Renal Flashcards
(296 cards)
1
Q
A 5-year-old boy presents with a short history of facial oedema that has now progressed to total body swelling involving the face, abdomen, scrotum, and feet. Other symptoms include nausea, vomiting, and abdominal pain. The parents report that the child had a viral illness with fever a few days before the development of the swelling. On examination, he has facial oedema, ascites, scrotal oedema, and pitting oedema of both legs up to the knees.
A
minimal change nephropathy
2
Q
A 42-year-old white man with no previous medical history presents to his primary care physician with progressively increasing oedema of both lower extremities. There is no family history of renal failure. The patient has pitting pedal oedema. Urinalysis reveals marked proteinuria (3+).
A
FSGS
3
Q
A 48-year-old man presents to his family doctor with a recent lower-extremity swelling that is gradually worsening. Over the last few weeks, he has also noticed puffiness under his eyes. A urinalysis demonstrates significant proteinuria, and a 24-hour urine collection confirms proteinuria of 12 g. He has no history of diabetes, macroscopic haematuria, or hypertension.
A
membranous nephropathy
4
Q
A 50-year-old man with a 15-year history of type 2 diabetes presents with oedema, fatigue, and impaired sensation in the lower extremities. He is found to have proteinuria, a reduced eGFR, anaemia, background diabetic retinopathy, and peripheral neuropathy
A
diabetic nephropathy
5
Q
A 23-year-old white man with an unremarkable past medical history presents to the clinic for a routine physical examination including a urine analysis required for his job. This shows invisible haematuria and mild proteinuria. The physical examination reveals no significant abnormal findings
A
IgA nephropathy, berger’s
6
Q
A 41-year-old woman is discharged from hospital following a diagnosis of community-acquired pneumonia, to be managed at home on amoxicillin. A day later she returns to the emergency department with a low-grade fever, widespread erythematous rash and pain throughout her joints and lower back, with her initial bloods showing a significantly elevated creatinine.
A
AIN
7
Q
A 20-year-old woman presents with a 5-day history of painless light brown coloured urine. She has experienced 3 episodes of this over the 5 days. There is no dyspareunia, urgency or pain elsewhere. As of now, she is afebrile though she alludes to being ill with a respiratory infection around three weeks ago.
A
post strep GN
8
Q
A concerned mother attends your GP surgery with her 7-year-old son. She is very concerned as she reports that ‘there is blood in his urine.’ Urine dipstick is ++++ for blood with no leukocytes, nitrates or protein. The boy reports that he first noticed the haematuria this morning. Physical examination is unremarkable, with normal heart and lung sounds and a soft non-tender abdomen. He is afebrile and does not have any symptoms of a urinary tract infection. His past medical history is unremarkable but his mother reports that he recently had a cold 2 days prior and has had several colds over the past year.
A
IgA nephropathy
9
Q
5 causes of nephrotic syndrome
A
primary glomerular disease
- minimal change
- FSGS
- membranous nephropathy
systemic
- diabetes
- amyloidosis
10
Q
nephritic syndrome causes
A
- post-strep glomerulonephritis
small vessel vasculitis
anti GBM disease
iga nephropathy
11
Q
causes of crescenteric nephritis or RPGN
A
- SVV small vessel vasculitis
- SLE
- anti GBM good pasture’s
- aggressive phase of other inflammatory nephritis
12
Q
acute intersitial nephritis causes AIN
A
Allergic
- drug
- autoimmune
Infective
-Toxic- noxious
13
Q
chronic interstitial nephritis causes
A
- AIN where the cause continues
- in assoc. with glomerulonephritis
- allergic/ immune- sarcoidosis, autoimmune-sjorgen
- infective
- toxic Ig light chains, heavy metals, Li
- development/ congenital - reflex nephropathy and renal dysplasias
- inhertied- metabolic, nephrocalcinosis
- ischaemia/ papillary necrosis- sickle cell, analgesic nephropathy
14
Q
haematuria causes
A
UTI stones tumours prostate gland disease -glomerulonephritis schistosomiasis
- not haematuria
- menstruation
- dyes in food
- transient haematuria from strenuous exercise
- if on warfarin more likely to get more significant
15
Q
signs of glomerulonephritis
A
haematuria proteinuria one of blood pressure oedema
16
Q
visible haematuria management
A
-exclude menstruation/ UTI
check BP, renal function
refer to urology for USS/ CT renal tracts/ cystoscopy
17
Q
persistent non visible haematuria diagnosis
A
need 2 out of 3 positive dipsticks
exclude menstruation and UTI
18
Q
persistent non visible haematuria and normal renal function and BP but over 40
A
refer to urology
19
Q
persistent non visible haematuria and normal renal function and BP but under 40 and symptomatic
A
refer to urology
20
Q
persistent non visisble haematuria and normal renal function and BP but under 40 and not symptomatic
A
keep under observation
-annual urinalysis and renal function and BP check
21
Q
persistent non visible haematuria and abnormal renal function and BP
A
refer to renal
22
Q
persistent non visible haematuria and fhx of renal disease or evidence of systemic disease
A
refer to renal
23
Q
inx options for haematuria
A
-hx
-urinalysis
-urine culture
-urine microscopy
BP
-renal function
-urine ACR
all patients >40 and persistent non visible haematuria get cystoscopy and imaging along with visible haematuria patients
24
Q
who to send to renal for haematuria
A
- hx of fhx of renal disease
- evidence of systemic disease
- abnormal BP or renal function
25
what is loin pain haematuria syndrome
-name given to the syndrome in which people suffer loin or flank pain and have blood in their urine, in whom no other cause is found
26
types of oedema
-localised
