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MBChB > Nephrology > Flashcards

Nephrology Flashcards

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1
Q

Give some secondary causes of glomerulonephritis

A 
Haematological: myeloma, CLL
Gastro: ALD, IBD, coeliac disease
Resp: bronchiectasis, lung cancer, TB 
Infectious disease: hepatitis, HIV, malaria, Abx
Rheum: SLE, RA, amyloid
Drugs: bisphosphonates, NSAIDs, heroin
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2
Q

What is key to the clinical diagnosis of GN?

A

Kidney biopsy (need 10-12 glomeruli)

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3
Q

Describe Rapidly Progressing Glomerulonephritis (RPGN)

A

Crescenteric damage
Rapid increase in sCr over days
Aggressive - progresses to ESRF in 80-90% without treatment

Causes:
ANCA vasculitis
Goodpastures Syndrome (anti-GBM)
Lupus nephritis
Infection associated (strept/staph) - happens weeks after infection
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4
Q

Describe nephritic syndrome

A

Haematuria and proteinuria
High BP, raising sCR
Associated with IgA, SLE, post-infective

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5
Q

Describe nephrotic syndrome

A

Proteinuria (PCR >300 or >3.5g/d of protein)
Low serum albumin (<30)
Oedema
(+hyperlipidaemia)

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6
Q

What is the most common primary glomerular disease?

A

IgA nephropathy

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7
Q

Describe IgA nephropathy

A

Most common primary glomerular disease
May be secondary due to coeliac disease/cirrhosis
May be precipitated by an infection - synpharyngitic (strept. infection + blood in urine at same time)
Abnormal/overproduction of IgA –> proliferation of mesangial cells

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8
Q

What are the effects of IgA nephropathy?

A

Haematuria
HTN
Proteinuria (varies with prognosis)

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9
Q

How is IgA nephropathy managed?

A

ACEi (reduce permeability of GBM)

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10
Q

How many people with IgA nephropathy will develop ESRF?

A

1/3

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11
Q

Describe Membranous Glomerulonephritis

A

A disease of adults - effects podocytes
Presents with nephrotic syndrome
10% secondary to malignancy, drugs

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12
Q

What Auto-Ab is associated with membranous glomerulonephritis?

A

Anti-phospholipase A2 receptor Ab (70%)

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13
Q

What is the history of membranous glomerulonephritis like?

A

1/3 will spontaneously remit in 12-18 months
1/3 will progress onto ESRF in 1-2 years
1/3 will have persistent proteinuria with maintained eGFR

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14
Q

Describe the management of membranous glomerulonephritis

A

Treat underlying condition
ACEi, statins, diuretics, salt restriction
Cyclosporin, ritixumab, alkylating agents (cyclosphosphamide), steroids

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15
Q

Describe minimal change disease

A

The commonest GN in children (90% <10y)
Generally idiopathic but may be due to malignancy ie lymphoma
Presents with nephrotic syndrome

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16
Q

What changes are seen on:
A) light microscopy
B) electron microscopy
in minimal change disease?

A

A) no changes on light microscopy

B) foot process fusion on electron microscopy

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17
Q

How is minimal change disease treated?

A

High dose steroids

50% will relapse

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18
Q

Give some functions of the kidney

A 
Metabolic waste excretion - urea, creatinine
Endocrine functions - Vit D, EPO, PTH
Drug metabolism/excretion
Control of solutes/fluid balance
BP control
Acid/base balance
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19
Q

Describe the Glomerular Filtration Barrier

A

Negatively charged - no protein in filtrate

Large molecules are maintained within capillaries

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20
Q

What is the normal amount of protein in the urine?

A

<150mg/24 hours

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21
Q

What type of protein is detected by urine dipsticks?

A

Albumin

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22
Q

Define renal clearance

A

(Urine concentration of substance x urine volume) / plasma concentration of substance

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23
Q

How else can renal clearance be known as?

A

Glomerular Filtration Rate

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24
Q

When calculating eGFR, what parameters are taken into context?

