Educational Objectives Faculty Disclosure Acknowledgements

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Educational Objectives Faculty Disclosure Acknowledgements Powered By Docstoc
					Volume 57, Issue 42                                                                                              November 14, 2009

                          From Family Medicine: Board Review Course, presented July 6-9, 2009, by the
                                 University of California, San Francisco, School of Medicine
   Shieva Khayam-Bashi, MD, Associate Clinical Professor, Department of Family and Community Medicine, University of
    California, San Francisco, School of Medicine, and Medical Director, Ward 4A/SNF, San Francisco General Hospital
                     Acute Kidney Disease                                (oliguria in adults, urine output of <400 mL/day; in chil-
Acute kidney injury: consider whether problem prerenal                   dren, <0.5 mL/kg per hr); anuria (urine output <100
                                                                         mL/day) usually associated with poorer prognosis, except
 (problem of flow to kidneys), postrenal (obstructive pro-
                                                                         in dehydration; mortality rates vary (25%-90%; in-hospital
 cess at level of ureter, bladder, or urethra), or intrinsic (“is it
                                                                         mortality, 50%); higher mortality rates usually seen in
 the kidneys?”); 66% of time, problem prerenal (10% of
                                                                         patients who require dialysis; complications — electrolyte
 time, postrenal; 33% of time, intrinsic)                                disorders (eg, hyperkalemia, metabolic acidosis); infec-
Case presentation: man 55 yr of age with diabetes, hyperten-             tions; gastrointestinal (GI) bleeding; arrhythmia; myocar-
 sion, and degenerative joint disease (DJD) presents with 3-             dial infarction (MI); pulmonary edema
 day history of nausea, vomiting, diarrhea, and low oral in-           Causes of acute kidney injury: volume depletion —
 take; becomes oliguric, anuric, confused, and complains of              decreased oral intake; vomiting; diarrhea; diuretic use; ana-
 pruritus; medications include benazepril, hydrochlorothia-              phylaxis; sepsis; MI; congestive heart failure (CHF); cir-
 zide, glipizide, and ibuprofen; physical examination —                  rhosis; signs of obstruction — patients often asymptomatic;
 dehydration; hypotension; tachycardia; tachypnea; hypoxia;              abdominal or flank pain; hematuria; sudden anuria; weight
 confusion; dry mucous membranes; rales on lung examina-                 loss or cancer symptoms (pelvic cancers lead to obstruction
 tion; no abdominal mass; normal prostate examination; no                of ureters, urethra, or bladder); agitation; intrinsic renal
 petechiae or purpura; laboratory studies — potassium high (6            problems — most commonly due to medications (eg, intra-
 mEq/L); sodium low (129 mEq/L); CO2 low (20 mEq/L); se-                 venous [IV] contrast, aminoglycosides, amphotericin, peni-
 rum urea nitrogen (BUN) high; creatinine high; treatment —              cillins, cephalosporins, sulfonamides); positive family
 normal saline boluses for hypotension; Foley catheter in-               history of kidney disease; personal renal history; autoim-
 serted to rule out obstruction (no urine excreted); no acute            mune disease and vasculitis (eg, lupus, Sjögren’s syn-
 changes on electrocardiography (ECG); hyperkalemia                      drome); viral diseases (eg, hepatitis B or C, HIV)
 treated with transcellular shifting-mediated mechanism of             Consequences of acute kidney injury: encephalopathy; ure-
 insulin and glucose, calcium, and sodium polystyrene to help            mic pericarditis; CHF and fluid overload (eg, pulmonary or
 bind potassium in gut; blood pressure (BP) medications and              peripheral edema, significant hypertension); acute platelet
 nonsteroidal anti-inflammatory drugs (NSAIDs) held; uri-                dysfunction; indications for dialysis
 nalysis (UA) showed concentrated urine, with no red blood             Physical examination: volume status; orthostatic vital signs;
 cells (RBCs), white blood cells (WBCs), or tubular cell casts           dry mucous membranes; pericardial rub (pericarditis;
 (acute tubular necrosis [ATN] ruled out); renal ultrasonogra-           emergent hemodialysis indicated); pulmonary edema; blad-
 phy (US) negative for hydronephrosis; patient's BP, urine               der distention; petechiae might suggest uremic syndrome
 output, mental status, BUN, and creatinine improved; man                or thrombotic thrombocytopenic purpura (TTP); palpable
 discharged after few days with diagnosis of acute kidney                purpura suggest vasculitis; pelvic and prostate examination
 injury (prerenal azotemia secondary to acute viral                    Laboratory studies: complete blood cell count (CBC); platelet
 gastroenteritis)                                                        count normal in acute kidney failure; chemistry panel (CHEM-
Acute kidney injury: rapid rise in creatinine over 2 wk; if             7); stat ECG; UA with microscopy; urine culture and renal US
 baseline creatinine <2.5 mg/dL, often defined as rise of                helpful; serum sodium and creatinine and urinary sodium and
 0.5 mg/dL; if baseline creatinine >2.5 mg/dL, defined as               creatinine (to calculate fractional excretion of sodium [FENa]);
 increase in creatinine >20%; can be nonoliguric or oliguric             x-ray of kidneys, ureter, and bladder optional; computed tomog-