| generalised- ascites, pleural effusion, facial - can with increased severity be in the genitalia and abdomen
27
inx for oedema
hx and exam
urinalysis
bloods- labumin
28
4 mechanisms of oedema
increased ECF
increased hydrostatic pressure
increased capillary permeability
lowered oncotic pressure
29
what can cause increased ECF
- sodium retention by kidneys renal failure
- heart failure
- nephrotic syndrome- low albumin
- liver failure
30
signs of general increased in hydrostatic pressure
-venous pressure is high in heart or renal failure
raised JVP
nephrotic syndrome - except get a normal JVP as intravascualr deplete
31
signs of local increased in hydrostatic pressure and cause
-venous pressure will be raised by DVT or venous insufficiency or by extrinsic obstruction such as pregnancy or tumour
-non pitting localised oedema- lymphoedema
also some infections, malignancy and radiation
32
causes of increased capillary permeability
infection
sepsis
protein leaks into the interstuitium which reduces the oncotic pressure gradient so draws fluid out
33
lowered oncotic pressure of blood
- low serum albumin due to reduced synthesis or increased loss
- assoc. with avid sodium retention by the kidneys
- liver failure is reduced synthesis
- nephrotic syndrome- increased loss of proteins
- malnutrition reduced synthesis
hold onto fluid
34
management of oedema
diuretics
salt and fluid restriction depending
compression
35
unilateral leg oedema suggests
a mechanical problem
36
oedema with hyponatraemia suggest
whole body sodium is increased but water is increased more - hypervolaemic hyponatraemia so needs restriction of water and salt but caution diuretics
37
proteinuria what does it signify
renal disease
| -protein in the urine always comes from the kidney
38
three main causes of proteinuria
-glomerular disease
increased protein production
low reabsorption at proximal tubule
39
main causes of proteinuria
- nephrotic syndrome
- glomerular disease -glomerulonephritis, diabetes
- CKD
- autoimmune- lupus, goodpasture
- urine infection
- systemic- congestive heart failure, eclampsia
- dehydration
- htn
40
less important causes of proteinuria
-fever
strenuous exercise
absent in the morning but occurs in the later in the day-orthostatic proteinuria
occurs only during a urine infection
41
inx proteinuria
-dipstick urine
42
indication for further inx of proteinuria
-proteinuria >100
haematuria- think glomerulonephritis
-raised serum creatnine/ low eGFR
-HTN
-symptoms of systemic disease eg vasculitis such as rash, arthralgia
-previous hx or fhx suggesting significant renal disease
43
further inx for proteinuria
quantify proteinuria creatinine
urine albumin creatinine ratio
uss of kidneys
consider referral renal biopsy
44
what is assoc, to proteinuria
cardiovascular disease
45
quantification of proteinuria inx
-PCR or ACR urine
46
what is normal protein loss in urine
about 0.3g/day
| but virtually no albumin
47
management of low level proteinuria
-absence of heavy proteinuria <1g day, haematuria, HTN, renal function, symptoms: monitor urine test and renal function at 6 month intervals
>1g consider renal biopsy
see flow chart
48
voiding symptoms
```
persistent dribbling
intermittent stream
straining
hesitancy
poor flow
bladder outflow obstruction
double voiding
```
49
storage symptoms
frequency
urgency
nocturia
incontinence
50
end stage renal failure symptoms
```
-thirst
twitching
pallor
fatigue
nausea
vomiting
bone pain
breathlessness
pigmentation
coma
confusion
```
51
causes of haematuria
-cysts
-tumours
-vascular malofrmations
-glomerular disease
0interstitial disease
-infection
-cancer
-stones
-trauma
-clotting disorders
-excerise
malnutrition
52
def of oliguria
<400
53
anuria def
<100
54
causes of oliguria/ anuria
urinary obstruction eg prostate, tumour, stone
lack of renal perfusion- aortic dissection
RPGN
55
AKI stage 1 is
creatinine >1.5-1.9
| urine <0.5 for >6 hours
56
AKI stage 2
creatinine 2-2.9
| urine <0.5 for 12 hours
57
AKI stage 3
>3 creatinine
| urine <0.3 for 24 hrs or anuric 12 hours
58
how do NSAIDs act at as predisposing drugs to AKI
NSAIDS inhibit prostaglandin production which inhibits the dilatation of the afferent arteriole
which is aimed at increasing glomerular pressure
59
how do ACEi act as predisposing drugs to AKI
ACEi inhibit angiotensin II production which prevents constriction of the efferent arteriole
which is aimed at increasing glomerular pressure
60
causes of AKI
usually multifactorial
-dehydration- SEVERE hypovolaemia
pre-existing renal damage
predisposing drugs
overall get decreased glomerular pressure that is required for proper filtration
61
predisposing drugs to AKI
```
-ACEi
NSAID
aminoglycosides
diuretics
IV contrast
```
62
classification of AKI
-pre-renal
renal
post-renal
63
pre renal causes for AKI
- circulation- systemic and local (RAS)
- bp
- cardiac ouput
- sepsis
- fluid balance reduced
- reduced arterial circualtion
- intrarenal microcirculation
- blood loss
- dehydration
- vascular occlusion
64
inx for AKI
1. renal u and e
2, urinalysis
3. renal USS
65
INX findings for pre-renal AKI
urine osmolality increases
sodium urine decreases- hold onto sodium
serum urea: creatinine increases
66
intrinisc renal AKI causes
- ATN acute tubular necrosis-prolonged pre-renal
- inflammation: glomerulonephritis, interstitial nephritis, pyelonephritis
- vascular- renal vein thrombosis, cholesterol emboli, renal infarction, malignant hypertension, recent angiography
67
Acute tubular necrosis pathology
-get an injury to the tubule which leads later to necrosis of the tubule and fibrosis
68
intrinisic renal AKI inx findings
urine osmolality decreased
| urine sodium increased- loose sodium
69
post-renal AKI causes
- neurological
- stones, crystals blocking
- kidneys, bladder
70
approach to the patient with oliguria
1. is it real- check bladder recordings?
