The Use of Selected Urine Chemistries in the Diagnosis of Kidney Disorders

Total Page:16

File Type:pdf, Size:1020Kb

The Use of Selected Urine Chemistries in the Diagnosis of Kidney Disorders CJASN ePress. Published on January 9, 2019 as doi: 10.2215/CJN.10330818 The Use of Selected Urine Chemistries in the Diagnosis of Kidney Disorders Biff F. Palmer1 and Deborah Joy Clegg2 Abstract Urinary chemistries vary widely in both health and disease and are affected by diet, volume status, medications, and disease states. When properly examined, these tests provide important insight into the mechanism and therapy of 1Division of various clinical disorders that are first detected by abnormalities in plasma chemistries. These tests cannot be Nephrology, interpreted in isolation, but instead require knowledge of key clinical information, such as medications, physical Department of examination, and plasma chemistries, to include kidney function. When used appropriately and with knowledge of Medicine, University of Texas Southwestern limitations, urine chemistries can provide important insight into the pathophysiology and treatment of a wide Medical Center, variety of disorders. Dallas, Texas; and Clin J Am Soc Nephrol 14: ccc–ccc, 2019. doi: https://doi.org/10.2215/CJN.10330818 2Department of Internal Medicine, University of California, Los Introduction values ,15 mEq/L. On the other hand, volume Angeles School of Urine chemistries can provide valuable insight into a expansion suppresses effector mechanisms and stimu- Medicine, Los wide range of clinical conditions. These tests are often lates release of atrial natriuretic peptide, leading to a Angeles, California underutilized because of the difficulty many physi- reduction in sodium reabsorption, causing urinary so- Correspondence: cians find in their interpretation. Whereas a basic dium concentration to be high. Thus, the urine sodium fi Dr. Biff F. Palmer, metabolic pro le obtained from a blood sample has concentrationisanindirectmeasureofvolumestatusand Department of Internal well defined normal values, there are no such values reflects the integrity of the kidney to regulate that status. Medicine, University for urine chemistries. Urinary excretion of electrolytes There are specific circumstances where measurement of Texas Southwestern vary widely as the kidney adjusts the rate of excretion of urine sodium no longer accurately reflects volume Medical Center, 5323 Harry Hines to match dietary intake and endogenous production. status. The urine sodium concentration is dependent on Boulevard, Dallas, The excretion of a dilute or concentrated urine or the amount of free water in the urine and is therefore TX 75390. Email: biff. administration of a drug can markedly alter the influenced by the rate of water reabsorption in the palmer@ concentration of urine electrolytes, potentially mis- kidneys. Under conditions of a water diuresis, the urine utsouthwestern.edu leading the clinician as to the absolute quantity in the sodium concentration may be reduced even though urine over a given amount of time. This review will be daily excretion is high, falsely suggesting the presence limited in scope and will concentrate on discussing the of a low volume state. Similarly, a concentrated urine clinical use and interpretation of urine chemistries to can increase urine sodium concentrationeventhoughthe include sodium, potassium, chloride, pH, creatinine, total amount of sodium is low, potentially masking the urea, and osmolality. Urine chemistries are best presence of volume contraction and falsely suggesting interpreted with knowledge of the clinical setting at euvolemia or volume expansion. The fractional excretion the time they are obtained. These tests can be di- of sodium (FENa)accountsfortheeffectofwater agnostic and offer mechanistic insight in the evalua- reabsorption in the kidney on urine sodium concentration: tion of AKI, volume status, disorders of plasma sodium and potassium, and acid-base disorders. FENa 5 ðUNa 3 PCreatinine=PNa 3 UCreatinineÞ 3 100% This formula expresses the percentage of filtered so- Urine Sodium dium excreted in the urine and provides a measure of Assessment of Effective Circulating Volume sodium handling that is independent of urinary con- Under normal conditions, sodium excretion by the centration. kidney equals dietary intake minus the small amount lost in sweat and feces, and typically ranges from 40 to 220 mEq/d. The ability to match dietary intake with Differentiation of Prerenal Azotemia versus Acute excretion enables extracellular fluid volume to be main- Tubular Necrosis tained within a narrow range. When effective circulatory Measurement of urine sodium concentration and volume is reduced, activation of effector mechanisms FENa are frequently utilized to determine whether such as sympathetic nerves and the renin-angiotensin- AKI is prerenal and correctable by restoring intravas- aldosterone system causes avid sodium retention in cular volume, or