Nephrology nephrology
The Best Review and Test Questions in Medicine:
• Clinical Evaluation of Kidney Function
• Fluids and Electrolytes • Acid-Base Disorders • Hypertension
®
Nephrology
• Chronic Tubulointerstitial Disorders • Glomerular Diseases
All New Content, Including 108 Multiple-Choice Questions
• Genetic Disorders and Kidney Disease • Acute Kidney Injury • Kidney Stones • The Kidney in Pregnancy • Chronic Kidney Disease
C u m u l at i v e
INDEX
Plus much more . . .
ISBN 978-1-938245-10-7
9 781938 245107
150521012
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Medical Knowledge Self-Assessment Program
16 AMA PRA Category 1 Credits™ available until Dec. 31, 2015.
9/27/12 2:01 PM
Table of Contents
Clinical Evaluation of Kidney Function Glomerular Filtration Rate . . . . . . . . . . . . . . . . . . . . . . . . . 1 Estimation of Glomerular Filtration Rate . . . . . . . . . . 1 Interpretation of the Urinalysis . . . . . . . . . . . . . . . . . . . . . 2 Urine Dipstick . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2 Urine Microscopy . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5 Measurement of Albumin and Protein Excretion. . . . . 6 Clinical Evaluation of Hematuria . . . . . . . . . . . . . . . . 7 Imaging Studies. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9 Kidney Biopsy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10
Fluids and Electrolytes Osmolality and Tonicity . . . . . . . . . . . . . . . . . . . . . . . . . . 10 Disorders of Serum Sodium . . . . . . . . . . . . . . . . . . . . . . . 10 Hyponatremia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10 Hypernatremia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15 Disorders of Serum Potassium . . . . . . . . . . . . . . . . . . . . . 17 Hypokalemia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17 Hyperkalemia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19 Disorders of Serum Phosphate . . . . . . . . . . . . . . . . . . . . . 22 Hypophosphatemia. . . . . . . . . . . . . . . . . . . . . . . . . . 22 Hyperphosphatemia . . . . . . . . . . . . . . . . . . . . . . . . . 22
Acid-Base Disorders General Approach . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22 Metabolic Acidosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23 Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23 Classification. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23 Metabolic Alkalosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30 Respiratory Acidosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31 Clinical Manifestations and Diagnosis . . . . . . . . . . . . 31 Treatment. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 32 Respiratory Alkalosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . 32
Hypertension Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33 Associated Complications. . . . . . . . . . . . . . . . . . . . . . . . . 33 End-Organ Damage . . . . . . . . . . . . . . . . . . . . . . . . . 33 Cardiovascular Risk. . . . . . . . . . . . . . . . . . . . . . . . . . 34 Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 34 History. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 34 Physical Examination . . . . . . . . . . . . . . . . . . . . . . . . 34 Laboratory Studies . . . . . . . . . . . . . . . . . . . . . . . . . . 35
Blood Pressure Measurement. . . . . . . . . . . . . . . . . . . . . . 35 Office Measurement . . . . . . . . . . . . . . . . . . . . . . . . . 35 Ambulatory Blood Pressure Monitoring . . . . . . . . . . 35 Electronic Blood Pressure Measurement . . . . . . . . . . 36 Home Blood Pressure Monitoring . . . . . . . . . . . . . . 37 Other Settings for Electronic Blood Pressure Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37 Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37 Prehypertension . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38 Essential Hypertension . . . . . . . . . . . . . . . . . . . . . . . 38 Secondary Hypertension. . . . . . . . . . . . . . . . . . . . . . 41 White Coat Hypertension . . . . . . . . . . . . . . . . . . . . . 42 Masked Hypertension. . . . . . . . . . . . . . . . . . . . . . . . 42 Resistant Hypertension . . . . . . . . . . . . . . . . . . . . . . . 43 Special Populations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43 Women. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43 Patients with Diabetes Mellitus . . . . . . . . . . . . . . . . . 43 Black Patients . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43 Older Patients. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43
Chronic Tubulointerstitial Disorders Pathophysiology and Epidemiology . . . . . . . . . . . . . . . . . 44 Clinical Manifestations . . . . . . . . . . . . . . . . . . . . . . . . . . . 44 Diagnosis and Evaluation. . . . . . . . . . . . . . . . . . . . . . . . . 44 Causes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46 Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48
