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11. Urinary > 10. Acute Kidney Injury and Glomerular Disease > Flashcards

10. Acute Kidney Injury and Glomerular Disease Flashcards

1
Q

What is oliguria?

A

Little urine.

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2
Q

What is oliguria defined as?

A

Less than 500ml of urine/day or less than 20ml/hour.

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3
Q

What is anuria?

A

No urine.

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4
Q

What is anuria defined as?

A

Less than 100ml of urine/day.

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5
Q

What does anuria suggest?

A

Blockage of urine flow.

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6
Q

What are the three types of acute kidney injury?

A

Pre-renal disease - decreased perfusion, post-renal failure - obstruction, intrinsic renal failure - damage to kidney.

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7
Q

What is pre-renal AKI caused by?

A

A reduction in renal perfusion.

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8
Q

What is a consequence of untreated pre-renal AKI?

A

Acute tubular necrosis.

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9
Q

What are the causes of reduced renal perfusion?

A

Reduced effective ECF volume, or impaired renal autoregulation.

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10
Q

What can reduce the effective ECF volume?

A

Hypovolaemia from blood or fluid loss. Systemic vasodilation from sepsis, cirrhosis, or anaphylaxis. Cardiac failure from LV dysfunction, valve disease, or tamponade.

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11
Q

What can cause impaired renal autoregulation?

A

Preglomerular vasoconstriction from sepsis, hypercalcaemia, hepatorenal syndrome, or drugs like NSAIDS. Postglomerular vasodilation from ACE inhibitors, or angiotensin II antagonists.

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12
Q

What does post-renal AKI indicate?

A

An obstruction to urine flow after the urine has left the tubules.

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13
Q

What are the three sites of obstruction that cause post-renal AKI?

A

Ureters (bilateral), bladder, urethra.

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14
Q

What causes obstruction within the lumen that causes post-renal AKI?

A

Calculi stones in renal pelves/urters, neck of bladder, urethra. Blood clots, papillary necrosis, tumour of renal pelvis, ureter, or bladder.

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15
Q

What causes obstruction within the wall that causes post-renal AKI?

A

Congenital - pelviureteric neuromuscular dysfunction, megaureter, neurogenic bladder. Ureteric stricture.

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16
Q

What causes pressure from the outside that causes post-renal AKI?

A

Prostatic hypertrophy, malignancy, aortic aneurysm, diverticulitis, accidental ligation or ureter in surgery.

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17
Q

What are the intrinsic causes of AKI?

A

Acute tubular necrosis, severe acute ischaemia, toxic acute tubular necrosis, glomerular and arteriolar disease, immune disease affecting the glomerulus, acute tubular-interstitial nephritis, inflammation of kidney intersticium.

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18
Q

What causes acute tubular necrosis?

A

Severe acute ischaemia and toxic acute tubular necrosis.

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19
Q

How does severe acute ischaemia cause acute tubular necrosis?

A

Pre-renal causes, the fall in renal perfusion causes necrosis if not treated.

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20
Q

How does toxic acute tubular necrosis cause acute tubular necrosis?

A

Nephrotoxins (endogenous or exogenous) damage the epithelial cells lining the tubules, and cause cell death and shedding into the lumen.

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21
Q

What are some nephrotoxic drugs?

A

Gentamicin, ACE inhibitors, angiotensin receptor blockers, NSAIDs.

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22
Q

How are NSAIDs nephrotoxic?

A

Prostaglandins normally cause vasodilation of the afferent arterioles in renal autoregulation. NSAIDs inhibit cyclooxygenase (COX) so prostaglandin production is inhibited too. There is unopposed vasoconstriction of afferent arterioles so reduced glomerular perfusion pressure and AKI.

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23
Q

What is acute glomerulonephritis simply?

A

An immune disease affecting the glomerulus.

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24
Q

What is primary acute glomerulonephritis?

A

Disease that only affects the kidneys.

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25
Q

What is secondary acute glomerulonephritis?