2. check circulation
3. fluid balance
4. drug chart
5. previous result and hx
6. uss and dipstick
71
elevated creatinine diff dx
1. aki
2. ckd
3. aki on background of ckd
72
KDIGO criteria for AKI 3
1. increase in serum creatinine by >26.5 micromol within 48 hours
2. increase in serum creatinine by >1.5 x baseline within the prior seven days
4. urine volume <0.5ml/kg for >6 hours
73
what suggest a dx of AKI rather than CKD
1. normal kidney size on USS
2. normal haemoglobin (RBC half life 120 days so wont be acute presentation)
3. normal PTH (also takes time to develop)
if in doubt assume AKI and inx promptly
74
pre renal AKI clinical features
-hypotensive, tachycardic, poor peripheral perfusion, delayed CRT, postural hypotension
75
management of pre-renal AKI
-fluid resus will work providing tubules intact
76
acute tubular necrosis causes
- when hypotension is very severe or prolonged, ATN may develop due to ischaemic injury
- prolonged pre-renal goes onto develop ATN
which is when urinary sodium begins to increase and osmolality decrease as can no longer absorb sodium and water back through tubules
also toxic causes
- drugs- aminoglycosides, cisplatin, tenofovir, methotrexate, iodinated contrast
- rhabdomyolysis
- myeloma light chains
- crystals
77
management of ATN
- fluid resuscitiation aggressive and early
| - once ATN has developed fluid resus alone will not be enough as kidney tubules take time to regenerate
78
mortality ATN
50% due to assoc. organ failure
79
Anti GBM immunofluorescence presentation
ribbon pattern
80
immune complex deposition disease presentation
| immunofluorescence
granular or starry sky pattern
81
vasculitis immunofluorescence presentation
negative
82
causes of RPGN
-vasculitis
anti GBM
post-infectious glomerulonephritis
83
post renal AKI causes
-obstruction
to flow in renal tract- NEEDS TO BE BILATERAL
-Most likely benign prostatic hypertrophy
-also tumours, external compression
84
presentaton of post-renal AKI
-anuria
or
-polyuria
85
systematic approach to patient with AKI
1. is the AKI renal- check renal function
2. could it be pre-renal failure
- access circualtory state eg BP,JVP, mucous membranes, check fluid balance, check medications eg any new medications
3. could it be post-renal
-bladder palpable?
-person at high risk eg male >60, hx of bladder cancer, loin pain, visible haematuria
order USS scan
4. could it be an intrinsic renal cause
Toxic ATN
AIN-eosinophilic count and leucocytes
glomerulonephritis- blood and protein
86
management of established AKI
-drug chart stop nephrotoxic drugs
-fluids
control intake of fluid, resus, match sodium loss, no potassium initially
-hyperkalaemia management
-acidosis give sodium bicarb if pH<7
-diet: low protein and phosphate
-prevent infection
-consider PPI reduce risk Upper GI bleeds
-treat obstruction if needed
others
-dialysis
87
what drugs need stopping in AKI
-NSAID
-AceI
-AMINOGLYCOSIDES
-ARB
diuretics
metformin
lithium
digoxin
88
indications in AKI for dialysis8
1. dangerous hyperkalaemia
2. pulmonary oedema
3. severe symptoms or complications
4. poor biochemical results and unlikely to recover function quickly
5. pericarditis
6. neurological signs eg uraemic encephalopathy
7. need for high fluid intake eg for nutrition during oliguria
8. to enable nutrition
89
dialysis of choice for AKI
haemodialysis
90
why is there a polyuric phase after AKI
-excess electrolytes and fluid retained during AKI but also because the tubules are recovering from injury so are less responsive to ADH/ ang so dont appropriately retain salt and water
91
management of after AKI Fluid
-rough guide is to ensure total fluid is equal to urinary volume from the day before
unless signs of overload
may also need to supplement bicarb, potassium
92
prognosis of AKI after
1. full recover
2. acute on chronic disease
3. AKI to ESRD
93
what do people with AKI die of 4
1. hyperkalaemia
2. pulmonary oedema
3. uraemia
4. infection
94
long term risks of aki
- recover often incomplete
- long term increased risk of ESRF
- poor outcomes are more likely with increasing severity and duration of the insult
95
biopsy sign of ATN
vacuolation
96
rf for aki
chronic kidney disease
other organ failure/chronic disease e.g. heart failure, liver disease, diabetes mellitus
history of acute kidney injury
use of drugs with nephrotoxic potential (e.g. NSAIDs, aminoglycosides, ACE inhibitors, angiotensin II receptor antagonists [ARBs] and diuretics) within the past week
use of iodinated contrast agents within the past week
age 65 years or over
97
CKD stages
```
1 >90
2 60-90
3 30-60
4 15-30
5 <15
```
98
eGFR variables
```
cage
Creatinine
age
gender
ethnicity
```
99
dx of CKD
eGFR of <60 on at least 2 occasions 90 days apart
abnormalities of kidney function or structure present for more than 3 months
irereversible deterioration of renal function
100
