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Applied Pathophysiology > Acute Kidney Disease > Flashcards

Acute Kidney Disease Flashcards

1
Q

What is Glomerular Hydrostatic Pressure?

A

the driving force behind glomerular filtration

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2
Q

How can you control how much gets through the glomerular system?

A

by squeezing down on afferent/efferent side

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3
Q

What is Acute Kidney Injury (AKI)?

A

ABRUPT (generally within 48 hrs) reduction in kidney function

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4
Q

What are the 4 results of Acute Kidney Injury (AKI)?

A
  1. Loss of excretory function of the kidneys (H2O and waste)
  2. Accumulation of metabolic waste products (e.g. K+, PO4), and a rapid rise in creatinine and urea
  3. A decline in urine output MAY occur
  4. Reduced ability to maintain fluid, electrolyte and acid- base balance
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5
Q

What are the Cellular & Metabolic Waste Products?

A

Accumulation of metabolic waste products, e.g. creatinine & urea

Skeletal Muscle –> Blood Creatine umol/L (60-100 umol/L) –> Kidney (Creatinine excreted in urine)

Protein Metabolism Blood Kidney
Protein –> AA –> NH3 –> (Liver) –> Urea mmol/L (2-7 mmol/L) –> Urea excreted in urine

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6
Q

Waste –> blood –> If we blood outflow (AKI)…what happens to the concentration of the waste in the bucket?

A

gets higher

(if kidney function stops working, urea rises)

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7
Q

How can we assess the degree of renal damage in AKI?

A

o Historically the retention of creatinine in the blood has been the GOLD STANDARD for assessing the degree of glomerular filtration impairment in patients with kidney damage

o Creatinine is a by-product of muscle metabolism and is steadily released into the blood

o Creatinine is freely filtered by the glomerulus and thus is an indicator of renal health. This relationship has been used mathematically to express the underlying degree of glomerular filtration (GFR). We assume in medicine that creatinine clearance ~= GFR !

o However, creatinine undergoes some degree of tubular secretion, as well as GFR; and thus this marker may overestimate GFR a little (but often ignored in clinical practice)

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8
Q

How do we assess the degree of renal damage in patients?

A

Method for estimating GFR as a CrCl = creatinine clearance

CrCL (ml/min/72kg) = (140-Age) x 80 / creatinine (umol/L) x 85% if female

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9
Q

What does The Cockcroft & Gault Equation for assessing the degree of renal damage in patients tell us?

A

higher age, poorer the function

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10
Q

Ex q for assessing the degree of renal damage in patients?

65 yo

creatinine = 124 umol/L

A

CrCL (ml/min/72kg) = (140-65 yo) x 80 / 124 umol/L = 48 mL/min/72 kg

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11
Q

Describe the eGFR (MDRD-4 *)

Modified Diet in Renal Disease formula

A

Developed for prognostication of renal disease

eGFR (mL/min/1.73 m2) = 175* × (Cr)-1.154 × (Age)-0.203 × (0.742 if female) × (1.212 if African American)

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12
Q

Ex q for eGFR (MDRD-4 *)

Modified Diet in Renal Disease formula

(Developed for prognostication of renal disease)

Cr = 124

Age = 65

A

eGFR = 175 * (124 umol/L-1.154 ) * (65yo -0.203) = 51 mL/min/1.73m2

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13
Q

What is the eGFR (MDRD-4 *)

Modified Diet in Renal Disease formula

used for?

A

Some will use this formula to assess the degree of renal damage in AKI or even proper dosing of drugs, however it has only been validated for staging the severity of chronic kidney disease (CKD)!

NEVER DESIGNED FOR DRUG DOSE

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14
Q

What are the limitations of using a creatinine in any renal function assessment for GFR?

