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Pathology - Y5 > AKI and CKD > Flashcards

AKI and CKD Flashcards

1
Q

What is the difference between AKI and CKD?

A

AKI:

  • Abrupt decline in GFR
  • Potentially reversible
  • Treatment targeted to precise diagnosis and reversal of disease

CKD:

  • Longstanding decline in GFR
  • Irreversible
  • Treatment targeted to prevention of complications of CKD and limitation of progression
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2
Q

Define AKI.

A

Defined as a rapid reduction in kidney function, leading to an inability to maintain electrolyte, acid-base and fluid homeostasis.

It is a medical emergency necessitating referral to a nephrologist for diagnosis and treatment.

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3
Q

What are the stages of AKI?

A

AKI Stage 1: Increase in sCr by ≥26 µmol/L, or by 1.5 to 1.9x the reference sCr.

AKI Stage 2: Increase in sCr by 2.0 to 2.9x the reference sCr.

AKI Stage 3: Increase in sCr by ≥3x the reference sCr, or increase by ≥354 µmol/L.

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4
Q

What are the three different types of AKI?

A

Pre-renal

Renal

Post-renal

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5
Q

What are features of pre-renal AKI?

A

Hallmark is reduced renal perfusion as part of generalised reduction in tissue perfusion or selective renal ischaemia.

No structural abnormality.

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6
Q

Which part of the normal response to reduced circulating volume fails in pre-renal AKI?

A

Normally:

  • Activation of central baroreceptors
  • Activation of RAS
  • Release of vasopressin
  • Activation of sympathetic system
  • Vasoconstriction, increased cardiac output, renal sodium retention

Pre-renal AKI occurs when normal adaptive mechanisms fail to maintain renal perfusion.

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7
Q

What are causes of pre-renal AKI?

A

True volume depletion

Hypotension

Oedematous states

Selective renal ischaemia

Drugs affecting glomerular blood flow

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8
Q

What is this?

A

Renal artery stenosis

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9
Q

Which drugs can predispose patients to develop pre-renal AKI?

A

NSAIDs

Calcineurin inhibitors

ACEi or ARBs

Diuretics

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10
Q

What is the difference between pre-renal AKI and acute tubular necrosis?

A

Pre-Renal AKI is not associated with structural renal damage and responds immediately to restoration of circulating volume.

Prolonged insult leads to ischaemic injury.

Acute Tubular Necrosis does not respond to restoration of circulating volume. Epithelial cell casts would be seen in the urine on microscopy. Will end up with an element of CKD.

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11
Q

A 68 year old man with previously normal renal function is found to have a creatinine of 624μmol/l. Renal ultrasound shows the following appearance in both kidneys. What is the likely cause of his AKI?

A

Benign prostatic hypertrophy

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12
Q

What are features of post-renal AKI?

A

Hallmark is physical obstruction to urine flow (intra-renal obstruction):

  • Ureteric obstruction (bilateral)
  • Prostatic/urethral obstruction
  • Blocked urinary catheter
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13
Q

What are common sites of obstruction in post-renal AKI?

A

Intra-renal obstruction

Ureteric obstruction (bilateral)

Prostatic/urethral obstruction

Blocked urinary catheter

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14
Q

What are different things which may cause obstruction in post-renal AKI?

A

Luminal: Stones, clots.

Mural: Malignancy (ureteric, bladder, prostate), BPH, urethral strictures.

Extrinsic compression: Malignancy (pelvic e.g. ovarian mass), prostatic hypertrophy.

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15
Q

What is the pathophysiology of obstructive uropathy?

A

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

Immediate relief of obstruction restores GFR with no structural damage e.g. via urethral catheter insertion provides immediate relief.

Alternative is subrapubic catheter if urethral not possible.

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16
Q

What does prolonged obstructive uropathy result in?

A

Glomerular ischaemia

Tubular damage

Long-term interstitial scarring

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17
Q

What is the cause of intrinsic renal AKI?

A

Pathophysiology is more diverse.

Hallmark is CELLULAR/INTRINSIC DAMAGE.

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18
Q

Where is the abnormality in intrinsic renal AKI?

A

Vascular disease (e.g. vasculitis).

Glomerular disease (e.g. glomerulonephritis).

Tubular disease (e.g. ATN).

Interstitial disease (e.g. analgesic nephropathy).

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19
Q

What are the most common causes of intrinsic renal AKI?

A

Direct tubular injury: Most commonly ischaemic.

Endogenous toxins:

  • Myoglobin
  • Immunoglobulins

Exogenous toxins - contrast, drugs:

  • Aminoglycosides
  • Amphotericin
  • Acyclovir
20
Q

What are common mechanisms of intrinsic renal injury?

A

Immune dysfunction causing renal inflammation:

  • Glomerulonephritis
  • Vasculitis

Infiltration/Abnormal protein deposition:

  • Amyloidosis
  • Lymphoma
  • Myeloma-related renal disease
21
Q

Which 2 measures can be used to predict severity of AKI?

A

The two measures used to define the severity of AKI are SERUM CREATININE and URINE OUTPUT

22
Q

Why do some cases of AKI resolve?

A

Acute wounds heal via four phases:

  • Haemostasis
  • Inflammation
  • Proliferation
  • Remodeling

Pathological responses to renal injury are characterized by imbalance between scarring and remodeling. Replacement of renal tissue by scar tissue results in chronic disease.