whether it is secondary to acute the kidneys, lowering urine sodium concentration to tubular necrosis, where administration of fluids might www.cjasn.org Vol 14 April, 2019 Copyright © 2019 by the American Society of Nephrology 1 2 Clinical Journal of the American Society of Nephrology be harmful by causing volume overload (1). A random The utility of the FEUrea to assess effective circulatory , urine sodium concentration of 15 mEq/L and a FENa of volume is lost when proximal reabsorption of salt and ,1% suggest the presence of a volume-responsive compo- water is impaired (22). This situation occurs after either nent to a reduced GFR. In patients with established acute administration of acetazolamide, an osmotic diuresis due tubular necrosis, loss of tubular function will prevent to administration of mannitol, glycosuria as in uncon- maximal sodium retention even when extracellular fluid trolled diabetes, or increased urea excretion resulting from volume depletion is present. These tests remain useful high protein intake or catabolism. Proximal tubule salt when evaluating a change in kidney function in patients with reabsorption may also be impaired in patients with cerebral previously stable CKD; however, the response to decreased salt wasting (23). kidney perfusion is delayed and the reduction in urine sodium The FEUrea has also been used to discriminate between will be less maximal as compared with normal kidneys (2) volume responsive azotemia and tubular necrosis in the (Supplemental Material, Case 1). absence of diuretic use. How this test compares to the FENa Therearesituationswheretheurinesodiumconcentra- for this purpose is difficult to determine because studies tion and FENa inadequately distinguish between azotemia included patients who were highly selected and excluded due to kidney parenchymal injury from volume responsive those with interstitial nephritis, GN, urinary obstruction, and azotemia (3). These conditions are characterized by vaso- exposure to radiocontrast material (19,20). Another potential constriction in the kidney causing a reduction in GFR and limitation of the FEUrea is its use in elderly patients and those filtered load of sodium in the setting where tubular with sepsis. Studies in experimental models show down- function remains relatively intact (4–12) (Figure 1). The regulation of urea transporters in the nephron with biochemical profile in the urine can change in a time endotoxemia and aging. This effect would tend to increase dependent manner from a prerenal picture to that of acute the FEUrea in septic and elderly patients even when volume tubular necrosis. Variability in timing of measurements depletion was the only cause of azotemia (24,25). likely explains disparities in the literature as to sensitivity Conditions in which volume contraction coexists with a and specificity of these tests in patients with AKI (13–15). The nonreabsorbable anion also cause urine sodium concentra- fi sensitivity and speci city of the FENa is greatest when tion and FENa to be increased. As discussed below, urinary applied to patients with oliguria and a reduced GFR (dis- chloride concentration is typically low in this setting. cussed further in Supplemental Material, Cases 1 and 2). In patients with severe congestive heart failure, advanced cirrhosis of the liver, and extensive burns, a reduction in the Urinary Chloride filtered load of sodium brought about by intense neurohu- Urinary excretion of chloride mirrors sodium excretion in moral activation can cause sodium retention in the kidneys to response to dietary intake. In a manner similar to sodium, the be of such a degree that urine sodium concentration and FENa urinary concentration of chloride and fractional excretion of remain low even when tubular necrosis is present, as chloride (FECL) can be used as indirect markers of effective manifested by granular casts and tubular cells in the urine circulatory volume. Despite these similarities, there are (16–19). Despite volume expansion, a low urinary sodium situations when the directional change in urinary concentration concentration is typically present early in acute GN when may differ, such that reliance solely on one or the other can lead tubular function is intact and the filtered load of sodium is to an erroneous assessment of effective volume status. These reduced because of the decrease in glomerular surface area differences are particularly evident when volume disturbances available for filtration (11). are accompanied by acid-base disorders (26). For this reason, Active diuretic use is another situation where the urine both urine sodium and chloride should be obtained when fl sodium concentration and FENa may not accurately re ect using urine electrolytes to assess volume or acid-base
Recommended publications
  • A Lady with Renal Stones
