Acute and Chronic renal Failure 1 Flashcards

1
Q

What is an AKI?

A

A potentially reversible abrupt decline in GFR with treatment targeted at diagnosis and reversal of disease.

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2
Q

What is CKD?

A

An irreversible longstanding decline in GFR with treatment aimed at prevention of complications and progression. (>3 months)

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3
Q

What is acute failure of kidneys?

A

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

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4
Q

Is an AKI an emergency?

A

Yes- immediate referral for management in nephrology

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5
Q

What are the stages of an 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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6
Q

What are the types of AKI?

A

Pre renal

Renal

Post Renal

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7
Q

What is a pre renal AKI?

A

Reduced tissue perfusion/ local ischaemia

NO structural abnormality

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8
Q

What is a normal response to reduced circulating volume?

A

Activation of central baroceptors activates RAS and there is a release of vasopressin and sympathetic system which causes vasoconstriction, increased cardiac output and renal sodium retention.

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9
Q

What are the causes of pre renal AKI?

A
True volume depletion
Hypotension
Oedematous states
Selective renal ischaemia
Drugs affecting glomerular blood flow

Renal artery stenosis

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10
Q

Which class of drugs may commonly predispose patients to developing pre-renal AKI?

A

ACEi

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11
Q
How do these drugs cuase pre renal AKI:
NSAIDS
ACEi/ARBs
Calcineurin inhibitors
Diuretics
A

NSAIDs - decrease afferent arteriolar dilatation
Calcineurin inhibitors - decrease afferent arteriolar dilatation
ACEi or ARBs - decrease efferent arteriolar constriction
Diuretics – affect tubular function, decrease preload

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12
Q

How can AKI lead to ATN?

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

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13
Q

What is the hallmark of post renal AKI?

A

Physical obstruction to urine flow.

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14
Q

What may cause post renal AKI?

A
(Intra-renal obstruction)
Ureteric obstruction (bilateral)
Prostatic / Urethral obstruction
Blocked urinary catheter
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15
Q

What is the pathophysiology of obstructive uropathy?

A

GFR is dependent on hydraulic pressure gradient
Obstruction results in increased tubular pressure
Immediate decline in GFR

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16
Q

How do you recover from obstructive uropathy?

A

Immediate relief of obstruction restores GFR fully, with no structural damage

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17
Q

What can prolonged obstruction cause?

A

Glomerular ischaemia
Tubular damage
Long term interstitial scarring

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18
Q

What is are the types of intrinsic 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

How does direct tubular injury occur?

A
Ischaemia
Endogenous toxins (Myoglobin, Igs)
Exogenous toxins (Aminoglycosides, amphotericin, acyclovir)
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20
Q

Patient has new onset AKI, haematuria and massive bruising. What is the likely diagnosis?

A

Rhabdomyolysis (Myoglobin is toxic)

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21
Q

A 40 year old female presents with a papular coalescing rash and AKI is diagnosed. What is the most likely cause of her renal failure from the following list?

A

Systemic Vasculitis

22
Q

What are common mechanisms of renal injury?

A
  1. Immune dysfunction (Renal inflammation):
    a. Glomerulonephritis
    b. Vasculitis
  2. Infiltration/ abnormal protein deposition:
    a. Amyloidosis
    b. Lymphoma
    c. Myeloma-related renal disease
23
Q

What are the important causes?

A

Pre-renal

ATN

24
Q

What are the non fatal outcomes of AKI?

A

Complete or partial recovery of renal function

Discharged with increasing creatinine

Discharged with a requirement for dialysis

25
Q

How do acute wounds heal?

A

Haemostasis
Inflammation
Proliferation
Remodeling

26
Q

What pathology stops renal resolution after an AKI?

A

Imbalance of scarring and remodelling

Replacement of renal tissue by scar tissue in chronic disease

27
Q

What is the process of getting CKD?

A

Increased Risk

Early Damage

Reduced GFR

Renal Failure

Death

28
Q

What are the stages of CKD?

A

1, Kidney damage with normal GFR, >90, 3.3 %

2, Mild GFR, 60-89, 3 %

3, Moderate GFR, 30-59, 4.3 %

4, Severe GFR, 15-29, 0.2 %

5, End-stage kidney failure, GFR <15 or dialysis, 0.2 %

29
Q

What are the causes of CKD?

