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YR5 Chemical Pathology > Assessment of Renal Function 2 > Flashcards

Assessment of Renal Function 2 Flashcards

1
Q

What is the difference between AKI and CKD?

A

AKI:

Abrupt decline in GFR

Potentially reversible

Tx targeted to precise dx + reversal of disease

CKD:

Longstanding decline in GFR

Irreversible

Tx targeted to prevention of complications of CKD + limitation of progression

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2
Q

Define AKI.

A

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

Medical emergency necessitating referral to a nephrologist for dx + tx

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3
Q

What are the stages of AKI?

A

1. Increase in sCr ≥ 26 µmol/L

or 1.5-1.9x reference sCr.

2: sCr 2.0-2.9x reference sCr.

3: sCr ≥3x reference sCr

or increase ≥ 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

Reduced renal perfusion:

as part of generalised reduction in tissue perfusion

or selective renal ischaemia.

No structural abnormality.

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6
Q

What is the normal response to reduced circulating volume ?

A

Activation of central baroreceptors

Activation of RAAS

Release of vasopressin

Activation of sympathetic system

Vasoconstriction, increased cardiac output, renal Na retention

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7
Q

When does pre-renal AKI occur?

A

When normal adaptive mechanisms fail to maintain renal perfusion when there is reduced circulating volume

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8
Q

What are 5 causes of pre-renal AKI?

A

True volume depletion (unable to drink)

Hypotension

Oedematous states (3 failures)

Selective renal ischaemia (e.g. RAS in atherosclerotic disease)

Drugs affecting glomerular blood flow

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9
Q

What is this?

A

Renal artery stenosis

(on RHS of image)

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10
Q

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

A

NSAIDs

Calcineurin inhibitors

ACEi or ARBs

Diuretics

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11
Q

How do NSAIDs predispose patients to developing pre-renal AKI? Give 2 examples

A

Decrease afferent arteriolar dilatation

Ibuprofen

Diclofenac

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12
Q

How do Calcineurin inhibitors predispose patients to developing pre-renal AKI? Give 2 examples

A

Decrease afferent arteriolar dilatation

Cyclosporine

Tacrolimus

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13
Q

How do ACEi or ARBs predispose patients to developing pre-renal AKI? Give 2 examples

A

Decrease efferent arteriolar constriction

Enalopril

Losartan

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14
Q

How do diuretics predispose patients to developing pre-renal AKI? Give an example

A

Affect tubular function, decrease preload

Loop: Furosemide

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15
Q

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

A

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

Prolonged insult leads to ischaemic injury.

ATN does NOT respond to restoration of circulating volume.

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16
Q

A 68M with previously normal renal function is found to have a creatinine of 624μmol/l.

Renal USS shows the following appearance in both kidneys. What is the likely cause of his AKI? What makes you think this?

A

Benign prostatic hypertrophy

Hydronephrosis in both kidneys, calyces very dilated, shows obstruction distal to kidneys

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17
Q

What causes post-renal AKI?

A

Physical obstruction to urine flow

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18
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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19
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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20
Q

What is the pathophysiology of obstructive uropathy?

A

GFR is dependent on the hydraulic pressure gradient.

Obstruction results in increased tubular pressure.

Results in an immediate decline in GFR.

Huge rise in Creatinine

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21
Q

Describe the recovery from obstructive uropathy

A

Immediate relief: Restores GFR with no structural damage e.g. via urethral catheter insertion (or subrapubic catheter)

Prolonged obstruction: structural damage

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22
Q

What does prolonged obstructive uropathy result in?

A

Glomerular ischaemia

Tubular damage

Long-term interstitial scarring

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23
Q

What is the cause of intrinsic renal AKI?

A

CELLULAR/ INTRINSIC DAMAGE.

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24
Q

Where is the abnormality in intrinsic renal AKI?

A

Vascular disease: vasculitis

Glomerular disease: glomerulonephritis

Tubular disease: ATN

Interstitial disease: analgesic nephropathy

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25
Q

What are the most common causes of direct tubular injury in intrinsic renal AKI?

A

Most commonly ischaemic.

Endogenous toxins: Myoglobin + Immunoglobulins

Exogenous toxins- contrast, drugs:

Aminoglycosides, Amphotericin, Acyclovir

26
Q

What are common conditions of immune dysfunction causing intrinsic renal injury?

A

Glomerulonephritis

Vasculitis

Cause renal inflammation

27
Q

What conditions lead to infiltration/ abnormal protein deposition causing intrinsic renal AKI?

A

Amyloidosis

Lymphoma

Myeloma-related renal disease

28
Q

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

A

SERUM CREATININE

URINE OUTPUT

29
Q

Why do some cases of AKI not resolve?

A

Acute wounds heal via 4 phases: Haemostasis, Inflammation, Proliferation, Re-modelling

Imbalance between scarring + remodelling:

Replacement of renal tissue by scar tissue

Results in chronic disease.

30
Q

What are the stages of CKD? What is the prevalence in the population of each?

A
  1. Kidney damage with normal GFR: >90ml/min Prev: 3.3%
  2. Mild decreased GFR: 60-89 ml/min
    Prev: 3%
  3. Moderate decreased GFR: 30-59 ml/min
    Prev: 4.3%
  4. Severe decreased GFR: 15-29 ml/min
    Prev: 0.2%
  5. End-stage kidney failure, GFR: <15 or dialysis
    Prev: 0.2%
31
Q

What are the 6 most common causes of CKD?

