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Medicine, Year 3, Metabolic Medicine > Clinical Topic 1: Acute Kidney Injury > Flashcards

Clinical Topic 1: Acute Kidney Injury Flashcards

1
Q

What are pre-renal causes of an AKI?

A
  • Hypovolaemia secondary to diarrhoea & vomiting, burns, major haemorrhage, shock, heart failure
  • Renal artery stenosis
  • Renal vein thrombosis
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2
Q

What drugs should definitively be stopped during an AKI, as it may worse it? 5 examples

What drugs should also be stopped during an AKI, which will increase in toxicity but not necessarily worsen the AKI?

A
  • NSAIDs
  • Aminoglycosides
  • ACE Inhibitors
  • ARBS
  • Diuretics
  • Digoxin
  • Metformin
  • Lithium
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3
Q

How can you prevent an AKI in patients about to have an investigation with contrast agent?

A

Give IV fluids before and after the investigation

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4
Q

What is the acute management of patients with Hyperkalaemia?

A
  • Calcium gluconate (first-line, to protect cardiac membrane)
  • Insulin/dextrose infusion and salbutamol (short term movement of K intracellularly)
  • Loop diuretics / Dialysis (to remove K+)
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5
Q

Is Aspirin safe to use during an AKI?

A

ONLY if low dose at 75mg OD

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6
Q

What are the two main causes of Renal Artery Stenosis? What do they characteristically appear like on renal arteriography?

A
  • Atherosclerosis: Narrowing of renal artery proximal to aorta
  • Renal fibromuscular dysplasia: “String of beads” appearance of renal artery distal to aorta
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7
Q

What abdominal examination finding is characteristic of renal artery stenosis?

A

Renal artery bruit

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8
Q

What is the pathophysiology of Renal Artery Stenosis? What are the symptoms / signs of this condition?

A

Reduced perfusion to kidneys causes activation of RAAS, leading to a persistent HTN. There is also atrophy and fibrosis of the kidney

Symptoms: Persistent HTN, headaches, blurry vision, possible stroke / MI

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9
Q

Oligouria is defined as what?

A

< 0.5 ml / kg / hr

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10
Q

What is Stage 1, 2 and 3 Acute Kidney Injury defined as?

A

Stage 1:
1.5-2x increase in Creatinine
<0.5ml/kg/hr for 6-12 hours

Stage 2:
2-2.9x increase in Creatinine
<0.5ml/kg/hr for >12 hours

Stage 3:
3x increase in Creatinine
<0.3ml/kg.hr for >24 hours OR
Anuria for >12 hours

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11
Q

What is the most common intra-renal AKI?

A

Acute Tubular Necrosis

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12
Q

Acute Tubular Necrosis commonly affects which aspects of the kidneys?

A

Proximal Convoluted Tubule

Thick Ascending Limb

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13
Q

What are the causes of Acute Tubular Necrosis? Toxic vs. Ischaemic

A
  • Ischaemic i.e. due to hypotension (shock, sepsis)

- Toxins i.e. aminoglycosides, myoglobin (rhabdomyolysis), anti-freeze, radio-contrast dye, uric acid

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14
Q

What are the clinical features of Acute Tubular Necrosis?

A

Muddy brown casts

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15
Q

In someone with Pre-renal failure, what is the sodium concentration of the urine likely to be? Why?

A

< 20 mmol / L

Renal tubular function is preserved so reabsorption of sodium is preserved and in fact increased

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16
Q

In someone with acute tubular necrosis, what is the sodium concentration of the urine likely to be? Why?

A

> 30 mmol / L

Renal tubular function is damaged hence reabsorption of sodium does not occur

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17
Q

In someone with Pre-renal failure, what is the osmolality of the urine likely to be? Why?

A

High

Renal tubular function is preserved so reabsorption of water occurs

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18
Q

In someone with acute tubular necrosis failure, what is the osmolality of the urine likely to be? Why?

A

Low

Renal tubular function is lost so rebabsorption of water does not occur hence is excreted in urine

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19
Q

What is the affect of ACEI on the afferent / efferent arterioles?

A

Vasodilation of efferent arteriole

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20
Q

What is the effect of NSAIDs on the afferent / efferent arterioles?

