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5 - Chemical Pathology > Kidney > Flashcards

Kidney Flashcards

1
Q

What are the indications for starting dialysis? (4)

A
  • Hyperkalaemia
  • Uraemia
  • Metabolic acidosis
  • Pulmonary oedema
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2
Q

When do you start dialysis in an anuric patient?

A

Only when they have indications

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3
Q

What complications can uraemia cause? (2)

A
  • Encephalopathy
  • Pericarditis
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4
Q

What is the pathophysiology of rhabdomyolysis?

A

Breakdown of muscle → release of CK

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5
Q

What is the key investigation in rhabdomyolysis?

A

CK

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6
Q

What is unique about the dipstick result in rhabdomyolysis?

A

+ve for blood but when observed under microscope there will be no RBCs - myoglobin

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7
Q

Why is rhabdomyolysis dangerous for the kidneys?

A

Risk of ARF as myoglobin is nephrotoxic

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8
Q

What is the management of rhabdomyolysis?

A

0.9% saline

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9
Q

What is the best measure of kidney function and what’s the normal value?

A

GFR = best measure of kidney (normal = 120ml/min)

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10
Q

How do we estimate GFR?

A

Using clearance - volume of plasma cleared of a marker substance per unit time

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11
Q

What is the formula for clearance?

A

Clearance = (urinary concentration of marker x volume) / plasma concentration of the marker

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12
Q

What are the 3 criteria for using a marker to estimate GFR? (3)

A
  • Freely filtered
  • Not bound to plasma proteins
  • Not reabsorbed / secreted by tubules
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13
Q

What is the gold-standard marker of GFR and why isn’t it used clinically?

A
  • Inulin is the gold-standard marker
  • Not used in clinical practice - requires an IV steady-state infusion
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14
Q

What are the characteristics of blood urea as a marker? (4)

A
  • Endogenous marker (by-product of protein metabolism)
  • Freely-filtered by variable reabsorption by tubular cells
  • Dependent on nutrition, GI bleeding, hepatic function
  • Not used as a marker of GFR but of dehydration
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15
Q

What are the key points about serum creatinine? (3)

A
  • Derived from muscle cells
  • Freely filtered, active secretion into tubules
  • CKD-EPI equation uses creatinine clearance to calculate eGFR - this is what we use in clinical practice
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16
Q

What are the characteristics of Cystatin C? (3)

A
  • Alternative endogenous marker to creatinine - generated by nucleated cells
  • Freely filtered, but almost completely reabsorbed
  • Not really used clinically
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17
Q

What is the gold standard for measuring proteinuria?

A

spot urine protein:creatinine ratio

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18
Q

Is 24-hour urine collection commonly used for measuring proteinuria?

A

no

19
Q

What is the gold standard imaging for kidney stones?

A

CTKUB (CT Kidneys, Ureters, Bladder)

20
Q

What is the basic definition of AKI?

A

Reduction in GFR over 1 week - reversible

21
Q

What are the three main categories of AKI? (3)

A
  • Pre-renal
  • Renal
  • Post-renal
22
Q

What is the main mechanism of pre-renal AKI?

A

Reduced renal perfusion

23
Q

What are the causes of pre-renal AKI? (7)

A
  • Shock
  • Renal artery stenosis
  • Haemorrhage
  • Hypotension
  • Calcineurin inhibitors
  • NSAIDs/ACIs/ARBs
  • Diuretics
24
Q

What are the two key adaptive mechanisms that maintain renal perfusion? (2)

A
  • Myogenic stretch - afferent arteriole if stretched constricts to reduce high pressure to the bowman’s capsule
  • Tubuloglomerular feedback - high Cl- in the distal tubule → constriction of afferent arteriole
25
Q

What are the key characteristics of pre-renal AKI? (3)

A
  • NO structural renal damage
  • Responds immediately to restoration of circulating volume
  • Often precipitated by starting an ACEi
26
Q

What is pre-renal AKI often precipitated by?

A

ACEi

27
Q

What is the key characteristic of renal AKI?

A

Structural renal damage is present

28
Q

What are the causes of renal AKI? (8) (MAGIC VAD)

A
  • M - Multiple Myeloma & Myoglobin
  • A - Amyloidosis & ATN
  • G - Glomerulonephritis
  • I - Interstitial disease
  • C - Contrast
  • V - Vasculitis
  • A - Aminoglycosides, Amphotericin, Aciclovir
  • D - Drugs (other nephrotoxic)
29
Q

What is the most common cause of ATN?

A

Most commonly caused by prolonged pre-renal AKI → ischaemic injury

30
Q

What are the obstructive causes of post-renal AKI? (4)

A
  • Renal stone
  • BPH
  • Transitional cell carcinoma
  • Extrinsic mass pressing on ureter
31
Q

What happens if post-renal AKI is managed quickly vs slowly? (2)

A
  • If managed quickly - restore GFR with no structural damage
  • If managed slowly - glomerular ischaemia & tubular damage
32
Q

What are the causes of CKD? (6)

A
  • DM (most common)
  • Hypertension
  • Atherosclerosis
  • Chronic glomerulonephritis
  • Prostate disease
  • PCKD
33
Q

Most common cause of CKD?

A

Diabetes

34
Q

What are the metabolic consequences of CKD? (4)

A
  • Metabolic acidosis
  • Hyperkalaemia
  • Normochromic anaemia
  • Secondary/tertiary hyperparathyroidism
35
Q

What are the major complications of CKD? (4)

A
  • Uraemia (leading to cardiomyopathy, encephalopathy)
  • Renal osteodystrophy
  • CVD (most likely to kill them, highly calcified plaques)
  • Bone disease
36
Q

What are the three types of bone disease in CKD? (3)

A
  • Osteitis fibrosa cystica → bone cysts, Brown’s tumours
  • Adynamic bone disease - resistance to PTH in bones → low bone turnover
  • Osteomalacia - inadequate mineralisation of bone
37
Q

What are the 6 key aspects that need management in CKD? (6)

Remember “AH HMVP” (Ah, Help My Vitamin P!)

A
  • A - Anaemia
  • H - Hyperkalaemia
  • H -Hyperparathyroidism
  • M - Metabolic acidosis
  • V - Vitamin D deficiency
  • P - Phosphate (Hyperphosphataemia)
38
Q

How is metabolic acidosis managed in CKD?

A

Oral sodium bicarbonate

39
Q

What is the management for hyperkalaemia in CKD?

A

Dietary management

40
Q

How is anaemia managed in CKD?

A

Artificial EPO (Erythropoietin)

41
Q

What are the two approaches to managing hyperphosphataemia in CKD? (2)

A
  • Dietary management
  • Phosphate binders
42
Q

How is Vitamin D deficiency managed in CKD?

A

1-alpha calcidol

43
Q

How is hyperparathyroidism managed in CKD?

A

Cinacalcet - increases sensitivity of calcium sensing receptors → decreased PTH

5 - Chemical Pathology (7 decks)

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