A

Age
Gender
Race
Plasma creatinine

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25
What is the unit for eGFR?
ml/min/1.73m^3
26
What things need to be taken into consideration when assessing a patient's eGFR?
Assumes stable renal function - not useful for AKI Can lose up to 50% renal function because eGFR starts to deteriorate Useful for drug dosing
27
How does eGFR correspond to staging of CKD?
``` >/= 90% + abnormality = stage 1 60-89 + abnormality = stage 2 30-59 = stage 3 (moderate impairment) 15-29 = stage 4 (severe impairment) <15 = stage 5 (advanced renal failure) ```
28
What is the mechanism of inheritance for adult polycystic kidney disease?
Autosomal dominant
29
What gene mutations are involved in adult polycystic kidney disease?
``` PKD 1 (chromosome 16) - 85% PKD 2 (chromosome 4) - 15% ```
30
What do PDK 1 and 2 genes encode?
Polycystin 1 & 2 Membrane protein involved in calcium regulation Present in renal tubular epithelia (+ liver and pancreas) Overexprssed in cyst cells
31
What is the natural history of adult polycystic kidney disease?
Cysts enlarge Kidney volume increases Some compensation initially eGFR starts to fall --> ~10y later kidneys fail
32
If a person has a FHx of adult polycystic kidney disease, how should they be investigated to see if they also have it?
Renal US at 21 Repeat at 30 if normal Age 15-30: 2 unilateral/bilateral cysts Age 30-59: 2 cysts in each kidney Age >60: 4 cysts in each kidney
33
If a person doesn't have a FHx of adult polycystic kidney disease, what is diagnostic for the condition?
>10 cysts in each kidney Renal enlargement Liver cyst
34
What are some of the clinical consequences associated with adult polycystic kidney disease?
50% risk of ESRD by 50 Cyst accidents - rupture, bleeding, infection ``` Other: HTN Intracranial aneurysm Aortic incompetence Mitral valve prolapse Colonic diverticular disease Liver/pancreatic cysts Hernia ```
35
Describe the management of adult polycystic kidney disease
``` Supportive Early detection and management of HTN Treat complications Manage extra-renal associations Renal replacement therapy ```
36
Describe Von Hippel Lindau Syndrome
Autosomal dominant | Multiple benign and malignant tumours
37
Describe Autosomal Recessive PKD
Affects children | Results in hepatic fibrosis
38
Describe Tuberous Sclerosis
Autosomal dominant Multiple benign tumours - brain, heart, eyes, kidney, skin Epilepsy and learning difficulties
39
Describe Medullary Cystic Disease
Autosomal dominant Cysts in medulla Small to normal sized kidneys Gout
40
Describe Alpert's Syndrome
Usually X-linked Second most common cause of inherited kidney disease Collagen 4 abnormality (Alpha 3/4/5 gene mutation) Deafness and renal failure (deafness first) Microscopic haematuria, proteinuria, ESRF
41
Describe Fabry's Disease
X-linked storage disorder Alpha galactosidase A deficiency resulting in accumulation of Gb3 in the glomeruli (podocytes) Proteinuria + ESRF (+neuropathy + cardiac and skin features)
42
Describe the diagnosis of Fabry's Disease
Alpha-Gal A activity in leucocytes | Renal biopsy - inclusion bodies of G3b
43
How is Fabry's Disease managed?
Enzyme replacement therapy
44
Describe the pathophysiology of diabetic nephropathy
``` Hyperglycaemia Volume expansion Intraglomerular hypertension Hyperfiltration (initially serum Cr decreases, so eGFR looks to improve) Proteinuria HTN + renal failure ```
45
How long does it take for diabetic nephropathy to occur following the development of diabetes?
Approximately 20 years
46
How should diabetic nephropathy be managed?
Tight glycemic control Good BP control - ACEi/ARB SGLT2 inhibitors
47
Describe renal artery stenosis
Stenosis of renal artery --> not enough blood supply to kidney --> kidney becomes fibrotic and shrinks down
48
What can cause progressive narrowing of the renal artery?
Atheroma
49
What happens if the renal perfusion has fallen to >20%?
GFR falls | Tissue oxygenation of cortex and medulla is maintained
50
What happens if the renal perfusion has fallen to >70%?
Cortical hypoxia --> microvascular damage and activation of inflammatory and oxidative pathways Parenchymal inflammation and fibrosis --> becomes irreversible Restoration of blood flow does not provide any benefit
51
Describe the management of renal artery stenosis
Good BP control (not with ACEi/ARB) Statin Good glycemic control if diabetic Smoking cessation, increased exercise, reduce NaCl intake Angioplasty
52
What are the indications for angioplasty in renal artery stenosis?
Rapidly deteriorating renal function Uncontrolled HTN on multiple agents Flash pulmonary oedema
53