    A lady with renal stones Dr KC Lo, Dr KY Lo, Dr SK Mak KWH History 53/F NSND, NKDA Good past health Complained of bilateral loin pain for few years No urinary symptoms/UTIs No haematuria Not on regular medications/vitamins No significant family history History Attended private practitioner in Feb, 2006: Blood test : Na/K 143/3.9 Ur/Cr 7.3/101 LFT N Urine test : RBC numerous/HPF WBC 5-8/HPF CXR unremarkable Given analgesics History Still on-and-off bilateral loin and lower chest pain Seek advice from Private Hospital: Blood test: WBC 3.2 Hb 12.9 Plt 139 Na/K 146/ 3.0 Ur/Cr 6.3/108 Ca2+/PO4 2.11/1.39 LFT unremarkable Urine test : RBC 6-8/HPF, WBC 0-1/HPF no cast KUB: bilateral renal stones (as told by patient) History ESWL done to right renal stone in 5/06, planned to have ESWL to left stone later But she then defaulted FU History This time admitted to our surgical ward complaining of similar bilateral lower chest wall pain (for six months) Had vomiting of undigested food 8 times per day for 1 day, no diarrhoea No fever Recent intake of herbs one week ago Physical exam BP 156/77 P 68 afebrile Hydration normal Chest, CVS unremarkable Local tenderness over bilateral lower chest wall Abdomen soft, mild epigastric tenderness, no rebound and guarding KUB Multiple tiny calcific densities projecting in bilateral renal areas with apparent distribution of the renal medulla bilateral medullary nephrocalcinosis CT Scan 1 yr ago in private CT Scan 1 yr ago in private Investigations WBC 3.1 HB 13.1 Plt 137 Na
    [Show full text]
  • Electrolyte and Acid-Base
    Special Feature American Society of Nephrology Quiz and Questionnaire 2013: Electrolyte and Acid-Base Biff F. Palmer,* Mark A. Perazella,† and Michael J. Choi‡ Abstract The Nephrology Quiz and Questionnaire (NQ&Q) remains an extremely popular session for attendees of the annual meeting of the American Society of Nephrology. As in past years, the conference hall was overflowing with interested audience members. Topics covered by expert discussants included electrolyte and acid-base disorders, *Department of Internal Medicine, glomerular disease, ESRD/dialysis, and transplantation. Complex cases representing each of these categories University of Texas along with single-best-answer questions were prepared by a panel of experts. Prior to the meeting, program Southwestern Medical directors of United States nephrology training programs answered questions through an Internet-based ques- Center, Dallas, Texas; † tionnaire. A new addition to the NQ&Q was participation in the questionnaire by nephrology fellows. To review Department of Internal Medicine, the process, members of the audience test their knowledge and judgment on a series of case-oriented questions Yale University School prepared and discussed by experts. Their answers are compared in real time using audience response devices with of Medicine, New the answers of nephrology fellows and training program directors. The correct and incorrect answers are then Haven, Connecticut; ‡ briefly discussed after the audience responses, and the results of the questionnaire are displayed. This article and Division of recapitulates the session and reproduces its educational value for the readers of CJASN. Enjoy the clinical cases Nephrology, Department of and expert discussions. Medicine, Johns Clin J Am Soc Nephrol 9: 1132–1137, 2014.
    [Show full text]
  • Renal Effects of Atrial Natriuretic Peptide Infusion in Young and Adult ~Ats'
    003 1-3998/88/2403-0333$02.00/0 PEDIATRIC RESEARCH Vol. 24, No. 3, 1988 Copyright O 1988 International Pediatric Research Foundation, Inc. Printed in U.S.A. Renal Effects of Atrial Natriuretic Peptide Infusion in Young and Adult ~ats' ROBERT L. CHEVALIER, R. ARIEL GOMEZ, ROBERT M. CAREY, MICHAEL J. PEACH, AND JOEL M. LINDEN WITH THE TECHNICAL ASSISTANCE OF CATHERINE E. JONES, NANCY V. RAGSDALE, AND BARBARA THORNHILL Departments of Pediatrics [R.L.C., A.R.G., C.E.J., B. T.], Internal Medicine [R.M.C., J.M. L., N. V.R.], Pharmacology [M.J.P.], and Physiology [J.M.L.], University of Virginia, School of Medicine, Charlottesville, Virginia 22908 ABSTRAm. The immature kidney appears to be less GFR, glomerular filtration rate responsive to atrial natriuretic peptide (ANP) than the MAP, mean arterial pressure mature kidney. It has been proposed that this difference UeC~pV,urinary cGMP excretion accounts for the limited ability of the young animal to UN,V, urinary sodium excretion excrete a sodium load. To delineate the effects of age on the renal response to exogenous ANP, Sprague-Dawley rats were anesthetized for study at 31-32 days of age, 35- 41 days of age, and adulthod. Synthetic rat A* was infused intravenously for 20 min at increasing doses rang- By comparison to the adult kidney, the immature kidney ing from 0.1 to 0.8 pg/kg/min, and mean arterial pressure, responds to volume expansion with a more limited diuresis and glomerular filtration rate, plasma ANP concentration, natriuresis (I). A number of factors have been implicated to urine flow rate, and urine sodium excretion were measured explain this phenomenon in the neonatal kidney, including a at each dose.