Glomerular Diseases Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48 Clinical Manifestations . . . . . . . . . . . . . . . . . . . . . . . . . . . 48 The Nephrotic Syndrome . . . . . . . . . . . . . . . . . . . . . 48 The Nephritic Syndrome . . . . . . . . . . . . . . . . . . . . . 48 Conditions that Cause the Nephrotic Syndrome . . . . . . . 49 Major Causes of the Nephrotic Syndrome with Kidney-Limited Disease . . . . . . . . . . . . . . . . . . . . . . 49 Systemic Diseases that Cause the Nephrotic Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 53 Conditions that Cause the Nephritic Syndrome . . . . . . . . 56 IgA Nephropathy . . . . . . . . . . . . . . . . . . . . . . . . . . . 56 Membranoproliferative Glomerulonephritis . . . . . . . 57 Hepatitis C Virus–Associated Glomerulonephritis . . . 58 Hepatitis B Virus–Associated Kidney Disease . . . . . . 58 Postinfectious Glomerulonephritis . . . . . . . . . . . . . . 58 Lupus Nephritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . 59 ix
Anti–Glomerular Basement Membrane Antibody Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 60 Small- and Medium-Vessel Vasculitis . . . . . . . . . . . . . 61 Cryoglobulinemic Vasculitis . . . . . . . . . . . . . . . . . . . 61 Thrombotic Microangiopathy. . . . . . . . . . . . . . . . . . 61
Clinical Manifestations . . . . . . . . . . . . . . . . . . . . . . . . . . . 75 Diagnosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 76 Acute Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 76 Risk Factor Evaluation and Subsequent Treatment. . . . . . 77
The Kidney in Pregnancy Genetic Disorders and Kidney Disease Kidney Cystic Disorders. . . . . . . . . . . . . . . . . . . . . . . . . . 63 Autosomal Dominant Polycystic Kidney Disease . . . . 63 Autosomal Recessive Polycystic Kidney Disease. . . . . 64 Tuberous Sclerosis Complex . . . . . . . . . . . . . . . . . . . 64 Medullary Cystic Kidney Disease. . . . . . . . . . . . . . . . 64 Noncystic Disorders. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 64 Alport Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . 64 Thin Glomerular Basement Membrane Disease. . . . . 65 Fabry Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65
Acute Kidney Injury Pathophysiology and Epidemiology . . . . . . . . . . . . . . . . . 65 Definition and Classification. . . . . . . . . . . . . . . . . . . . . . . 65 Clinical Manifestations and Diagnosis . . . . . . . . . . . . . . . 65 Causes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 67 Prerenal Azotemia . . . . . . . . . . . . . . . . . . . . . . . . . . 67 Intrinsic Kidney Diseases. . . . . . . . . . . . . . . . . . . . . . 67 Postrenal Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . 72 Acute Kidney Injury in Specific Clinical Settings. . . . . . . . 72 Critical Care . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 72 Cardiovascular Disease . . . . . . . . . . . . . . . . . . . . . . . 72 Liver Disease. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73 Malignancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73 HIV Infection. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 74
Normal Physiologic Changes in Pregnancy . . . . . . . . . . . 77 Hemodynamic Changes . . . . . . . . . . . . . . . . . . . . . . 77 Changes in the Urinary Tract . . . . . . . . . . . . . . . . . . 77 Changes in Acid-Base Regulation . . . . . . . . . . . . . . . 77 Changes in Water Homeostasis . . . . . . . . . . . . . . . . . 77 Hypertensive Disorders Associated with Pregnancy . . . . . 78 Chronic Hypertension . . . . . . . . . . . . . . . . . . . . . . . 78 Gestational Hypertension . . . . . . . . . . . . . . . . . . . . . 79 Preeclampsia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79 Kidney Disease in the Pregnant Patient . . . . . . . . . . . . . . 80 Diabetes Mellitus . . . . . . . . . . . . . . . . . . . . . . . . . . . 80 Systemic Lupus Erythematosus . . . . . . . . . . . . . . . . . 80 Management of End-Stage Kidney Disease During Pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 80
Chronic Kidney Disease Pathophysiology and Epidemiology . . . . . . . . . . . . . . . . . 81 Screening. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 81 Clinical Manifestations . . . . . . . . . . . . . . . . . . . . . . . . . . . 82 Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 83 Prevention of Progression . . . . . . . . . . . . . . . . . . . . . 83 Complications. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 86 Special Considerations . . . . . . . . . . . . . . . . . . . . . . . 90 Treatment of End-Stage Kidney Disease. . . . . . . . . . . . . . 90 Dialysis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 91 Kidney Transplantation . . . . . . . . . . . . . . . . . . . . . . . 92
