Renal Function Flashcards

1
Q

Blood urea nitrogen

  • relationship to GFR
  • define uremia and azotemia
A
  • urea is filtered and partially reabsorbed by the nephron, which means that BUN always slightly underestimates the GFR
  • Reabsorption increases with hypovolemia; thus BUN underestimates the GFR even more in hypovolemic states
  • An increase in BUN = azotemia
  • uremia refers to the toxic effects of elevated BUN
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2
Q

GFR calculation

A
  • Creatinine passes freely through glomerulus and a small amount is secreted by tubules; the latter increases with increasing serum [Cr]
  • Creatinine overestimates GFR

ClearanceCr = UCr/PCr x VUr/time(minutes)

UCr is urine creatinine (mg/dL)

VUr is volume of urine (mL, collected over 24 hours)

PCr is plasma creatinine (mg/dL)

Units for ClCr are mL/min with 80-120 mL/min being normal

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3
Q

Problems with using creatinine clearance to estimate GFR

A
  • relationship between GFR and creatinine is nonlinear: mild impairment in GFR does not cause much increase in creatinine
  • When GFR is 1/2 normal, creatinine begins to linearly reflect changes in GFR
  • Nonglomerular influences upon creatinine; creatinine concentration is increased by muscle mass, muscle activity, muscle injury (trauma, surgery), and protein intake
  • Creatinine decreases with age and is influenced by race, sex, medications
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4
Q

Other calcuations for GFR

A
  • Modification of Diet in Renal Disease (MDRD) Study equations is most widely used, but is being replaced by:
    • Chronic Kidney Disease Epidemiologic Collaborative (CKD EPI) equation in many labs
  • MDRD equation is invalid at high GFR (eGFR over 60 mL/min/1.73 m2)
  • CKD EPI equation is valid over the whole eGFR range
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5
Q

BUN/Creatinine ratio

A
  • Normal is 10:1
  • Prerenal azotemia: ratio is increased, frequently > 20:1, in renal hypoperfusion (2/2 hypovolemia, hypotension)
  • Ratio is maintained near normal in intrarenal causes of renal failure
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6
Q

Cystatin C

A
  • Freely filtered by glomerulus and completely reabsorbed by proximal tubule
  • at least as good as serum creatinine for estimating the GFR and less dependent on age, sex, or muscle mass
  • Strong predictor of cardiovascular mortality in patients with chronic renal disease
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7
Q

Normal proteinuria

A

Does not exceed 150 mg/day (mainly Tamm-Horsfall protein)

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8
Q

Significant proteinuria

  • level
  • method
  • compared to creatinine clearance
  • dipstick
A
  • > 300 mg/day
  • based on 24 hour urine collection
  • random urine samples (“spot urine”)
    • can be misleading because protein handling by kidney varies throughout the day
    • when compared to simultaneous urine creatinine determination, the spot urine protein measurement is as good as the 24 hour urine
  • urine dipstick result (1+ to 3+) is semiquantitative and most sensitive to albumin; not sensitive enough to detect microalbuminuria
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9
Q

Microalbumin assay

A
  • capable of detecting as little as 0.3 mg/dL of albumin (dipstick sensitive to ~30 mg/dL)
  • microalbuminuria defined by albumin:creatinine ratio (mg/G) of a spot urine rather than a 24 hour collection
  • possible source of confusion - protein:creatinine ratio is reported as mg/mg
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10
Q

urine Beta2 microglobulin and lysozyme assays

A
  • these proteins are freely filtered by the glomerulus and then completely reabsorbed by the normally functioning proximal convoluted tubule
  • presence in the urine suggests tubular dysfunction
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11
Q

Laboratory screening for chronic kidney disease

  • who gets screened
  • what tests are done
  • define CKD
A
  • Annual testing for those at high risk for CKD, including patients with:
    • diabetes mellitus
    • HTN
    • family history of renal disease
  • High risk groups should get
    • eGFR
    • microalbuminuria screen (urine albumin: creatinine ratio)
  • Chronic kidney disease defined by:
    • GFR <60 mL/minute/1.73 m2 of body surface area
    • albuminuria for 3 or more consecutive months
  • Stage categorizations:
    • Stage 1: kidney damage (albuminuria) without decreased GFR (GFR > 90 mL/min/1.73 m2​ or dialysis)
    • Stage 2: kidney damage with a mild decrease in GFR (GFR 60-89 mL/min/1.73 m2​ or dialysis)
    • Stage 3: moderate decrease in GFR (GFR 30-59 mL/min/1.73 m2​ or dialysis)
    • Stage 4: severe decrease in GFR (GFR 15- 29 mL/min/1.73 m2​ or dialysis)
    • Stage 5: renal failure (GFR < 15 mL/min/1.73 m2 or dialysis)
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12
Q

Laboratory evaluation in acute renal failure

Prerenal ARF

A
  • Result of decreased renal perfusion
  • A sustained benefit by expansion of intravascular volume with colloid is characteristic
  • BUN/Cr ratio usually elevated
  • Fractional excretion of sodium (FENa) low (<1%)
  • “Inactive” urine sediment
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13
Q

Laboratory evaluation in acute renal failure

postrenal ARF

A
  • bilateral obstruction of the renal collecting system
  • BUN:Cr ratio often elevated
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14
Q

Laboratory evaluation in acute renal failure

Intrarenal ARF

A
  • Injury to the nephron (glomeruli, tubules, vessels, or interstitium)
  • ATN is most common cause of intrarenal ARF
  • Most common causes of ATN are
    • ischemia
    • nephrotoxins
    • acute glomerulonephritis
  • Usually normal BUN/Cr ratio
  • FENa > 1%
  • Urine may show “active” sediment:
    • dysmorphic RBCs and RBC casts in glomerulonephritis
    • coarse granular casts in ATN, GN, or interstitial nephritis
    • WBC casts in pyelonephritis
    • eosinophils in acute allergic interstitial nephritis
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15
Q

Acute renal failure (ARF): prerenal vs renal

A
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16
Q

Causes of Prerenal acute renal failure

A
  • Hypovolemia
  • CHF
  • Cirrhosis
  • NSAIDs
  • ACE inhibitors
  • Vasopressors
17
Q

Causes of acute renal failure

A
  • ATN
    • ischemia
    • acute GN
    • contrast media
    • aminoglycosides
    • amphotericin
    • tumor lysis syndrome
    • rhabdomyolysis
  • Acute glomerular injury
    • penicillamine
    • cyclosporine
    • acute GN
    • thrombotic microangiopathy
    • malignant HTN
  • Acute tubulointerstitial nephritis (NSAIDs)
  • Vasculitis
18
Q

Causes of postrenal acute renal failure

A
19
Q

Hepatorenal syndrome

A
  • Progressive renal impairment in patients with endstage liver disease in the absence of another identifiable cause
    • shock
    • bacterial sepsis
    • nephrotoxin exposure
    • spontaneous bacterial peritonitis
  • often follows profound fluid shifts such as occur in the treatment of ascites