A

Kidneys are involved as part of systemic process, systemic lupus erythematosus, vasculitis.

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26
Q

What is acute tubulo-interstitial nephritis?

A

Inflammation of the kidney interstitium.

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27
Q

What causes acute tubulointerstital nephritis?

A

Infection like acute pyelonephritis (ascending bacterial infection), or toxin induced from nephrotoxic drugs.

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28
Q

What are the features of cardiac failure that can be identified with overloading kidneys?

A

Gallop rhythm, raised BP, raised JVP, pulmonary oedema (basal crackles and dyspnoea), peripheral oedema (sacral, ankle).

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29
Q

What are the signs indicative of sepsis in AKI investigation?

A

Pyrexia (hot) and rigors (feel shivery with raised temperature), vasodilation causing warm peripheral, bounding pulse, rapid capillary refill, hypotension.

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30
Q

What are the signs indicative of urinary tract obstruction in AKI investigation?

A

Anuria, single functioning kidney, history of renal stones, prostatism or previous pelvis/abdominal surgery, palpable bladder, pelvic/abdominal masses, enlarged prostate.

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31
Q

What are the serum biochemistry results of urea and creatinine in AKI?

A

Raised urea and raised creatinine.

32
Q

What are the serum biochemistry finding of potassium, sodium, calcium, and phosphate levels in AKI?

A

Hyperkalaemia, hyponatraemia, hypocalcaemia, and hyperphosphataemia.

33
Q

What are the ECG changes in hyperkalaemia?

A

Tall T waves, small/absent P waves, increased PR interval, widened QRS complex, sine wave pattern, asystole.

34
Q

What does dipstick testing show in AKI?

A

Blood, protein, and leucocytes.

35
Q

How do dipstick tests vary with the cause of AKI?

A

Positive proteinuria and haematuria if caused by glomerulonephritis, negative if from pre-renal or ATN.

36
Q

What are the microscopy findings of pre-renal AKI?

A

Hyaline casts - aggregations of protein seen in concentration urine.

37
Q

What are the microscopy findings of acute tubular necrosis?

A

Muddy brown casts.

38
Q

What are the microscopy findings of rapidly progressive glomerulonephritis?

A

Red blood cell casts.

39
Q

What are the results of soluble immunological tests with AKI?

A

Circulating antibodies: anti-nuclear antibody raised in systemic lupus erythematosus, anti-neutrophil cytoplasmic antibody raised in systemic vasculitis, anti-glomerular basement membrane antibodies raised in Goodpasture’s disease.

40
Q

What are the findings of ultrasound scanning in AKI?

A

Renal size change, hydronephritis, presence of obstruction.

41
Q

What are the findings of chest X ray in AKI?

A

Pulmonary oedema.

42
Q

When are biopsies used in AKI?

A

When pre-renal and post-renal AKI have been ruled out and a confident diagnosis of ATN can’t be made or systemic inflammatory symptoms or signs are present.

43
Q

What is the treatment of pre-renal failure AKI?

A

Volume correction, so fluids are administered to correct hypovolaemia or diuretics given in heart failure.

44
Q

What is the treatment of post-renal failure AKI?

A

Urological intervention to re-establish urine flow.

45
Q

What is the treatment of acute tubular necrosis?

A

Supportive treatment, aim to maintain good kidney perfusion and avoid nephrotoxins.

46
Q

When is dialysis initiated?

A

When kidneys can no longer adequately excrete sale, water, and potassium.

47
Q

How is asymptomatic glomerular disease detected?

A

Incidentally by dipstick urinalysis.

48
Q

How is asymptomatic glomerular disease investigated?

A

Cystoscopy and renal biopsy (not mandatory).

49
Q

What is microscopic haematuria caused by?

A

Renal stones or tumours, arteriovenous malformations, glomerular disease.

50
Q

What is macroscopic haematuria caused by?

A

Non-nephrotic proteinuria.

