DOCSLIB.ORG

Uremic Acidosis

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Uremic Acidosis View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Kidney International, Vol. 34 (1988), pp. 278—287 NEPHROLOGY FORUM Uremic acidosis Principal discussant: DAVID G. WARNOCK San Francisco Veterans Administration Medical center, San Francisco, california mg/dl; and glucose, 145 mg/dl. Urinalysis revealed a specific gravity of 1.010; pH 6.0; trace protein; occasional white blood cells; and no red Editors blood cells, casts, or crystals. A 12-hour urine collection disclosed 638 JORDAN J. COHEN mg of creatinine and a creatinine clearance of 13 mI/mm. The patient had dialysis twice via a subclavian catheter, and an JOHN T. HARRINGTON arteriovenous fistula was constructed. All antihypertensive medications JEROME P. KA55IRER were discontinued and the patient was discharged on a regimen of NIcoLAos E. MADIA5 furosemide, aluminum hydroxide, and allopurinol. Despite discontinuation of calcitriol and calcium carbonate, the patient's serum calcium remained above 10 mg/dl. The serum PTH level Managing Editor was 4200 dEq/ml when the serum calcium was 10.3 mg/dl. Some CHERYL J. ZU5MAN suppression of the serum PTH level was obtained (to 2400 pJEq/ml) when the serum calcium was raised to 11 mg/dl, but this decrease was followed by rebound of the PTH to the previous level. Subperiosteal University of Chicago Pritzker School of Medicine resorption was not seen on radiographs of the hands, but a sonogram of the neck revealed 2 large (2 x 1.5 cm), solid, cystic parathyroid masses. and A subtotal parathyroidectomy (3.5 glands) therefore was performed. At Tufts University School of Medicine the time of surgery, arterial blood gas measurements revealed a pH of 7.38, PaCO2 of 35 mm Hg, and a plasma bicarbonate of 20.4 mEq/liter. Since surgery, the serum calcium level has remained below 10 mg/dl, and renal function has stabilized with a creatinine clearance of 18 mI/mm. The total co2 stabilized at 22 mEq/liter while the patient was taking furosemide, aluminum hydroxide, and allopurinol. Repeated Case presentation measurement of the PTH level was 800 lEq/ml. The most recent evaluation revealed a creatinine clearance of 14 ml/min; sodium, 144 A 62-year-old male with a 22-year history of albuminuria and pro- mEg/liter; potassium, 5.2 mEg/liter; chloride, 107 mEg/liter; carbon gressive renal insufficiency was admitted to the hospital for placement dioxide, 22 mEg/liter; anion gap, 15 mEg/liter; calcium, 9.0 mg/dl; of a vascular access preparatory to dialysis. The left kidney had been phosphate, 4.6 mg/dl; BUN, 74 mg/dl; and creatinine, 5.9 mg/dl. found to be hypoplastic when proteinuria was first noted. The causes of his renal failure were presumed to be chronic glomerulonephritis and hypertension. The patient complained of nocturnal pruritis at the time of admission but no other symptoms. Discussion The medical history was otherwise unremarkable except for several episodes of acute gout. Medications being taken prior to admission Da. DAVtD G. WARNOCK (Chief, Nephrology Section, San included minoxidil, furosemide, metoprolol, allopurinol, calcitriol, alu- Francisco Veterans Administration Medical Center, and Pro- minum hydroxide, and calcium carbonate. Physical examination revealed a blood pressure of 96/60 mm Hg; fessor of Medicine and Pharmacology, University of Califor- pulse, 98 beats/mm; respiratory rate, 20/mm; and oral temperature, nia, San Francisco, California): The patient presented today 94°F. The sclerae were pale and anicteric, and the pupils were equally has clearly established chronic renal insufficiency and surgically reactive. The fundi revealed arteriovenous nicking but no hemorrhages proved diffuse hyperparathyroidism. Although the exact cause or exudates. The chest was clear, cardiac examination revealed an S4 gallop but no murmurs or rubs. The jugular venous pressure was normal of renal insufficiency has not been documented, it is notable and peripheral edema was not present. The abdomen revealed nothat his course has stabilized since he had a subtotal parathy- organomegaly, tenderness, or masses. Guaiac test of the stool wasroidectomy 1.5 years ago. At the time of surgery, determina- negative, and the neurologic examination was unremarkable. Several tions of arterial blood gases documented a mild metabolic excoriated areas were