    [Show full text]
  • Guidelines for Approach to a Child with Metabolic Acidosis (Including RTA)
    Guidelines for approach to a child with Metabolic acidosis (including RTA) Children’s Kidney Centre University Hospital of Wales Cardiff CF14 4XW DISCLAIMER: These guidelines were produced in good faith by the authors reviewing available evidence/opinion. They were designed for use by paediatric nephrologists at the University Hospital of Wales, Cardiff for children under their care. They are neither policies nor protocols but are intended to serve only as guidelines. They are not intended to replace clinical judgment or dictate care of individual patients. Responsibility and decision-making (including checking drug doses) for a specific patient lie with the physician and staff caring for that particular patient. Version 1, S. Hegde/Sept 2007 Metabolic acidosis ormal acid base balance Maintaining normal PH is essential for cellular enzymatic and other metabolic functions and normal growth and development. Although it is the intracellular PH that matter for cell function, we measure extra cellular PH as 1. It is easier to measure 2. It parallels changes in intracellular PH 3. Subject to more variation because of lesser number of buffers extra cellularly. Normal PH is maintained by intra and extra cellular buffers, lungs and kidneys. Buffers attenuate changes in PH when acid or alkali is added to the body and they act by either accepting or donating Hydrogen ions. Buffers function as base when acid is added or as acid when base is added to body. Main buffers include either bicarbonate or non-bicarbonate (proteins, phosphates and bone). Source of acid load: 1. CO2- Weak acid produced from normal metabolism, dealt with by lungs pretty rapidly(within hours) 2.
    [Show full text]
  • Urate-2- C Transport in the Rat Nephron
    Urate-2-14C transport in the rat nephron Ronald A. Kramp, … , William E. Lassiter, Carl W. Gottschalk J Clin Invest. 1971;50(1):35-48. https://doi.org/10.1172/JCI106482. Research Article Intrarenal transport of urate-2-14C was studied in anesthetized rats using the microinjection technic. During saline diuresis, small volumes of urate-2-14C (0.24-0.48 mM) and inulin-3H were injected into surface proximal and distal convoluted tubules, and ureteral urine was collected serially. Total (74-96%) and direct (57-84%) urate recovery increased significantly the more distal the puncture site. Delayed recovery (±20%) remained approximately the same regardless of localization of the microinjection. After proximal injections, total and direct recoveries of urate-2-14C were significantly higher in rats treated with probenecid, pyrazinoate, or PAH than during saline diuresis alone, while the excretion rates were comparable after distal injection. Delayed recovery was not altered by drug administration. The decreased proximal reabsorption of urate is presumably due to an effect of the drugs on the luminal membrane of the nephron. For perfusion at high urate concentrations, nonradioactive urate was added to the injectate (0.89-1.78 mM). Urate-2-14C recovery was almost complete and there was no delayed excretion, demonstrating saturation kinetics. These findings are compatible with a carrier-mediated mechanism for urate transport probably located at the luminal border of the proximal tubular epithelium. No definitive evidence for urate secretion was found in these studies. Find the latest version: https://jci.me/106482/pdf Urate-2-14C Transport in the Rat Nephron RONALD A.