A

Vasoconstriction of afferent arteriole

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21
Q

How does angiotensin II act to increase the filtration fraction in the kidney?

A

Vasoconstriction of efferent arteriole

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22
Q

What is the MoA of spirinolactone?

A

Aldosterone antagonist / K+ sparring diuretic

23
Q

Is there a response to fluid challenge in Acute Tubular Necrosis and Pre-renal AKI?

A

Acute Tubular Necrosis - Yes

Pre-Renal AKI - No

24
Q

How do you calculate the anion gap?

A

Na + K - Cl - HCO3

25
Q

Which substance can be used to achieve the most accurate measurement of the glomerular filtration rate?

A

Inulin

26
Q

What does the urine appear like in Pre-renal uraemia and Acute Tubular Necrosis?

A

Pre-renal Uraemia - Bland sediment

Acute tubular necrosis - Muddy brown casts

27
Q

How can you prevent Tumour Lysis syndrome in cancer patients? In what cancer patients does it typically present?

A

Allopurinol
Rasburicase

Typically presents in Leukaemia / Lymphoma patients

28
Q

What medications are capable of causing Acute Interstitial Nephritis?

A

NSAIDs
Penicillin
Diuretics

29
Q

What is Acute Interstitial Nephritis? What are the symptoms

A

Inflammation of the interstitium, caused by Eosinophil and Neutrophil infiltration. Gives an “allergic” presentation with raised eosinophils, FEVER, RASH and oliguria

30
Q

All diabetic patients require annual screening for their kidneys by what test?

A

Albumin:creatinine ratio (ACR) in early morning specimens

31
Q

What are the clinical features of NephrOtic syndrome?

A

PrOteinuria
HypOalbuminaemia
Oedema
Hyperlipidaemia (Oh so fat)

32
Q

If Nephrotic syndrome is diagnosed in children, what is the assumed condition?

A

Minimal change disease

33
Q

State 5 Nephrotic syndromes

A

Minimal change disease
Membranous nephropathy
Focal segmental glomerulosclerosis

Amyloidosis
Diabetic nephropathy

34
Q

If a child is diagnosed with Minimal Change Disease but is unresponsive for steroids, what is the next course of action?

A

Kidney biopsy

35
Q

What is the general management for Nephrotic Syndrome?

A
  • Restrict salt intake, prescribe loop diuretics
  • Treat hypertension with ACEI / ARB if appropriate
  • Treat underlying cause

*If serum albumin < 20 g/L -> consider anticoagulation

36
Q

In Minimal Change Disease, what is the characteristic finding on histology?

A

Fusion of podocyte foot processes

37
Q

In Minimal Change Disease, what is the treatment?

A

Corticosteroids

38
Q

In Minimal Change Disease, what is it associated with?

A

Hodgkin’s Lymphoma, NSAID use

39
Q

In Membranous Nephropathy, what is the characteristic finding on histology?

A

Basement membrane thickening due to IgG complex deposition

40
Q

In Membranous Nephropathy, what is the treatment?

A

1/3 -> resolve by themselves
1/3 -> require cytotoxic drugs
1/3 -> lead to CKD

41
Q

Why is clotting impaired in Nephrotic Syndrome?

A

Loss of antithrombin III and plasminogen in urine

42
Q

What are the clinical features of Nephritic Syndrome?

A
  • Hypertension
  • Haematuria
  • Oligouria
  • Proteinuria
43
Q

Give three examples of Nephritic syndromes

A

IgA nephropathy
Alport syndrome
Rapidly progressive GN

44
Q

What are the clinical features of IgA nephropathy and Post-streptococcal glomerulonephritis?

A

IgA - followed by a URTI few days ago

PSGN - followed by a URTI few weeks ago

45
Q

Give examples of 2 conditions which have both Nephrotic and Nephritic features

A

Post-streptococcal glomerulonephritis

Membranoproliferative glomerulonephritis

46
Q

Which Membranoproliferative glomerulonephritis is associated with Hepatitis C?

A

Type 1

47
Q

What is the most common Nephrotic syndrome in adults?

A

Focal Segmental Glomerulosclerosis

48
Q

Haemolytic uraemic syndrome is commonly caused by what?

