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Renal,Urinary And Male Reproductive Systems > Renal Function Tests & AKI > Flashcards

Renal Function Tests & AKI Flashcards

1
Q

What are the functions of kidney?

A
  1. Filtration
  2. Excretion
  3. Reabsorption
  4. Secretion
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2
Q

Renal function tests categories:

A
  1. Glomerular filtration rate assessment
  2. Blood tests
  3. Urine tests
  4. Tubular function tests
  5. Imaging
  6. Renal Biopsy
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3
Q

What is GFR? How is it done?

A

It is the measure of the rate at which the kidneys filter blood per minute.

There are two methods:
Direct measurement : Using inulin clearence
Estimated GFR:
a) Creatinine based estimations b) Cystatin C based estimations

Also sometimes Creatinine clearance level is used

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4
Q

What is the gold standard for measuring GFR and why?

A

Inulin clearance

Because Inulin is not affected by other physiological activities , and neither secreted nor reabsorbed by the kidneys

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5
Q

How is Estimated GFR based on creatinine and cystatin C done?

A

Serum Creatinine or Cystatin C is taken and the value is inserted in formulas that include variables such as age, sex, ethnicity

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6
Q

What is the normal value of GFR?

A

> 90ml/min/1.73m2

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7
Q

How is creatinine clearance measured ? Normal values?

A

Serum creatinine and Urine creatinine ( urine collected over 24 hrs- downfall) are measured and put in a formula

Men: 95-135ml/min
Women: 85-125ml/min

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8
Q

Normal values for serum creatinine?

A

Men: 0.6-1.3mg/dl
Women: 0.5-1.2 mg/dl

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9
Q

Blood tests in evaluation of renal function involve?

A
  1. BUN test
  2. Serum electrolytes test ( Na+,K+,Cl-, Hco3-, Ca2+)
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10
Q

Normal values for BUN?

A

7- 20 mg/dl

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11
Q

Urinary tests of renal function involve?

A

Urinalysis
Physical properties : color, odor, clarity
Chemical properties: Dip stick- pH, proteins, sugar, bilirubin
Microscopic : Casts, crystals, wbc, rbc

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12
Q

Tubular function tests include?

A
  1. Fractional excretion of sodium ( FeNa)
  2. Acid-base balance tests
  3. Water deprivation test
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13
Q

How is Fractional excretion of sodium done and significance?

A

Both Serum and urine sodium and creatinine levels are measured and inserted in a formula

It helps to distinguish between AKI by pre-renal FeNa < 1% ( kidney is preserving sodium due to decreased blood volume)
or intrinsic renal causes FeNa >2% ( kidney can not preserve sodium due to intrinsic injury)

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14
Q

Significance of water deprivation test in renal function assessment

A

It helps in distinguishing between central and nephrotic diabetes insipidus

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15
Q

What are imaging tests used in Renal function assessment?

A
  1. Ultrasound
  2. CT and MRI
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16
Q

Describe arterial renal blood flow

A

Abdominal aorta- Renal artery- segmental arteries- interlobar arteries- arcuate arteries- cortical radiate arteries ( interlobular)- afferent arterioles

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17
Q

What are the problems caused by AKI?

A
  1. Accumulation of wastes in the body: Urea, Creatinine
  2. Increased fluid retention: edema, SOB
  3. Decreased urine output
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18
Q

Name the categories of causes of AKI

A
  1. Pre-renal
  2. Intra renal
  3. Post- renal
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19
Q

Key causes of pre-renal AKI

A
  1. Hypovolemia
    a) Decreased effective arterial blood volume
    b) Decreased actual blood volume
  2. Vascular abnormalities
    a) Blockage of renal vessels by emboli
    b) Renal artery stenosis
  3. Hepatorenal syndrome
  4. Medication induced
20
Q

Which conditions can bring about decrease in EABV as pre- renal AKI cause?

A
  1. Cardiorenal syndrome: In CHF the heart fails to pump blood to the body, this decreases MAP therefore decreasing EABV which in turn decreases perfusion to the kidneys hence AKI
  2. Hypoalbuminemia
    a) Liver failure : Here the liver fails to produce Albumin therefore water can not be retained in blood vessels causing third spacing of fluid hence decreased EABV

b) Nephrotic syndrome: Injury to the kidneys therefore excreting Albumin in the urine

  1. Pancreatitis: Severe inflammation of the pancreas lead to release of cytokines which cause vasodilation and vessels to become leaky, there for causing third spacing hence decreased EABV
  2. Sepsis: Systemic inflammation lead to vasodilation as well as leaky blood vessels this causes hypotension hence decreased perfusion to the kidneys
21
Q

Which conditions bring about decrease in Actual blood volume as pre - renal AKI cause?