Kidney Stones Types of Kidney Stones . . . . . . . . . . . . . . . . . . . . . . . . . . 74 Calcium Stones. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 74 Struvite Stones . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 75 Uric Acid Stones. . . . . . . . . . . . . . . . . . . . . . . . . . . . 75 Cystine Stones . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 75
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Bibliography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 94 Self-Assessment Test . . . . . . . . . . . . . . . . . . . . . . . . . 97 Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 183
Nephrology
Clinical Evaluation of Kidney Function Glomerular Filtration Rate Glomerular filtration rate (GFR) is the parameter most frequently used to assess kidney function and monitor disease progression. GFR can be estimated by mathematical equations based on the serum creatinine level or, in special circumstances, by methods such as creatinine clearance measurement or radionuclide kidney clearance scanning.
Estimation of Glomerular Filtration Rate Serum Indicators of Kidney Function Measurement of the serum creatinine level has historically been used to evaluate kidney function. The relationship between GFR and serum creatinine is not linear, but inversely proportional (Figure 1). A 50% reduction in GFR results in a doubling of the serum creatinine level once steady state conditions are attained. At high levels of GFR, small changes in the serum creatinine level may reflect large changes in GFR. At low levels of GFR, large changes in the serum creatinine level reflect relatively smaller changes in GFR. In patients who become functionally anephric (for
F I G U R E 1 . The relationship between serum creatinine and glomerular filtration rate. Example A illustrates that a small increase in the serum creatinine level in the reference range (in this case, 0.8 to 1.2 mg/dL [70.7-106 micromoles/L]) reflects a relatively large change in GFR (120 to 78 mL/min/1.73 m2). Example B illustrates that a relatively greater increase in the serum creatinine level (in the high range of 3.0 to 4.5 mg/dL [265-398 micromoles/L]) reflects a proportionately smaller change in GFR (35 to 22 mL/min/1.73 m2). GFR = glomerular filtration rate.
example, from profound acute kidney injury), the serum creatinine level typically increases 1.0 to 1.5 mg/dL (88.4133 micromoles/L) per day. Although serum creatinine is one of the most commonly used markers of GFR, it is an imperfect measure of kidney function. Reduction of muscle mass, as seen in amputees and patients with malnutrition or muscle wasting, can result in a lower serum creatinine level without a corresponding change in GFR. Younger persons, men, and black persons often have higher muscle mass and higher serum creatinine levels at a given level of GFR compared with older persons with decreased muscle mass. Patients with advanced liver disease produce lower levels of precursors of serum creatinine and often have muscle wasting, with a correspondingly lower serum creatinine level at a particular level of GFR. Finally, serum creatinine overestimates kidney function in elderly persons, especially women. Certain medications, including cimetidine and trimethoprim, block tubular secretion of creatinine and result in a higher serum creatinine level without a change in GFR. The nephrotic syndrome is associated with increased tubular secretion of creatinine, leading to overestimation of GFR. The colorimetric assay for serum creatinine cross-reacts with cefoxitin, flucytosine, and acetoacetate, leading to falsely high values. Elevated bilirubin levels interfere with the colorimetric assay, resulting in falsely low values of serum creatinine. Serum cystatin C is an alternative marker of GFR that is less influenced by age, gender, muscle mass, and body weight compared with serum creatinine. Serum cystatin C is more sensitive in identifying milder decrements in kidney function than serum creatinine. Serum levels, however, are affected by thyroid status, inflammation, diabetic status, and corticosteroid use. The clinical utility of serum cystatin C remains to be established, and it is not clear whether serum cystatin C will replace the serum creatinine level as a marker of GFR. Blood urea nitrogen (BUN) is derived from the metabolism of proteins. Although widely used, BUN concentration is a poor marker of kidney function for several reasons: it is not produced at a constant rate; it is reabsorbed along the tubules; and alterations in kidney blood flow markedly influence tubular reabsorption and excretion. BUN should not be used in isolation to predict kidney function. Urea clearances significantly underestimate GFR but may be useful in estimating GFR when it is less than 15 mL/min/1.73 m2. Table 1 outlines several factors unrelated to the kidney that can affect BUN and serum creatinine levels. 1
Clinical Evaluation of Kidney Function
TA B L E 1 .
