Eosinophils in Urine - PowerPoint

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      Shahzad Qureshi M.D.
     Division of Nephrology
 Loyola University Medical Center
 Define and review classification of ARF
 Epidemiology of ARF
 Measurement of kidney function
 Pathophysiology of ARF
 Management and treatment of ARF
 Review clinical cases
            What is ARF?
A) Increase in serum Creatinine 0.5mg/dL.

B) An increase in serum Creatinine of more
  then 50% from baseline.

C) A reduction in the calculated Creatinine
  Clearance of 50%
        RIFLE Classification
2004 ADQI group classification
 Risk (R) -Increase Cr x1.5 or Decrease GFR x
  25% or UO <0.5 ml/kg/hr x 6hrs
 Injury (I)- Increase Cr x2.0 or Decrease GFR x
  50% or UO <0.5 ml/kg/hr x 12hrs
 Failure (F)- Increase Cr x3.0 or Decrease GFR
  x75% or anuria x 12 hours
 Loss (L)- Persistent ARF, complete loss of kidney
  function x 4 weeks (needing RRT)
 End Stage Kidney Disease (E)- Loss of kidney
  function x 3 months
Measurement of Kidney
           Serum Creatinine
 Serum creatinine is a reflection of creatinine
 Creatinine production is determined by muscle
  mass and must be interpreted with respect to pt’s
  age, weight and sex.
 Creatinine is filtered and secreted and tends to
  over estimate GFR.
 Certain diseases and medications interfere with
  correlation between serum Cr and GFR. (i.e..
  Acute glomerulonephritis, trimethoprim,
    Serum Creatinine (cont.)
Cockcroft-Gault equation
Cr Cx= (140 - age y)(weight kg)(0.85 if
 female)/(72 X serum creatinine mol/L)

MDRD (Modified Diet and Renal Disease)
GFR, in mL/min per 1.73 mm2 = 186.3 X ((serum
 creatinine) exp[-1.154]) X (Age exp[-0.203]) X
 (0.742 if female) X (1.21 if African American)
    Serum Creatinine (cont.)
 None of the equations accurately determine
  GFR in ARF. (Assume Cr is stable)
 More accurate techniques involve nuclear
  medicine studies and GFR scans.
 New biochemical markers investigated (i.e..
  Cystatin C)
 5 % of hospitalized patients dev. ARF.
 0.5% of these patients require dialysis.
 20% of critical care admissions dev. ARF.
 Hospital acquired ARF usually develops in
  the setting of ICU secondary to multisystem
  organ failure.
Causes of ARF in Hospitalized
45% ATN
 Ischemia, Nephrotoxins
21% Prerenal
 CHF, volume depletion, sepsis
10% Urinary obstruction
4% Glomerulonephritis or vasculitis
2% AIN
1% Atheroemboli
 Mortality rates range from 7-80% depending on
  patients other co morbidities.
 This rate has remained unchanged since the advent
  of dialysis because of increasing age and co
  morbid conditions.
 Most common cause of death associated with ARF
  are sepsis, cardiac failure and respiratory failure.
 Mortality rates are lower for nonoliguric
  (>400ml/day) then oliguric ARF (<400 ml/day).
 1) As an adaptive response to severe volume
  depletion and hypotension with structurally and
  functionally intact nephrons. (Pre renal azotemia)
 2) In response to cytoxic or ischemic insults to the
  kidney with structural and functional damage.
  (Intrinsic Renal failure)
 3) With obstruction to passage of urine. (Post
  obstructive uropathy)
   Nausea? Vomiting? Diarrhea?
   Hx of heart disease, liver disease,
    previous renal disease, kidney stones,
   Any recent illnesses?
   Any edema, change in
   Any new medications?
   Any recent radiology studies?
   Rashes?
                Physical Exam
 Volume Status
   – Mucus membranes, orthostatics
 Cardiovascular
   – JVD, rubs
 Pulmonary
   – Decreased breath sounds
   – Rales
 Rash (Allergic interstitial nephritis, Livedo reticularis)
 Large prostate
 Extremities (Skin turgor, Edema)
               Workup for ARF
 Urine
    – Urine sediment (U/A): casts, cells, protein
    – Urine electrolytes (UNa and UUN) and urine Cr to
      calculate FeNa/FeUrea
    – Urine osmolarity
    – Urine protein
    – Urine eosinophils
   Kidney U/S - r/o hydronephrosis
A 75yo man, NH resident, with
Alzheimer’s dementia admitted for
aspiration pneumonia. BUN 50 and Cr 2.6
                        A. ATN from Abx
                        B. Glomerulo-
                        C. Dehydration
                        D. AIN from