A
  • Only for adult patients (>18 years of age)
  • Assumes a steady-state serum creatinine value! During AKI the actual creatinine may be rising dramatically ever day! Any calculated CrCl or eGFR value is thus a MOVING TARGET!
  • Patients with muscle wasting medical conditions (e.g. muscular dystrophy (MD), multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS) may have an underproduction of creatinine; and thus the formula will give you erroneous results
  • A few drugs may compete with creatinine for tubular secretion and thus may ‘falsely’ elevate serum creatinine in patients (e.g. trimethoprim/ sulfamethoxazole)
  • IN PEDIATRICS, WE USE THE SCHWARTZ EQUATION: CrCl(ml/min/1.73m2)= [Length(cm) * k] /creatinine, where k = 0.7 for adolescent males 13 - 18 years old for example (but not used in neonatsology, i.e. < 1 mo of age)
  • NOT TESTED ON THIS POINT
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15
Q

GFR averages ________ in young healthy adults 18 - 22 years of age

A

120 -140 mL/min/72kg

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16
Q

GFR gradually declines with age to _______ at age 65 years of age

A

~ 50 - 60 mL/min/72kg

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17
Q

We expect a GFR in an otherwise healthy, normal 80 y.o. to be
________

A

~ 30 - 40 mL/min/72kg

(may explain that: more sensitive to drugs, the older you are)

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18
Q

Pediatrics – GFR is ____ _____ to accurately assess!

A

very difficult

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19
Q

Explain the Classification of kidney damage

A

Normal Kidneys

Acute Kidney Injury (AKI) - < 7 days

Acute Kidney Disease (AKD) - < 3 months
GFR <60mL/min/1.73m2

Chronic Kidney Disease (CKD) - >/ 3 months
GFR <60mL/min/1.73m2
and has 5 stages based on
GFR & Albuminuria

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20
Q

What is the duration of creatinine elevation on defining kidney damage!

Evidence of Acute Kidney Injury

A

rapid rise in creatinine & then goes away after 7 days from renal injury

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21
Q

What is the duration of creatinine elevation on defining kidney damage!

Evidence of Acute Kidney Disease

A

rapid rise in creatinine & then stays for ~month and then goes away after 3 months from renal injury

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22
Q

What is the duration of creatinine elevation on defining kidney damage!

Evidence of Chronic Kidney Disease

A

rapid rise in creatinine & then stays constant from renal injury

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23
Q

What is the profile in Acute Kidney Injury?
As reflected by the biomarkers creatinine & urea

A

Plasma Creatinine rises & Urea rises as well (but not as much)

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24
Q

Definition of Acute Kidney Injury (AKI):

A

o a rise in creatinine and decline in urine output that has developed within hours to days

o an increase in creatinine by > 27 mmol/L within 48 hours, or e.g. baseline Cr = 100 mmol/L jumps to 130 mmol/L

o an increase >/ 1.5 times in creatinine from their presumed baseline (in last 7 days), or e.g. baseline Cr = 30 mmol/L jumps to 45 mmol/L (dCr=15)

o a decrease in urine output (U.O.) by < 0.5 mL/kg/h over 6 hours
e.g. 80 kg patient with U.O. falls < 40 mL/h over 6
hours or described as less than 240 mL in 6 hours

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25
Q

How common is AKI?

A
  • Community – about 1% of patients presenting to hospital have an AKI
  • Hospitalized - occurs in only about 2 – 5 %
  • Adult ICU –arises in more than 50% of cases
  • Pediatric ICU – arises in 30% of cases (12% develop severe AKI)
  • AKI is associated with an increased risk of morbidity and mortality
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26
Q

What are the Risk Factors for AKI?

A
  • Male
  • African American
  • Pre-existing CKD
  • Age>65yrs
  • Volume depletion (diarrhea, vomiting or dehydration)
  • Sepsis
  • Critical Illness
  • Nephrotoxic drugs
  • Hypotension
  • Diabetes mellitus
  • Acute heart failure
  • Chronic Diseases (heart, liver, lung) * Albuminuria
  • Major surgery
  • Cardiac surgery
  • Trauma
  • Cancer
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27
Q

What is the prognosis of an episode of AKI?