Factors Altering Blood Urea Nitrogen and Serum Creatinine Levels Independent of Kidney Function Decreased
Increased
Blood urea nitrogen
Muscle wasting; protein malnutrition; cirrhosis
Poor kidney perfusion (volume depletion, chronic heart failure, cirrhosis); gastrointestinal bleeding; hyperalimentation; hypercatabolic states
Serum creatinine
Decreased muscle mass; cirrhosis
Tubular secretion blocked (trimethoprim, cimetidine); interference of assay (ketones, bilirubin, flucytosine, cephalosporins); overproduction (creatine ingestion, rhabdomyolysis, sustained exercise)
Methods for Estimating Glomerular Filtration Rate The National Kidney Foundation Kidney Disease Outcomes Quality Initiative (NKF KDOQI) recommends the use of mathematical equations to estimate GFR (Table 2). These equations should only be used when the serum creatinine level has been stable for at least 24 to 48 hours. The Modification of Diet in Renal Disease (MDRD) study equation has been validated in multiple populations with chronic kidney disease (CKD); however, this equation frequently underestimates GFR when it is greater than 60 mL/min/1.73 m2. The Chronic Kidney Disease Epidemiology (CKD-EPI) Collaboration equation performs better at higher (normal) values of GFR. Accurate estimation of GFR is important for appropriate adjustment of drug dosing, particularly in the elderly population and in patients with kidney disease. Historically, drug dosing guidelines were developed based on the estimated creatinine clearance derived from the Cockcroft-Gault equation. This equation takes into account lean body weight, age, and gender. Simulation studies show a high concordance rate between the estimates via the Cockcroft-Gault and MDRD study equations for drug dosing. Most clinical laboratories employ the MDRD study equation to estimate GFR, and higher levels of GFR are reported as “>60 mL/min/1.73 m2.” This practice raises concern because physicians may ignore other signs or symptoms of CKD, such as proteinuria, after erroneously assuming that the GFR is normal. Conversely, the benefits of labeling a patient with a stable GFR around 55 mL/min/1.73 m2 (apart from guiding appropriate drug dosing) as having stage 3 CKD when there are no other signs of kidney disease remain unclear. Estimation equations are less accurate when there are extremes in age and weight, in the setting of pregnancy, and in patients who have undergone amputation or have underlying cirrhosis. In these circumstances, a 24-hour urine collection for creatinine clearance should be used to estimate GFR. Because creatinine is secreted by renal tubules, creatinine clearance overestimates GFR. Inaccuracies arise with over- or undercollection of urine. Observed creatinine excretion can be compared with expected excretion to assess the accuracy of the sample. The expected excretion of creatinine is 20 to 2
25 mg/kg/24 h (177-221 mmol/kg/24 h) for men and 15 to 20 mg/kg/24 h (133-177 mmol/kg/24 h) for women. GFR can be measured very precisely using radionuclide kidney clearance scanning, which measures clearance of radiolabeled iothalamate or diethylenetriamine pentaacetic acid (DTPA). The complexity and cost of these methods limit use in clinical practice, but they may be of value when there is a need to precisely measure GFR. KEY POINTS
• Most clinical laboratories employ the Modification of Diet in Renal Disease study equation to estimate the glomerular filtration rate (GFR), and higher levels of GFR are often reported as “>60 mL/min/1.73 m2.” • Observed creatinine excretion can be compared with expected excretion to assess the accuracy of a 24-hour urine collection. • Glomerular filtration rate can be measured very precisely using radionuclide kidney clearance scanning.
