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Renal > RenalKidney Disease > Flashcards

RenalKidney Disease Flashcards

1
Q

what is Acute tubular necrosis

A
  • damage and death of the epithelial cells of the renal tubules due to ischaemia or toxins
  • most common cause of acute kidney injury
  • epithelial cells can regenerate
  • 7-21 days to recover.
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2
Q

Symptoms of Acute tubular necrosis

A
  • Oligouria/anuria
  • Hypotension
  • Tachycardia
  • Poor oral intake and anorexia
  • malaise
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3
Q

Causes of Acute tubular necrosis

A
  • Low renal perfusion
  • major surgery
  • exposure to nephrotoxins/radio contrast
  • underlying renal disease
  • infection
  • Muscle trauma
  • cardiac arrest/mechanical ventilaation
  • DM
  • multiple myeloma
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4
Q

What U&E results would you expect to see in acute tubular necrosis

A
  • raised creatnine
  • raised urea
  • hyperkalaemia
  • Urea:createnine ratio 10:1
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5
Q

What would you see on a VBG for acute tubular necrosis

A

Metabolic acidosis

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6
Q

What urinary results would you expect to see in acute tubular necrosis

A
  • Elevated urine sodium level
  • Urine osmolality <450
  • epithelial cell/muddy brown casts
  • urinary myoglobin elevated
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7
Q

Management of acute tubular necrosis

A
  • Supportive care:
  • stop nephrotoxic agents
  • correct hypovolaemia
  • If severe, renal replacement therapy
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8
Q

Complications of acute tubular necrosis

A
  • hyperkalaemia
  • metabolic acidosis
  • anaemia
  • end stage renal disease
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9
Q

What is cranial diabetes insipidus

A

deficiency of antidiuretic hormone

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10
Q

What is nephrogenic diabetes insipidus

A

Insensitivity to anti-diuretic hormone

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11
Q

Causes of Cranial Diabetes insipidus

A
  • Idiopathic
  • Post head injury
  • Pituitary surgery
  • Craniopharyngiomas
  • Haemochromatosis
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12
Q

Causes of nephrogenic diabetes insipidus

A
  • genetic
  • electrolytes: hypercalcaemia, hypokalaemia
  • Drugs: demecocylcine, lithium
    Tubulointerstitial disease: obstruction, sickle cell, pyelonephritis
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13
Q

Symptoms of Diabetes Insipidus

A
  • Polyuria
  • extreme polydipsia
  • nocturia
  • symptoms of hypernatraemia
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14
Q

Symptoms of hypernatraemia

A
  • Irritability
  • Restlessness
  • Lethargy
  • Spasticity
  • Hyper-reflexia
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15
Q

What would you expect to see in serum and urinary osmolality in diabetes insipidus

A
  • Urine <300 (>700 excludes diabetes insipidus)

- Serum normal or elevated

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16
Q

What would you expect to see in U&Es in diabetes insipidus

A

Normal or elevated

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17
Q

Would you see urinary glucose on dipstick in diabetes insipidus

A

no - serum glucose would also be normal

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18
Q

What is the desmoporessin stimulation test

A

Distinguishes between cranial and nephrogenic diabetes insipidus

Patients are given desmopressin 2 micrograms subcutaneously, and serum osmolality, urine osmolality, and urine volumes are measured hourly over the next 4 hours.

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19
Q

In the desmopression stimulation test, what would you expect to see in cranial diabetes insipidus

A

> 50% increase in urine osmolality following desmopressin

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20
Q

In the desmopression stimulation test, what would you expect to see in nephrogenic diabetes insipidus

A

no or <50% increase in urine osmolality following desmopressin

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21
Q

Differentials of Diabetes insipidus

A
  • psychogenic polydipsia
  • chronic DM
  • Hyperosmolar hyperglycaemic state
  • diuretics
  • hypercalcaemia
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22
Q

Management of cranial diabetes insipidus

A

desmopression

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23
Q

Management of nephrogenic diabetes insipidus

A
  • Drink freely in response to thirst
  • Treat underlying cause
  • sodium restriction or hydrochlorothiazide or indometacin
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24
Q

AKI criteria

A
  • Rise in createnine of >26 in 24 hours
  • . 50% rise in createnine over 7 days
  • Fall in urine output to less than 0.5ml/kg/hour for more than 6 hours
  • 25% + fall in eGFR in 7 days
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25
Q

Risk factor for AKIs

A
  1. Emergency surgery
  2. intraperitoneal surgery
  3. CKD if eGFR <60
  4. Diabetes
  5. HF
  6. age >65
  7. liver disease
  8. Use of nephrotoxic drugs
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26
Q

when to refer an AKI to a nephrologist

A
  1. Renal tranplant
  2. ITU patient with unknown cause
  3. Vasculitis/ glomerulonephritis/ tubulointerstitial nephritis/ myeloma
  4. AKI with no known cause
  5. Inadequate response to treatment
  6. Complications of AKI
  7. Stage 3 AKI (see guideline for details)
  8. CKD stage 4 or 5
  9. Qualify for renal replacement
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27
Q