main causes of CKD
```
diabetes mellitus
interstitial disease
glomerular disease
hypertension
systemic inflammatory disease
renovascular disease
cogenital and inherited
unknown
```
101
clinical features CKD
```
<15 gfr
-tired
breathless
renal anaemia
pruuritus
anorexia
weight loss
n and v
```
102
risk factors for developing ESRD
```
-severity
proteinuria
haematuria
high BP
young age
```
103
inx
```
blood tests
urinalysis and proteinuria
ACR
HEPATitis testing
renal USS
CT/ MRI angiography
```
104
referral CKD to nephrologist
- eGFR <30
- rapid deterioration >25% from past yr
- significant proteinuria unless known to be due to diabetes ACR >70
- ACR >30 with non visible haemturia
- HTN that remains poorly controlled despite 4 medications
- suspicion of renal involvement in multisystem disease
105
AKI def
1.5 x baseline 7days
cr 26.5 in 48hrs
0.5 urine for 6hrs ?
106
when to refer to renal unit -immediate
```
suspect acute renal failure
oliguria
obstruction
ARF on CRF
severe new renal failure
```
107
cause ckd 4-5
```
often multifactorial
diabetes and renal artery stenosis
inflammation eg glomerulonephritis
circulatory
obstruction
inherited eg pkd
```
108
management CKD 3
-assess- features, urinalysis, medication, PMH
-monitoring: aim to keep BP <140/90
management of CVD- stain
refer for specialist
-proteinuria
haematuria
rapid deteriorating renal function
young age
fhx of renal failure
poorly controlled HTN
109
CKD managemenet
```
-BP control
<130/80 if albuminuria
ACEi if proteinuria
bicarbonate for acidosis
dietary avoid potassium
salt restriction
avoid high protein diet
```
110
complications of CKD
```
-HTN
potassium
acidosis
anaemia
renal osteodystrophy
CVD risk
malnutrition
```
111
acidosis rx in ckd
sodium bicarb
| avoid too much protein
112
anaemia of ckd is
normochromic normocytic anaemia
make sure from renal and not another cause
113
anaemia pathology CKD
recombinant EPO
IV iron
-definiciency of EPO
decreased response to EPO, toxic effect of uraemia, reduced RBC survival
114
renal osteodystrophy pathology
low vitamin D
high PTH- high phosphate levels stimualte PTH
decreased calcium absortion
osteoclastic bone resporption
115
rx of renal bone disease
phosphate binders eg calcium carbonate
| calcitriol alfacalcidol
116
drugs to stop taking on sick days
```
ACEi
ARB
NSAID
diuretics
metformin
```
117
indications for dialysis
```
fluid overload- acute pulmonary oedema
hyperkalaemia
uraemia-encephalopathy
metabolic acidosis
bleeding diathesis
```
118
ESRD options
conservative treatments
| dialysis
119
types of dialysis
```
hospital haemodialysis
home haemodialysis
peritoneal dialysis
-continuous ambulatory peritoneal
automated peritoneal dialysis
```
120
haemodialysis preparation
-anticoagulation
-vascular access
monitoring
121
SE haemodialysis
```
hypotension
muscle cramps
bacteraemia
hypotension
cardiac arrhythymias
haemorrhage
air embolism
dialyser
pulmonary oedema
sepsis
```
122
types of haemodialysis
haemofiltration-mostly AKI
| haemodiafiltration- haemodialysis and ultrafiltration
123
continuous ambulatory peritoneal dialysis
-4 x 2L fluid exchanges dialy
4-6 hrs with a gap overnight
each bag takes 30-60 minutes
124
automated peritoneal dialysis
overnight 8-9hrs as sleep
125
disadvantages of peritoneal dialysis
```
peritoneal infection
peritonitis
catheter site exit infection
ultrafiltration failure
sclerosing pertinoitis
```
126
contraindication to PD
```
major abdo surgery
peritoneal adhesions
inguinal hernias
severe respiratory compromise
inability to perform the technique safely and hygenically
```
127
sclerosing peritonitis is
major complication of PD usually by staph epidermidis or bowel organism
-abdo pain, fever, cloudy PD
antibiotics needed
128
ESRD definition
implies a level of renal function at which death is likely within weeks or months
symptoms
129
immunosuppression for transplant
triple therapy
1. MMF mycophenalate mofetil or azathioprine
2. tacrolimus or cyclosporine
3. relatively low dose prednisolone
130
risks of immunosuppression therapy for transplant
1. increased SCC risk
2. cardio toxicity
3. renal failure nephrotoxicity
131
rejection from transplant
5 days to 2 weeks
- give high dose steroids
- tubulointerstitial inflammatory infiltrates
132
what is hyper-acute rejection
minutes to hours
due to pre-existing antibodies
HLA type 1 antigens
type II reaction
133
complication of transplant
1. ischaemia reperfusion injury- interruption of blood supply, build up toxicities, organ damage
2. delayed graft function- more common cadaveric so may need dialysis initially - oliguric after transplant
3. technical problems
4. acute rejection
<6 months post-transplant
signs and symptoms of infection
mismatched HLA
rise in creatinine
5. chronic rejection >6 months both antibody and cell mediaated mechanism cause fibrosis or due to recurrence of original disease