A

E. Coli 0157:H7

49
Q

What is the first-line treatment for Rhabdomyolysis?

A

0.9% NaCl IV

50
Q

ACUTE KIDNEY INJURY

  1. What are the causes of AKI?
  2. What is the definition of Stage 1, 2, 3 AKI?
  3. What are the risk factors of an AKI?
  4. What are the investigations for an AKI?
  5. How do you manage an AKI?
  6. How do you manage hyperkalemia in a patient with AKI?
  7. What are complications of patients with AKI?
  8. What is the most common cause of Acute Kidney Injury?
A
  1. Pre-renal: renal artery stenosis, dehydration, hypotension, heart failure

Renal: Acute tubular necrosis, acute interstitial nephritis, rhabdomyolysis, glomerulonephritis

Post-renal: Kidney stones, BPH / Prostate cancer, kidney stones, urethral stricture, abdominal / pelvic mass

2.
Stage 1: <0.5ml / kg / hr for 6-12 hours
Stage 2: <0.5ml / kg / hr for >12 hours
Stage 3: <0.3ml / kg / hr for >24 hours or anuria for 12 hours

  1. Acute illness i.e. infection, surgical operation, CKD, heart failure, diabetes, old age, cognitive impairment, recent contrast agent, previous AKI, drugs (NSAIDs, ACEIs, ARBs, aminoglycosides, diuretics)
  2. Urinalysis for protein, U&Es, blood, glucose, leukocytes. Renal US if ?obstruction or unknown cause
  3. Fluid rehydration, especially for pre-renal AKIs. Stop any nephrotoxic medications i.e. ACEIs, ARBs, NSAIDs, aminoglycosides. Relieve post-renal obstructions i.e. catheterising the patient
  4. Calcium gluconate to stabilise the cardiac membrane, an insulin / dextrose infusion + salbutamol to shift potassium extracellularly to intracellularly, and finally Calcium resonium, loop diuretics or dialysis to remove potassium from body
  5. Hyperkalaemia, uraemia, encephalopathy, pericarditis
  6. Acute Tubular Necrosis
51
Q

ACUTE TUBULAR NECROSIS

  1. What are some causes of Acute Tubular Necrosis?
  2. What is classically seen in ATN on urinalysis?
  3. What is the Urinary Sodium or Urinary Osmolality for ATN?
A
  1. Ischaemic causes, i.e. Shock, sepsis. Toxic causes, i.e. Aminoglycosides, Myoglobin / Rhabdomyolysis, Radiocontrast dye, Uric acid
  2. Brown muddy casts
  3. High urinary sodium, low urine osmolality
52
Q

ACUTE INTERSTITIAL NEPHRITIS

  1. What is it?
  2. What type of hypersensitivity reaction is it?
  3. What typically causes it?
  4. What are the classic features?
  5. What is seen on urinalysis?
  6. How is it managed?
A
  1. A hypersensitivity reaction of inflammation of the interstitium (space between cells and tubules in kidneys)
  2. Type 1 or 4 Hypersensitivity reaction
  3. NSAIDs, penicillin, diuretics
  4. FEVER, EOSINOPHILIA, RASH (allergic picture)
  5. Sterile pyuria, WC casts
  6. Treat underlying cause, steroids to reduce inflammation
53
Q

RHABDOMYOLYSIS

  1. What is it?
  2. What are the symptoms?
  3. What are the investigations?
  4. What is the management?
A
  1. When skeletal muscle tissue breaks down, releasing the products into the blood
  2. Muscle aches, fatigue, confusion, red urine
  3. Elevated creatine kinase, myoglobinuria, U&Es (hyperkalaemia), 12-lead ECG
  4. IV Fluids, IV Sodium bicarbonate, IV mannitol and correct the hyperkalaemia
54
Q

DIABETIC NEPHROPATHY

  1. What is it?
  2. What is the main feature on urinalysis?
  3. How are patients screened for it?
  4. How is it managed?
A
  1. The most common cause of CKD in UK
  2. Proteinuria
  3. Early morning sample of albumin:creatitine ratio
  4. Monitor HTN, have good glycaemic control, and ACEI

Medicine, Year 3, Metabolic Medicine (9 decks)

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