Interpretation of the Urinalysis Dipstick analysis and microscopic examination of the urine are indicated in the clinical evaluation of kidney function for both acute and chronic kidney disease (Table 3, on page 4). The sample is best collected without contamination, which requires a “clean catch” midstream collection or a bladder catheterization. The specimen should ideally be examined within 1 hour of being produced to minimize the breakdown of formed elements.
Urine Dipstick Specific Gravity Specific gravity is the ratio of the weight of urine to an equal quantity of the weight of water. The typical range is 1.005 to 1.030 but can vary depending on hydration status and the capacity of an individual’s kidneys to maximally dilute and concentrate the urine. Table 4 (on page 4) illustrates the approximate urine osmolality that corresponds to a given value of urine specific gravity. pH Ingestion of a typical high-protein American diet results in consumption of a high “acid-ash” content and the need to
This self-assessment test contains one-best-answer multiple-choice questions. Please read these directions carefully before answering the questions. Answers, critiques, and bibliographies immediately follow these multiple-choice questions. The American College of Physicians is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians. The American College of Physicians designates MKSAP 16 Nephrology for a maximum of 16 AMA PRA Category 1 CreditsTM. Physicians should claim only the credit commensurate with the extent of their participation in the activity.
Earn “Same-Day” CME Credits Online For the first time, print subscribers can enter their answers online to earn CME credits in 24 hours or less. You can submit your answers using online answer sheets that are provided at mksap.acponline.org, where a record of your MKSAP 16 credits will be available. To earn CME credits, you need to answer all of the questions in a test and earn a score of at least 50% correct (number of correct answers divided by the total number of questions). Take any of the following approaches: ‚ Use the printed answer sheet at the back of this book to record your answers. Go to mksap.acponline.org, access the appropriate online answer sheet, transcribe your answers, and submit your test for same-day CME credits. There is no additional fee for this service. ‚ Go to mksap.acponline.org, access the appropriate online answer sheet, directly enter your answers, and submit your test for same-day CME credits. There is no additional fee for this service. ‚ Pay a $10 processing fee per answer sheet and submit the printed answer sheet at the back of this book by mail or fax, as instructed on the answer sheet. Make sure you calculate your score and fax the answer sheet to 215-351-2799 or mail the answer sheet to Member and Customer Service, American College of Physicians, 190 N. Independence Mall West, Philadelphia, PA 19106-1572, using the courtesy envelope provided in your MKSAP 16 slipcase. You will need your 10-digit order number and 8-digit ACP ID number, which are printed on your packing slip. Please allow 4 to 6 weeks for your score report to be emailed back to you. Be sure to include your email address for a response. If you do not have a 10-digit order number and 8-digit ACP ID number or if you need help creating a username and password to access the MKSAP 16 online answer sheets, go to mksap.acponline.org or email custserv@acponline.org. CME credit is available from the publication date of December 31, 2012, until December 31, 2015. You may submit your answer sheets at any time during this period.
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Self-Assessment Test
Nephrology Self-Assessment Test
Each of the numbered items is followed by lettered answers. Select the ONE lettered answer that is BEST in each case.