6. infections- CMV especially
7. CMV
8. anastomosis damage or infection
9. arterial thrombosis
10. cardiac event at transplantation
immunosuppression risks
134
BK virus transplant
```
also called polyomavirus
only causes problems in transplant
most people who carry it have no symptoms
biopsy
Blood PCR testing
urine cells
attacks transplant
```
balance risk of developing this on immunosuppression
-reduce immunosuppressive drugs
135
AIN causes
allergic
NSAID, PPI, antibiotics-penicillin, allopurinol, furosemide
```
immune-autoimmune
-TINU syndrome-tubulointerstitial nephritis and uveitis
-AIN only
sjorgen syndrome
sarcoidosis
transplant rejection
```
infective
toxic- drugs most common
136
inx for AIN
```
-eosinophilia
leucocytes
drug induced generalised signs of drug hypersensitivity
white cell cast
sterile urine
biopsy shows inflammation
```
137
management AIN
withdrawal of drug
high dose steroids
treat cause
138
chronic interstitial nephritis is
renal dysfunction with firbosis and infiltration of the renal parenchyma by lymphocytes, plasma cells and macrophages
139
cause chronic interstitial nephritis
-persistent AIN
glomerulonephritis
immune
-sarcoidosis, sjorgen ,chronic transplant rejection, SLE
myeloma-bence jones protein -cast nephropathy
posions eg lead poisoning
drugs eg gentamicin, chemo, tenofovir, all drugs from AIN, lithium, ciclosporin, tacrolimus
infection
inherited
-VUR, renal dysplasias, wilson disease, sickle cell
metabolic- hypokalaemia, calcium phosphate crystals
unknown sometimes especially Asian race in UK
140
cast nephropathy causes
-form casts seen in
| loop diuretics, myeloma
141
fanconi syndrome is
renal glycosuria in normal blood sugars
damage to proximal tubules
crystals form in proximal tubules
excess glucose, uric acid,phosphates being excreted
142
signs of CIN
```
HTN
small kidneys
CKD
impaired concentration abilities
sodium and water deplete
```
143
CIN management
supportive
correct acidosis and hyperkalaemia
renal replacement therapy if irreversible renal damage has occurred
144
ATN causes
1. prolonged pre-renal aki
2. severe infection- v.low BP
3. toxicity
4. myeloma
5. crystals
6. rhabdomyolysis
145
nephrotic to nephritis
minimal change
FSGS
Membranous nephropathy
diabetic nephropathy
MCGN
Post strep
vasculitis
GBM
146
nephrotic syndrome triad
heavy proteinuria >3.5g/24hrs
hypoalbuminuria <30g/l
peripheral oedema formation - due to avid sodium and fluid retention by the kidneys
147
cause nephrotic
damage to podocyte or non inflammatory architectyal alterations of the glomerulus
148
minimal change disease
```
normal glomeruli on micoroscopy
can get podocyte foot process effacement
most common cause children
in adults assoc. to NSAID nand hodgkin
high dose steroids
```
149
FSGS focal segmental golmeruli sclerosis
```
focal scarring
idiopathic, HIV, reflux nephropathy, obesity
primary= idiopathic- treat with steroids
secondary- gradual onset, causal, ACEi
variable response to steroids
may progress to renal failure
tends to be younger people
```
150
membranous nephropathy
usually idiopathic, some drugs, rarely malignancy
more common elderly
1/3 progress to renal failure
thickened glomerular capillary walls and basement membrane
basememnt membrane spikes on silver staining
immune complex deposition
often primary in adults and secondary in children
151
amyloidosis
early manifestation often
amyloid protein depositis
more common elderly
152
SLE
usually young women
153
management nephrotic syndrome
diet control salt intake
diuretics often loop
-careful and stop if signs of increasing creatinine or hypovolaemia
```
ACEI
anticoagulation
statin
infection
steroids and PPI
```
154
nephrotic oedema 2 main factors
sodium retention directly by renal
secondary sodium retention in which the low plasma oncotic pressure due to hypoalbuminaemia promotes the movement of fluid from the vascular space into the interstitium
155
complications of nephrotic syndrome
```
susceptibility to infection
increased risk DVT
high cholesterol
hypercoaguability
protein malnutrition
hypovolaemia
AKI
```
156
nephritic syndrome presentation
haematuria- often non visible
hypertension
reduction in renal function
157
pathology nephritic syndrome
inflammation in the glomeruli which damages and disrupts the glomerular basement membrane GBM, allowing red blood cells to enter the urinary space
allows RBC to enter into the urinary space
increased permeability
158
RPGN presentations
1. post strep- ASOT, c3, c4
2. anti GBM
3. small vessel vasculitis - ANCA
4. lupus- ds DNA ANA c3 c4
159
mild glomerulonephritis presentations
1. IgA nephropathy IgA and HSP
2. mesangiocapillary glomerulonephritis MCGN- c3, c4 hiv, hep b, ANA dsDNA
3. Alport syndrome -genetic screening, hearing test
160
RPGN crescenteric nephritis
severe and rapid nephritic syndrome
exhibits many cellular "crescents"