present on the arms and back. Laboratory studies showed a hematocrit of 30.5%; white blood cell acidosis with appropriate respiratory adaptation, despite ad- count, 8900 mm3 with a normal differential; platelet count, 177,000 vanced renal insufficiency with a creatinine clearance of 13 mm3; BUN, 108 mg/dl; creatinine, 6.8 mg/dl; sodium, 141 mEq/liter; ml/min. For the purposes of our discussion of uremic acidosis, potassium, 3.0 mEq/liter; chloride, 106 mEq/liter; carbon dioxide, 24the questions we need to address include: (1) What is uremic mEg/liter; anion gap, 11 mEg/liter; calcium, 11.0 mg/dl; phosphate, 4,8acidosis? (2) What are the pathophysiologic processes that cause acidosis to develop in the setting of chronic renal insuf- Presentation of the Forum is made possible by grants from Pfizer;ficiency? (3) What are the renal and extrarenal adaptations to Incorporated; Merck Sharp & Dohme; Sandoz, Incorporated; and E. R. chronic renal insufficiency that defend acid-base homeostasis? Squibb & Sons, Incorporated. The case presentation is instructive, particularly if we ask why © 1988 by the International Society of Nephrology acidosis was so mild in this patient. 278 Nephrology Forum: Uremic acidosis 279 Clinical features of uremnic acidosis ganic-acid anions that have not been completely oxidized) with their daily production, just as they are not able to excrete the Chronic progressive renal disease usually results in somedaily endogenous acid load [2]; the retention of these acid degree of systemic acidosis when the glomerular filtration rateanions and hydrogen ions generates the so-called anion-gap is reduced to 25 mllmin or less [1]. Metabolic acid productionmetabolic acidosis characteristic of uremia [10]. generally is not increased in patients with chronic renal insuf- ficiency [2]; therefore the development of acidosis reflects an Patho genesis of uremic acidosis impairment in the renal acidification mechanisms [3] as well as If serum bicarbonate levels in uremic patients are raised some limitations in the renal homeostatic responses to acidosis.towards normal, the urine pH rises and the already reduced Reduced bicarbonate reabsorption [4] and impaired ammoniarenal net acid excretion falls further. At times, overt production [5] are thought to be the underlying disturbances inbicarbonaturia occurs [4]. In the absence of bicarbonate sup- the renal acidification process characteristic of uremic acidosis.plementation, however, the urine pH usually is less than 5.4. Hyperchloremic metabolic acidosis can develop early in theThis finding suggests that the ability of the distal nephron to course of renal disease but the acidosis "converts" to anacidify the urine (that is, maintain a normal pH gradient) is anion-gap form when the glomerular filtration rate falls below 20intact in chronic renal failure. Furthermore, the capacity of the mLfmin [6]. Hyperchloremic metabolic acidosis, well describeddistal nephron's proton secretory systems to respond to an in patients with tubulointerstitial disease [3, 6], also has beenincrease in buffer delivery (such as that following administra- seen in patients with primary glomerular disease [7]. One of thetion of a phosphate load) is also well maintained (reviewed in classic studies analyzing metabolic acidosis in patients withRef. 11). There is an important distinction, however, between chronic renal insufficiency was done here at the New Englandsimple acidification of the urine and renal net acid excretion Medical Center. In a retrospective analysis of 138 ambulatory(defined as the sum of ammonium excretion and titratable acid patients with stable renal function, Widmer, Gerhardt, Har-minus the excretion of bicarbonate). Unlike patients with distal rington, and Cohen examined the relationships between serumrenal tubular acidosis, in whom the primary acidification defect electrolytes and renal function, as assessed by serum creatinineresides in the distal proton secretory mechanisms, patients with measurements [7]. The study excluded patients with vomiting,chronic renal insufficiency appear to have impaired renal net diarrhea, or volume depletion and those who had receivedacid excretion because of inadequate or inappropriate delivery diuretics, alkali, steroids, potassium-exchange resins, or antac-of buffer to the distal nephron acidification sites. I will now ids. Patients also were