Indications for dialysis

A

hyperkalaemia
metabolic acidosis
complications of uraemia
fluid overload (pulmonary oedema)

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28
Q

Pre-renal causes of AKI

A
  • hypovolaemia: D&V, sepsis, dehydration

- Renal artery stenosis

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29
Q

Intrinsic causes of AKI

A
  • glomerulonephritis
  • acute tubular necrosis (ATN)
  • acute interstitial nephritis (AIN), respectively
  • rhabdomyolysis
  • tumour lysis syndrome
  • Drugs; NSAIDs, contrast
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30
Q

Post-renal causes of AKI

A
  • kidney stone in ureter or bladder
  • benign prostatic hyperplasia
  • external compression of the ureter
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31
Q

Investigation for AKI

A
  • U&Es
  • urinalysis
  • Renal USS if no cause can be identified
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32
Q

Drugs that should be stopped in AKI

A
  • NSAIDs
  • Aminoglycosides
  • ACE inhibitors
  • Angiotensin II receptor antagonists
  • Diuretics
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33
Q

Drugs that may have to be stopped in AKI

A
  • increased risk of toxicity (but doesn’t usually worsen AKI itself)
    • Metformin
    • Lithium
    • Digoxin
34
Q

Management of hyperkalaemia

A
  • calcium gluconate
  • IV insulin + dextrose
  • nebulised salbutamol
  • Calcium resonium (orally or enema)
  • Loop diuretics
  • Dialysis
35
Q

What causes visible haematuria shortly following URTI

A

IgA nephropathy - Bergers

36
Q

what causes (haematuria) and proteinurea 1-2w following an URTI

A

post-streptococcal glomerulonephritis

37
Q

What is the most common nephrotic syndrome in a child

A

Minimal change disease

38
Q

Features of minimal change disease

A
  • nephrotic syndrome
  • normotension - hypertension is rare
  • highly selective proteinuria*
  • renal biopsy: electron microscopy shows fusion of podocyte
39
Q

Management of minimal change disease

A
  • steroids (80%)
  • If steroid refractory - renal biopsy
  • cylophosphamide
40
Q

Prognosis of minimal change disease

A
  • 1/3 have just one episode
  • 1/3 have infrequent relapses
  • 1/3 have frequent relapses which stop before adulthood
41
Q

What are the complications of nephrotic syndrome

A
  • Infection: immunoglobulin loss
  • VTE:antithrombin III and plasminogen in the urine.
  • hyperlipidaemia
  • hypocalcaemia`: vitamin D and binding protein lost in urine
  • acute renal failure
42
Q

What are common causes of CKD

A
  • diabetic nephropathy
  • chronic glomerulonephritis
  • chronic pyelonephritis
  • hypertension
  • adult polycystic kidney disease
43
Q

What are you most likely to die of on dialysis

A

Ischaemic heart disease

44
Q

What are the acute complications of AKI

A
  • hyperkalaemia
  • acidosis
  • pulmonary oedema
  • bleeding
45
Q

When to refer an AKI to a nephrologist

A
  • Uraemic complications
  • CKD 4/5
  • If you’re ? intrinsic renal disease
  • Progressive renal failure - Cr>300 or increase >100
  • Severe metabolic acidaemia <7.2
  • pulmonary oedema
  • Refractory hyperkalaemia >6.5
46
Q

Management of AKI

A
  • stop nephrotoxic drugs
  • Monitor createnine
  • ? K/Na restriction
  • Treat udnerlying cayse
47
Q

Which toxins can cause acute tubular necrosis

A 
Radiology contrast dye
Gentamycin
NSAIDs
Lithium
Heroin
48
Q

What is interstitial nephritis

A
  • inflammation of the space between cells and tubules (the interstitium) within the kidney
  • different to glomerulonephritis, where there is inflammation around the glomerulus
49
Q

What are the main types of interstitial nephritis

A
  • acute interstitial nephritis

- chronic tubulointerstitial nephritis.

50
Q

What is acute interstitial nephritis a result of

A
  • presents with acute kidney injury and hypertension
  • acute inflammation of the tubules and interstitium
  • usually caused by a hypersensitivity reaction
51
Q

In acute interstitial nephritis, what is the hypersensitivity reaction usually in response to

A

Drugs (e.g. NSAIDS or antibiotics)

Infection

52
Q

As acute interstitial nephritis is often a hypersensitivity, what other features may you see

A

Rash
Fever
Eosinophilia

53
Q

What is the management of acute interstitial nephritis

A
  • treating the underlying cause

- Steroids: reduce inflammation & improve recovery.