                    Educational Objectives                             committee to disclose relevant financial relationships within
                                                                       the past 12 months that might create any personal conflicts of
  The goal of this program is to improve management of acute
                                                                       interest. Any identified conflicts were resolved to ensure that
  and chronic kidney disease. After hearing and assimilating this
                                                                       this educational activity promotes quality in health care and
  program, the clinician will be better able to:
                                                                       not a proprietary business or commercial interest. For this pro-
     1. List intrinsic renal problems that lead to acute kidney        gram, Dr. Khayam-Bashi and the planning committee reported
         injury.                                                       nothing to disclose.
     2. Identify causes of acute kidney injury, based on urinal-
         ysis with microscopy.                                                            Acknowledgements
     3. Perform appropriate laboratory studies to evaluate kid-        Dr. Khayam-Bashi spoke in San Francisco, CA, at Family
         ney function.                                                 Medicine: Board Review Course, presented July 6-9, 2009,
     4. Use appropriate methods to accurately screen for               by the University of California, San Francisco, School of
         proteinuria.                                                  Medicine. The Audio-Digest Foundation thanks Dr. Khayam-
     5. Counsel patients about therapy and lifestyle modification.     Bashi and the University of California, San Francisco,
                                                                       School of Medicine for their cooperation in the production
                       Faculty Disclosure                              of this program.
  In adherence to ACCME Standards for Commercial Support,
  Audio-Digest requires all faculty and members of the planning
                                          AUDIO-DIGEST FAMILY PRACTICE 57:42