excluded who had multiple myeloma, oraddress the defects in the renal excretion of ammonium and who had undergone adrenalectomy or parathyroidectomy. Ob-reabsorption of bicarbonate, which are the central factors viously these patients were highly selected; many of the pa-responsible for the development of acidosis in chronic renal tients in a typical renal clinic would not meet these criteria, butinsufficiency. the goal of the investigators was to determine the relationship Ammonium excretion. A major factor in the limitation of between the various serum electrolytes and renal function in therenal net acid excretion in chronic renal insufficiency is inade- steady state. The final analysis included 41 patients who werequate renal ammonium excretion. Although there is an adaptive 16 to 73 years old. There were 25 men
Load more

Recommended publications
  • Surgeons, Columbia University, New York City) (Received for Publication August 9, 1932)
    THE ADDIS SEDIMENT COUNT IN NORMAL CHILDREN By JOHN D. LYTTLE (From the Babies Hospit and the Department of Pediatrics, Colege of Physicians and Surgeons, Columbia University, New York City) (Received for publication August 9, 1932) THE METHOD In 1925 Addis (1) described a method by which, in a concentrated acid urine, the rate of excretion of protein, casts and red and white cells could be determined. His method, with certain modifications, has been followed here. All of the counts were made on the 12 hour night specimen from 7 or 8 P.M. to 7 or 8 A.M. Addis recommended that fluids be restricted during, and for 12 hours preceding the collection, since in dilute and alkaline urine hyaline casts dissolve and red cells may be completely lysed. With children this rigid restriction of fluid proved impossible. Withholding fluid during the afternoon and night except for 200 cc. at the evening meal, gave urines of such concentration and acidity that they were suitable for a count. Most children had an early supper and col- lections were started at 7 or 8 P.M. Under these conditions, the urinary pH was between 5.0 and 6.0 and the specific gravity usually well above 1.020. The specimens were treated as described by Addis: "the con- centrated night urine is thoroughly mixed by repeated inversion of the rubber-stoppered bottle and a 10 cc. sample is transferred to a special graduated tube, and centrifugalized for five minutes at 1,800 revolutions per minute. The supernatant urine is decanted and pipetted down to a known volume which varies with the amount of sediment as judged by direct observation.
    [Show full text]
  • Arterial Blood Gases: Acid-Base Balance
    EDUCATIONAL COMMENTARY – ARTERIAL BLOOD GASES: ACID-BASE BALANCE Educational commentary is provided through our affiliation with the American Society for Clinical Pathology (ASCP). To obtain FREE CME/CMLE credits click on Earn CE Credits under Continuing Education on the left side of the screen. **Florida licensees, please note: This exercise will appear in CE Broker under the specialty of Blood Gas Analysis. LEARNING OUTCOMES On completion of this exercise, the participant should be able to • identify the important buffering systems in the human body. • explain the Henderson-Hasselbalch equation and its relationship to the bicarbonate/carbonic acid buffer system. • explain the different acid-base disorders, causes associated with them, and compensatory measures. • evaluate acid-base status using patient pH and pCO2 and bicarbonate levels. Introduction Arterial blood gas values are an important tool for assessing oxygenation and ventilation, evaluating acid- base status, and monitoring the effectiveness of therapy. The human body produces a daily net excess of acid through normal metabolic processes: cellular metabolism produces carbonic, sulfuric, and phosphoric acids. Under normal conditions, the body buffers accumulated hydrogen ions (H+) through a variety of buffering systems, the respiratory center, and kidneys to maintain a plasma pH of between 7.35 and 7.45. This tight maintenance of blood pH is essential: even slight changes in pH can alter the functioning of enzymes, the cellular uptake and use of metabolites, and the uptake and release of oxygen. Although diagnoses are made by physicians, laboratory professionals must be able to interpret arterial blood gas values to judge the validity of the laboratory results they report.