54
Q

What is Chronic Tubulointerstitial Nephritis

A
  • chronic inflammation of the tubules and interstitium
  • Presents as CKD
  • underlying autoimmune, infectious, iatrogenic and granulomatous disease causes.
55
Q

What is the management of Chronic Tubulointerstitial Nephritis

A

treat underlying cause

steroids guided by a specialist

56
Q

What is nephritis

A

Very non-specific term that refers to inflammation of the kidneys

57
Q

What is Nephritic syndrome or acute nephritic syndrome

A
  • Group of symptoms, NOT a diagnosis

- Patients fit a clinical picture of inflammation of the kidneys

58
Q

What are the common features that fit a nephritis syndrome

A
  • Haematuria: microscopic or macroscopic
  • Oliguria
  • Proteinuria: nephritic syndrome <3g / 24 hours. Any more –> nephrotic syndrome.
  • Fluid retention
59
Q

what is oligouria

A

significantly reduced urine output.

60
Q

What is nephrotic syndrome

A
  • refers to a group of symptoms without specifying the underlying cause
61
Q

What criteria must be met to call symptoms nephrotic syndrome

A
  • Peripheral oedema
  • Proteinuria more than 3g / 24 hours
  • Serum albumin less than 25g / L
  • Hypercholesterolaemia
62
Q

What is Glomeruloscelrosis

A
  • Process of scar tissue formation in the glomerulus

- NOT a diagnosis in itself

63
Q

What causes glomerulosclerosis

A
  • Any type of glomerulonephritis
  • obstructive uropathy
  • focal segmental glomerulosclerosis.
64
Q

How are most types of glomerulonephritis treated

A
  • Immunosuppression (e.g. steroids)

- Blood pressure control by blocking renin-angiotensin system (i.e. ACEi or ARBs)

65
Q

What does nephrotic syndrome predispose patients to

A
  • thrombosis
  • hypertension
  • high cholesterol.
66
Q

What is the most common cause of nephrotic syndrome in children

A

Minimal change disease:

  • Idiopathic (no identified cause)
  • Treated successfully with steroids
67
Q

What is the most common cause of nephrotic syndrome in adults

A

focal segmental glomerulosclerosis

68
Q

What is IgA nephropathy (AKA Berger’s disease)

A

Most common cause of primary glomerulonephritis (not caused by another disease)
Peak age at presentation is in the 20s

69
Q

What are the key features of IgA nephropathy (AKA Berger’s disease)

A
  • Painless haematuria, usually following URTI (or gastroenteritis)
  • Proteinurea: <2-3 g/day
70
Q

What might you see on urine microscopy and culture in IgA nephropathy (AKA Berger’s disease)

A
  • dysmorphic erythrocytes
  • rarely red cell casts
  • no bacterial growth
71
Q

What is Membranous glomerulonephritis

A
  • Most common type of glomerulonephritis overall
  • bimodal peak in age in the 20s and 60s.
  • The majority (~70%) are idiopathic
  • Can be secondary to malignancy, rheumatoid disorders and drugs (e.g. NSAIDS)
72
Q

What do you see on histology of membranous glomerulonephritis

A

“IgG and complement deposits on the basement membrane”

73
Q

What do you see on histology of IgA nephropathy (AKA Berger’s disease)

A

“IgA deposits and glomerular mesangial proliferation”

74
Q

What is Post streptococcal glomerulonephritis (AKA diffuse proliferative glomerulonephritis)

A
  • 1-3 weeks after a streptococcal infection (e.g. tonsillitis or impetigo)
  • They develop a nephritic syndrome
  • There is usually a full recovery
75
Q

What is goodpastures syndrome

A
  • Anti-GBM (glomerular basement membrane) antibodies attack glomerulus and pulmonary basement membranes. This causes glomerulonephritis and pulmonary haemorrhage.
76
Q

What is the presentation of goodpastures disasee

A
  • AKI
  • Haemoptysis
  • Oedema
  • Oligourea
  • SOB
  • Cough
  • Fever
  • Nausea
  • crackles on lungs
77
Q

What investigations should you complete if suspecting Goodpastures disease

A
  • U&Es
  • Renal biopsy
  • Anti-glomerular basement membrane anti-body titre
  • ANCA: Anti-neutrophil cytoplasmic antibodies
  • Serum complement (C3 & C4)
  • Clotting screen prior to renal biopsy
78
Q

Why do we do serum complement (C3 & C4) in renal disease

A

Necessary to rule out nephritic syndrome related to lupus, infection, endocarditis, or cryoglobulinaemia

79
Q

What may you see on renal biopsy in goodpastures disease

A
  • crescentic glomerulonephritis

- linear IgG staining on immunofluorescence

80
Q

What is Rapidly progressive glomerulonephritis

A

Histology shows “crescentic glomerulonephritis”
It presents with a very acute illness with sick patients but it responds well to treatment
Often secondary to Goodpasture syndrome

81
Q

What is the management of crescentic glomerulonephritis?

A

Without treatment, the disease progresses to end-stage kidney disease within a few months. Prednisolone and cyclophosphamide are generally effective in patients before severe renal damage occurs.

Renal (4 decks)

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