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Biochemistry > Chemical Pathology Of Renal Disease > Flashcards

Chemical Pathology Of Renal Disease Flashcards

1
Q

ADD CLINICAL CASES TO TEST

A

—

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3
Q

What are the homeostasis functions of the kidneys?

A

Waste products of metabolism
Fluid/electrolyte balance
Acid-base balance
Removal of drugs and toxins

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4
Q

What are the endocrine functions of kidney?

A

RAAS
Erythropoietin production
Hydroxylation of vitamin D

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5
Q

Which functions of the kidneys are effected by AKI and CKD?

A

AKI= excretion and homeostasis in early AKI

CKD= endocrine and then excretion later in CKD

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6
Q

How are the different stages of AKI defined? Which stages is associated with increased in-hospital mortality?

A

Stage 1:
Serum creatinine: >=26.5 micro mol/L in 48 hrs or 1.5-1.9 x baseline
Urine output: <0.5ml/kg/h for 6-12 hours

Stage 2:
Serum creatinine: 2.0-2.9 x baseline
Urine output: <0.5ml/kg/h for >12 hrs

Stage 3:
Serum creatinine: >=3 x baseline or rise in >=353.g micromols/L or need for renal replacement therapy regardless of creatinine levels
Urine output: <0.3ml/kg/h for >24hrs

Stage 2

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7
Q

What are the causes of AKI?

A

Renal underperfusion

Intrinsic renal damage

Obstruction

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8
Q

What is the most common cause of AKI in hospitalised patients and why is this?

A

Renal underperfusion

Due to causes being associated with hosptial setting:

Hypovolaemia (trauma/GI bleed)

Sepsis (afferent arteriole vasodilation)

Renal artery stenosis/atherosclerosis

Pump failure (HF)

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9
Q

Why does intrinsic renal damage occur?

A

Ischaemia

Nephrotoxins

Infection (pyelonephritis

Trauma

Early stage inflammation causes of CKD (glomerulonephritis)

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10
Q

When is post-obstructive diuresis occur and what are the potential problems?

A

When catheter inserted to relieve retained urine in renal obstruction

Can then cause pre-renal injury due to fluid depletion associated with the diuresis= need to ensure fluids being replaced

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11
Q

What are the stages involved in AKI development?

A

Pre-renal cause (hypovolaemia/sepsis/renal artery stenosis) leads to renal underoperfusion

Pre-renal renal failure leads to prolonged renal underperfusion which can cause acute tubular necrosis

Acute tubular necrosis can lead to intrinsic renal failure

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12
Q

What are the precipitating factors of glomerular damage leading to intrinsic renal failure?

A

Trauma

Toxins

Infection

Infarction

Inflammation

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13
Q

What are the most common causes of AKI in patients?

A

Hypovolaemia and sepsis

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14
Q

How can you differentiate between a pre-renal renal failure and intrinsic renal AKI?

A 
Pre-renal 
Low urine vol
Urine:plasma osmolality= high i.e. trying to preserve water (concentrated urine) 
Urine sodium conc= low 
Plasma sodium= high 
Serum elevation of urea >> creatinine

Intrinsic
Initially high= due to kidney being unable to reabsorbed water and electrolytes
Urine:plasma osmolality= low or similar
Urine sodium conc= high
Plasma sodium= low
Serum elevation urea=creatinine

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15
Q

What is the most specific test for differentiating between pre-renal and intrinsic renal AKI? What would the results be and why?

A

Urine sodium concentration

Pre-renal= LOW
Aldosterone being released to retain sodium

Intrinsic damage= HIGH
Kidney unable to reabsorb sodium

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16
Q

How does the treatment of pre-renal AKI differ from intrinsic renal damage? Why is this?

A

Pre-renal= fluid cures
Due to low fluid volume being the reason for underperfusion

Intrinsic= fluid kills
Kidney unable to clear the fluid which lead to fluid overload

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17
Q

What are the biochemical features of intrinsic AKI?

A

Retain acidic waste products= acidosis

Retain Potassium

Retain nitrogenous waste products
I.e. leads to uraemic symptoms= nausea, malaise, confusion

Retain salt and water = decreased GFR

18
Q

What serum concentration of potassium is life-threatening?

A

> 8mmol/L

19
Q

How would someone with intrinsic AKI present?

A

Hyperkalaemia metabolic acidosis

Malaise + nausea

Hyponatraemia due to fluid retention

Fluid overload

20
Q

How is AKI managed?

A

Determine whether pre-renal, intrinsic or post-renal causes

Identify underlying cause

Stop ACEi/ARBs/NSAIDs

Correct life-threading fluid and electrolytes and acid base abnormalities

Restore renal perfusion if pre-renal

Haemofiltration or dialysis to support renal function in life threatening AKI

21
Q

When is restoration of renal perfusion in pre-renal AKI contraindicated and why?

