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Renal Tubular Acidosis Clinical DIMENSION Renal Tubular Acidosis Abigail S. Brown, BSN, RN, CCRN Renal tubular acidosis is a relatively uncommon clinical syndrome characterized by the inability of the kidney to adequately excrete hydrogen ions, retain adequate bicarbonate, or both. This syndrome can be categorized into 3 separate disorders, each with unique clinical characteristics. Although an uncommon finding, prompt and inexpensive tests can lead to early intervention and subsequently reduce complications from persistent renal dysfunction. The purpose of this article was to bring awareness of the clinical manifestations, diagnosis, and treatments of renal tubular acidosis to critical care nurses. Keywords: Renal disease, Renal physiology, Renal tubular acidosis [DIMENS CRIT CARE NURS. 2010;29(3):112/119] INTRODUCTION AND BACKGROUND general weakness over the past month. Examination results Renal tubular acidosis (RTA) is a relatively uncommon were relatively benign aside from general, diffuse muscle clinical syndrome characterized by the inability of the kidney weakness, dry buccal mucosa, and dry eyes. Her medical to adequately excrete hydrogen ions, retain adequate and surgical history were unremarkable except for an bicarbonate, or both.1,2 First illustrated in 1935, this approximate 6-month history of dry eyes that which was syndrome was further delineated as RTA in 1951.2 Renal unrelieved by over-the-counter eye drops. Her current tubular acidosis syndrome is manifested in the presence of a medications were only over-the-counter eye drops (artifi- relatively normal glomerular filtration rate, normal plasma cial tears). She denied any known allergies to medications anion gap, and a hyperchloremic metabolic acidosis.2-4 and denied the use of alcohol or tobacco products. Renal tubular acidosis can additionally be categorized into Laboratory testing revealed the following: 3 separate disorders, each with unique clinical character- & Chemistry: sodium (Na+), 135 mmol/L; potassium (K+), 2.1 istics. The 3 disorders include (1) proximal RTA (type 2), mmol/L; chloride (Clj), 112 mmol/L; phosphate (PO j), (2) distal RTA (type 1), and (3) hyperaldosteronism- 4 2.6 mg/dL; blood urea nitrogen (BUN), 15 mg/dL; associated RTA (type 4). Although an uncommon finding, creatinine (Cr), 0.9 mg/dL; calcium (Ca2+), 9.4 mg/dL; prompt and inexpensive tests can lead to targeted inter- carbon dioxide, (CO2) 15 mmol/L vention and reduce complications from persistent renal + j j & Serum anion gap (Na j [Cl + HCO3 ]): 8 dysfunction. The purpose of this article was to bring j & Arterial blood gas: pH 7.28; PCO ,47mmHg;HCO , awareness of the clinical manifestations, diagnosis, and 2 3 16 mmol/L; PO ,120 mm Hg treatments of RTA to critical care nurses. Two case studies 2 & Urinalysis: pH 7.1 illustrate the crucial elements in the diagnosis and sub- & Sodium, urine random: 82 mEq/L sequent treatment of RTA. & Potassium, urine random: 26 mEq/L & CASE STUDIES Chloride, urine random: 78 mEq/L & 24-Hour urinary anion gap 30 Ruling in RTA Further diagnostic testing included a positive rheumatoid A 46-year-old white woman presented to the emergency factor (IgM) and positive antiYRo/SS-A. Through an ophthal- department with complaints of progressively worsening mologist referral, a diagnosis of bilateral keratoconjunctivitis 112 Dimensions of Critical Care Nursing Vol. 29 / No. 3 Copyright @ 2010 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. Renal Tubular Acidosis sicca was made. Subsequent salivary gland biopsy of the & Clostridium difficileYpositive stool antigens lower lip confirmed Sjo¨ gren syndrome as the presenting & Urinalysis: positive for leukoesterase and nitrogen, pH 7.2 diagnosis. The patient was diagnosed as having Sjo¨ gren She was subsequently admitted to the intensive care syndrome associated with hypokalemia and distal RTA. unit with the diagnosis of change in mental status due to Although Sjo¨ gren syndrome primarily affects women older dehydration, C difficile, UTI, hypophosphatemia, and hypo- than 40 years and those with a family history of Sjo¨gren kalemia. The treatment plan included a course of antibiotics syndrome, it is a relatively uncommon clinical disorder.2 for her UTI and C difficile, intravenous rehydration with 0.9% saline, and replacement of both potassium and The patient was diagnosed as having phosphorous. Sjögren syndrome associated with Over the course of her hospitalization, the frequency of stools decreased, but she became increasingly somno- hypokalemia and distal RTA. lent. Further laboratory testing revealed the following: & Chemistry: Na+, 157 mmol/L; K+, 2.7 mmol/L; Clj, j 144 mmol/L; HCO3 , 8 mmol/L; BUN, 47 mg/dL; Ruling Out RTA j creatine, 1.2 mg/dL; Ca2+,9.6mg/dL;PO ,1.4mg/dL A 66-year-old white woman presented to the emergency 4 & Serum anion gap: 5 department with a 1- to 2-day history of mental status & Complete blood count: white blood cell, 12.8; hemo- change, confusion, lethargy, and 3-day history of nausea globin, 11.5; hematocrit, 33.9; platelet, 142 and diarrhea. Her medical history was significant for & Arterial blood gas: pH 7.27; PCO2,19mmHg; bladder cancer with multiple bladder surgeries, ileal j HCO , 9 mmol/L; PO , 149 mm Hg conduit, recurrent urinary tract infections (UTIs), chronic 3 2 & Sodium, urine random: 45 mEq/L obstructive pulmonary disease, and bipolar disorder. Her & Potassium, urine random: 11 mEq/L current medications include albuterol, dicyclomine (Bentyl), & Chloride, urine random: 61 mEq/L clonazepam, venlafaxine hydrochloride (Effexor), lopera- & Urinary anion gap: j27 mide (Imodium), potassium, mirtazapine (Remeron), quetia- pine (Seroquel), carbamazepine (Tegretol), and trazodone. The laboratory results illustrated a hyperchloremic, She had no known allergies to medications. She reported use non-anion gap metabolic acidosis. The differential diagnoses of alcohol in the past but denied alcohol or tobacco use for her presenting laboratory results and physical examina- within the past 12 months. tion included renal or gastrointestinal (GI) wasting via Further questioning revealed approximately 6 to 8 diarrhea, proximal RTA, distal RTA, primary hyperpar- episodes of large, liquid stools for the past 3 days despite athyroidism, aldosterone deficiency, Addison disease, aldos- self-treatment with Imodium. She reported the stool to be terone insensitivity, and/or ureteroileostomy.4-6 To rule out light brown in color, without obvious blood. She denied a blockage to her ileal conduit, an ileal conduit loopogram abdominal pain, vomiting, and recent weight loss, but was obtained with results of no extraluminal contrast admitted to a poor appetite over the past few days. Upon observed (negative). The result of her urinary anion gap physical examination, she was found to be drowsy yet ({urine [Na+]+urine[K+]} j urine [Clj])2,4 was normal oriented. She was pale and thin in appearance. Initial vital (j27), supporting a diagnosis of GI wasting via diarrhea as signs displayed a pulse rate of 110 beats per minute, blood being a likely cause of her hyperchloremic, non-anion gap pressure of 90/54 mm Hg, and a respiratory rate of 18 metabolic acidosis. Her serum bicarbonate corrected over breaths per minute. The monitor displayed sinus tachycar- the following days with an intravenous administration of dia. Lungs were clear to auscultation, and her abdomen dextrose with sodium bicarbonate, while continuing to was nontender and flat, with hyperactive bowel sounds. An replete her potassium and phosphorous. Over the following ileal conduit was noted to her right lower abdomen, week, she became increasingly alert, had minimal diarrhea, drainage bag intact, with a small amount of cloudy, amber and was eventually transferred to the floor. urine present. Initial laboratory testing was obtained, which revealed the following: PATHOGENESIS & Chemistry: Na+, 136 mmol/L; K+, 2.0 mmol/L; Clj, j j 120 mmol/L; HCO3 ,19mmol/L;PO4 ,1.1mg/dL; Renal Acidification BUN, 29 mg/dL; creatine, 1.0 mg/dL; Ca2+, 10.6 mg/dL The kidneys play a vital role in the homeostasis of acid- & Serum anion gap: 7 base balance throughout the body. This role is mainly seen & Complete blood count: white blood cells, 8K/2L; he- through both the proximal convoluted tubule and the moglobin, 11.8 g/dL; hematocrit, 35.3%; platelet, 379 K/2L distal nephron. With normal, steady-state conditions, May/June 2010 113 Copyright @ 2010 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. Renal Tubular Acidosis approximately 0.8 to 1 mEq per kilogram of nonvolatile port defect, as in Fanconi syndrome.10 Both inherited and acid is generated daily, primarily as a by-product of secondary (acquired) disorders for proximal RTA are metabolism from dietary protein.7 This acid load is listed in Table 1.2,7,8 Inherited disorders, which result excreted through the urine in the presence of sufficient in accumulation of endogenous metabolites and subse- buffering compounds, which include ammonia and phos- quent tubular injury, include Wilson disease, cystinosis, phate. As the systemic acid load increases, there is a tyrosinemia, fructose intolerance, glycogen storage dis- subsequent increase in ammonium production and excre- ease type I, Lowe syndrome, and galactosemia, which are tion. Failure to excrete adequate amounts of ammonium all related to Fanconi syndrome.8 Fanconi syndrome is directly contributes to the development of metabolic thoughttobedirectlyassociatedwithadeficitinATP acidosis. production in
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