A
  • The number of irreversibly lost nephrons in AKI determines the long- term prognosis of kidney function (Kellum-JA, 2021)
  • AKI has a poor, but variable prognosis depending on the clinical setting, underlying cause and patient comorbidities
  • High mortality of 35 - 90% depending on underlying illness (not all homogenous)
  • 90% recover enough renal function to live normal lives, but 50% of them may have ongoing defects in kidney function
  • ~ 25% will go on to develop CKD
  • ~12.5% will go on to require life-long dialysis

(don’t memorize %’s)

28
Q

What is the clinical presentations of kidney damage?

A

o May be ACUTE (hours to days- AKI), SUBACUTE (weeks - AKD), or chronic (over 3 months-CKD). Our focus will be on ACUTE KIDNEY INJURY (AKI)

o For any rise in creatinine & urea and the associated urine outputs, they can take on ONE of THREE forms:
o Anuric, i.e. < 100 mL/day
o Oliguric, i.e. < 500 mL/day (< 0.5 mL/kg/h of urine output)
o Non-oliguric, i.e. > 500 mL/day

o Manifestations of kidney disease -
1. Evidence of reduce renal function, i.e. elevated creatinine & urea,
edema, hyperkalemia (K+), & hyperphosphatemia (PO43-)
2. Evidence of kidney damage (e.g., gross hematuria, proteinuria)
3. Abnormal radiological findings on kidney imaging
4. Requirement for some form of dialysis

29
Q

For any rise in creatinine & urea and the associated urine outputs, they can take on ONE of THREE forms:

A

o Anuric, i.e. < 100 mL/day

o Oliguric, i.e. < 500 mL/day (< 0.5 mL/kg/h of urine output)

o Non-oliguric, i.e. > 500 mL/day

30
Q

Manifestations of kidney disease -

A
  1. Evidence of reduce renal function, i.e. elevated creatinine & urea, edema, hyperkalemia (K+), & hyperphosphatemia (PO43-)
  2. Evidence of kidney damage (e.g., gross hematuria, proteinuria)
  3. Abnormal radiological findings on kidney imaging
  4. Requirement for some form of dialysis
31
Q

____ will turn off urine output & then comes back as the drug is metabolized

A

NSAIDS

32
Q

What are the 3 Mechanistic Etiologies of AKI?

A
  1. Intrinsic Renal AKI
  2. Pre-Renal AKI
  3. Post-Renal AKI
33
Q

Intrinsic Renal AKI:

A

Intrinsic causes:
- Glomerular nephritis tubular interstitial (ATN) Embolic

Structural damage within the kidney!

34
Q

Pre-Renal AKI:

A

Prerenal causes:
- Volume depletion
- Low cardiac output
- Renal vascular dis.

Decreased renal blood flow!

35
Q

Post-Renal AKI:

A

Postrenal causes:
- flow obstruction

Obstruction to outflow!

36
Q

Rises in creatinine have many etiologies…

A

o The terms Pre-Renal, Intrinsic-Renal, and Post-Renal are used to group COMMON PATHOPHYSIOLOGIC FEATURES. All forms of AKI can be classified into one of these 3.

o By identifying the type of AKI from its presentation; one can more quickly establish the cause. This allows for more rapid treatment intervention and may minimize any further kidney damage

o Caveat –NOT all elevations in creatinine are from AKI. Watch for FALSE ELEVATIONS in creatinine when specific drugs are added that compete for tubular secretion!

37
Q

Which common pathophysiologic features correspond to unique clinical causes of Pre-Renal (of AKI)?

A
  • Dehydration/hypovolemia
  • Hemorrhage
  • Drugs
  • Decreased effective circulation volume: Heart failure, Liver failure
38
Q

Which common pathophysiologic features correspond to unique clinical causes of Intrinsic Renal (AKI)?

A
  • Nephrotic syndrome
  • Glomerular disease
  • Interstitial
  • Tubular
  • Vascular
39
Q

Which common pathophysiologic features correspond to unique clinical causes of Post-Renal (AKI)?