    [Show full text]
  • Clinical Features, Genetic Background, and Outcome in Infants with Urinary Tract Infection and Type IV Renal Tubular Acidosis
    www.nature.com/pr CLINICAL RESEARCH ARTICLE Clinical features, genetic background, and outcome in infants with urinary tract infection and type IV renal tubular acidosis Min-Hua Tseng1, Jing-Long Huang2, Shih-Ming Huang3, Jeng-Daw Tsai4,5,6,7, Tai-Wei Wu8, Wen-Lang Fan9, Jhao-Jhuang Ding1,10 and Shih-Hua Lin11 BACKGROUND: Type IV renal tubular acidosis (RTA) is a severe complication of urinary tract infection (UTI) in infants. A detailed clinical and molecular analysis is still lacking. METHODS: Infants with UTI who exhibited features of type IV RTA were prospectively enrolled. Clinical, laboratory, and image characteristics and sequencing of genes responsible for phenotype were determined with follow-up. RESULTS: The study cohort included 12 infants (9 males, age 1–8 months). All exhibited typical type IV RTA such as hyperkalemia with low transtubular potassium gradient, hyperchloremic metabolic acidosis with positive urine anion gap, hypovolemic hyponatremia with renal salt wasting, and high plasma renin and aldosterone levels. Seven had hyperkalemia-related arrhythmia and two of them developed life-threatening ventricular tachycardia. With prompt therapy, all clinical and biochemical abnormalities resolved within 1 week. Five had normal urinary tract anatomy, and three of them carried genetic variants on NR3C2. Three variants, c.1645T>G (S549A), c.538G>A (V180I), and c.1-2C>G, on NR3C2 were identified in four patients. During follow-up, none of them had recurrent type IV RTA, but four developed renal scaring. CONCLUSIONS: Genetic mutation on NR3C2 may contribute to the development of type IV RTA as a complication of UTI in infants fi 1234567890();,: without identi able risk factors, such as urinary tract anomalies.
    [Show full text]
  • Atrial Natriuretic Peptide and Blood Volume During Red Cell Transfusion
    Archives ofDisease in Childhood 1991; 66: 395-397 395 Atrial natriuretic peptide and blood volume during Arch Dis Child: first published as 10.1136/adc.66.4_Spec_No.395 on 1 April 1991. Downloaded from red cell transfusion in preterm infants W Rascher, N Lingens, M Bald, 0 Linderkamp Abstract 1710 g (range 650-2660). All infants were in Because raised plasma concentrations of good clinical condition. Four were mechanically atrial natriuretic peptide indicate volume ventilated through an intratracheal tube. None expansion, we studied the effect of red cell had renal disease, shock, sepsis or were being transfusion on plasma atrial natriuretic pep- treated with diuretics. The volume of trans- tide concentration, packed cell volume, and fused red cells was calculated to raise the packed intravascular volume in eight preterm infants. cell volume to 0-45 (haemoglobin to 155 g/l). Red cell transfusion increased red cell mass, The transfusion rate averaged 0-05 (0 01) packed cell volume and erythrocyte count, ml/min/kg. but decreased plasma volume. Total blood Before and one hour after red cell transfusion volume, plasma atrial natriuretic peptide con- blood was drawn in EDTA coated tubes (1 5-2 centration, urine flow rate, and urinary ml) for determination of plasma atrial natriur- sodium excretion did not change. etic peptide and haemoglobin concentrations We conclude that a slow transfusion of packed cell volume, haemoglobin F concentra- less than 10 ml red cells/kg body weight does tion, and plasma osmolality. In addition 0 5 ml not cause volume expansion with subsequent blood was drawn in plastic tubes for measure- atrial natriuretic peptide release thereby ment of serum sodium, potassium and creati- affecting the cardiovascular system.
    [Show full text]
  • Hypernatremia Due to Urea-Induced Osmotic Diuresis: Physiology at The
    Educational Forum Hypernatremia due to Urea-Induced Osmotic Diuresis: Physiology at the Bedside Sonali Vadi, Kenneth Yim1 Private Practitioner, Mumbai, Maharashtra, India, 1Director of Inpatient Hemodialysis‑Davita Dialysis, University of Maryland Midtown Campus, Maryland, USA Abstract Hypernatremia secondary to urea‑induced solute diuresis is due to the renal excretion of electrolyte‑free water. This concept is explained here step‑wise physiologically with the help of a clinical vignette. Keywords: Electrolyte‑free water clearance, hypernatremia, hypertonicity, osmotic diuresis, urea BACKGROUND Her initial laboratory data are presented in Table 1 and electrolyte trends during the hospital stay are summarized in Equation between solutes and water determines serum sodium Table 2. levels. Increased urinary solute load in the form of urea nitrogen leads to urea‑induced osmotic diuresis with increased Acute issues at hand free water loss and ensued hypernatremia. Diagnostic 1. What is the cause of her renal dysfunction? CLINICAL VIGNETTE 2. Why is she hypernatremic? A 70‑year‑old woman was found unconscious at home. As Treatment per her family members, she complained of abdominal pain 1. Should she be urgently dialyzed? and diarrhea for 1 week’s duration. Her baseline mental 2. How should her hypernatremia be managed? status was noted to be alert and oriented three days prior to presentation. Her medical history was significant for DISCUSSION hypertension and osteoarthritis. There was no prior history of renal dysfunction. She has been a heavy alcohol drinker. This complex pathological situation has been de‑coded Her medications included ibuprofen and cyclobenzaprine step‑wise in a question format, with answers to each in two for osteoarthritis; lisinopril and felodipine for hypertension; parts.
