in a former paper.1 Conditions in which edema commonly appears are summarized in Table 1. Although clinical edema usually involves more than one physiologic mechanism, it is not difficult to determine the predominant disturbance. Table 2 illustrates the physiologic mechanisms of clinical edema. Physiologically, edema is an excessive accumulation of interstitial fluid. Clinically, it may be latent or manifest, and, by its nature, localized or generalizing. These terms, with the exception of generalizing, have been defined, and may be accepted. By generalizing edema is meant a condi- tion in which edema is at first local in its appearance, but in which, as the process extends, edema will become general, causing anasarca. The degree of edema in any area is limited by tissue tension and the sites of its first appearance and later spread are partly determined by gravity. CARDIAC EDEMA Generalizing edema is an early manifestation of cardiac failure. It is usually considered to be evidence of inadequacy of the right ventricu- lar musculature (back pressure theory). Peripheral edema may be accompanied by pulmonary edema in cases where there is simultaneous left ventricular failure. Actually, the genesis of cardiac edema may depend more on sodium retention2,3'4 due to "forward cardiac failure" and renal constriction than on venous back pressure alone. -
Managing Hyponatremia in Patients with Syndrome of Inappropriate Antidiuretic Hormone Secretion
REVIEW Managing Hyponatremia in Patients With Syndrome of Inappropriate Antidiuretic Hormone Secretion Joseph G. Verbalis, MD Division of Endocrinology and Metabolism, Department of Medicine, Georgetown University Medical Center, Washington DC. J.G. Verbalis received an honorarium funded by an unrestricted educational grant from Otsuka America Pharmaceuticals, Inc., for time and expertise spent in the composition of this article. No editorial assistance was provided. No other conflicts exist. This review will address the management of hyponatremia caused by the syndrome of inappropriate antidiuretic hormone secretion (SIADH) in hospitalized patients. To do so requires an understanding of the pathogenesis and diagnosis of SIADH, as well as currently available treatment options. The review will be structured as responses to a series of questions, followed by a presentation of an algorithm for determining the most appropriate treatments for individual patients with SIADH based on their presenting symptoms. Journal of Hospital Medicine 2010;5:S18–S26. VC 2010 Society of Hospital Medicine. Why is SIADH Important to Hospitalists? What Causes Hyponatremia in Patients with SIADH? Disorders of body fluids, and particularly hyponatremia, are Hyponatremia can be caused by 1 of 2 potential disruptions among the most commonly encountered problems in clinical in fluid balance: dilution from retained water, or depletion medicine, affecting up to 30% of hospitalized patients. In a from electrolyte losses in excess of water. Dilutional hypo- study of 303,577 laboratory samples collected from 120,137 natremias are associated with either a normal (euvolemic) patients, the prevalence of hyponatremia (serum [Naþ] <135 or an increased (hypervolemic) extracellular fluid (ECF) vol- mmol/L) on initial presentation to a healthcare provider was ume, whereas depletional hyponatremias generally are asso- 28.2% among those treated in an acute hospital care setting, ciated with a decreased ECF volume (hypovolemic). -
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. -
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. -
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. -
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. -
Anasarca As the Presenting Symptom of Juvenile Dermatomyositis: a Case Series Emily E