A
  • Prostatic hypertrophy
  • Bladder outlet obstruction
  • Kidney Stones
  • Strictures
  • Tumor
  • Thrombosis
  • Fibrosis
40
Q

How can one differentiate the various forms of AKI?

A
  • Examination of urinary sediment
  • Examination of urinary sodium, osmolality and specific gravity
  • Another useful test is:
    Fractional excretion of sodium (FeNa)
  • Examining changes in creatinine & urea to identify the possible etiology of the AKI
41
Q

Examination of urinary sediment:

A
  • HYALINE CASTS are usually present in dehydration, exercise, or with diuretic therapy. But non-specific for disease.
  • EPITHELIAL CASTS may occur with tubular necrosis
  • RBC’s, AND RBC CASTS are a sign of bleeding into the kidney tubule, or possibly from glomerulonephritis (bleeding occurring high up in nephron)
  • WBC’s, AND LEUKOCYTE CASTS suggest pyelonephritis, or glomerulonephritis
  • NITRITES are suggestive of the presence of bacteriuria (bacterial infection)
  • LEUKOCYTE ESTERASE suggests urinary bacterial infection
42
Q

Examination of urinary sodium, osmolality and specific gravity for Pre-renal AKI:

A

Pre-renal AKI

 Urinary sodium < 10 mmol/L (tells you it’s trying to hang onto Na+)
 Urinary osmolality > 500 mOsm/kg
 Urine specific gravity > 1.020

A CONCENTRATED URINE
- only present if not getting enough BF to the urine

43
Q

Examination of urinary sodium, osmolality and specific gravity for Intrinsic AKI:

A

 Urinary sodium > 40 mmol/L (can’t hang onto Na+)
 Urinary osmolality < 350 mOsm/kg
 Urine specific gravity < 1.010

AN INABILITY TO CONCENTRATE URINE

44
Q

Examination of urinary sodium, osmolality and specific gravity for Post-Renal AKI:

A

 May be completely normal in concentrating ability

45
Q

Another useful test is:

Fractional excretion of sodium (FeNa):

A

A standard part of AKI work-up for pre-renal causes. FeNa measures the ratio of SODIUM EXCRETED IN THE URINE compared to the SODIUM AVAILABLE FOR FILTRATION by the kidney (GFR)

FeNa = s-creatinine x u-Na+ / u-creatinine x s-Na+

FeNa < 1%

FeNa > 3%

46
Q

What does FeNa < 1% mean?

A

in oliguric/anuric patients = pre-renal AKI, as an increased reabsorption of Na is the appropriate response of functioning nephrons to the state of decreased renal perfusion

(low FeNa –> trying to hang onto Na+)

47
Q

What does FeNa > 3% mean?

A

may be consistent with an Intrinsic form of AKI*, due to inappropriate Na excretion in the setting of tubular damage (i.e. losing Na). Inability to concentrate their urine.

(increase FeNa –> lost Na+)

48
Q

How can we identify pre-renal injury?

A

Plasma Creatinine rising & Urea rising as well (from a hemorrhage for ex)

49
Q

Pre-renal injury -

A

UREA increases disproportionately in the serum compared with CREATININE due to enhanced proximal tubular REABSORPTION of urea that FOLLOWS transport of Na+ & H2O

(Urea follows Na+ & H20)

(decreases BF to kidneys)

50
Q

Profiles in Acute Kidney Injury

Suggestive of pre-renal injury

A

Urea/Creatinine Ratio:

Urea * 1000 / Creatinine = > 100 / 1 (normal ratio)

Note: ONLY interpret in the absence of gastrointestinal bleeding, since urea gets reabsorbed from blood in the Gut

(check if they’re bleeding - if not, can say pre-natal)

51
Q

Profiles in Acute Kidney Injury

We can identify intrinsic-renal injury

A

Plasma Creatinine rising

Urea Rising as well

Urea/Creatinine Ratio:

Urea * 1000 / Creatinine

A flat Urea/Creatinine ratio is suggestive of an Intrinsic profile of AKI (or possibly Post-renal)
- nothing wrong with kidney itself (urea & creatinine is blocked)

52
Q

Specific background on the various forms of AKI

Pre-renal AKI:

A

o Caused by decreased blood perfusion to the kidney, reducing renal blood flow, and thus GFR falls off

o Decreased perfusion can arise from blood volume depleted states (such as acute hemorrhage, diarrhea, vomiting, or dehydration)

o Can also occur in hypervolemic state, but with low effective circulating blood volume to the kidney, e.g. severe heart failure, or liver failure precipitating kidney failure! i.e. Cardiorenal syndrome or Hepatorenal syndrome

o Caused by some drugs of renal vascular autoregulation

o Essentially a normal urinalysis, no cells, no proteinuria, u-Na+ <10, u- specific gravity > 1.020, FeNa+ <1%, Urea/Creatinine ratio > 100/1

o Decreasing urine output is always the case, either:
- Oliguria < 500 mL/day or < 0.5 mL/kg/h, or
- Anuria < 100 mL/day

(will never see someone with a normal urine output with pre-natal)

53
Q

Specific background on the various forms of AKI

Post-renal disease AKI, or obstructive uropathy:

A

o Mechanical obstruction may occur anywhere along the urinary collecting system, including the renal pelvis, ureters, bladder, or urethra – need to perform a renal ultrasound to detect hydronephrosis

o Stone disease, stricture, tumors, thrombosis, fibrosis, prostatic hypertrophy

o Obstruction may be unilateral, or bilateral*

o Only bilateral (obstructive) disease results in oliguria and severely elevated urea & creatinines

o Abrupt parallel rise in creatinine & urea (urea/creatinine ratio is flat), and an abrupt decline in urine volume

o Essentially a normal urinalysis with no/few RBC’s or WBC’s cells, no casts, and no/minimal proteinuria; but may have crystals in the urine suggestive of the mechanism of the obstruction (urate, calcium phosphate, etc)
- caused by crystal disease

54
Q

Clinical Etiologies of AKI

A

slide 41 (draw)

55
Q

Urinary profiles of intrinsic renal injury

A

slide 42 (draw chart)

56
Q

_____ ____ is the exception with Intrinsic disease to have low u-sodium!

A

Nephrotic syndrome

57
Q

Intrinsic renal disease

Nephrotic Syndrome & AKI

A

 The triggering of an excessive amount of protein released into the urine; from increased glomerular permeability

 As a result, severe systemic hypoalbuminemia develops

 Loss of protein occurs because of changes to the CAPILLARY ENDOTHELIAL CELLS, the GLOMERULAR BASEMENT MEMBRANE (GBM), or the PODOCYTES (don’t memorize)

58
Q

Diseases that progress to nephrotic syndrome are grouped into three major categories:

A
  • ANTIBODY-MEDIATED DISEASES (e.g., lupus, membranoproliferative glomerulonephritis, and membranous nephropathy);
  • METABOLIC DISORDERS (e.g., diabetes, amyloidosis, and Fabry disease) and
  • PODOCYTOPATHIES (e.g., minimal change disease, and focal segmental glomerulosclerosis)
59
Q

Intrinsic renal disease

Tubular damage – also referred to as acute tubular necrosis (ATN)

A

Approximately 85% of all cases of intrinsic AKI are caused by ATN
- 50% are a result of renal ischemia
- 35% are the result of exposure to direct tubular toxins

Tubular ‘toxin’ damage can be the result of:
- Endogenous causes (e.g. hemolysis, rhabdomyolysis, uric acid)
- Exogenous causes (e.g. contrast dye, aminoglycosides)

Renal tubular epithelial cell injury is the hallmark of an initiation phase that leads to a reduction in GFR

Site of Tubular epithelial cell injury - loop of henle?