presentation
- non visible haematuria
- severe nephritic syndrome
- acute onset of haematuria, HTN, oedema
- pulmonary haemorrhages good pastures
- systemic features vasculitis
161
main causes of RPGN
post strep
vasculitis
anti GBM
Lupus
162
treatment of RPGN
pulse methylprednisolone then daily oral prednisolone
IV cyclphosphamide or rituximab
plasmapharesis
163
IgA nephropathy
```
common disease
most common worlwide
often slowly evolving over decades
can occur as HSP
IgA deposited in the mesangium of glomeruli
```
164
post- strep GN
```
-10-14 days after strep throat
fluid retention
hypertension
oedema
haematuria
reduced GFR
diffuse proliferation of cells on renal biopsy
```
165
small vessel vasculitis
usually assoc. with antibodies to neutrophil granule enzyme ANCA
other systemic features
-microscopic polyangiitis
wegner disease
if severe can cause crescenteric nephritis
166
MCGN mesangiocapillary glomerulonpehritis
either
| can be caused by persistent infection or other diseases or occur alone
167
IgA presentation
```
-most common asymptomatic
visible haematuria
dark brown urine
discomfort in kidneys
rarely sa nephrotic syndrome
hypertension
young male
occurs with or a few days after resp infection
```
168
diagnosis of IgA nephropathy
hx of passing blood at same time as infection
urinalysis blood
bloods= raised IgA
renal biopsy- immune deposits
169
management of IgA nephropathy
1. ACEi
2. Steroids if haematuria and either renal dysfunction, proteinuria
3. fish oil
4. immunosuppression- cyclophosphamide, cyclosporin -most not needed
5. 1/3 develop CKD and need dialysis and some need transplant
170
prognosis Iga NEPHROPATHY
1/3 devlop chronic kd
171
vasculitis pathology
ANCA antibodies to neutrophil cytoplasmic antigens, granule enzymes such as myeloperoxidase
172
presentation of 2 main small vessel vasculitis
- wegner granulomatosis with polyanggitis-sinusitis
- MPA microscopic polyangiitis -kidney, gut and skin
- HSP; children, abdo pain, rash, haematuria, weakness
173
dx of SVV
ANCA positive
antibodies to myeloperoxidase
biopsy
174
presentation of SVV
systemically unwell
renal
RPGN
pulmonary haemorrhage, rash
175
management of SVV
-cyclophosphamide, steroids and plasma exchange
176
post strep GN
```
asymptoamtic
microscopic haematuria
full blown acute nephritic- headahce, malaise
light brown urine
children
oedema gross haematuria and HTN
usually 1-3 weeks after strep throat
```
177
inx for post-strep GN
```
in children
-urinalysis
serology antibodies
renal function
no biopsy
```
178
biopsy signs of post strep GN
diffuse GN
starry night
neutrophils
deposition of IgG and c2
179
diff dx for post-strep GN
need to consider if lasts beyond 2 weeks
membranoproliferative GN -lasts longer
IgA nephropathy -shorter time interval
180
management post -strep GN
supportive
181
minimal change disease
```
often hx of recent viral illness
oedematous puffy child
facial oedema, abdominal and scrotum
HTN is rare
can have nausea and vomiting
```
182
diagnosis of MCD
dont biopsy in children-trial steroids first
biopsy appears normal on light microscopy
on electron microscopy can see podocyte foot processes
183
causes of MCD
```
-infectious
90% cause unknown
allergic reaction
asoc. to other disease
drugs eg ibuprofen
hodgkin's
```
184
prognosis MCD
1/3 frequent relapse
1/3infrequent relapse
1/3 only one episode
185
management MCD
give high dose of prednisolone
if dont respond
-wrong disease or
-need a combination of treatment
186
relapsing MCD treatment
cylophosphamide 8-12 week course of drug can prevent relapses for many months or years
in patients with frequent relapses
cyclosporin
tacrolimus
187
FSGS pathology
| 2 types
diseases that damage the glomeruli in small areas and leave scarring = secondary FSGS
primary FSGS= occurs without any known reason- idiopathic
188
biopsy of FSGS shows
only some / focal areas of glomeruli show scarring
189
assoc. to primary FSGS
WEST AFRICA
| apoliprotein 1
190
secondary FSGS causes
-presents with more modest proteinuria than primary
1. HUS
2. cholesterol emboli
3. toxins
4. genetic
5. HIV, severe obesity
191
presentation of FSGS
nephrotic
all ages
sometimes responds to steroid treatmnet- not always
kidney function can be abnormal
can cause complete kidney destruction and need dialysis
can come back after transplantation
192
diff dx FSGS
can be mistaken for MCD if biopsy taken of a normal part of glomeruli
193
primary FSGS treatment
steroids
194
secondary FSGS treatment
depends on cause
| ACEI to prevent progression
195
membranous nephropathy pathology
in membranous nephropathy the filtering layer becomes thickened and there is a protein leak into the urine
- attack on the cells within the glomerulus that make the GBM known as podocytes
- most common cause of nephrotic syndrome in caucasian adults
- antibodies attack podocytes
196