  raphy (CT) of abdomen for masses or symptoms suggestive of              Nephritis: interstitial — clinical clues include fever, rash,
  cancer; ECG in hyperkalemia—ventricular tachycardia or ven-                and eosinophilia in blood; urine sediment; protein in
  tricular fibrillation can be sudden or gradual; peaked T waves             urine; consider viral testing (for, eg, cytomegalovirus
  with prolonged PR intervals; with progression, P waves lost and            [CMV], HIV, hepatitis B virus [HBV]) and autoimmune
  QRS intervals widen with peaked T waves; FENa—indicates                    testing (for, eg, sarcoidosis, Sjögren’s syndrome); consult
  how well kidneys retain sodium in setting of dehydration; (uri-            nephrologist before treating; glomerulonephritis —
  nary sodium/plasma sodium) ÷ (urinary creatinine/plasma cre-               clinical clues include preexisting infection (eg, Strepto-
  atinine) x 100; obtain urinary and plasma values at same time of           coccus), rash, arthritis; urine sediment; RBC casts; pro-
  day; <1% usually suggests prerenal etiology (>1% usually sug-              tein in urine; look for infections (eg, HIV, hepatitis B and
  gests ATN); FENa often elevated by diuretic use, or decreased              C); in patients with rash or arthritis, look for cryoglobuli-
  due to certain intrinsic renal problems (eg, acute glomerulone-            nemia or lupus; consider multiple myeloma in patients
  phritis, ATN, rhabdomyolysis, contrast nephropathy, sepsis); pa-           >40 yr of age (perform urine and serum protein electro-
  tients with chronic kidney disease can have chronically elevated           phoresis); consult nephrologist
  FENa; fractional excretion of urea—useful in patients with re-          Vasculitis: clinical clues include fever, constitutional symp-
  cent use of diuretic; (urinary urea/plasma urea) ÷ (urinary creat-         toms, rash, respiratory symptoms; RBC casts; autoim-
  inine/plasma creatinine) x 100; <35% usually suggests prerenal             mune testing, testing for HIV, hepatitis B and C
  etiology (>35% usually suggests ATN); more reliable than              Summary of acute renal failure: adjust doses of all drugs;
  FENa; if clinical setting suggests prerenal etiology, low urinary       choose lowest dosing; diuretics for converting oliguric to
  sodium and low fractional excretion of sodium confirm prerenal          nonoliguric renal failure no longer used (benefits unclear
  etiology; FENa can be low in acute glomerulonephritis or vas-           and may worsen mortality); no benefit of low doses of do-
  cular disorder; in intrinsic renal problems, urinary sodium high;       pamine; prevention of contrast nephropathy — in patients
  UA with microscopy—tubular epithelial cell casts usually indi-          with risk factors for acute renal failure (eg, advanced age,
  cate ATN, and sometimes acute interstitial nephritis; white cell        chronic kidney or liver disease), hold metformin, diuretics,
  casts without bacteria often indicative of interstitial nephritis       and NSAIDs for 2 days; start IV fluids or advise high oral
  (most commonly caused by drugs; ask nephrologist to look for            fluid intake 1 day before; giving sodium bicarbonate 1 hr
  >10% eosinophils), but sometimes seen in chronic glomerulo-             before and 6 hr after may be beneficial (data conflicting);
  nephritis; red cell casts indicative of glomerulonephritis; hyaline     acetylcysteine (eg, Mucomyst; 600 mg bid) 1 day before
  casts nonspecific (often seen in prerenal cases); oval fat bodies       and on day of study (controversial)
  indicative of nephrotic syndrome; when urine dipstick positive                        Chronic Kidney Disease (CKD)
  for blood (eg, 1+, 2+, or 3+) with no RBCs on UA microscopy,          Screening for CKD: screen patients with risk factors (eg, di-
  consider rhabdomyolysis (reversible cause of acute renal failure;       abetes, hypertension, age >60 yr); positive family history,
  irreversible if missed) and check serum creatine kinase                 history of recurrent urinary tract infection (UTI) or obstruc-
Treatment: manage consequences; consider need for emer-                   tion, or systemic illness (eg, autoimmune disease, vasculi-
  gent hemodialysis; give IV fluids unless patient volume                 tis) less common risk factors; reasons for screening — to
  overloaded; inserting Foley catheter helpful for ruling out             slow disease progression; to prevent or reduce risk for car-
  distal obstruction of urethra (flush catheter with normal sa-           diovascular disease; check BP and creatinine; CHEM-7;
  line to clear any obstructive sediment or clot)                         random urine sample for protein or albumin to creatinine
Indications for emergent hemodialysis: hyperkalemia; meta-                ratio; UA with microscopy
  bolic acidosis; CHF; uremic encephalopathy; pericarditis;             Estimated glomerular filtration rate (eGFR): normal GFR,
  BUN and creatinine values alone not indication for dialysis;            95 to 120 mL/min per 1.73 m2; GFR decreases with age; re-
  certain drug overdoses; ECG of pericarditis — diffuse ST                nal dysfunction can occur despite normal creatinine; eGFR
  segment elevations with audible rub; PR interval depressions            better measure of kidneys’ ability to filter, and helps detect
Treatment before dialysis: hyperkalemia — treat with glu-                 early kidney disease; calculation based on age, sex, and
  cose and insulin or IV calcium; sodium polystyrene                      ethnicity (ie, black or white)
  (Kayexalate); furosemide; check ECG and monitor;                      Screening for proteinuria: can detect kidney disease even before
  CHF — treat with O2 and diuresis; severe acidosis — treat               changes in eGFR occur; proteinuria associated with more rapid
  with sodium bicarbonate; NSAIDs and anticoagulants con-                 decline of kidney function; reducing proteinuria slows progres-
  traindicated in patients with uremic pericarditis; avoid —              sion of CKD; treat with ACE inhibitor or angiotensin receptor
  potassium, potassium-sparing diuretics, angiotensin-con-                blocker (ARB); urine dipstick detects large amounts (>300 mg)
  verting enzyme (ACE) inhibitors, NSAIDs, and IV contrast                of protein (albumin); measure albumin directly in patients with
Postrenal causes: masses; tumors; stones; anticholinergic drugs           microalbuminuria; 24-hr urine collection gold standard for pro-
  (eg, tricyclic antidepressants; diphenhydramine [eg, Benadryl])         tein, but inconvenient and prone to error; measure protein or al-
Intrinsic renal causes: aortic dissection; 90% of time, due to            bumin to creatinine ratio; normal urinary protein to creatinine
     ATN (often induced by hypotension); most common prob-                ratio, <200 mg to 1 g (for albumin, <30 mg to 1 g); microalbu-
     lems due to nephrotoxic drugs and rhabdomyolysis (treat              minuria, 30 to 300 mg of albumin to 1 g of creatinine; macroal-
     with hydration and IV bicarbonate); acute interstitial               buminuria, >300 mg of albumin to 1 g of creatinine; in patients
     nephritis — can develop as late as 10 to 30 days after last          with protein in urine, obtain total protein to creatinine ratio; in
     drug dose; drug history important; only 33% of patients             patients with risk factors and positive dipstick (protein >30 mg),
     have eosinophils in urine (diagnostic finding); vascular —           perform albumin or total protein to creatinine ratio; perform 24-
     less likely; emboli from left heart; aortic atheroma; postaor-       hr urine for patients “in extremes” (eg, extremes of age or
     tic surgery; left heart endocarditis; atrial fibrillation; renal     weight, high muscle mass) or with malnutrition, muscle dis-
     artery stenosis (consider in young people with refractory hy-        eases, paraplegia, vegetarianism, pregnancy
     pertension) or thrombosis; glomerulonephritis; autoimmune          Diagnosing CKD: presence of kidney damage for 3 mo (based
     diseases; renal infiltration (rare)                                  on abnormal structure on imaging study or abnormal func-
                                                AUDIO-DIGEST FAMILY PRACTICE 57:42