    [Show full text]
  • 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.
    [Show full text]
  • Albuminuria Versus Egfr
    Albuminuria versus GFR as markers of diabetic CKD progression KDIGO Controversies Conference: “Diabetic Kidney Disease” New Delhi, March 2012 Richard J MacIsaac PhD FRACP Director of Endocrinology & Diabetes, St Vincent's Hospital Professorial Fellow, University of Melbourne Evolution of Diabetic CKD Incipient Overt Nephropathy Nephropathy GFR 100 Log AER (ml/min) GFR 10 15 20 yrs Normoalbuminuria Microalbuminuria Macroalbuminuria (AER < 20 µµµg/min) (AER 20-200 µµµg/min) (AER > 200 µµµg/min) Stages of CKD Stage eGFR Description Predominant (ml/min/1.73 m2) AER status 1 > 90 Kidney damage with normal/high GFR Normo- Micro- 2 60-89 Kidney damage with mild reduction in GFR Micro- 3 30-59 Kidney damage with moderate reduction in Micro/Macro- GFR 4 15-29 Kidney damage with severe reduction in Macro- GFR 5 < 15 Kidney failure Albuminuria versus GFR as markers of diabetic CKD progression 1. Albuminuria as a predictor of diabetic CKD 2. GFR as a predictor of diabetic CKD 3. Albuminuria & GFR uncoupling/coupling 4. Summary Albuminuria as a marker of diabetic CKD progression • High Variability M N • Low Specificity • Spontaneous Regression µ • Δ AER ≠ Δ GFR Higher levels of urinary albumin excretion within the normal range predict faster decline in glomerular filtration rate in diabetic patients Babazono T et al. Diabetes Care 2009;32:1518-1520 Albuminuria versus GFR as markers of diabetic CKD progression 1. Albuminuria as a predictor of diabetic CKD 2. GFR as a predictor of diabetic CKD 3. ALbuminuria & GFR uncoupling/coupling 4. Summary GFR as
    [Show full text]
  • Renal Tubular Acidosis in Children: State of the Art, Diagnosis and Treatment
    www.medigraphic.org.mx Bol Med Hosp Infant Mex 2013;70(3):178-193 REVIEW ARTICLE Renal tubular acidosis in children: state of the art, diagnosis and treatment Ricardo Muñoz-Arizpe,1 Laura Escobar,2 Mara Medeiros3 ABSTRACT Overdiagnosis of renal tubular acidosis (RTA) has been recently detected in Mexican children, perhaps due to diagnostic errors as well as due to a lack of knowledge regarding the pathophysiology and molecular biochemistry involved in this illness. The objective of the present study is to facilitate the knowledge and diagnosis of RTA, a clinical condition infrequently seen worldwide. RTA is an alteration of the acid-base equilibrium due to a bicarbonate wasting in the proximal renal tubules [proximal RTA, (pRTA) or type 2 RTA] or due to a distal nephron hy- drogen ion excretion defect [distal RTA (dRTA) or type 1 RTA]. Hyperkalemic, or type 4 RTA, is due to alterations in aldosterone metabolism. RTA may be primary, secondary, acquired or hereditary and frequently presents secondary to an array of systemic diseases, usually accom- panied by multiple renal tubular defects. The main defect occurs in the transmembrane transporters such as carbonic anhydrase (CA I and + - - + - II), H -ATPase, HCO3 /Cl (AE1) exchanger and Na /HCO3 (NBCe1) cotransporter. Diagnosis should include the presence of hyperchloremic metabolic acidosis with normal serum anion gap (done in an arterial or arterialized blood sample), lack of appetite, polyuria, thirst, growth failure, and rickets; nephrocalcinosis and renal stones (in dRTA); abnormal urine anion gap and abnormal urine/serum pCO2 gradient. Diagnosis of a primary systemic disease must be made in cases of secondary RTA.