A

Heart failure

Leads to fluid overload

22
Q

What is CDK and what are the main causes?

A

Gradual irreversible change in kidney function

DM 
Hypertension 
Polycystic kidney disease 
Recurrent pyelonephritis 
Glomerulonephritis 
Interstitial nephritis 
Multisystem disease
Drugs
23
Q

How is CDK monitored?

A

24 hr urine collection for protein to determine GFR

Estimated GFR

Creatine (in end stage)

Albumin/creatine ratio

24
Q

Why is GFR used in early stages of CDK and creatine used in late stages?

A

Can loose 50% of kidney function before creatinine changes

EGFR changes less in later stages whereas creatinine changes a lot

25
Q

How is eGFR used to stage CKD?

A 
>90= stage 1 
60-90= stage 2 
45-60= stage 3a 
30-44= stage 3b 
15-30= stage 4 
<15= stage 5

NOTE= the 1st number of the range values is half of the upper value in previous stage range after stage 1 i.e. 90/2= 45

26
Q

At what stage of CKD does a patient present with clinical consequences? Which clinical signs are associated with the stages?

A 
3a= hypertension and increase CVD risk 
3b= low calcium and secondary increase PTH (due to problems with vitamin D hydroxylation) 
4= anaemia(due to erythropoietin prod)/anorexia/high phosphate 
5= salt and water retention/acidosis/high potassium
27
Q

What are the biochemical changes associated with CKD stage 3-4?

A

Elevate creatine
Reduced eGFR
Elevated ACR
Reduced 1-alpha hydroxylation of vitamin D = decreased amount of active vitamin D present
Reduced erythropoietin production (renal anaemia)
Elevated lipids and triglyceride (increased CVD risk)
Impaired immune function

28
Q

Why are hypocalcaemia and secondary hyperparathyroidism associated with stage 3-4 CKD?

A

Decreased 1-alpha hydroxylation of vitamin D leads to impaired calcium absorption in GIT= hypocalcaemia

Hypocalcaemia detected by parathyroid gland which stimulates increased production of PTH to promote increase osteoclast function to increase bone resorption to release calcium

29
Q

What are the biochemical changes associated with stage 4-5 CKD?

A

Elevate creatinine and urea= leads to uraemic symptoms

High phosphate

Acidosis

Hyperkalaemia= only presents in later stages due to increased gut-losses offsetting it until that point

30
Q

How does the site of kidney damage influence the water balance in CKD?

A

Glomerular damage:
Little glomerular filtrate= little urine produce (oliguria) i.e. fluid overload

Healthy nephron in disease kidney
Tubules unable to reabsorb electrolytes or water i.e. osmotic diuresis + polyuria

Tubular damage
Ineffective water reabsoprtion i.e. polyuria

31
Q

Is a CKD patient more likely to present with polyuria or oliguria?

A

Polyuria

Oliguria only present in later stages of CKD

32
Q

What are the 2 possible mechanism contributing to renal bone disease?

A
  1. Decreased 1-alpha hydroxylation= decreased plasma calcium and increased PTH
  2. Decreased GFR
    - increased plasma phosphate= increase calcium/phosphate products
    - metabolic acidosis= dissolves bone buffers
33
Q

What bone diseases are associated with CKD and why?

A

Osteomalacia = decreased plasma calcium

Osteitis fibrosa = increased bone resorption

Metastatic calcification= increase calcium/phosphate products

Osteoporosis= bone decay due to dissolved bone buffers

34
Q

How is CKD stage 2-3a managed?

A

Monitor patients via eGFR + ACR/ BP + lipids/ bone profile + PTH in stage 3a

Treat causes (diabetes, hypertension, recurrent UTI)

Avoid precipitates of AKI

Block slow progression by blocking RAAS if ACR via ACEi/ARB

35
Q

How is stage 3b-5 CKD managed?

A

Endocrine abnormalities:
Alfacalcidol= corrects calcium and prevens tertiary hyperparathyroidism
Erythropoietin
Phosphate binders= decreases risk of metastatic calcification
Modified diet to decreased potassium
Fluids

Bicarbonate to correct acid-base disturbances

Renal replacement therapy i.e. haemodialysis or peritoneal dialysis

36
Q

What is tertiary hyperparathyroidism?

A

Excessive production of PTH due to long-standing secondary hyperparathyroidism

37
Q

What are the different causes of renal tubular disorders?

A

Specific transport defects i.e. glucose/amino acids/phosphates

Global tubular defect i.e. fanconi syndrome

Renal tubular acidosis i.e. causes acid/base and electrolytes disturbances

Biochemistry (5 decks)

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