Renal Flashcards

1
Q

What are the 2 main types of dialysis?

A

Haemodialysis
Peritoneal dialysis

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2
Q

What is required for haemodialysis?

A

Dialysis machine (patient’s blood is pumped OUTSIDE body through this machine)

Vascular access is required via an AV fistula (longterm), or a temporary CVC

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3
Q

What happens inside a haemodialysis machine (broadly)?

A

Blood flows through tiny semi-permeable tubes surrounded by a dialysis solution (dialysate)
Filtration occurs via osmosis + diffusion- dialysis fluid contains solutes at a similar level to the level they would be in a healthy patient’s blood
Can add bicarbonate (to combat acidosis), EPO + drugs if needed
Heparin always added

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4
Q

How often should haemodialysis be performed?

A

4h treatment 3x per week

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5
Q

How many weeks does an AV fistula take to mature?

A

6-8w

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6
Q

How does peritoneal dialysis work?

A

Dialysis solution injected into abdo cavity through a permanent catheter.

High dextrose conc. of the solution draws waste products from blood into abdo cavity across the peritoneum.

After several hours of dwell time, the solution is drained, removing waste products from body, + exchanged for new dialysis solution.

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7
Q

What is continuous ambulatory peritoneal dialysis (CAPD)?

A

Patient operated- each exchange 30-40 mins + each dwell time 4-8h.
Patient can do normal activities with dialysis solution inside their abdomen

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8
Q

What is automated peritoneal dialysis (APD)?

A

dialysis machine fills + drains the abdomen while patient is sleeping, performing 3-5 exchanges over 8-10h each night

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9
Q

Give 5 complications of haemodialysis

A

Site infection
Stenosis at site
Bleeding
AV access steal syndrome
Dialysis disequilibrium syndrome

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10
Q

What is Steal syndrome?

A

painful ischemia of the hand secondary to AV fistula or graft shunting blood away from the distal limb

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11
Q

What is Dialysis disequilibrium syndrome?

A

acute cerebral oedema secondary to rapid extraction of osmotically active substances (e.g., urea, NaCl) from the blood

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12
Q

Give 3 advantages of PD

A

Offers more flexibility (can be done overnight
Is better tolerated by patients
Less expensive

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13
Q

What is a Tesio line?

A

Tunneled dual lumen central line
Used as a ‘bridge’ before an AV fistula can be put in
1 lumen enters the right atrium, the other sits outside the RA in the vena cava
Both lumens exit the body

(with a central line, only 1 lumen enters the skin)

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14
Q

Why is a normal vein unsuitable for haemodialysis, and why is an AV fistula used?

A

Normal vein would easily collapse/ thrombose with recurrent venepuncture
Vein in an AV fistula hypertrophies in response to turbulent flow of blood from artery + so can withstand repeated venepuncture

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15
Q

What are the most common causes of AKI?

A

STOP

Sepsis/ dehydration

Toxins (NSAIDs, Nephrotoxic drugs)

Obstruction in the urinary tract

Parenchymal kidney disease

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16
Q

What are the most common causes of CKD?

A

Diabetic nephropathy

HTN

(PKD)

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17
Q

What are the primary functions of the kidney?

A

Salt + water balance

Acid base homeostasis

Endocrine function: vitamin D, EPO, renin-angiotensin system

Excrete waste

Electrolyte homeostasis

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18
Q

What symptoms might you expect from someone in CKD? (7)

A

Anaemia: SOB, fatigue, LoC, headache

Uraemia: encephalopathy, N+V, confusion, pruritis, pericarditis

Fluid overload: pedal oedema, pleural effusion, ascites, tiredness

Hyperkalaemia: palpitations, cardiac arrest, asymptomatic

Acidosis: N+V, tiredness

Increased drug action: opioid side effects

Reduced urine output

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19
Q

List 5 indications for emergency dialysis

A

A – Acidosis

E – Electrolyte imbalance (K+ >6.5, refractory to medical Mx)

I – Intoxication (certain drugs require dialysis to clear the blood)

O – Overload of fluid (refractory to diuretic Tx)

U – Uraemic encephalopathy + pericarditis

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20
Q

What mnemonic can be used for drugs that can be dialysed out?

A

BLAST
Barbiturates
Lithium
Alcohol
Salicylates
Theophylline

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21
Q

What diet should be followed in patients with very low creatinine clearance?