    Hyaline Casts
         Pre Renal Azotemia
 Impaired renal blood flow as a result of true
  intravascular depletion, decreased effective
  circulating volume to the kidneys, or agents that
  impair renal blood flow.
 Urine and blood studies are helpful in diagnosing
  pre renal ARF.
 Hyaline casts can be seen (Not an abnormal
 Treat with fluid boluses or continuous IVF,
  monitor urine output.
                 Prerenal Causes
   Intravascular volume depletion
     – Hemorrhage
     – Vomiting, diarrhea
     – “Third spacing”
     – Diuretics
   Reduced Cardiac output
     – Cardiogenic shock, CHF, tamponade, huge PE....
   Systemic vasodilation
     – Sepsis
     – Anaphylaxis, Antihypertensive drugs
   Renal vasoconstriction
     - Hepatorenal syndrome
   Medications
     - ACE-I, NSAIDS
                Urine Indices in ARF
                  Pre Renal      Intrinsic ATN   Post Renal
                    > 500            < 350         < 350

   Na (meq/L)       < 20             > 40           > 40

Bun/Cr (mg/dL)     > 20:1           < 10:1         < 10:1
      FENa          < 1%            >3%            >3%
      FEUrea        <35%            >55%           >55%
                 Hyaline casts      Brown,         Bland
                  Acute Renal Failure
                            Urinary Indices
            PR              PR              ATN

500              40              40

350              20              20

      ATN             ATN              PR

   UOsm               (U/P)Cr           UNa             FENa
 (mOsm/L)                             (mEq/L)
               What is FENa
   The fraction of filtered
    sodium excreted in the
FeNa = (urine Na x plasma Cr)
       (plasma Na x urine Cr)
    ARF syndromes with Low
 Pre renal ARF
 Vasoconstriction Mediated Intrinsic Renal Failure
      -Tacrolimus, cyclosporine, cocaine
      - Hepatorenal syndrome
      - Radiocontrast Injury
      - Rhabdomyolysis
      - Sepsis (early), burn injury
      - Acute Glomerulonephritis
 Calculating FeNa after pt has
        gotten Lasix...
  Caution with calculating FeNa if pt has gotten Loop
   Diuretics in past 24-48 h
 Loop diuretics cause natriuresis (incr urinary Na excretion)
   that raises U Na-even if pt is prerenal
 So if FeNa>1%, you don’t know if this is because pt is
   euvolemic or because Lasix increased the U Na
 So helpful if FeNa still <1%, but not if FeNa >1%
1. Fractional Excretion of Lithium (endogenous)
2. Fractional Excretion of Uric Acid
3. Fractional Excretion of Urea
Nurse pages you and states your patient
has not urinated in 8 hours….
    What do you want to do?”
• Examine pt: Dry? Septic (vasodilated)?
•Check I/Os (has pt been drinking?)
•Insert Foley and measure PVR
•Flush foley (sediment can obstruct outflow)
• Give IV BOLUS (250-500cc IVF), see if pt urinates
in next 30-60 min
   –If pt urinates, then the pt was dry
   –If pt doesn’t urinate, then pt’s either REALLY dry or in
   renal failure
•Check UA, urine lytes, urine osmolarity, BMP
•Consider Renal U/S if reasonable
     Post Obstructive Uropathy
   Occurs if both urinary outflow tracts are
    obstructed or outflow tract of solitary kidney is
   Patients with SUDDEN ONSET of anuria are
    likely to have post obstructive uropathy.
   Primary causes include BPH, prostate and cervical
    cancer, stones, strictures and retroperitoneal
   Bladder catheterization and Renal U/S to assess
   Can have obstruction w/o hydronephrosis on U/S
   Monitor for post obstructive diuresis, hemorrhagic
 You evaluate a 60 yo man who undergoes fem-
 pop bypass for severe PVD now with oliguria
 and rapidly increasing BUN, Cr.

A.   ATN              Brown, “Muddy” casts
B.   Acute glomerulonephritis
C.   Contrast Induced Nephropathy
D.   Post-Obstructive uropathy
     Intrinsic Acute Renal Failure
1.    Tubular (ATN)
2.    Interstitial (AIN)
3.    Glomerular (Glomerulonephritis)
4.    Vascular
 Most common cause of ARF in hospitalized
 Contrast and aminoglycosides most often
  associated with nonischemic ATN.
 3 phases:
  1) Initiation phase- Renal injury lasting
                       hours to days.
  2) Maintenance phase- Lasts days to
                    weeks. GFR and U.O at lowest.
  3) Recovery Phase- Postacute tubular necrosis
  diuresis. Can still exp. uremia and hypovolemia as
  tubular function not completely restored.
Tubular-Cell Injury and Repair in Ischemic Acute Renal Failure.

