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Nephrology > Kidney Clearance and Acute Kidney Injury > Flashcards

Kidney Clearance and Acute Kidney Injury Flashcards

1
Q

What drugs or chemicals increase afferent-arteriolar resistance?

A
  • NSAIDS (inhibiting prostaglandin-mediated vasodilation)
    • Adenosine
    • Thromboxane
    • Norepinephrine
    • Endothelin
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2
Q

What drugs or chemicals increase efferent-arteriolar resistance?

A

• Angiotensin II is pretty alone here

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3
Q

What are the forces that determine the rate of glomerular filtration at a single nephron? SNGFR

A

• SNGFR = glomerular filtration at the level of a single nephron
• Determined by starling forces
○ Glomerular capillary hydrostatic pressure (P-gc)
○ Glomerular capillary oncotic pressure (Pi-gc)
○ Tubular hydrostatic pressure (P-t)
○ Oncotic pressure in the tubule
○ K-f - accounts for surface area and permeability of glomerular capillary membrane

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4
Q

Is the net pressure favoring glomerular filtration the same from beginning to end of glomerular capillary?

A

• No. filtration is more earlier in the capillary beause oncotic pressure of the capillary increases as more filtration occurs

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5
Q

GFR is maintained by what actions of the afferent and efferent arteriole? What processes determine those actions?

A

• Vasodilation of afferent arteriole
○ Prostaglandins E2 and I2, and NO are vasodilatory on the afferent arteriole
• Vasoconstriction of efferent arteriole
○ Angiotensin II is the main constrictor

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6
Q

What can we assume about SNGFR?

A
  • Assume SNGFR is proportional to P-Gc (glomerular capillary pressure)
    • The other determinants are very little
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7
Q

Which starling forces favor filtration and which oppose filtration

A

• P-gc and Pi-t favor glomerular filtration
○ Capillary hydrostatic pressure and tubular oncotic pressure
• Pi-gc and P-t oppose glomerular filtration
○ Capillary oncotic pressure and tubular hydrostatic pressure
• Assume Pi-t is 0 as most large proteins don’t filter into the tubules
• Assume SNGFR is proportional to P-Gc (glomerular capillary pressure)

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8
Q

How do you calculate SNGFR?

A
  • SNGFR = glomerular filtration at the level of a single nephron
    • SNGFR = [(P-gc - P-t) - (Pi-gc - Pi-t)]* K-f
    • Balance of push and pull, push being hydrostatic and pull being oncotic
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9
Q

What is the clearance formula used to estimate GFR?

A
  • Cl-x = U-x*V/P-x
    • For the clearance of creatinine use urinary creatinine and plasma creatinine and the volume of excretion
    • Volume is usually a certain volume in a given collection period, and is expressed in ml/min
    • Plasma creatinine comes from a blood draw, urine creatinine comes from the 24-hour collection
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10
Q

How do you go about calculating creatinine clearance with the following info? Plasma creatinine = 2mg/dL, 24-hr urine volume of 1500mL, urine-creatinine = 100mg/dL

A 
• Cl-cr = U-cr*V/P-cr
	• V = 1500/1440=1.0417 ml/min
	• U-cr = 100
	• P-cr = 2
		○ Cl-cr = 100*1.0417=104.17 
		○ 104.17/2=52.085 
	• Thus creatinine clearance in this patient is 52ml/min, which is an overestimate of GFR
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11
Q

Can you use creatinine clearance when patients are not in steady state?

A

• NO, this method assumes steady state, and when creatinine is creeping up you can’t use it for the function of GFR estimation

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12
Q

What is creatinine and what is it used for?

A

• Creatinine is most commonly used for GFR estimation
• Nonenzymatic breakdown product of creatine that is in high and mostly stable concentrations in human muscle and other tissues
• Creatinine production reflects muscle mass
○ 18-22 mg/kg/day in men and 15-19 mg/kg/day in women
§ Less or more in body builders or frail old ladies
• Creatinine is freely filtered, not reabsorbed but is secreted
○ Thus creatinine is a GFR overestimator by about 10-20%

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13
Q

What is the Cockcroft and Gault formula and what does it give you?

A

• Gives you creatinine clearance, a way to quickly estimate what it should be
○ Creatinine clearance = (A140-agewieght)/72*Serum-cr
○ Clearance is expressed as ml/min
○ A is 1.0 for males, 0.85 for females
○ Age (years)
○ Weight (kg)
○ Serum-cr expressed in mg/dL

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14
Q

What are the clinical plasma-based estimates of GFR?

