Renal 2 Flashcards

1
Q

Compare and contrast AKI and CKD in terms of:

a) GFR
b) Reversibility
c) Targets of treatment

A

a) AKI abrupt decline, CKD longstanding decline
b) AKI reversible, CKD irreversible
c) AKI treatment targeted to precise cause of AKI, CKD treatment targeted to prevention of complications of CKD

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2
Q

Define AKI

A

Rapid reduction in kidney function, leading to inability to maintain electrolyte, acid-base and fluid homeostasis

Raised creatinine, decreased urine output

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3
Q

3 types of AKI

A

Pre-renal
Post-renal
Intrinsic renal

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4
Q

What is the hallmark of pre-renal AKI?

A

Reduced renal perfusion pressure (w/o structural abnormalities)

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5
Q

5 causes of pre-renal AKI

A

True volume depletion e.g. haemorrhage

Hypotension

Oedematous state

Selective renal ischaemia e.g. renal artery stenosis

DRUGS e.g. ACEi, ARBs, NSAIDS, diuretics, calcineurin inhibitors

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6
Q

What is a key difference between AKI and acute tubular necrosis?

A

No structural renal damage in AKI, but prolonged AKI –> ATN –> renal damage

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7
Q

How does the response to restoration of normal circulating volume differ in AKI and ATN?

A

AKI resolves with restoration of normal circulating volume, ATN doesn’t

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8
Q

What key finding would you see on urine microscopy in ATN?

A

Epithelial cell casts

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9
Q

Describe the normal renal response to reduced circulating volume

A
Low pressure detected by baroreceptors
RAAS activated
Vasopressin release
SNS activated
Vasoconstriction, increased cardiac output, renal Na retention
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10
Q

Name and explain the two mechanisms by which renal blood flow remains constant despite varying pressure

A

Myogenic Stretch – if the afferent arteriole gets stretched due to high pressure, it will constrict to reduce the transmission of that high pressure into the Bowman’s capsule, thereby keeping the GFR steady

Tubuloglomerular Feedback – high chloride concentration in the early distal tubule (sign of high GFR) stimulates constriction of the afferent arteriole which lowers GFR and reduced chloride level in the distal tubule

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11
Q

Causes of post-renal AKI

A

Ureteric obstruction (bilateral)
Prostatic / urethral obstruction
Blocked urinary catheter
Retroperitoneal fibrosis / Ormond’s disease

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12
Q

Pathophysiology of post-renal AKI

A

GFR is dependent on the hydraulic pressure gradient
Obstruction results in increased tubular pressure
This results in an immediate decline in GFR

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13
Q

3 mechanisms of renal injury that cause intrinsic renal AKI (with examples)

A

Direct Tubular Injury (Common) – ischaemia or toxins:

  • Most commonly ischaemic
  • Endogenous toxins –> myoglobin (i.e. rhabdomyolysis from muscle injury), immunoglobulins
  • Exogenous toxins –> contrast medium > aminoglycosides, amphotericin, aciclovir

Immune dysfunction causing renal inflammation (Common)

  • Glomerulonephritis
  • Vasculitis (i.e. 40yo presenting with systemic purpura and AKI diagnosis)

Infiltration/Abnormal Protein Deposition

  • Amyloidosis (causes nephrotic syndrome)
  • Lymphoma
  • Multiple Myeloma
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14
Q

Most common intrinsic renal cause of AKI?

A

Acute tubular necrosis

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15
Q

Why do some AKIs resolve and others don’t?

A

Pathological responses are characterised by an imbalance between scarring and remodelling

Replacement of renal tissue by scar tissue results in chronic disease

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16
Q

Causes of CKD

A
DIABETES
HYPERTENSION
Chronic Glomerulonephritis
Infective or obstructive uropathy
Polycystic kidney disease
17
Q

Give some homeostatic, hormonal and cardiovascular consequences of CKD

A

Progressive failure of homeostatic function

  • Acidosis
  • Hyperkalaemia

Progressive failure of hormonal function

  • Anaemia
  • Renal bone disease

Cardiovascular disease

  • Vascular calcification (renal osteodystrophy)
  • Uraemic cardiomyopathy

Uraemia and death

18
Q

Describe the consequences of renal acidosis in CKD

Treatment?

A

Metabolic acidosis (failure of renal excretion of protons) leads to:

  • Muscle and protein degradation
  • Osteopaenia due to mobilisation of bone calcium (because protons can be stored in bone)
  • Cardiac dysfunction

TREATMENT: oral sodium bicarbonate

19
Q

Describe the consequences of hyperkalaemia in CKD

A

Cardiac arrhythmias

Muscle weakness

20
Q

What sort of anaemia do you get in CKD and how?

A

Normochromic, normocytic anaemia

Because get loss of EPO-producing cells as GFR declines

21
Q

How do you treat anaemia of CKD?

A

Artificial erythropoiesis-stimulating agents (ESAs) e.g.

	Erythropoietin alfa (Eprex)
	Erythropoietin beta (NeoRecormon)
	Darbopoietin (Aranesp)
22
Q

4 types of renal bone disease in CKD

A

Osteitis fibrosa cystica
Osteomalacia
Adynamic bone disease
Renal osteodystrophy

23
Q

Pathophysiology of renal osteodystrophy

A

Unable to: excrete phosphate from kidneys / make vitamin D

FGF-23/klotho produced –> lower vitamin D –> 2nd HPT

Excess phosphate –> complexes with Ca2+ –> hypocalcaemia

Phosphate-calcium crystals deposit –> renal osteodystrophy

24
Q

Pathophysiology of osteitis fibrosa cystica

A

Caused by osteoclastic resorption of calcified bone and replacement by fibrous tissue

This is a feature of hyperparathyroidism

25
Q

Pathophysiology of osteomalacia

A

Insufficient mineralisation of bone osteoid because body is trying to mobilise calcium from the bone

26
Q

Pathophysiology of adynamic bone disease

A

Excessive suppression of PTH (from overtreatment) results in low turnover and reduced osteoid

27
Q

Management of renal bone disease

A

Phosphate control (bring it down): dietary, phosphate binders

Vitamin D receptor activators:
• 1-alpha calcidol
• Paricalcitol

Direct PTH suppression

28
Q

Treatment of CKD

A

Transplantation
Haemodialysis
Peritoneal dialysis

29
Q

Indications for dialysis in CKD

A

Refractory hyperkalaemia

Refractory fluid overload

Metabolic acidosis

Uraemic symptoms (encephalopathy, nausea, pruritis, malaise, pericarditis)

CKD stage 5 (GFR <15mL/min)