        Thadhani, R. et al. N Engl J Med 1996;334:1448-1460
 Reverse underlying causes and correct fluid
  and electrolyte balances
 Treatment is supportive.
 Drugs such as mannitol, loop diuretics,
  dopamine and CCB successful in promoting
  diuresis in animals but not in humans.
 Dialysis as needed (IHD vs. CRRT)
60yo woman with h/o OA has labs
drawn BUN=24, Cr 1.8. U/A reveals
20 WBC, no bacteria. What is the cause
of ARF?
                       A. Pre renal azotemia
                          secondary to UTI
                       B. ATN secondary to
                       C. AIN secondary to
                          NSAID use
                       D. Acute
    Acute Interstitial Nephritis
70% Drug hypersensitivity
 30% Antibiotics: PCNs (Methicillin), Cephalosporins,
 Sulfa drugs
 Allopurinol...

15% Infection
 Strep, Legionella, CMV, other bact/viruses
8% Idiopathic
6% Autoimmune Dz (Sarcoid, Tubulointerstitial
                    AIN from Drugs
Renal damage is NOT dose-dependent
May take wks after initial exposure to drug
 Up to 18 mos to get AIN from NSAIDS!
But only 3-5 d to develop AIN after second exposure to drug

 Fever (27%)
 Serum Eosinophilia (23%)
 Maculopapular rash (15%)

   Bland sediment or WBCs, sterile pyuria most commonly seen
   WBC Casts are common
   Urine eosinophils on Wright’s or Hansel’s Stain
    - Also see urine eos in RPGN, renal atheroemboli...

   Treatment is to remove offending agents. Most patients recover complete
    kidney function w/I one year.
You evaluate a 32yo woman with oliguria, hematuria
and rapidly increasing BUN/Cr a few days after
experiencing a viral URI. U/A reveals…

                               A. ATN
                               B. Acute
                               C. Acute interstitial
                               D. Pre renal Azotemia

       RBC CASTS
    Acute Glomerulonephritis
Nephrotic Syndromes
  1° Disorders - Minimal Change Disease
                - Membranous Nephropathy
                - FSGS
  2° Disorders- DM
              - SLE
              - Hepatitis B
              - Amyloid
              - Heroin
      Nephrotic Syndromes
 Edema (Anasarca)
 Proteinuria (>3.5gm/24hrs)
 Lipidemia
 Can have normal serum creatinine (Not
 Usually do NOT see RBC casts
            Nephritic Syndromes
Type 1: Anti-GBM dz (Anti GBM Ab positive)
- Goodpasture’s Disease
- Anti-GBM

Type 2: Immune complex (Low compliment, elevated ESR)
 IgA nephropathy (Normal Compliment levels)
 Postinfectious glomerulonephritis
 Lupus nephritis
 Mixed cryoglobulinemia

Type 3: Pauci-immune (ANCA positive, assoc with vasculitis)
 Wegner’s Disease
 Microscopic Polyangitis
 Churg-Strauss
         Nephritic Syndromes
   Fever
   Oliguria
   Hematuria
   Htn
   RBC casts
   Proteinuria (1-2grams usually)
   Treatment varies based on underlying disease
68y/o male with baseline Cr=1.2 underwent
angiogram 3 days prior for ACS. Now pt has
Cr=2.0 and blanching rash.

     A.   Renal Artery Stenosis
     B.   Contrast-Induced Nephropathy
     C.   Abdominal Aortic Aneurysm
     D.   Cholesterol Atheroemboli
      Renal Atheroembolic Dz
1% of Cardiac caths: atheromatous debris scraped from the
  aortic wall will embolize
   – Retinal
   – Cerebral
   – Skin (Livedo Reticularis, Purple toes)
   – Renal (ARF)
   – Gut (Mesenteric ischemia)
 Cr will NOT improve with IVF
 Diagnosis of exclusion: will NOT show up on MRI or
  Renal U/S; WILL show up on renal bx
 Tx: supportive
You are called to evaluate a 45
 y/o female in the ER admitted
for heart palpatations. BUN 80,
      Cr 3.0, Potassium 6.5

       What do you do?
    Treatment of Hyperkalemia
 EKG/Telemetry
 Calcium Gluconate
 Glucose and Insulin
 Sodium Bicarbonate
 Diuretics (Lasix)
 Cation-exchange resins (Kayexalate)
 Dialysis
             Case (cont.)
 You admit the pt to telemetry and give
  appropriate medications.
 You recheck labs 4h later and BUN=105,
  Cr=4.0, K=7.0. Suddenly the pt starts to
 Now what?
 Acute Indications for Dialysis

 Acidosis (metabolic)
 Electrolytes (hyperkalemia)
 Ingestion of drugs/Ischemia
 Overload (fluid)
 Uremia
An excess in the blood of urea, creatinine and other
nitrogenous end products with signs and symptoms listed .
   General
    – Fatigue, weakness
    – Pruritis
   Mental status change
    – Uremic encephalopathy
    – Seizures
    – Asterixis
   GI disturbance
    – Anorexia, early satiety, N/V,
 Uremic Pericarditis
 Plt dysfunction/bleeding

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