Item 1 A 41-year-old woman is evaluated during a follow-up visit for high blood pressure. She is a vegetarian and does not smoke cigarettes. She feels well except for an occasional tension headache. She takes no medications. On physical examination, blood pressure is 162/100 mm Hg, which is similar to the values measured at her initial visit. Other vital signs are normal. BMI is 21. The remainder of the examination is unremarkable. Laboratory studies reveal normal electrolytes, complete blood count, fasting glucose, and fasting lipid profile as well as normal kidney function. Electrocardiogram is unremarkable. Which of the following is the most appropriate next step in the management of this patient’s hypertension? (A) (B) (C) (D)
Combination drug therapy Lifestyle modifications Single-drug therapy Reevaluate patient in 2 weeks
Item 2 A 52-year-old woman is evaluated for a 2-day history of right flank pain, mild nausea, and fever. She has autosomal dominant polycystic kidney disease. On physical examination, the patient appears ill. Temperature is 38.6 °C (101.4 °F), blood pressure is 149/94 mm Hg, pulse rate is 92/min, and respiration rate is 20/min. BMI is 26. Abdominal examination reveals right costovertebral angle tenderness on palpation; the abdomen is nondistended, and bowel sounds are normal. Laboratory studies reveal a leukocyte count of 13,000/µL (13 × 109/L), a serum creatinine level of 1.9 mg/dL (168 µmol/L), and negative urine culture results. On kidney ultrasound, the left kidney is 16.2 cm, and the right kidney is 16.9 cm; multiple bilateral intraparenchymal cysts are noted. Which of the following is the most appropriate treatment for this patient? (A) (B) (C) (D)
Amoxicillin Cephalexin Ciprofloxacin Nitrofurantoin
Item 3 A 51-year-old man is being followed in the hospital after receiving chemotherapy for acute myeloid leukemia 1 day ago. Kidney function was normal at the start of his treatment, which consisted of normal saline at a rate of 200 mL/h and rasburicase on the day of chemotherapy. He reports no symptoms except for some fatigue and nausea. He has no shortness of breath or fever. On physical examination, the patient is afebrile. Blood pressure is 122/70 mm Hg, pulse rate is 72/min, and
respiration rate is 12/min. BMI is 25. Some bruising is noted on the skin. There is no jugular venous distention. Heart rate is regular. Lungs are clear to auscultation. There is no edema. Urine output has been around 50 mL/h. Laboratory studies: Albumin 3.2 g/dL (32 g/L) Blood urea nitrogen 14 mg/dL (5.0 mmol/L) Calcium 9 mg/dL (2.3 mmol/L) Serum creatinine 1.0 mg/dL (88.4 µmol/L) (baseline: 0.9 mg/dL [79.6 µmol/L]) Electrolytes Sodium 139 meq/L (139 mmol/L) Potassium 5.2 meq/L (5.2 mmol/L) Chloride 100 meq/L (100 mmol/L) Bicarbonate 25 meq/L (25 mmol/L) Phosphorus 5.7 mg/dL (1.84 mmol/L) Uric acid 7.1 mg/dL (0.42 mmol/L) Which of the following is the most appropriate next step in management? (A) Add sodium bicarbonate to intravenous fluid at current rate (B) Add sodium polystyrene sulfonate (C) Increase intravenous saline rate (D) Substitute allopurinol for rasburicase
Item 4 A 31-year-old woman is seen to discuss treatment of her progressive chronic kidney disease resulting from membranoproliferative glomerulonephritis. She has had a steady decline in kidney function and is approaching the need for kidney replacement therapy. Her identical twin sister has agreed to donate a kidney but is currently pregnant, and donation will likely not be possible for at least a year. She is otherwise doing well and is actively involved in her medical care. In discussing future treatment options, she has expressed a desire to pursue peritoneal dialysis should kidney replacement therapy be needed before the availability of the transplant from her sister. Medications are epoetin alfa, sevelamer, amlodipine, and sodium bicarbonate. On physical examination, blood pressure is 126/78 mm Hg. BMI is 24. Cardiac examination is normal without a rub. Lungs are clear. Abdominal examination is normal, with no evidence of prior surgery. There is no asterixis. Trace edema is present. Laboratory studies reveal a blood urea nitrogen level of 88 mg/dL (31.4 mmol/L), a serum creatinine level of 4.7 mg/dL (415 µmol/L), and a urine protein–creatinine ratio of 3.3 mg/mg. In counseling this patient, which of the following is the most appropriate recommendation for management? (A) Plan for hemodialysis when needed (B) Plan for peritoneal dialysis when needed 99
Self-Assessment Test
Directions
Answers and Critiques Answer:
A