    [Show full text]
  • TITLE: Acid-Base Disorders PRESENTER: Brenda Suh-Lailam
    TITLE: Acid-Base Disorders PRESENTER: Brenda Suh-Lailam Slide 1: Hello, my name is Brenda Suh-Lailam. I am an Assistant Director of Clinical Chemistry and Mass Spectrometry at Ann & Robert H. Lurie Children’s Hospital of Chicago, and an Assistant Professor of Pathology at Northwestern Feinberg School of Medicine. Welcome to this Pearl of Laboratory Medicine on “Acid-Base Disorders.” Slide 2: During metabolism, the body produces hydrogen ions which affect metabolic processes if concentration is not regulated. To maintain pH within physiologic limits, there are several buffer systems that help regulate hydrogen ion concentration. For example, bicarbonate, plasma proteins, and hemoglobin buffer systems. The bicarbonate buffer system is the major buffer system in the blood. Slide 3: In the bicarbonate buffer system, bicarbonate, which is the metabolic component, is controlled by the kidneys. Carbon dioxide is the respiratory component and is controlled by the lungs. Changes in the respiratory and metabolic components, as depicted here, can lead to a decrease in pH termed acidosis, or an increase in pH termed alkalosis. Slide 4: Because the bicarbonate buffer system is the major buffer system of blood, estimation of pH using the Henderson-Hasselbalch equation is usually performed, expressed as a ratio of bicarbonate and carbon dioxide. Where pKa is the pH at which the concentration of protonated and unprotonated species are equal, and 0.0307 is the solubility coefficient of carbon dioxide. Four variables are present in this equation; knowing three variables allows for calculation of the fourth. Since pKa is a constant, and pH and carbon dioxide are measured during blood gas analysis, bicarbonate can, therefore, be determined using this equation.
    [Show full text]
  • Approach to Acute Kidney Injury: Differentiation of Prerenal, Postrenal and Intrinsic Renal Disease, Acute Tubular Necrosis and Renal Vascular Disease
    Acute Kidney Injury, Renal Vascular Disease Renal Genital Urianry System 2019 APPROACH TO ACUTE KIDNEY INJURY: DIFFERENTIATION OF PRERENAL, POSTRENAL AND INTRINSIC RENAL DISEASE, ACUTE TUBULAR NECROSIS AND RENAL VASCULAR DISEASE Biff F. Palmer, MD, Office: H5.112; Phone 87848 Email: [email protected] LEARNING OBJECTIVES • Given laboratory tests results and radiographic imaging, be able to diagnose a patients with an increased serum creatinine concentration as having post-renal renal disease and list the common clinical etiologies of urinary obstruction • Given laboratory tests results and radiographic imaging, be able to diagnose a patients with an increased serum creatinine concentration as having pre-renal kidney injury • Given pertinent aspects of the history, physical examination, serum and urine electrolytes, and urinalysis in any patient, be able to distinguish pre-renal renal failure from intrinsic renal disease • Given urine and plasma concentrations of sodium and creatinine in any patient, be able to calculate the fractional excretion of sodium (FENa) and interpret the results • List the renal syndromes associated with use of NSAID’s • List the characteristics of thromboembolic disease of the kidney, multiple choesterol emboli syndrome, renal vein thrombosis, and renal artery stenosis After determining chronicity and assessing the level of renal function, one should attempt to classify the patient with renal disease into one of several syndromes based on the renal structures most affected: pre-renal, post-renal or intrinsic renal disease. This classification is based on the information obtained in the history, physical examination, laboratory tests and selected imaging studies. It is particularly important to identify prerenal and postrenal disorders because theses disorders are often readily reversible.