A

Diabetes

Atherosclerotic renal disease

HTN

Chronic Glomerulonephritis

Infective or obstructive uropathy

PKD

32
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 + Death

33
Q

What is renal acidosis?

pathophysiology? consequence? treatment?

A

Metabolic acidosis.

Failure of renal excretion of protons.

Results in:

Muscle + protein degradation

Osteopenia due to mobilization of bone calcium

Cardiac dysfunction

Tx: Sodium bicarbonate PO

34
Q

What are common ECG findings in hyperkalaemia? What may this progress to?

A

Tall tented T-wave

Flattening of P-wave

Widened QRS

VT + VF

35
Q

What is anaemia of chronic renal disease?

A

Progressive decline in EPO-producing cells with loss of renal parenchyma.

Usually when GFR < 30mL/min.

Normochromic, normocytic anaemia.

36
Q

What are 3 erythropoiesis-stimulating agents (ESAs) and what do they treat?

A

Erythropoietin alfa (Eprex)

Erythropoietin beta (NeoRecormon)

Darbopoietin (Aranesp)

Anaemia of CKD

37
Q

What are 5 reasons for CKD not responding to ESA treatment?

A

Iron deficiency

TB

Malignancy

B12 + folate deficiency

Hyperparathyroidism

38
Q

What is renal bone disease?

A

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

Osteitis fibrosa

Osteomalacia

Adynamic bone disease

Mixed osteodystrophy

39
Q

What is the pathophysiology of renal bone disease?

A

Unable to excrete phosphate from kidneys (despite high PTH).

Phosphate retention stimulates production of FGF23 + Klotho (lowers levels of activated vit D).

Unable to make activated vit D (no 1a-hydroxylase).

Phosphate retention + low levels of activated vit D leads to hypocalcaemia. Phosphate retention also causes end-organ resistance to PTH, which further leads to hypocalcaemia.

Hypocalcaemia leads to increased PTH (2 HPT) + eventually leads to autonomous secretion + 3 HPT.

Increased phosphate in blood complexes with calcium, which lowers free calcium in blood.

In response to high circulating PTH, bone will become resistant to PTH.

40
Q

What is osteitis fibrosa?

A

Osteoclastic resorption of calcified bone + replacement by fibrous tissue

Due to 2 HPT

Lesions (Brown tumours) of fibrous tissue

41
Q

What is osteomalacia?

A

Insufficient mineralization of bone osteoid

Due to low active Vit D

42
Q

What is adynamic bone disease?

A

Excessive suppression of PTH results in low turnover + reduced osteoid

43
Q

What are management strategies for renal bone disease?

A

Phosphate control:

Dietary + Phosphate binders

Vit D receptor activators:

1-alpha calcidol + Paricalcitol

(As can’t hydroxylate)

Direct PTH suppression:

Cinacalcet

44
Q

What is the most important consequence of CKD?

A

Cardiovascular disease

45
Q

What is the association between GFR and cardiac events?

A

Risk of cardiac event is directly predicted by GFR.

As eGFR reduces, risk of mortality massively increases

46
Q

How does atherosclerosis arise in CKD?

A

Role of traditional RFs less well defined in patients with renal disease

Though control of Cholesterol + HTN shown to slow progression/ risks

47
Q

What is vascular calcification?

A

Renal vascular lesions characterised by heavily calcified plaques

(rather than traditional lipid-rich atheroma)

48
Q

What is this?

A

Vascular calcification

LAD = WHITE due to being full of calcium

49
Q

What are the 3 phases of uraemic cardiomyopathy?

A

Left ventricle (LV) hypertrophy

LV dilatation

LV dysfunction

50
Q

What are contraindications for renal transplant? What are not contraindications for renal transplant?

A

CI: Active sepsis

Not CI: HIV, BMI >30, >65, any malignant disease are not CI (depends on disease).

51
Q

What is haemodialysis?

A

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

~3x/ week for ~6h.

Home dialysis possible

52
Q

What is peritoneal dialysis?

A

Peritoneal cavity is filled with fluid + peritoneal membrane is used as dialysing membrane.

Can be done at home.

53
Q

Patient has new onset AKI. What is the likely diagnosis?

A

Rhabdomyolysis

Fall, long lie, muscle breakdown

Myoglobin in urine

54
Q

A 40F presents with a rash and AKI is diagnosed. What is the most likely cause of her renal failure?

A

Systemic vasculitis

Non blanching rash, young, no other insult

55
Q

What measures can be used to predict risk of outcomes in CKD?

A

eGFR

Albumin : Creatinine ratio (ACR)

56
Q

List 5 functions of the kidney

A

Excretion of water-soluble waste

Water balance

Electrolyte balance

Acid-base homeostasis

Endocrine functions: produces EPO + renin, hydroxylates Vit D

57
Q

What is a major cause of hyperkalaemia in patients with CKD?

A

Dietary intake

High K+ found in milk, chocolate, dried fruits, tomatoes

58
Q

Why does hyperkalaemia cause pathology? In which CKD patients is this particularly common? What medications can precipitate it?

A

K+ is the major intracellular cation

Hyperkalaemia causes membrane depolarisation: cardiac + muscle disruption

Diabetic CKD patients

ACEi, Spironolactone, Potassium sparing diuretics

59
Q

How do you distinguish Anaemia of chronic renal disease from other common causes of anaemia?

A

Iron deficiency: microcytic

B12 +/- folate deficiency: macrocytic

60
Q

Why is uraemic cardiomyopathy uncommon in the UK?

A

Uraemia is a consequence of end stage CKD

Patients receive dialysis

In LIC there is less access to dialysis so is more common

YR5 Chemical Pathology (16 decks)

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