 tion), or eGFR <60 mL/min per 1.73 m2 for 3 mo; end-stage                       mend aggressive targets (eg, LDL <100 mg/dL, triglycerides
 renal disease — eGFR <15 mL/min per 1.73 m2 (kidney fail-                        <200 mg/dL); hypertension — ACE inhibitors and ARBs
 ure); need for dialysis or transplantation; stages — stage 5                     preferentially lower glomerular pressures and reduce protein-
 most severe; stage 3, eGFR, 30 to 60 mL/min per 1.73 m2;                         uria; in patients with normal urine protein, target BP, <130/80
 eGFR underestimates renal function at normal creatinine lev-                     mm Hg; in patients with protein in urine, target BP, <125/75
 els (eg, creatinine of 0.6 mg/dL may correlate with stage 1                      mm Hg; when starting ACE inhibitors in CKD patients, GFR
 eGFR value; creatinine of 0.9 mg/dL may correlate with                           initially decreases, and creatinine increases mildly (30%;
 lower eGFR); eGFR values <60 mL/min per 1.73 m2 reliable;                        check CHEM-7 1-2 wk after initiating therapy; do not discon-
 CKD commonly caused by diabetic kidney disease, vascular                         tinue therapy unless increase does not stabilize; monitor);
 problem (eg, hypertension, large vessel disease), and glomer-                    anemia — normochromic; normocytic; hypoproliferative;
 ular diseases (eg, tubular interstitial disease, drug toxicities);               caused by low erythropoietin; reduces quality of life; causes
 in patients with risk factors for parenterally transmitted dis-                  fatigue and can lead to cardiomyopathy from left ventricular
 eases consider eg, HIV, hepatitis B and C, associated kidney                     hypertrophy; correction of anemia may help improve CKD;
 diseases; in patients with rash, consider lupus and cryoglobu-                   recommended hemoglobin (Hb) target, 10 g/dL to 12 g/dL;
 linemia; laboratory studies — recent UA; CHEM-7; urine
                                                                                  check ferritin and supplement with iron if indicated; give
 protein or albumin to creatinine ratio; renal US — may show
 stones, hydronephrosis, or cysts; small hyperechoic kidneys                      erythropoietin to predialysis patients if Hb <10 g/dL; renal
 generally indicate CKD; large kidneys may be associated with                     osteodystrophy — common; early CKD patients have hyper-
 hydronephrosis (obstructive process), or infiltrating process                    phosphatemia and increased parathyroid hormone (PTH), re-
 (eg, sarcoidosis or lymphoma); size disparity between kidneys                    sulting in increased bone turnover, decreased bone strength,
 indicates renal vascular disease (eg, fibromuscular dysplasia                    and fractures; check PTH and restrict dietary phosphate in-
 or renal artery thrombosis); slow progression of CKD by con-                     take; treat with calcium acetate and vitamin D; refractory pa-
 trolling BP, glucose, and proteinuria                                            tients may need surgical treatment to remove parathyroid
Complications: hyperkalemia; hyperphosphatemia; hypocalce-                       Nutrition and lifestyle: CKD patients at risk for malnutri-
 mia (secondary hyperparathyroidism); hyponatremia; de-                           tion; study showed patients on restricted protein diet did
 creased immunoglobulins; dyslipidemia — coronary artery                          not fare better; refer patients to nutritionist and consult ne-
 disease number 1 cause of mortality in patients with CKD;                        phrologist; be aggressive about tobacco smoking cessa-
 animal studies suggest dyslipidemia can worsen kidney func-                      tion; social support and screening for depression
 tion; recent meta-analysis of 13 small studies showed lipid re-                 When to refer to nephrologist: underlying cause unclear after
 duction might preserve GFR; patients with CKD tend to have                       work-up; need for biopsy; diagnosis unclear; stage 3 or 4 CKD;
 high triglycerides and elevated low-density lipoprotein (LDL)                    rapid progression of CKD or superimposed acute kidney fail-
 to high-density lipoprotein (HDL) ratios; guidelines recom-                      ure; or useful resources