23
Q

What are the stages of CKD?

A

Stage 1: Kidney damage with normal GFR: >90ml/min; Prevalence: 3.3%

Stage 2: Mild decreased GFR: 60-89ml/min; Prevalence: 3%

Stage 3: Moderate decreased GFR: 30-59ml/min; Prevalence: 4.3%

Stage 4: Severe decreased GFR: 15-29ml/min; Prevalence: 0.2%

Stage 5: End-stage kidney failure, GFR: <15 or dialysis; Prevalence 0.2%

24
Q

What are the most common causes of CKD?

A

Diabetes

Atherosclerotic renal disease

Hypertension

Chronic Glomerulonephritis

Infective or obstructive uropathy

Polycystic kidney disease

25
Q

What are the four broad categories of consequences of CKD?

A

Progressive failure of homeostatic function:

  • Acidosis
  • Hyperkalaemia

Progressive failure of hormonal function:

  • Anaemia
  • Renal Bone Disease

Cardiovascular disease:

  • Vascular calcification
  • Uraemic cardiomyopathy

Uraemia and Death

26
Q

What is renal acidosis?

A

Metabolic acidosis. Failure of renal excretion of protons.

Results in:

  • Muscle and protein degradation
  • Osteopenia due to mobilization of bone calcium
  • Cardiac dysfunction

Treated with oral sodium bicarbonate.

27
Q

What are common ECG findings in hyperkalaemia?

A

Tall tented T-wave

Loss of P-wave

Widened QRS

28
Q

What is anaemia of chronic renal disease?

A

Progressive decline in erythropoietin-producing cells with loss of renal parenchyma. Usually noted when GFR<30mL/min.

Normochromic, normocytic anaemia.

Distinguish from other causes of anaemia, which are common:

  • Iron deficiency
  • B12 and/or folate deficiency
29
Q

What are some erythropoiesis-stimulating agents (ESAs) and what do they treat?

A

Anaemia of CKD:

  • Erythropoietin alfa (Eprex)
  • Erythropoietin beta (NeoRecormon)
  • Darbopoietin (Aranesp)
30
Q

What are reasons for CKD not responding to ESA treatment?

A
  • Iron deficiency
  • TB
  • Malignancy
  • B12 and folate deficiency
  • Hyperparathyroidism
31
Q

What is renal bone disease?

A

Complex entity resulting in reduced bone density, bone pain and fractures:

  • Osteitis fibrosa
  • Osteomalacia
  • Adynamic bone disease
  • Mixed osteodystrophy
32
Q

What is the pathophysiology of renal bone disease?

A

You are unable to excrete phosphate from the kidneys (even though PTH is high). You are also unable to make activated vitamin D (as no 1a-hydroxylase). The phosphate retention stimulates production of FGF23 and Klotho which also lowers the levels of activated vitamin D.

The phosphate retention and low levels of activated vit D leads to hypocalcaemia. There is also end-organ resistance to PTH due to phosphate retention, which further leads to hypocalcaemia. The hypocalcaemia leads to increased PTH (secondary hyperparathyroidism) and eventually you get autonomous secretion and end up with tertiary hyperPTH.

The increased phosphate in the blood will complex with calcium, which lowers the amount of free calcium in the blood. In response to the high levels of circulating PTH, the bone will become resistant to PTH.

33
Q

What is osteitis fibrosa?

A

Osteoclastic resorption of calcified bone and replacement by fibrous tissue

Hyperparathyroidism

Lesions: Brown tumours

34
Q

What is osteomalacia?

A

Insufficient mineralization of bone osteoid

35
Q

What is adynamic bone disease?

A

Excessive suppression of PTH results in low turnover and reduced osteoid

36
Q

What is the management of renal bone disease?

A

Phosphate control:

  • Dietary
  • Phosphate binders

Vit D receptor activators:

  • 1-alpha calcidol
  • Paricalcitol

Direct PTH suppression:

  • Cinacalcet
37
Q

What is the most important consequence of CKD?

A

Cardiovascular disease

38
Q

What is the association between GFR and cardiac events?

A

Risk of cardiac event is directly predicted by GFR.

39
Q

What is atherosclerosis?

A

Role of traditional risk factors less well defined in patients with renal disease:

  • Cholesterol
  • Hypertension
40
Q

What is vascular calcification?

A

Renal vascular lesions are frequently characterised by heavily calcified plaques, rather than traditional lipid-rich atheroma.

41
Q

What is this?

A

Vascular calcification

42
Q

What is uraemic cardiomyopathy?

A

Three phases:

  • Left ventricle (LV) hypertrophy
  • LV dilatation
  • LV dysfunction
43
Q

What are contraindications for renal transplant?

A

Active sepsis

HIV-positive, BMI >30, aged >65 is not a contraindication, any malignant disease are not contraindications (depends on the disease).

44
Q

What is haemodialysis?

A

Blood is passed through a dialyser which removed most waste products.

It is done about 3x per week for around 6 hours.

You can have home dialysis.

45
Q

What is peritoneal dialysis?

A

This can be done at home.

The peritoneal cavity is filled with fluid and the peritoneal membrane is used as the dialysing membrane.

Pathology - Y5 (59 decks)

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