A
  1. Excessive Vomiting
  2. Severe diarrhea
  3. Severe dehydration; decreased water intake
  4. Burns
  5. Blood loss: Trauma, GI bleeding, surgery
22
Q

What can bring about Renal blockage ?

A

Renal emboli from conditions such Atrial fibrillation which cause blood stasis therefore cause clotting of blood

23
Q

What can bring about Renal stenosis?

A
  1. Renal Artherosclerosis
  2. Fibromuscular dysplasia
24
Q

Explain Hepatorenal syndrome of pre-renal AKI

A
  1. Here there is severe liver failure leading to portal hypertension.
    In portal hypertension the liver produces vasodilators such as cytokines and nitric oxide in order to increase blood flow , these compounds cause systemic vasodilatory effects, which in turn causes a decrease in kidney perfusion.

Decreased perfusion causes decreased GFR, the kidney responds by activating the RAAAS, the Angiotensin II induces vasoconstriction which further pulls blood away from non- vital organs which include the kidneys, causing ischemia and eventually necrosis of tubular cells.

  1. In liver failure, the fails to produce albumin, thus fluid can not be retained in the blood vessels, this leads to third-spacing of fluid in the body leading to a decrease in effective arterial blood volume and hence decreased GFR. The kidneys respond by activating the RAAAS, which further exacerbates the problem.
25
Q

Explain medication induced Pre-renal AKI

A
  1. NSAIDs : Ibuprofen, asprin- They work by inhibiting cycloxygenase enzymes ( COX 1&2) which are essential for prostaglandin production, which plays a key role in inflammation, fever and pain.
    Prostaglandin helps in dilation of afferent arterioles therefore increasing perfusion to the glomeruli. Decreasing prostaglandins lead to afferent arterioles constriction therefore decreased perfusion and decreased GFR, thus increased accumulation of wastes in the body which is a hallmark of AKI
  2. Diuretics: such as furosemide if not well monitored can lead to dehydration hence decreased kidney perfusion
  3. ACE inhibitors / ARBs: This drug alters the effect of Angiotensin on efferent arterioles leading to efferent arteriole dilation hence decreased GFR .
26
Q

What are the categories of intra renal causes of AKI

A
  1. Acute tubular necrosis
  2. Acute interstitial nephritis
  3. Glomerular nephritis
  4. Thrombotic microangiopathies
27
Q

What causes acute tubular necrosis?

A
  1. Decreased blood flow: This causes decreased perfusion to nephrons hence leading to ischemia, if it persists it leads to necrosis of tubular cells disrupting their reabsorption and secretory function.
  2. Drugs: nephrotoxic drugs cause direct injury to the tubular cells, these include Aminoglycosides, vancomycin, contrast dyes
  3. Hemolysis and Rhabdomyolysis : These lead to direct injury to tubules as well as obstruction.
    Hemolysis releases hemoglobin which is nephrotoxic esp if not bound to haptoglibin and iron increases free radical damage to the tubule cells.
    Myoglobin from rhabdomyolysis can cause tubular obstruction and nephrotoxicity
  4. Chemotherapy and tumor lysis syndrome: uric acid produces here can cause direct nephrotoxicity and tubular obstruction as it crystallizes in the tubular cells
  5. Multiple myeloma: Production light chain proteins can deposition in renal tubules and cause direct injury
28
Q

What cause Acute Interstitial nephritis?

A
  1. Drugs: Beta lactams, Protein pump inhibitors
  2. Infections: Streptococcus, CMV, HIV
  3. Infiltrative diseases: Sarcoidosis , amyloidosis
  4. Autoimmune Disease: SLE
29
Q

What are causes of Post renal AKI / Obstructive nephropathy?

A
  1. Upper Urinary tract: Ureters; Renal calculus, tumor
  2. Lower Urinary tract:

Bladder and Urethra : In men Benign Prostatic Hyperplasia, Neurogenic bladder, medications- anticholinergics, bladder stones

30
Q

Pathophysiology of pre-renal AKI

A

Decreased perfusion cause decreased GFR, this results in less blood being filtered therefore Increase in BUN and Creatinine.
However, because the renal tubules are functional, the Urea can still be reabsorbed, as well as Sodium and water. Also, the Creatinine can still be secreted and excreted. Decrease in GFR triggers the activation of RAAAS. This caused sodium and water retention. All this results in:

  1. Much more BUN in the blood than Creatinine hence ; BUN/Cr ratio >/= 20:1
  2. FeNa<1%
  3. Urine osmolality > 500 ( concentrated urine)
  4. Decreased urea in the urine
31
Q