51
Q

What is the quality of episodic macroscopic haematuria associated wit glomerular disease?

A

Often brown or smoking in colour rather than red. Clots are usual.

52
Q

What are some causes of macroscopic haematuria?

A

Glomerular disease, haemoglobinuria, myoglobinuria, and consumption of food dyes.

53
Q

What is the most common glomerular cause of macroscopic haematuria?

A

IgA nephropathy.

54
Q

What is nephrotic syndrome?

A

A non-specific disorder, where the kidneys are damaged, leaking a large amount of protein into the urine.

55
Q

What is the classic triad of findings in nephrotic syndrome?

A

Proteinuria, hypoalbuminaemia, oedema.

56
Q

How is a renal biopsy taken?

A

Using an ultrasound-guided needle which is aimed at the bottom of the kidney to take a piece of the cortex (not medullar where there is no glomeruli).

57
Q

What are the causes of nephrotic syndrome?

A

Minimal change glomerulonephritis, focal segmental glomerulosclerosis, membranous glomerulonephritis.

58
Q

What is nephritic syndrome?

A

A collection of signs and symptoms associated with disorders affecting the kidneys, characterised by having small pores in the podocytes of the glomerulus large enough to permit proteins and red blood cells.

59
Q

What are the characteristics of nephritic syndrome?

A

Rapid onset, oliguria, hypertension, generalised oedema, haematuria with smoky brown urine, normal serum albumin, variable renal impairment, urine contains protein and red blood cell casts.

60
Q

How does the onset of nephrotic and nephritic syndrome differ?

A

Nephrotic is insidious, nephritic is abrupt.

61
Q

How do nephrotic and nephritic syndrome differ in terms of oedema?

A

Very very present in nephrotic syndrome, less so, but still present, in nephritic syndrome.

62
Q

How do nephrotic and nephritic syndrome differ in terms of blood pressure?

A

Nephrotic syndrome doesn’t affect blood pressure, but it is raised in nephritic blood pressure.

63
Q

How do nephrotic and nephritic syndrome differ in terms of JVP?

A

Nephrotic has normal or lowered JVP, nephritic has raised JVP.

64
Q

How do nephrotic and nephritic syndrome differ in terms of proteinuria?

A

Very severe in nephrotic syndrome, less so, but still present, in nephritic syndrome.

65
Q

How do nephrotic and nephritic syndrome differ in terms of haematuria?

A

Nephrotic syndrome may or may not have haematuria, nephritic syndrome has sever haematuria.

66
Q

How do nephrotic and nephritic syndrome differ in terms of red cell casts?

A

Absent in nephrotic syndrome, present in nephritic.

67
Q

How do nephrotic and nephritic syndrome differ in terms of serum albumin?

A

Decreased in nephrotic syndrome, normal or slightly decreased in nephritic.

68
Q

What is rapidly progressive glomerulonephritis?

A

A clinical situation in which glomerular injury is so sever that renal function deteriorates over days.

69
Q

How may a patient with rapidly progressive glomerulonephritis present?

A

As a uraemic emergency with evidence of extrarenal disease.

70
Q

What is rapidly progressive glomerulonephritis associated with?

A

Crescentic glomerulonephritis.

71
Q

What is needed to diagnose rapidly progressive glomerulonephritis?

A

A renal biopsy.

72
Q

What is the course of many forms of glomerulonephritis?

A

Slowly progressive renal impairment, including hypertension, dipstick abnormalities, and uraemic syndrome.

73
Q

What is the associated kidney appearance of glomerulonephritis?

A

Small, smooth, shrunken kidneys.

74
Q

Why are renal biopsies not performed with chronic renal failure?

A

They are hazardous without providing diagnostic material.

75
Q

What are the symptoms of chronic renal failure?

A

Tiredness and lethargy, breathlessness, nauseas and vomiting, aches and pains, sleep reversal, nocturia, restless legs, itching, chest pains, seizures and coma.

11. Urinary (12 decks)

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