                        Suggested Reading                                        ate therapy and contrast-induced nephropathy. Am J Kidney Dis
                                                                                 54:390, 2009; Solomon R: Contrast-induced acute kidney injury
Kleinknecht D: Interstitial nephritis, the nephrotic syndrome, and
                                                                                 (CIAKI). Radiol Clin North Am 47:783, 2009; Thakar CV et al: In-
chronic renal failure secondary to nonsteroidal anti-inflammatory
                                                                                 cidence and outcomes of acute kidney injury in intensive care units: a
drugs. Semin Nephrol 15:228, 1995; Levin A et al: Canadian Society
                                                                                 Veterans Administration study. Crit Care Med 37:2552, 2009; Trivedi
of Nephrology. Guidelines for the management of chronic kidney dis-
                                                                                 H et al: High-dose N-acetylcysteine for the prevention of contrast-in-
ease. CMAJ 179:1154, 2008; Lines S et al: Acute kidney injury. Clin
                                                                                 duced nephropathy. Am J Med 122:874, 2009; van Heyningen C:
Med 9:273, 2009; Schwarz A et al: The outcome of acute interstitial
                                                                                 Lipid metabolism and causal pathways for cardiovascular disease in
nephritis: risk factors for the transition from acute to chronic intersti-
                                                                                 chronic kidney disease. Curr Opin Lipidol 20:440, 2009.
tial nephritis. Clin Nephrol 54:179, 2000; Singh D: Sodium bicarbon-

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                                        AUDIO-DIGEST FAMILY PRACTICE 57:42

                                 To test online, go to and sign in to online services.
            To submit a test form by mail or fax, complete Pretest section before listening and Posttest section after listening.
   1. Choose the correct statement about acute kidney injury.
         (A)   Characterized by rapid rise in creatinine over 1 mo
         (B)   Can be nonoliguric or oliguric
         (C)   Anuria usually associated with good prognosis
         (D)   Mortality rates lower in patients who require dialysis

   2. Intrinsic renal problems that lead to acute kidney injury are most commonly caused by:
         (A) Pelvic cancer                                             (C) Congestive heart failure
         (B) Vomiting                                                  (D) Medications

   3. Values for fractional excretion of sodium are often elevated by:
         (A) Diuretic use                                              (C) Rhabdomyolysis
         (B) Acute glomerulonephritis                                  (D) Sepsis

   4. Which of the following findings on urinalysis with microscopy is most commonly indicative of interstitial nephritis?
         (A) Tubular epithelial cell casts                             (C) Red blood cell casts
         (B) White blood cell casts                                    (D) Hyaline casts

   5. Which of the following is not an independent indication for emergent hemodialysis?
         (A)   Hyperkalemia
         (B)   Uremic encephalopathy
         (C)   Abnormal serum urea nitrogen and creatinine levels
         (D)   Metabolic acidosis

   6. Using diuretics to convert oliguric renal failure to nonoliguric renal failure may worsen mortality.
         (A) True                                                      (B) False

   7. Choose the correct statement about screening for proteinuria.
         (A)   Can detect kidney disease even before changes in estimated glomerular filtration rate (eGFR) occur
         (B)   Normal urinary protein to creatinine ratio <200 mg to 1 g
         (C)   24-hr urine collection is gold standard, but prone to error
         (D)   All the above

   8. A patient with an eGFR measurement of 45 mL/min per 1.73 m2 would most likely be diagnosed with _______ chronic
      kidney disease (CKD).
         (A) Stage 1                         (B) Stage 2                       (C) Stage 3                        (D) Stage 4

   9. In patients with CKD, what is the recommended target level of low-density lipoprotein?
         (A) <175 mg/dL                      (B) <150 mg/dL                    (C) <125 mg/dL                     (D) <100 mg/dL

  10. In patients with CKD, angiotensin-converting enzyme inhibitor therapy should be discontinued if elevations in creatinine
         (A) True                                                      (B) False

Answers to Audio-Digest Family Practice Volume 57, Issue 40: 1-B, 2-C, 3-D, 4-D, 5-C, 6-A, 7-B, 8-A, 9-B, 10-A

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                                    2009 Audio-Digest Foundation • ISSN 0271-1362 •
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