    [Show full text]
  • Abim Certification Exam: Nephrology
    7/12/16 Disclosures • I am site PI for the REPRISE study evaluating efficacy of ABIM CERTIFICATION tolvaptan in autosomal dominant polycystic kidney EXAM: NEPHROLOGY disease (Otsuka pharmaceuticals) JULY 2016 UCSF CME Division of NephroloGy Department of Medicine Meyeon Park, MD MAS As s is tant Pr ofes s or Roadmap for today • Glomerular diseases (30 min) ---------Scheduled 15 min break------- • Common electrolyte abnormalities (30 min) • Acid-base (45 min) • Acute kidney injury (20 min) GLOMERULAR DISEASES • Secondary hypertension (10 min) 1 7/12/16 Case Laboratory studies A 74 yo man is evaluated for a 5-month history of sinusitis • Hemoglobin 11.5 g/dl and intermittent otitis media. He has lost 9 lbs (4.1 kg) • Leukocyte count 10.8x10^9 /L and has occasional joint pains. • Blood urea nitrogen 28 mg/dl Physical exam: Afebrile • Creatinine 1.6 m/dl HEENT: crusting in right nares; opaque right tympanic • Albumin 3.8 g/dl membrane; bilateral maxillary sinus tenderness • C3 100 mg/dl CV: 2/6 systolic murmur • C4 32 mg/dl Lungs: rhonchi • Urinalysis: 18 dysmorphic erythrocytes and 1 erythrocyte Extremities: 2+ edema bilateral lower ext cast/hpf • CXR: nodule in RUL, hazy density in LLL Case Question Case answer review A. Antinuclear antibody – lupus nephritis – wrong age / Which one of the following studies is most appropriate? sex – low complements A. Antinuclear antibody B. Anti-glomerular basement membrane antibody – wrong B. Anti-glomerular basement membrane antibody history; usually younger men; no respiratory C. Myeloperoxidase antineutrophil cytoplasmic antibody involvement D. Proteinase-3 antineutrophil cytoplasmic antibody C. Myeloperoxidase ANCA – can exist in granulomatous E.
    [Show full text]
  • Near and Far
    CLINICAL CARE CONUNDRUMS Near and Far The approach to clinical conundrums by an expert clinician is revealed through the presentation of an actual patient’s case in an approach typical of a morning report. Similar to patient care, sequential pieces of information are provided to the clinician, who is unfamiliar with the case. The focus is on the thought processes of both the clinical team caring for the patient and the discussant. This icon represents the patient’s case. Each paragraph that follows represents the discussant’s thoughts. Adam Gray, MD1,2, Sean Lockwood, MD1,2, Aibek E. Mirrakhimov, MD1, Allan C. Gelber, MD3, Reza Manesh, MD3* 1Department of Medicine, University of Kentucky College of Medicine, Lexington, Kentucky; 2Department of Medicine, Lexington Veterans Affairs Medical Center, Lexington, Kentucky; 3Department of Medicine, Johns Hopkins Hospital and Johns Hopkins University School of Medicine, Balti- more, Maryland. A previously healthy 30-year-old woman presented to but no fever, weight loss, dyspnea, dysphagia, visual chang- the emergency department with 2 weeks of weakness. es, paresthesias, bowel or bladder incontinence, back pain, or preceding gastrointestinal or respiratory illness. She had True muscle weakness must be distinguished from the more experienced diffuse intermittent hives, most prominent in her common causes of asthenia. Many systemic disorders pro- chest and upper arms, for the past several weeks. duce fatigue, with resulting functional limitation that is often interpreted by patients as weakness. Initial history should fo- History certainly supports true weakness but will need to be cus on conditions producing fatigue, such as cardiopulmonary confirmed on examination. The distribution began as proximal disease, anemia, connective tissue disease, depression or ca- but now appears diffuse.