60
Q

Intrinsic renal disease

Glomerulonephritis (GMN):

A

 Glomerular disease can result from many inherited or acquired disorders and can manifest in a variety of ways, ranging in severity from asymptomatic urinary abnormalities to AKI and end-stage kidney disease (ESRD)

 May present with concurrent protein-losing disease!
 Glomerular disease should be suspected when hematuria and/or proteinuria are seen on urinalysis

 With GMN, inflammation within the glomerulus leads not only to the passage of inflammatory cells, such as leukocytes and RBCs, but also of protein into the renal tubule

61
Q

Intrinsic renal disease

Normal kidney vs. Glomerulonephritis

A

Glomerulonephritis - intense inflammation

62
Q

Clinical Case 1 – type of AKI?

46 yo, 75kg female presents to hospital after 2 days of severe nausea and vomiting. No fever, or elevated WBC. BP = 90 / 60 mmHg,
HR = 120 bpm

AKI is suspected: Creatinine has increased from 80 umol/L to 160 umol/L after 48 hours on this admission; and now Urea = 22 mmol/L

Urea/Creat ratio = 22*1000/160 = 138 (norm 100/1)
Urine output is less than 50 mL for the last 6 hours (=8.3 mL/kg or 0.11 mL/kg/h)

Urinalysis unremarkable (no protein, no RBC’s, no casts) FeNa < 1%, u-Na= 8 mmol/L, u-specific gravity = 1.030

A

= Pre-Natal

63
Q

Clinical Case 2 – type of AKI?

An 18 yo, 75kg male patient presented with swelling in the face, legs and scrotal area; which developed 8 days after a case of tonsillitis

AKI is suspected: Creatinine has increased from 60 umol/L to 180 umol/L over 48 hours; and now Urea = 17 mmol/L

Urea/Creat ratio = 17*1000/180 = 94 (norm 100/1)
Urine output is less than 50 mL for the last 6 hours (=8.3 mL/kg or 0.11 mL/kg/h)

Urinalysis revealed ++ hematuria (RBC’s, RBC casts) and ++ proteinuria (2 g/day)

FeNa 4%, u-sodium = 50 mmol/L, u-specific gravity = 1.010

A

= Intrinsic AKI from acute post-streptococcal glomerulonephritis
- dilate urine, losing Na+ ?

64
Q

Clinical Case 3 – type of AKI?

65 yo, 80kg male presents to hospital swelling of face, feet and hands.

No fever, no elevated WBC. BP = 110 mmHg / 70 mmHg, HR = 85 bpm

AKI is suspected: Creatinine has increased from 80 umol/L to 150 umol/L after 48 hour on this admission; and now Urea = 15.2 mmol/L

Urea/Creat ratio = 15.2*1000/150 = 101 (norm 100/1)
Urine output is less than 100 mL for the last 6 hours (=17 mL/h or 0.2 mL/kg/h)

Urinalysis ++ 3.2 g/day protein, no RBC’s, no WBC’s
FeNa = 0.5%, u-sodium = 10 mmol/L, and u-specific gravity =1.035

A

= Intrinsic AKI = nephrotic syndrome

65
Q

Clinical Case 4 – type of AKI?

80yo, 65kg male presents a 2 day history in hospital of difficulty voiding, colicky abdominal pain, and a feeling of abdominal fullness

Past medical history of benign prostatic hypertrophy. No fever, no elevated WBC. BP = 115 mmHg / 80 mmHg, HR = 110 bpm

AKI is suspected: Creatinine has increased from 110 umol/L to 200 umol/L in the last 48 hours. Urea = 21 mmol/L

Urea/Creat ratio = 21*1000/200 = 105 (norm 100/1)
Urine output has been zero for the last 6 hours (minimal earlier)

Urinalysis unremarkable except for a few RBC’s, no WBC’s, no casts
Earlier his FeNa = 2%, u-sodium = 20 mmol/L, u-specific gravity = 1.015

A

= Pre-Renal AKI –> Obstructive renal

Applied Pathophysiology (34 decks)

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