A

Low phosphate
(eg. avoid chocolate, shellfish, nuts)

Low K+ (avoid chocolate, bananas etc)

Fluid restricted (avoid alcohol + too much tea/ coffee)

Low salt (avoid processed foods)

Can take phosphate binders if diet restriction alone doesn’t succeed

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22
Q

Name 1 phosphate binder

A

Sevelamer

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23
Q

How does CKD affect phosphate and vitamin D?

A

1-alpha hydroxylation normally occurs in kidneys → leads to LOW vitamin D

kidneys normally excrete phosphate → leads to HIGH phosphate

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24
Q

What problems arise from high phosphate and low vitamin D in CKD?

A

High phosphate level ‘drags’ calcium from bones→ osteomalacia

Low calcium: due to lack of vitamin D + high phosphate

Secondary hyperparathyroidism: due to low calcium, high phosphate + low vitamin D

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25
Define acute kidney injury
Sudden decrease in GFR manifested by an increase in serum creatinine or oliguria over a period of hours/ weeks
26
What causes should be excluded first in AKI? Why?
Pre renal (hypovolaemia, sepsis) + post renal (stones, cancer) Renal causes require a biopsy
27
How can AKI secondary to blood loss be differentiated into pre-renal and renal cause?
Pre: LOW urinary Na+ (hypovolaemia: kidneys hold on) Renal: HIGH urinary Na+ (ischaemia of tubules: loss)
28
How are intrinsic renal causes of AKI classified?
Glomerulonephritis: MCD, Membranous GN ATN: affects tubules AIN: affects surrounding tissue Vascular: small (microangiopathic- HUS, TTP) or large (obstructive- thrombosis/ emboli)
29
What is nephritic syndrome?
Subtype of intrinsic AKI with BLOOD + PROTEIN in urine indicative of glomerular disease
30
What is nephrotic syndrome?
Proteinuria (>3.5g/ 1.73m^2 body surface area/ 24h) Hypoalbuminaemia (<30g/L) Oedema (+ Hyperlipidaemia)
31
What causes the high level of proteinuria in nephrotic syndrome?
Injury of the podocyte (provides most of the protein filter barrier of the glomerulus)
32
Give 3 primary renal diseases presenting with nephrotic syndrome
Minimal change disease Membranous glomerulonephritis Focal Segmental Glomerular Sclerosis
33
Give 2 systemic causes presenting with nephrotic syndrome
Diabetes Amyloidosis
34
What is chronic kidney disease?
Decrease in GFR present >3 months
35
Which 4 variables are used in the modification of diet in renal disease (MDRD) formula for eGFR?
Creatinine (serum) Age Gender Ethnicity
36
List 3 factors that will affect the MDRD estimation of GFR
Pregnancy Muscle mass (e.g. amputees (lower Cr), body-builders (higher Cr)) Eating red meat 12h prior to the sample being taken
37
What is Proliferative glomerulonephritis characterised by?
Increased no. cells in glomerulus Presents with NEPHRITIC syndrome
38
What is Non-proliferative glomerulonephritis characterised by?
Lack of glomerular cell proliferation Presents with NEPHROTIC syndrome
39
Give 6 causes of proliferative glomerulonephritis
IgA nephropathy Post-infectious glomerulonephritis Membranoproliferative glomerulonephritis Rapidly progressive glomerulonephritis (RPGN) Anti-GBM disease Vasculitic disorders (GPA + microscopic polyangitis)
40
What is IgA nephropathy aka? In which patient group is it usually seen?
Bergers disease Most common form of glomerulonephritis in adults Often young adults
41
How does IgA nephropathy usually present?
Haematuria 24-48h after URTI
42
Mx of IgA nephropathy with isolated hematuria, no/ min. proteinuria (<500-1000 mg/day) and normal GFR
No Tx needed F/U to check renal function
43
Mx of IgA nephropathy with persistent proteinuria (>500-1000 mg/day), and normal/ slightly reduced GFR
ACE inhibitors
44
Mx of IgA nephropathy with active disease (falling GFR) or failure to respond to ACEi
High dose Prednisolone
45
What is the prognosis in IgA nephropathy?
25% develop ESRF within 20-25y
46
What investigations are required for IgA nephropathy?