    [Show full text]
  • Atrial Natriuretic Peptide and Furosemide Effects on Hydraulic Pressure in the Renal Papilla
    Kidney International, Vol. 34 (1988), pp. 36—42 Atrial natriuretic peptide and furosemide effects on hydraulic pressure in the renal papilla RAMON E. MENDEZ, B. RENTZ DUNN, JULIA L. TROY, and BARRY M. BRENNER The Harvard Center for the Study of Kidney Diseases, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA Atrial natriuretic peptide and furosemide effects on hydraulic pressure pre-renal arterial clamping prior to, or during, ANP administra- in the renal papilla. Atrial peptides (ANP) have been shown to prefer- tion has been shown to markedly blunt or abolish the natriuresis entially increase blood flow tojuxtamedullary nephrons and to augment vasa recta blood flow. To determine the effect of this alteration in[1,9,4]. Since clamping also prevented an ANP-induced rise in intrarenal blood flow distribution on pressure relationships in innerGFR, the enhancement of GFR by ANP was felt to be a primary medullary structures and their significance as a determinant of ANP- factor responsible for its natriuretic effect [11. However, several induced natriuresis, we measured hydraulic pressures in vascular and studies have demonstrated increases in renal sodium excretion tubule elements of the renal papilla exposed in Munich-Wistar rats in in the absence of discernable changes in whole kidney hemo- vivo during an euvolemic baseline period and again during an experi- mental period. Rats in Group 1 received intravenous infusion of rANP dynamics [6, 7, 10]. On the other hand, an additional hemody- [4-27], administered as a 4 sg/kg prime and 0.5 gIkg/min continuous namic mechanism which might be operative lies in the renal infusion, and were maintained euvolemic by plasma replacement.vasodilatory properties of ANP, in particular its ability to Infusion of ANP resulted in significant natriuresis, diuresis and increase increase vasa recta blood flow [11, 10].
    [Show full text]
  • Table of Contents (PDF)
    CJASNClinical Journal of the American Society of Nephrology February 2018 c Vol. 13 c No. 2 Patient Voice 193 Accountability of Dialysis Facilities in Transplant Referral: CMS Needs to Collect National Data on Dialysis Facility Kidney Transplant Referrals Kevin John Fowler See related article on page 282. Editorials 195 The Urine Anion Gap in Context Daniel Batlle, Sheeba Habeeb Ba Aqeel, and Alonso Marquez See related article on page 205. 198 Why Nomenclature for Pharmacist-Led Interventions Matters: Conquering the State of Confusion Amy Barton Pai See related article on page 231. 201 Persistent Hematuria in ANCA Vasculitis: Ominous or Innocuous? Shannon L. Mahoney and Patrick H. Nachman See related article on page 251. 203 Employment among Patients on Dialysis: An Unfulfilled Promise Ayman Hallab and Jay B. Wish See related article on page 265. Original Articles Acid/Base and Electrolyte Disorders 205 Urine Anion Gap to Predict Urine Ammonium and Related Outcomes in Kidney Disease Kalani L. Raphael, Sarah Gilligan, and Joachim H. Ix See related editorial on page 195. Chronic Kidney Disease 213 Nondepressive Psychosocial Factors and CKD Outcomes in Black Americans Joseph Lunyera, Clemontina A. Davenport, Nrupen A. Bhavsar, Mario Sims, Julia Scialla, Jane Pendergast, Rasheeda Hall, Crystal C. Tyson, Jennifer St. Clair Russell, Wei Wang, Adolfo Correa, L. Ebony Boulware, and Clarissa J. Diamantidis 223 Association between Urine Ammonium and Urine TGF-b1inCKD Kalani L. Raphael, Sarah Gilligan, Thomas H. Hostetter, Tom Greene, and Srinivasan Beddhu 231 Medication Therapy Management after Hospitalization in CKD: A Randomized Clinical Trial Katherine R. Tuttle, Radica Z. Alicic, Robert A.
    [Show full text]