Educational Objective: Manage newly diagnosed stage 2 hypertension. Combination drug therapy is indicated for this patient with newly diagnosed stage 2 hypertension. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) guidelines classify stage 2 hypertension as a systolic blood pressure of ≥160 mm Hg or a diastolic blood pressure of ≥100 mm Hg. According to the JNC 7, in the absence of comorbidities or compelling indications, the blood pressure goal in patients younger than 80 years is 140/90 mm Hg. In patients whose blood pressure goal requires reductions of systolic pressure more than 20 mm Hg and of diastolic pressure more than 10 mm Hg, the JNC 7 indicates that combination therapy can shorten the time needed for medication adjustment and increase the likelihood of achieving the blood pressure goal, while reducing the number of visits needed for drug titrations. Initial treatment with two antihypertensive agents is therefore warranted in this patient who has blood pressure measurements at least 22/10 mm Hg above goal. Several nondrug approaches are useful in lowering blood pressure, including weight loss if the patient is overweight, salt reduction, physical activity of at least 30 minutes per day at least 3 days per week, and a reduction in alcohol consumption. However, lifestyle modifications alone in this patient with a normal BMI who has good health habits will likely not adequately lower her blood pressure to the targeted goal. Monotherapy is unlikely to be effective in patients whose blood pressure is more than 20 mm Hg above the blood pressure goal. This patient has newly diagnosed stage 2 hypertension, with blood pressure measurements that are unlikely to be controlled with a single agent. A follow-up visit in 2 to 4 weeks to reevaluate this patient is also indicated; however, this is in addition to initiating treatment for her stage 2 hypertension. KEY POINT
• Initial treatment with two antihypertensive agents may be warranted in patients whose blood pressure is more than 20 mm Hg above the blood pressure goal.
Council for High Blood Pressure Research and the Councils on Clinical Cardiology and Epidemiology and Prevention [erratum in Circulation. 2007;116(5):e121]. Circulation. 2007;115(21):27612788. [PMID: 17502569]
Item 2
Answer:
C
Educational Objective: Treat infected cysts in a patient with autosomal dominant polycystic kidney disease. Ciprofloxacin is appropriate treatment for this patient with probable infected kidney cysts. She has autosomal dominant polycystic kidney disease (ADPKD) and now has flank pain and fever. Patients with ADPKD can have infected cysts without any abnormal findings on urinalysis or culture because the infected cyst(s) may not communicate with the rest of the urinary tract. With high suspicion of an infected cyst (flank pain and fever), treatment should consist of an antibiotic with an appropriate antimicrobial coverage spectrum for urinary tract pathogens and with good cystic penetration, such as ciprofloxacin. In this case, treatment should be continued for 2 to 4 weeks. In patients with ADPKD, nitrofurantoin, cephalosporins, or penicillins are not considered appropriate antibiotic choices given their poor cystic penetration. Patients with ADPKD who have cystic hemorrhage can have flank pain and low-grade fever that may mimic infection; however, this patient’s degree of fever with an elevated leukocyte count is out of proportion for what would be expected for a ruptured hemorrhagic cyst, suggesting infection. KEY POINT
• Patients with autosomal dominant polycystic kidney disease can have infected kidney cysts without abnormal findings on urinalysis or culture. Bibliography Sallée M, Rafat C, Zahar JR, et al. Cyst infections in patients with autosomal dominant polycystic kidney disease. Clin J Am Soc Nephrol. 2009;4(7):1183-1189. [PMID: 19470662]
Item 3
Answer:
C
Educational Objective: Prevent tumor lysis syndrome.
Bibliography Rosendorff C, Black HR, Cannon CP, et al; American Heart Association Council for High Blood Pressure Research; American Heart Association Council on Clinical Cardiology; American Heart Association Council on Epidemiology and Prevention. Treatment of hypertension in the prevention and management of ischemic heart disease: a scientific statement from the American Heart Association
An increase in the intravenous saline rate is appropriate. This patient with acute myeloid leukemia received chemotherapy 1 day ago and is at risk for tumor lysis syndrome. Manifestations include acute kidney injury and arrhythmias resulting from the release of potassium, phosphorus, and 131
Answers and Critiques
Item 1