    [Show full text]
  • Acid-Base Physiology & Anesthesia
    ACID-BASE PHYSIOLOGY & ANESTHESIA Lyon Lee DVM PhD DACVA Introductions • Abnormal acid-base changes are a result of a disease process. They are not the disease. • Abnormal acid base disorder predicts the outcome of the case but often is not a direct cause of the mortality, but rather is an epiphenomenon. • Disorders of acid base balance result from disorders of primary regulating organs (lungs or kidneys etc), exogenous drugs or fluids that change the ability to maintain normal acid base balance. • An acid is a hydrogen ion or proton donor, and a substance which causes a rise in H+ concentration on being added to water. • A base is a hydrogen ion or proton acceptor, and a substance which causes a rise in OH- concentration when added to water. • Strength of acids or bases refers to their ability to donate and accept H+ ions respectively. • When hydrochloric acid is dissolved in water all or almost all of the H in the acid is released as H+. • When lactic acid is dissolved in water a considerable quantity remains as lactic acid molecules. • Lactic acid is, therefore, said to be a weaker acid than hydrochloric acid, but the lactate ion possess a stronger conjugate base than hydrochlorate. • The stronger the acid, the weaker its conjugate base, that is, the less ability of the base to accept H+, therefore termed, ‘strong acid’ • Carbonic acid ionizes less than lactic acid and so is weaker than lactic acid, therefore termed, ‘weak acid’. • Thus lactic acid might be referred to as weak when considered in relation to hydrochloric acid but strong when compared to carbonic acid.
    [Show full text]
  • Hyperkalemia: This Time, Not the Usual Suspect
    TUBULAR QUIZ Port J Nephrol Hypert 2018; 32(4): 395-397 • Advance Access publication 4 January 2019 Hyperkalemia: this time, not the usual suspect Anna Lima, Pedro Campos, Ana Gaspar, Afonso Santos, Patricia Carrilho Department of Nephrology, Hospital Prof Dr Fernando Fonseca, Lisbon, Portugal Received for publication: Dec 18, 2018 Accepted in revised form: Jan 4, 2019 A 49-year-old Caucasian male was admitted to the acidosis, one important step to search for the cause is emergency department with a three-day history of to calculate the anion gap.1 In this case the anion gap abdominal pain and nausea. These episodes were fre- was normal (AG= Na – (CL+HCO3) =12mmol/L). The next quent and, in the previous four months, he had noticed step was to calculate the urinary anion gap (UAG= (Na+ fatigue, more severe in the lower limbs, and symptoms + K+) – Cl-= 74mmol/L), which was highly positive. So, compatible with postural hypotension. He had no fever we were in presence of a metabolic acidosis with non- or any other symptoms. Lab tests requested by his increased anion gap, positive UAG, hyperkalemia and general practitioner six weeks earlier had revealed acidic urine (pH 5) in a patient with normal renal function hyperkalemia, without other relevant changes. He had matching a type IV (distal) renal tubular acidosis.2 followed a low-potassium diet since then. Past medical history included active smoking habits, intravenous There are many causes for hyperkalemic distal renal drug use (he suspended seventeen years ago), and tubular acidosis, the most common of which is diabetes changed bowel habits with alternating obstipation and mellitus (by definition a hyporeninemic hypoaldoster- diarrhea.
    [Show full text]
  • Proteinuria and Albuminuria: What’S the Difference? Cynthia A
    EXPERTQ&A Proteinuria and Albuminuria: What’s the Difference? Cynthia A. Smith, DNP, CNN-NP, FNP-BC, APRN, FNKF What exactly is the difference between TABLE Q the protein-to-creatinine ratio and the Persistent Albuminuria Categories microalbumin in the lab report? How do they compare? Category Description UACR For the non-nephrology provider, the options for A1 Normal to mildly < 30 mg/g evaluating urine protein or albumin can seem con- increased (< 3 mg/mmol) fusing. The first thing to understand is the impor- tance of assessing for proteinuria, an established A2 Moderately 30-300 mg/g marker for chronic kidney disease (CKD). Higher increased (3-30 mg/mmol) protein levels are associated with more rapid pro- A3 Severely > 300 mg/g gression of CKD to end-stage renal disease and in- increased (> 30 mg/mmol) creased risk for cardiovascular events and mortality in both the nondiabetic and diabetic populations. Abbreviation: UACR, urine albumin-to-creatinine ratio. Monitoring proteinuria levels can also aid in evaluat- Source: KDIGO. Kidney Int. 2012.1 ing response to treatment.1 Proteinuria and albuminuria are not the same low-up testing. While the UACR is typically reported thing. Proteinuria indicates an elevated presence as mg/g, it can also be reported in mg/mmol.1 Other of protein in the urine (normal excretion should be options include the spot urine protein-to-creatinine < 150 mg/d), while albuminuria is defined as an “ab- ratio (UPCR) and a manual reading of a reagent strip normal loss of albumin in the urine.”1 Albumin is a (urine dipstick test) for total protein.