A

• Obtain plasma sample and measure the concentration of substances normally cleared by kidney to gauge GFR
• Creatinine is most commonly used for this
• Rising plasma creatinine indicates worsening renal function
• Measured daily in hospitalized patients and every visit for outpatients
• Use the Cockcroft and Gault formula
○ Creatinine clearance = (A140-agewieght)/72*Serum-cr
○ Clearance is expressed as ml/min
○ A is 1.0 for males, 0.85 for females
○ Age (years)
○ Weight (kg)
○ Serum-cr expressed in mg/dL

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15
Q

What is the clearance of urea like?

A
  • Urea is a nitrogenous waste endogenously produced, freely filtered and not secreted. IT IS REABSORBED THOUGH
    • Thus, urea clearance is a GFR underestimator
    • BUN is the urea concentration in the blood
    • BUN is affected by renal clearance, rate of protein catabolism, dietary protein intake. So it’s a rough estimate
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16
Q

If a substance is produced by the body at a constant rate and the only method of clearance of that substance was urine, how can you use plasma and urine levels of that substance to calculate GFR?

A
  • GFR = (Urine-substance*Volume)/Plasma-substance
    • GFR (ml/min)
    • Plasma-substance (mg/100mL)
    • Urine-substance (mg/100mL)
    • Volume (ml/min)
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17
Q

What is the most accurate estimation for GFR by using clearance measurements?

A
  • Inulin. A polysaccharide that is freely filtered and not reabsorbed or secreted
    • You have to give IV because inulin is not produced in humans
    • 125-iodothalamate is also used
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18
Q

How do you calculate the amount of a substance eliminated in the kidney?

A

• X-e is the product of urine concentration of X (U-x) and the urine flow rate (V)
○ Cl-x = (U-x)*V/(P-x)
• Only for substances freely filtered and not secreted or reabsorbed…so this is an estimation only for most substances
• Thus the use of clearance to estimate GFR

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19
Q

What can be calculated by clearance at the whole kidney level?

A

• Renal blood flow and GFR
• Clearance of a substance defined as the volume of plasma from which all of substance X is removed
• Can be calculated by amount of subastnce eliminated (X-e) and the mean plasma concentration of X (P-x)
○ Cl-x = (X-e)/(P-x), ml/min

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20
Q

What is normal GFR?

A
  • 115-125ml/minute in men

* Lower 100s or even 90 for women

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21
Q

For any substance, what do you call it when that substance increases in the body or decreases?

A
  • Positive balance = less out than in
    • Negative balance = more out than in
    • External balance = input and output
    • Internal balance = shift ICF vs. ECF
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22
Q

What are the constituents of a balance sheet?

A

• IN(mL), OUT(mL)
○ Example IN = fluid, flood, metabolism, total
○ Example OUT = insensible fluid loss, stool, urine, total

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23
Q

What are some biochemical differences you can use to differentiate Pre-renal AKI and ATN?

A

• Urine Na
○ 20 is ATN
• Ucr/Pcr
○ >20 is pre-renal and 2 in ATN

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24
Q

How do you treat AKI?

A

• Treatment is dependent on the cause of injury
○ Prerenal = optimize renal perfusion
○ Postrenal = relieve obstruction
• Treat before ATN, but if you see ATN, treat flouid and electrolyte disturbances medically at first
• If medical treatment fails use renal replacement therapy (dialysis)

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25
Q

What are the concerning complications of Acute Kidney Injury?

A
  • The injury messes with fluid balance and electrolye regulation
    • Complications are volume overload (pulmonary edema, heart failure), electrolyte abnormalities (hyperkalemia and acidosis), uremia symptoms
    • MORTALITY IS HIGH 60% often due to infections and gastrointestinal bleeding
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26
Q

What urinalysis test results are expected in Pre-renal azotemia?

A
  • SG = high
    • Blood dip = negative
    • Protein dip = negative
    • Microscopic = negative
27
Q

What urinalysis test results are expected in Acute Tubular Necrosis?

A
  • SG = isosmotic
    • Blood dip = negative OR positive
    • Protein dip = negative
    • Microscopic = coarse, granular casts and visible tubular epithelial cells
28
Q

What urinalysis test results are expected in Glomerulonephritis?

A
  • SG = normal to high
    • Blood dip = positive
    • Protein dip = positive
    • Microscopic = RBCs and RBC casts
29
Q

What urinalysis test results are expected in vasculitis?

A
  • SG = normal or high
    • Blood dip = positive
    • Protein dip = positive
    • Microscopic = RBCs and RBC casts
30
Q

How is a microscopic exam of urinalysis done?

A
  • Centrifuge 10-15mL of fresh urine 450g for 5min
    • Supernatant decanted and sediment is resuspended in small volume
    • Microscopic evaluation done by light microscope
31
Q

What urinalysis test results are expected in obstruction?