causes of membranous nephropathy
-2/3 idiopathic (anti PLA2)
-arthritis lupus
drugs pencillamine, gold, captopril
cancer
infections hepatitis
toxins eg mercury, formaldehyde
197
histology of membranous nephropathy
thickened GBM
subepithelial spikes
PLA2
198
presentation of membranous nephropathy
asymptomatic
proteinuria
peripheral oedema
hypercoaguable state
199
prognosis membranous nephropathy
5-15% remission
30-40% partial remission
25% disease will progress and cause slow loss of function , lead to ESRF
200
factors that increase the chance of loss of kidney function
```
male >50
high proteinuria
kidney biopsy scarring
BP not well controlled
kidney function abnormal at dx
hepatitis - known cause cant be cured
```
201
management membranous nephropathy
```
-monitoring
steroids
-immunosuppressive cyclophosphamide, cyclosporin
bp treatment
diuretics
```
202
mesangiocapillary glomerulonephritis pathology
pattern of injury seen on renal biopsy characterised by an increase in mesangial cellularity with thickening of glomerular capillary walls
203
presentation MCGN
nephrotic or nephritis
204
types of MCGN
```
1st= deposition of IG into glomeruli, assoc. to chronic infections
2nd= deposition of complement into glomeruli , assoc. inherited or acquired abnormalities in complement pathway, dense deposit disease
```
205
treatment of MCGN
immunoglobulin type eg MMF, cyclophosphamide
| complement type eg eculizumab
206
lupus markers
ANA
| anti DS DNA
207
management of Lupus
```
MMF
cyclophosphamide
azathioprine
cytotoxic agents
anti B cell antibodies rituximab
```
208
thiazides side effects
hyponatraemia
hypocalciuria
hypokalaemia
209
action thiazides
inhibit reabsorption of NaCl in tubules
210
loop diuretics action
inhibit reabsorption of NaCL in loop henle
211
spironalactone
aldosterone antagonist
| inhibits sodium potassium exhange
212
SE of loop diuretics
```
hypercalciuria
hyponatraemia
hypokalaemia
hypomagnesia
ototoxic
```
213
Ace inhibitors side effects
```
hypotension
dry cough
rash
hyperkalaemia
renal dysfunction
```
214
calcium channel side effects
constipation in verapamil
| bradycardia
215
drugs to avoid in renal failure
```
ACEi
ARB
gentamicin
nitrofurantoin
NSAID
opiates
heparin LMWH use UFH
vancomycin
```
216
alport syndrome pathology
defect in type 4 collagen
GBM deteriorates with time leading to progressive loss of glomeruli often with deafness
rare
loss of alport protein- autoimmune
217
histology alport
basket weaving
| thick and thin GBM
218
presentation of alport
```
male
renal problems
sensorineural hearing loss
women only get partial symptoms if carriers
x-linked worse in me
```
219
thin GBM disease
often runs in families
benign familial haematuria
thin GBM
some also carry one copy of alport protein gene mutation
220
benign familial haematuria
-inherited cause for blood appearing in urine
| often related to Thin GBM
221
nail patella syndrome
-poorly formed nails
2. patella missing
3. elbows often dont straighten properly
4. iliac horns
5. scolitosis
6. abnormality GBM
7. glaucoma
autosomal dominant
get nephrotic syndrome
LMX1B-collagen
222
good pasture's disease is
an autoimmune condition in which there can be severe inflammation affecting kidneys and lungs
antibodies develop against the a3 chain of type 4 collagen
young patients
223
anti GBM presentation
```
-haematuria
nephritic
renal failure
RPGN can get more severe features
signs of kidney failure
lung haemorrhages
dry cough and minor breathlessness
haemoptysis
```
224
diagnosis anti GBM
early symptoms often vague
biopsy
anti GBM antibodies
check for ANCA
225
management AntiGBM
steroids
cyclphosphamide
plasma exchange
226
DIABETIC NEPHROPATHY
late microvascular complication of diabetes mellitus
typically appears more than 20yrs type 1 dm
most already have diabetic retinopathy and neuropathy
227
phases of diabetic nephropathy
phase1= hyperfiltration
-elevated GFR
hypertension
microalbuminuria
```
phase 2= over diabetic neuropathy
-overt proteinuria
dipstick test positive
BP can start to lose dip at night
GFR starts to go back to normal
```
phase 3= incipient nephropathy
htn
proteinuria
npehortic syndrome
phase 4
progressive renal failure
CKD
228
histo features of diabetic nephropathy
mesangial expansion in glomerulus
slit diaphragm break down and protein leak
kimmelstiel- nodules of matrix
arterio hyalinolysis
229
risk factors diabetic nephropathy
poor diabetic control
duration of diabetes
presence of retinopathy and other microvascular complications
fhx susceptibility to HTN
230
diagnosis of diabetic nephropathy
ACR urine albumin creatinine ratio more sensitive
GFR renal function
if atypical then renal biopsy might be considered aka rapid onset not indicating diabetic nephropathy
231
prevention of diabetic nephropathy
blood sugars control
bp control
ACEI for proteinuria
diet protein restrict
232