    [Show full text]
  • Understanding What It Means to Have Protein in Your Urine Understanding What It Means to Have Protein in Your Urine
    UNDERSTANDINGUnderstanding WHAT ITYour MEANS TO HAVE Hemodialysis PROTEINAccess Options IN YOUR URINE 2 AAKP: Understanding What It Means to Have Protein in Your Urine Understanding What It Means to Have Protein in Your Urine The kidneys are best known for making urine. This rather simple description does not tell the whole story. This brochure describes other important functions of the kidneys; including keeping protein in the blood and not letting any of the protein in the liquid (plasma) part of blood escape into the urine. Proteinuria is when “Proteinuria” is when kidneys allow proteins to kidneys appear in the urine and be lost from the body. allow Proteinuria is almost never normal, but it can proteins to be normal - rarely - in some healthy, active appear in the urine children or young adults. and be The kidneys are paired organs located on either lost from the body. side of the backbone. They are located at the Proteinuria level of the lowest part of the rib cage. They are is almost the size of an adult fist (4.5 – 5 inches in length). never Together the two kidneys receive a quarter of normal, but it can the blood that is pumped from the heart every be normal minute. This large blood flow is needed in order - rarely - for the kidneys to do one of the kidneys’ main in some jobs: healthy, active • remove waste products in the blood every children day or young adults. • keep the body in balance by eliminating the extra fluids and salts we consume on a regular basis.
    [Show full text]
  • Distal Renal Tubular Acidosis and Diabetes Insipidus Leading to the Diagnosis of Sjögren's Syndrome
    The Medicine Forum Volume 17 Article 15 2016 Distal Renal Tubular Acidosis and Diabetes Insipidus Leading to the Diagnosis Of Sjögren's Syndrome Loheetha Ragupathi, MD Thomas Jefferson University, [email protected] Elijah Grillo, MD Thomas Jefferson University, [email protected] Jonathan Yadlosky, MD Thomas Jefferson University, [email protected] Ravi Sunderkrishnan, MD Thomas Jefferson University, [email protected] Follow this and additional works at: https://jdc.jefferson.edu/tmf Part of the Internal Medicine Commons, and the Nephrology Commons Let us know how access to this document benefits ouy Recommended Citation Ragupathi, MD, Loheetha; Grillo, MD, Elijah; Yadlosky, MD, Jonathan; and Sunderkrishnan, MD, Ravi (2016) "Distal Renal Tubular Acidosis and Diabetes Insipidus Leading to the Diagnosis Of Sjögren's Syndrome," The Medicine Forum: Vol. 17 , Article 15. DOI: https://doi.org/10.29046/TMF.017.1.016 Available at: https://jdc.jefferson.edu/tmf/vol17/iss1/15 This Article is brought to you for free and open access by the Jefferson Digital Commons. The Jefferson Digital Commons is a service of Thomas Jefferson University's Center for Teaching and Learning (CTL). The Commons is a showcase for Jefferson books and journals, peer-reviewed scholarly publications, unique historical collections from the University archives, and teaching tools. The Jefferson Digital Commons allows researchers and interested readers anywhere in the world to learn about and keep up to date with Jefferson scholarship. This article has been accepted for inclusion in The Medicine Forum by an authorized administrator of the Jefferson Digital Commons. For more information, please contact: [email protected].
    [Show full text]