Pathophysiology of Intra renal AKI

A

Damage to tubular cells leads to formation of casts within the tubules due to necrosis of tubular cells, this causes increase in hydrostatic pressure in the tubule therefore decreasing the GFR.
Decreased GFR leads to increase in BUN and creatinine in the blood.
But since the tubules are damaged, they cannot reabsorb urea nor secrete creatinine.
Therefore the amount of creatinine in the blood significantly increases as compared to that of BUN.
Also, sodium and water can not be reabsorbed. The tubules can not respond to the RAAAS either. All this results to:

  1. BUN/Cr ratio < 15:1
  2. FeNa> 2%
  3. Urine osmolality decreases < 350
  4. Increased Sodium and urea in the urine
32
Q

Pathophysiology of post renal AKI
Early vs Late

A

In Early post renal AKI
The results are just like pre-renal AKI
This is because:
Obstruction in lower or upper urinary tract cause a build up of back pressure in the tubules therefore lowering the GFR
This results in increase in BUN and creatinine in the blood.
But since the tubular cells are still functional Urea can still be reabsorbed and creatinine can still be excreted. The tubular cells can also respond to RAAAS and reabsorb sodium and water.

In Late Post renal AKI results are just like intrarenal AKI
This is because ; with time, due to the excessive build up of back pressure, the tubules will swell up and compress the blood vessels surrounding them, this leads to ischemia and eventually necrosis of the tubular cells. Due to that, decreased GFR will cause an increase in BUN and creatinine in the blood but the tubular cells are not functional therefore BUN can not be reabsorbed and creatinine can not be secreted. Also, they can not respond to RAAAS system thus water and sodium are not reabsorbed.

33
Q

What are the complications associated with AKI

A
  1. Uremia
    - This cause platelet dysfunction which leads to bleeding
    - It causes pericarditis which lead to pleural effusion and in severe cases cause cardiac tamponade
    - It causes Seizures, Encephalopathy, Asterixis
  2. Metabolic acidosis
  3. Electrolyte disturbances: Hyperkalemia causing Arrthmias etc
  4. Drugs accumulation
  5. Volume overload: Fluid retention causing pulmonary edema, peripheral edema
34
Q

Using KDIGO guidelines of diagnosis of AKI, how can you diagnose AKI?

A

Serum creatinine
a) >/= +0.3 mg/dl within 48hrs
b) >/=+1.5* baseline within 7 days

Urine output: Less than 0.5ml/kg/hr for 6 hrs

35
Q

What other diagnostic methods are used in AKI?

A
  1. History
  2. Lab tests: BUN, Creatinine
  3. Urinalysis
  4. Imaging studies: US, CT AP
  5. Renal biopsy
36
Q

In case of post-renal AKI, what is expected in imaging studies?

A

Ultrasound shows Hydronephrosis

37
Q

In case of AKI on CKD, what can be seen in imaging studies?

A

Atrophic kidneys

38
Q

In which case can we see muddy brown casts In Urinary analysis ?

A

In ATN

39
Q

Presence of eosinophils in urine analysis may indicate?

A

Acute Interstitial nephritis

40
Q

In treatment of AKI, what should be done for pulmonary edema caused by CHF?

A

Immediate treatment, using diuretics, oxygen, IV vasodilators, inotropes or dialysis

41
Q

How to resolve AKI caused by hepatorenal syndrome?

A

Octreotide to reduce vasodilators secretion on splanchnic vessels

Midodrine to induce vasoconstriction therefore increasing blood pressure

Albumin

42
Q

How to resolve AKI caused by sepsis?

A
  1. Antibiotics
  2. Iv fluids
  3. Vasopressors
43
Q

Treatment of AKI due to intrarenal causes, how to determine ATN?

A
  1. Stop nephrotoxins
  2. Rhabdomyolysis- IVF
  3. Tumor lysis syndrome- Rasburinase

How to determine ATN; use furosemide test, the absence of diuretic response indicates ATN

44
Q

Treatment of intrarenal AKI- AIN and GN

A
  1. Stop nephrotoxins
  2. Steroids
45
Q

Treatment of post renal AKI

A
  1. BPH :
    a) Alpha 1 blockers to relax the sphincter muscles to relax
    b) 5 alpha reductase inhibitors to decrease size of the prostate gland
    c) catheterization; foley catheter
  2. Tumor/ Stone
    a) Stent
    b) Percutaneous nephrostomy
  3. Discontinuation of anti-cholinergics
46
Q

In AKI complications Dialysis is used in the following

A

A- acidosis
E- electrolyte imbalance ( Hyperkalemia )
I- Intoxication by drugs
O- overload of fluids
U- uremia

47
Q

For Dialysis in management of AKI,
Which patients are for
Continuous Renal replacement therapy ( CRRT) vs intermittent hemodialysis ( IHD)

A

CRRT- hemodynamically unstable patients, already have hypotension
IHD- hemodynamically stable

Renal,Urinary And Male Reproductive Systems (3 decks)

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