A
Diabetes
Atherosclerotic renal disease
Hypertension
Chronic Glomerulonephritis
Infective or obstructive uropathy
Polycystic kidney disease
30
Q

What are the functions of the kidney?

A

Excretion of water-soluble waste

Water balance

Electrolyte balance

Acid-base homeostasis

Endocrine functions (EPO, RAS, Vit D)

31
Q

What are the consequences of CKD?

A

Progressive loss of homeostatic function (acidosis and hyperkalaemia)

Progressive failure of hormonal function (Anaemia, renal bone disease)

Cardiovascular disease (vascular calcification, uraemic cardiomyopathy)

Uraemia and death

32
Q

What does renal acidosis cause?

A

Muscle and protein degradation

Osteopenia due to mobilization of bone calcium

Cardiac dysfunction

33
Q

What is the treatment of renal acidosis?

A

NaHCO3, PO

34
Q

What is potassium used for?

A

Major intracellular cation
Membrane depolarisation
Cardiac function
Muscle function

35
Q

What medications can cause hyperkalaemia?

A

ACEi
Spirinolactone
Potassium sparing diuretics

36
Q

What is anaemia of chronic renal disease?

A

Normochromic, normocytic anaemia

Usually noted when GFR<30mL/min

(Loss of EPO cells)

37
Q

What are the ESAs (Erythropoiesis- stimulating agents)?

A
Erythropoietin alfa (Eprex)
Erythropoietin beta (NeoRecormon)
Darbopoietin (Aranesp)
38
Q

Your patient with CKD has been started on an ESA but does not respond. What could be the cause?

A
TB
Malignancy
(Chronic Disease)
B12/ Folate/ IDA
Hyper-parathyroidism
39
Q

What are the renal bone diseases?

A

Osteitis fibrosa
Osteomalacia
Adynamic bone disease
Mixed osteodystrophy

40
Q

What is osteitis fibrosa?

A

Osteoclastic resorption of calcified bone and replacement by fibrous tissue

Comes with hyperparathyroidism

41
Q

What is osteomalacia?

A

Insufficient mineralisation of bone osteoid

42
Q

What is adynamic bone disease?

A

Excessive suppression of PTH results in low turnover and reduced osteoid

43
Q

What is the treatment of renal bone disease?

A

Phosphate control: dietary, phosphate binders

Vit D receptor activators: 1-alpha calcidol, paricalcitol

Direct PTH suppression: Cinacalcet

44
Q

What is associated with atherosclerosis?

A

Cholesterol

Hypertension

45
Q

What are the 3 phases of uraemic cardiomyopathy?

A

Left ventricle (LV) hypertrophy

LV dilatation

LV dysfunction

46
Q

What are relative contraindications to renal transplant?

A

Conditions: Untreated coronary artery disease, HIV, Chronic Hep B/C

Age >65 years

Previous Malignancy

Obesity/ Co morbidity

47
Q

What are absolute contraindications to renal transplant?

A

Untreated malignancy

Active infection

Untreated HIV infection or AIDS

any condition where life expectancy is under two years.

48
Q

What two measures do we use to define acute kidney injury?

A

Creatinine and Urine output

49
Q

How is AKI defined using creatinine and urine output?

A

Stage 1:
1.5–1.9 times baseline OR ⩾0.3 mg/dl (⩾26.5 μmol/l) increase
UO = <0.5 ml/kg/h for 6–12 hours

Stage 2:
2.0–2.9 times baseline
UO = <0.5 ml/kg/h for ⩾12 hours

Stage 3:
3.0 times baseline OR Increase in serum creatinine to ⩾4.0 mg/dl (⩾353.6 μmol/l)*
UO = <0.3 ml/kg/h for ⩾24 hours OR Anuria for ⩾12 hours

*OR Initiation of renal replacement therapy OR, In patients <18 years, decrease in eGFR to <35 ml/min per 1.73 m2

50
Q

What measures aid prognosis in CKD?

A

eGFR

ACR (Albumin-Creatinine Ration) in the urine

51
Q

What foods can cause hyperkalaemia in CKD?

A

Tomatoes
Chocolate
Dried fruits

DIET RESTRICTION IS IMPORTANT