A
  • SG = isosmotic
    • Blood dip = negative
    • Protein dip = negative
    • Microscopic = negative or normal, waxy, fine granular casts
32
Q

What urinalysis test results are expected in Acute Interstitial Nephritis?

A 
• SG = isosmotic
	• Blood dip = negative OR positive
	• Protein dip = negative OR positive
	• Microscopic = WBC casts and eosinophils
	•
33
Q

What are the urinalysis patterns indicative of Obstruction?

A

• Tonicity usually isotonic or hypotonic, usually heme is negative unless superimposed infection, micro may be benign or show RBC and WBC evidence of superimposed infection

34
Q

What are the urinalysis patterns indicative of Acute Tubular Necrosis?

A

• Typically isotonic, variable heme pigment (positive from hemolysis or rhabdomyolysis), pigmented coarsely ganular casts and renal tubular epithelial cells

35
Q

What are the urinalysis patterns indicative of vascular disease?

A

• Variable tonicity, positive or negative heme pigments

36
Q

What are the urinalysis patterns indicative of Acute Interstitial Nephritis (AIN)?

A

• Isotonic urine, could be positive or negative heme pigment, WBC casts, eosinophils if allergic interstitial nephritis

37
Q

What are the urinalysis patterns indicative of glomerulonephritis?

A

• Variable tonicity, positive heme pigment, sediment exam reveals RBC alone and RBC casts

38
Q

What are the urinalysis patterns indicative of prerenal azotemia?

A

• High specific gravity, no heme pigment, normal sediment (waxy or finely granular casts if seen)

39
Q

What goes into the macroscopic exam part of urinalysis?

A
  • Direct, visual observation of collected urine
    • Fresh urine should be pale to dark yellow in coloer
    • Ill patients may have cloudy or turbid urine
    • RBCs in urine look red or cola colored (brown)
40
Q

What goes into the microscopic exam of urinalysis?

A
  • Used for ID of formed elements like cells, casts and crystals
    • Cells = WBCs, RBCs, bacterial, epithelial
    • Casts = mucoproteins from tubule epithelium, hyaline casts have no cells and are normal findings, but RBC and WBC casts are “snapshots” of bleeding or inflammation going on (glomerulonephritis or AIN respectively)
41
Q

What goes into the dipstick analysis part of urinalysis?

A
  • Long thin strips of inert plastic, with square reaction pads that provide color readouts based on biochemical reactions with urine
    • Glucose, protein, heme, bilirubin, ketones, leukocyte (esterase and nitrite)
42
Q

How does a good clinician use the H and P to ddx AKI?

A
  • Evidence for pre-renal, renal, or post-renal AKI
    • Intravascular volume depletion = weight loss, flat neck veins, postural changes in blood pressure or pulse - all suggest pre-renal AKI
    • Cardiac dysfunction = edema, pulmonary rales, S3 gallop - suggesting pre-renal cuase AKI
    • History of insults = exposure to hypotension, surgery with lots of blood loss, transfusion reactions, radio contrast from CTs
    • Evidence of obstruction = anuria, intermittent anuria or large swings in urine flow rate
    • Evidence of allergic causes = rash, fever, rash + fever associated with drug like ampicillin - suggests allergic interstitial nephritis
43
Q

How does a good clinician use urinalysis and sediment examination to ddx AKI?

A

• MUST be performed on all patients with AKI
• Provides info on tonicity of urine and presence or absence of casts or heme pigments or RBCs
• High tonicity when the kidney retains water due to increased ADH by way of pre-renal statea sn SIADH
• Heme pigments but no microscopic RBC evidence suggests rhabdomyoloysis or hemolysis
• Urinalysis has 3 components
○ Macroscopic/gross exam
○ Dipstick chemical analysis
○ Microscopic exam

44
Q

Once renal blood flow is insufficient what happens to the tubular epithelium?

A
  • Ischemia. They usually die, slough off, allow for backleak of tubular stuff into the interstitium and the sloughed cells cause further obstruction and back pressure. No bueno
    • This ischemia likely also blocks autoregulation of blood flow, resulting in a lower threshold of hypotension to cuase further ischemic events
45
Q

What are two pretty serious complications of ischemic AKI by way of ATN?

A
  • Infections b/c of decreased leukocyte function

* Gastrointestinal tract hemorrhage because of increased acid secretion

46
Q

What does oliguric mean?

A

• Oliguria or hypouresis is the low output of urine. In humans, it is clinically classified as an output more than 80 ml/day but less than 400ml/day.

47
Q

What might cause intrinsic renal disease through affecting the vasculature?