Describe amyloidosis
Deposition of highly stable insoluble proteinous material in the extracellular space
54
What stain can be used to identify amyloid, and what will it stain?
Congo Red Stain | Apple green birefringence
55
What are the two types of amyloid?
AA amyloid: inflammation/infection | AL amyloid: immunoglobulin fragments - myeloma
56
How should amyloidosis be treated?
AA amyloid: treat underlying inflammatory/infection | AL amyloid: treat underlying haematological malignancy
57
In SLE, what can autoantibodies be directed against?
DNA Histones snRNPs Transcriptional/translational machinery
58
Describe lupus nephritis
Auto-antibodies against dsDNA or nucleosomes Form intravascular immune complexes or attach to GBM Activates complement Renal damage
59
How should lupus nephritis be managed?
Renal biopsy to confirm diagnosis + stage | Immunosuppression - steroids, retuximab, cyclophosphamide
60
Define Acute Kidney Injury
Decline of renal excretory function over hours/days which is recognised by an increase in serum urea and creatinine
61
What are the three classifications of AKI?
Pre-renal: circulatory failure Renal: the cells of the kidney Post-renal: obstruction
62
Give some pre-renal causes of AKI
``` Hypotension Hypovolaemia Hypoxic Hypoperfusion Sepsis Drugs/toxins ```
63
Give some causes of post-renal AKI
``` Obstruction: Calculi Tumours Lymph nodes Prostate ```
64
Give some causes of renal AKI
Acute tubular necrosis GN Rhabdomyolysis Gentamicin
65
Describe acute tubular necrosis
``` Usually reversible Under-perfusion of tubules and/or direct toxicity Hypotension Sepsis Toxins ```
66
Give some endogenous toxins that can cause acute tubular necrosis
``` Myoglobin Haemoglobin Immunoglobin Calcium Urate ```
67
Give some exogenous toxins that can cause acute tubular necrosis
Drugs: ACEi, NSAIDs, gentamicin Contrast Poisons: metals, antifreeze
68
How does ACEi exacerbate AKI?
Inhibits production of ACE | Don't get efferent arteriole constriction
69
How do NSAIDs exacerbate AKI?
Inhibits production of prostaglandins | Don't get afferent arteriole dilation
70
What two drugs should always be stopped in a patient with AKI?
ACEi | NSAIDs
71
Describe the investigations required in a patient with suspected AKI
Bloods: urea, creatinine, potassium Urine output Clinical assessment: BP, JVP, oedema, heart sounds
72
Describe the initial treatment of a patient with AKI
Treat hyperkalaemia Treat pulmonary oedema Remove cause - NSAIDs, ACEi, sepsis Exclude obstruction (renal US), and consider renal causes
73
What are some components of a GN screen?
ANCA ANA Immunoglobulins Bence-Jones proteins
74
How should hyperkalaemia be managed?
Reduce reabsorption of K from gut - calcium resonium Calcium gluconate - stabilises cardiac membrane Insulin+dextrose - moves K into cells
75
What are the absolute indications of RRT in a patient with AKI?
Refractory K >/= 6.5mmol/L | Refractory pulmonary oedema
76
What are the relative indications of RRT in a patient with AKI?
Acidosis pH<7.1 Uraemia esp if urea >40 Pericarditis, endocarditis Toxins (lithium)
77
Define CKD
Kidney damage or GFR >60ml/min/1.73m^3 for >3 months
78
Describe stable CKD
eGFR is not changing
79
Describe unstable CKD
eGFR is changing
80
What can cause a protein result of +1 on dipstick?
Fever, exercise, normal
81
How can proteinuria be quantified?
Comparing [protein] to [creatinine]
82
What is a normal ACR result?
<2.5
83
What is a normal PCR result?
<20
84
How does ACR relate to PCR?
ACR is around 2/3 of PCR result
85
Give some symptoms of CKD
``` Pruritis Nausea, anorexia, weight loss Fatigue Leg swelling Breathlessness Nocturia Joint/bone pain Confusion ```
86
Give some signs of CKD
``` Peripheral and pulmonary oedema Pericardial rub Rash/excoriation HTN Tachypnoea Cachexia Pallor/lemon yellow tinge ```
87
How can the progression of CKD be slowed down?
``` Aggressive BP control with ACEi and ARB Good glycemic control Diet Smoking cessation Lowering cholesterol - statins Treating acidosis ```
88
When is anaemia common in CKD?
When eGFR <30ml/min/1.73m^3
89
What should be replaced first if a patient with CKD has anaemia?
Folate, B12, iron
90
What is the target Hb in a patient with CKD?
100-120g/l
91
What phosphate binders can be used in secondary hyperparathyroidism?
Calcium: calcium carbonate/acetate | Non-calcium: aluminium
92
What is the target phosphate concentration in a patient with secondary hyperparathyroidism?
0.9-1.5mmol/L
93
If a patient has hyperparathyroidism secondary to CKD, what vitamin D replacement should they be given?
Alfacalcidol

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