Schildt and De Ranieri Pediatric Rheumatology (2021) 19:120 https://doi.org/10.1186/s12969-021-00604-3 CASE REPORT Open Access Anasarca as the presenting symptom of juvenile dermatomyositis: a case series Emily E. Schildt and Deirdre De Ranieri* Abstract Background: Juvenile Dermatomyositis (JDM) is an autoimmune disease that typically presents with classic skin rashes and proximal muscle weakness. Anasarca is a rare manifestation of this disease and is associated with a more severe and refractory course, requiring increased immunosuppression. Early recognition of this atypical presentation of JDM may lead to earlier treatment and better outcomes. Case presentation: We present two female patients, ages 11 years old and 4 years old, who presented to the ED with anasarca and were subsequently diagnosed with JDM. Both patients required ICU-level care and significant immunosuppression, including prolonged courses of IV methylprednisolone, IVIG, and Rituximab. Conclusions: Anasarca is a rare presentation of Juvenile Dermatomyositis, but it is important for clinicians to recognize this manifestation of the disease. Early recognition and treatment will lead to better outcomes in these children and hopefully decrease the need for prolonged hospitalization and ICU level care. Keywords: Juvenile dermatomyositis, Anasarca, Generalized edema, Vascular permeability, Muscle enzymes, Myositis, Immunosuppression Background We describe two patients with a final diagnosis of Ju- Juvenile dermatomyositis (JDM) is the most common venile Dermatomyositis who presented with anasarca, chronic inflammatory myopathy of childhood. It is an both of whom required ICU-level care. Anasarca is a autoimmune disease that primarily affects the muscles rare presentation of this disease but can be life- and skin but can also affect the blood vessels, manifest- threatening, and expedient identification and treatment ing as localized edema. -
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, -
2015 Diagnostic Criteria for TAFRO (Thrombocytopenia-Anasarca-Fever-Renal Insufficiency-Organomegaly) Syndrome
2015 diagnostic criteria for TAFRO (Thrombocytopenia-anasarca-fever-renal insufficiency-organomegaly) syndrome Masaki Y. et al. Int J Hematol, 2016, 103:686-692 This research was originally published in International Journal of Hematology, Masaki Y, et al., Proposed diagnostic criteria, disease severity classification and treatment strategy for TAFRO syndrome. 2015 version. Int J Hematol. 2016, 103:686-92 © 2016 by The Japanese Society of Hematology. Reproduced with permission. http://link.springer.com/article/10.1007%2Fs12185-016-1979-1. A. Major categories (1) Anasarca, including pleural effusion, ascites and general edema (2) Thrombocytopenia; defined as a pre-treatment platelet count ≤100,000/μl (3) Systemic inflammation, defined as fever of unknown etiology above 37.5 °C and/or serum C-reactive protein concentration ≥2 mg/dl B. Minor categories (1) Castleman’s disease-like features on lymph node biopsy (2) Reticulin myelofibrosis and/or increased number of megakaryocytes in bone marrow (3) Mild organomegaly, including hepatomegaly, splenomegaly and lymphadenopathy (4) Progressive renal insufficiency C. Diseases to be excluded (1) Malignancies, including lymphoma, myeloma, mesothelioma, etc. (2) Autoimmune disorders, including systemic lupus erythematosus (SLE), ANCA-associated vasculitis, etc. (3) Infectious disorders, including acid fast bacterial infection, rickettsial disease, lyme disease, severe fever with thrombocytopenia syndrome (SFTS), etc. (4) POEMS syndrome (5) IgG4-related disease (6) Hepatic cirrhosis (7) Thrombotic thrombocytopenic -
An Unusual Case of Postpartum Anasarca an Unusual Case of Postpartum Anasarca
JSAFOG CASE REPORT An Unusual Case of Postpartum Anasarca An Unusual Case of Postpartum Anasarca 1Jai Inder Singh, 2Randhir Puri, 3KG Kiran 1Major, Graded Specialist, Medicine, Military Hospital, Belgaum, Karnataka, India 2Colonel, Department of Obstetrics and Gynecology, Military Hospital, Belgaum, Karnataka, India 3Colonel, Commanding Officer, Military Hospital, Belgaum, Karnataka, India Correspondence: Major, Jai Inder Singh, Medical specialist, Military Hospital, Belgaum Camp, Karnataka-590009, India Phone: +919343979290, +918312423852, e-mail: [email protected] Abstract A 21-year-old lady, primipara presented with breathlessness on exertion and generalized swelling of three weeks duration. Clinical examination revealed anasarca and features of cardiac failure. After evaluation, a diagnosis of peripartum cardiomyopathy was established based on echocardiographic