A

• Cholesterol emboli, renal vein thrombosis

48
Q

What are the two different buckets of ATN physiology?

A

• Acute tubular necrosis
○ Vascular and tubular
• Vascular = decrease in RBF and decrease in Kf (glomerular permeability)
• Tubular = obstruction by cellular debris, backleak of glomerular filtrate

49
Q

What might cause intrinsic renal disease through affecting the tubules?

A

• Ischemic or nephrotoxic acute tubular necrosis

50
Q

What might cause intrinsic renal disease through affecting the interstitium?

A

• Acute interstitial nephritis, allergic interstitial nephritis, infection, myeloma kidney

51
Q

What might cause intrinsic renal disease through affecting the glomerulus?

A

• Acute glomerulonephritis, hemolytic uremic syndrome

52
Q

What effect on the urine chemistry does obstruction usually have?

A

• Tubular function is messed up in sodium and water handeling
• Impaired tubular sodium reabsorption
• HIGH urinary sodium concentrations >40mEq/L
• Impaired water reabsorption so low urine creatinine concentrations
○ Ucr/Pcr

53
Q

What are the four overall categories of intrinsic renal disease?

A
  • Vessels, glomeruli, interstitium, tubules

* Most common is ATN or acute tubular necrosis by way of ischemia or nephrotoxins

54
Q

How do you diagnose obstruction as the cause of post-renal azotemia?

A
  • Renal ultrasound
    • Looks like expansion of the collecting system (hydronephrosis) in 98% of cases
    • Foley catheter relief suggests urethral obstruction
    • Post-voidal volume over 150mL is concerning
55
Q

What are some causes of extraureteral post-renal azotemia?

A

• Carcinoma of cervix, endometriosis, retroperitoneal fibrosis, ureteral ligation

56
Q

What are some causes of intraureteral post-renal azotemia?

A

• Stones, blood clots, sloughed papilla

57
Q

In pre-renal azotemia what are the expected sodium and creatinine levels?

A

• Urine sodium concencration low (20)
• Another way of looking at this is the FENa or the fractional excretion of sodium
○ (Urine-sodium/Plasma-sodium)/(Urine-creatinine/Plasma creatinine) * 100%
○ FENa is expressed as a percentage

58
Q

If you have a presentation of anuria or intermittent urine flow, what should you be thinking?

A

• Obstructive-caused AKI, or post-renal azotemia
• Could also be from neurologic causes or deficits
• The causes here can be categorized in ureter, bladder, urethral
○ Ureter = intraureteral or extraureteral
○ Bladder = outlet obstruction
○ Urethral = obstruction

59
Q

What is the equation relating Urine and Plasma sodium and

creatinine?

A

• FENa or the fractional excretion of sodium
• (Urine-sodium/Plasma-sodium)/(Urine-creatinine/Plasma creatinine) * 100%
• FENa is expressed as a percentage
○ If FENa is

60
Q

What is the flow chart for ddx of Pre-Renal azotemia?

A
  • Hypovolemic vs. Hypervolemic
    • If hypovolemic: renal losses, third space losses, GI losses, Hemorrhage
    • If hypervolemic: reduced cardiac output vs. systemic arterial vasodilation
    • If reduced cardiac output: CHF, MI, Valvular disease, Pericardial Tamponade
    • If systemic arterial vasodilation: Cirrhosis, Sepsis, Medication, Autonomic Neuropathy
61
Q

What is “normal blood flow” to the kidneys?

A

• Up to 25% of cardiac output. The result is more than 1 liter of blood blow per minute (5L per minute in normal adult)
• You need this blood flow to maintain GFR AND maintain oxygen supply required for ion transport in the kidney epithelium itself
○ Thus prolonged pre-renal azotemia results eventually in Acute Tubular Necrosis
• Thus, prerenal azotemia is the most common cause of an abrupt fall in GFR in a hospitalized patient

62
Q

Hypovolemia is a common cause of pre-renal azotemia, but hypervolemic states can do the same thing…?

A
  • Yes, CHF and cirrhosis are the best two examples of hypervolemic states (more than the heart or liver can handle) but there is backflow enough to keep the kidneys from being adequately perfused
    • Low effective arterial blood volume EABV
63
Q

Describe the classification scheme for Acute Renal Failure

A
  • First step is Pre-renal vs. Renal vs. Post renal causes
    • If Renal: vascular? Glomerulonephritis? Interstitial nephritis? Tubular necrosis?
    • If Tubular necrosis: ischemia? Toxins? Pigments?
    • THE MOST COMMON CUASE OF AKI IS PRE-RENAL IN ABOUT 70% OF CASES

Nephrology (14 decks)

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