Renal biopsy (definitive): increased no. mesangial cells Urinalysis: haematuria
47
What is Post-infectious glomerulonephritis most commonly associated with?
Group A beta-haemolytic Streptococcus infection (usually Strep. pyogenes)
48
How does Post-infectious glomerulonephritis usually present?
Gross haematuria Proteinuria + Oedema Oliguria Headache + malaise 1-2w after strep infection
49
What is the pathophysiology of Post-streptococcal glomerulonephritis?
immune complex (IgG, IgM + C3) deposition in the glomeruli.
50
What investigations can be used for Post-streptococcal glomerulonephritis?
anti-streptolysin titre (ASOT). low C3 Biopsy Diffuse proliferative + exudative glomeronephritis EM: subepithelial humps- lumpy complex deposition
51
Mx and prognosis in post-streptococcal glomerulonephritis
Self limiting Good prognosis
52
What is Membranoproliferative glomerulonephritis?
group of immune-mediated disorders characterised by GBM thickening + proliferative changes on light microscopy.
53
Membranoproliferative glomerulonephritis is associated with which 2 diseases
Hepatitis C SLE
54
How can membranoproliferative glomerulonephritis present?
Nephrotic syndrome Haematuria Proteinuria
55
Give 3 typical findings on renal biopsy in membranoproliferative glomerulonephritis
Thickened basement membrane Thickened mesangium “Tram tracking” appearance: electron dense material deposition
56
Mx for membranoproliferative glomerulonephritis
Children (with nephrotic-range proteinuria): corticosteroids Adults: dipyridamole + aspirin Kidney transplantation for patients with ESRF
57
What is Rapidly progressive glomerulonephritis (RPGN) aka?
Crescentic glomerulonephritis
58
What is RPGN?
rapid loss of renal function a/w formation of epithelial crescents in the majority of glomeruli within weeks-months
59
List 4 causes of RPGN
Goodpasture's syndrome Wegener's granulomatosis SLE Microscopic polyarteritis
60
How does RPGN present?
Nephritic syndrome: haematuria with red cell casts, proteinuria, HTN, oliguria Features specific to underlying cause (e.g. haemoptysis with Goodpasture's, vasculitic rash or sinusitis with Wegener's)
61
What is Anti-GBM antibody disease aka?
Goodpasture's syndrome if lungs + kidneys involved
62
What is Goodpasture's syndrome?
small-vessel vasculitis a/w pulmonary haemorrhage + rapidly progressive glomerulonephritis. Caused by anti-GBM antibodies against type IV collagen.
63
Describe epidemiology of Goodpasture's syndrome
M > F 2:1 Bimodal 20-30 + 60-70 HLA DR2 association
64
How does Goodpasture's syndrome usually present?
Pulmonary haemorrhage: Haemoptysis RPGN: rapid onset AKI= nephritis → proteinuria + haematuria
65
What investigations can be used for Goodpasture's syndrome?
Immunohistochemistry: Linear IgG deposits along basement membrane Antibodies: anti-GBM antibodies
66
Mx for Goodpasture's syndrome
Prednisolone Plasmapheresis Cyclophosphamide
67
Give 5 risk factors for pulmonary haemorrhage in Goodpasture's syndrome
Smoking LRTI Pulmonary oedema Inhalation of hydrocarbons Young males
68
What are the small vessel ANCA-associated vasculitides?
Microscopic polyangiitis (MPA) Granulomatosis with polyangiitis (GPA-Wegener’s granulomatosis) Eosinophilic granulomatosis with polyangiitis (EGPA- Churg-Strauss syndrome)
69
What is the pathophysiology of the ANCA associated vasculitides?
Anti-neutrophil cytoplasmic antibodies target myeloperoxidase + proteinase 3
70
What is GPA characterised by?
necrotising vasculitis with granulomas Affects ENT, lungs, kidneys, skin, eyes, nervous system
71
How does GPA present?
FLAW ENT: nasal crusting + discharge, otitis media, sensorineural deafness Pulmonary: cough, dyspnoea, haemoptysis Renal: haematuria, proteinuria, nephritic syndrome
72
Ix for GPA
Biopsy: leukocytoclastic vasculitis with necrotic changes + granulomatous inflammation ANCA serology
73
Mx for GPA
Induction: Methylprednisolone, Prednisolone + Rituximab/ Cyclophosphamide Maintenance: Prednisolone + Rituximab/ Methotrexate