findings of dilated cardiac chambers and poor left ventricular function. She responded well to treatment. The case is being reported for the diagnostic dilemma and rarity. Keywords: Anasarca, peripartum cardiomyopathy, systolic dysfunction, echocardiography. INTRODUCTION pleural effusion, ascites and mild hepatomegaly. Laboratory examination revealed microcytic hypochromic anemia (Hb = Peripartum cardiomyopathy (PPCM) is a type of dilated 8.2 gm/dl). Urine analysis showed presence of albumin 2 +, 8-10 cardiomyopathy in women with no past history of cardiac pus cells and 4-6 RBC’s/hpf. Twenty four hour urine protein disease and requires a high index of suspicion for diagnosis. was 1.12 gm and urine culture was sterile. Renal/liver function It is a disease of uncertain etiology and can worsen during tests, serum proteins, albumin and cholesterol were within normal future pregnancies. Symptomatic patients should receive limits. Chest X-ray showed cardiomegaly and bilateral pleural therapy for cardiac failure. -
Parasites in Liver & Biliary Tree
Parasites in Liver & Biliary tree Luis S. Marsano, MD Professor of Medicine Division of Gastroenterology, Hepatology and Nutrition University of Louisville & Louisville VAMC 2011 Parasites in Liver & Biliary Tree Hepatic Biliary Tree • Protozoa • Protozoa – E. histolytica – Cryptosporidiasis – Malaria – Microsporidiasis – Babesiosis – Isosporidiasis – African Trypanosomiasis – Protothecosis – S. American Trypanosomiasis • Trematodes – Visceral Leishmaniasis – Fascioliasis – Toxoplasmosis – Clonorchiasis • Cestodes – Opistorchiasis – Echynococcosis • Nematodes • Trematodes – Ascariasis – Schistosomiasis • Nematodes – Toxocariasis – Hepatic Capillariasis – Strongyloidiasis – Filariasis Parasites in the Liver Entamoeba histolytica • Organism: E. histolytica is a Protozoa Sarcodina that infects 1‐ 5% of world population and causes 100000 deaths/y. – (E. dispar & E. moshkovskii are morphologically identical but only commensal; PCR or ELISA in stool needed to differentiate). • Distribution: worldwide; more in tropics and areas with poor sanitation. • Location: colonic lumen; may invade crypts and capillaries. More in cecum, ascending, and sigmoid. • Forms: trophozoites (20 mcm) or cysts (10‐20 mcm). Erytrophagocytosis is diagnostic for E. histolytica trophozoite. • Virulence: may increase with immunosuppressant drugs, malnutrition, burns, pregnancy and puerperium. Entamoeba histolytica • Clinical forms: – I) asymptomatic; – II) symptomatic: • A. Intestinal: – a) Dysenteric, – b) Nondysenteric colitis. • B. Extraintestinal: – a) Hepatic: i) acute -
Obstruction of the Urinary Tract 2567
Chapter 540 ◆ Obstruction of the Urinary Tract 2567 Table 540-1 Types and Causes of Urinary Tract Obstruction LOCATION CAUSE Infundibula Congenital Calculi Inflammatory (tuberculosis) Traumatic Postsurgical Neoplastic Renal pelvis Congenital (infundibulopelvic stenosis) Inflammatory (tuberculosis) Calculi Neoplasia (Wilms tumor, neuroblastoma) Ureteropelvic junction Congenital stenosis Chapter 540 Calculi Neoplasia Inflammatory Obstruction of the Postsurgical Traumatic Ureter Congenital obstructive megaureter Urinary Tract Midureteral structure Jack S. Elder Ureteral ectopia Ureterocele Retrocaval ureter Ureteral fibroepithelial polyps Most childhood obstructive lesions are congenital, although urinary Ureteral valves tract obstruction can be caused by trauma, neoplasia, calculi, inflam- Calculi matory processes, or surgical procedures. Obstructive lesions occur at Postsurgical any level from the urethral meatus to the calyceal infundibula (Table Extrinsic compression 540-1). The pathophysiologic effects of obstruction depend on its level, Neoplasia (neuroblastoma, lymphoma, and other retroperitoneal or pelvic the extent of involvement, the child’s age at onset, and whether it is tumors) acute or chronic. Inflammatory (Crohn disease, chronic granulomatous disease) ETIOLOGY Hematoma, urinoma Ureteral obstruction occurring early in fetal life results in renal dys- Lymphocele plasia, ranging from multicystic kidney, which is associated with ure- Retroperitoneal fibrosis teral or pelvic atresia (see Fig. 537-2 in Chapter 537), to various