management diabetic nephropathy no proteinuria
```
monitoring
aim BP <130/80
hba1c <7
diet advice
stop smoking
```
233
management diabetic nephropathy proteinuria
```
close monitoring
monitor urine protein
aim BP <125/75
further BP drugs
cholesterol
ACEI
```
234
who needs a renal biopsy for diabetic with kidney problems
1. Type 1dm <10 yrs failing kidneys
2. rapid progression proteinuria
3. rapid deterioration renal function
4. absence retinopathy
5. presence severe haematuria
6. additional systemic symptoms such as weight loss
235
polycycstic kidney disease presentation
```
abdominal pain
early satiety
palpable mass
urinary tract infection
haematuria
hypertension
asymptomatic initially
renal failure
```
236
PKD pathology
autosomal dominant inherited
50% with PKD1 progresss to ESRD
PKD2 tends to be milder
237
dx PKD
-USS
cyts not detectable till in 20s
so cant use for screening in teens
can also be hepatic cysts
MRI
berry aneurysm if fhx of them sudden death or high risk job
renal function
can be fairly normal till late stage
238
management pkd
tolvaptan
ADH vasopressin V2 receptor antagonist
slows rate of growth of cyst and GFR loss
risk of dehydration due to polyuria
50% dialysis and renal transplant
239
complications of PKD
1. hepatic cysts= hepatomegaly
2. diverticulosis
3. berry aneurysms- subarachnoid haemorrhages
4. ovarian cysts
5. mitral valve prolapse
6. kidney stones
240
infantile PKD pathology
```
autosomal recessive
rare
different gene
PKHD1 gene fibrocystin
also cysts in liver
pulmonary fibrosis
severe illness
```
241
alport syndrome pathology
```
x-linked young men
recessive
women as carriers get a lesser disease
due to lyonisation get inactivation in some cells
collagen 4 absent or normal
```
242
histology alport
basket weave
243
presentation alport
deafness sensorineural
eye involvement -lenticonus of lens
progressive haematuria, proteinuria then renal failure in teens
244
management alport
acei limit progression
245
renal anaemia is
normochromic normocytic anaemia
| due to deficiency in EPO
246
management of renal anaemia
look for contributing causes- dont assume renal
need to ensure IRON replete before giving EPO
erythropoiesis stimulating agents 2-3 injections a week
IV iron
247
se of EPO treatment
```
HTN
encephalopathy
bone aches
urticaria
pure red cell aplasia- antibodies develop
```
248
haemoglobin target for renal anaemia
100-110
| avoid predisposing to thrombosis
249
renal artery stenosis pathology
arteriosclerosis of renal arteries
reduction in renal perfusion pressure activates the RAS system
increase in angII
vasoconstriction and increased aldosterone so retain sodium
global renal ischaemia leads to shrinkage of kidney
>70% stenosis haemodynamically significant effects
most common cause secondary HTN
250
main cause of RAS in young patients
fibromuscular dysplasia
-uncommon
-hypertrophy of the media which narrows artery
more often women <50
distal main renal artery or the intra-renal branches
251
presentation of RAS
usually HTN
classic but rare presentation is with recurrent episodes of sudden flashing lights
flash pulmonary oedema-usually at night
252
RAS is more likely if
```
severe HTN
asymmetrical kidneys
flash pulmonary oedema
peripheral vascular disease of lower limbs
renal impairment
renal function has deteriorated on ACEi
```
253
inx RAS
```
dipstick
blood- hypokalaemia secondary aldosteronism increased renin
MRI/ CT angiography
USS
RENAL ARTERIOGRAPHY GOLD STANDARD
```
254
Management RAS
-fibromuscular dysplasia patients often resond to balloon dilatation
1st line
-medical therapy
2nd line
interventions
angioplasty - balloon
255
indications for management angioplasty RAS
```
young <40
BP intractable
flash pulmonary oedema
malignant HTN
deteriorating renal function
```
256
what is ischaemic nephropathy
CKD that results from RAS
257
acute renal infarction
sudden occlusion of the renal arteries
loin pain, non visible haematuria
severe HTN
can be caused by thrombosis of a renal artery or thromboemboli from a distant source
258
thrombotic microangiopathy pathology
diseases are assoc. with platelet thromboses in small blood vessels
damage to endothelium
plateelt thromboses in small vessels
259
causes of thrombotic microangiopathy
```
HUS
TTP
DIC
malignancy
systemic sclerosis
PET
```
260
diagnosis
BLood film
- microangiopathic haemolytic anaemia MAHA
- schistocytes= fragments of RBC
blood
raised LDH
elevated unconjugated bilirubin
thrombocytopaenia
261
thrombotic thrombocytopaenia purpura pathology
haematological, CNS and renal pathology
-autoimmune disorder against antibodies to ADAMTS-13
this is involved in regulating platelet aggregation
low serum ADAMTS 13
USUALLY helps to break down vWF larger versions
so get abnormal build up of large vWF
262
presentation of TTP
```
-MAHA
thrombocytopaenia purpura
neurological manifestations
fever
renal disease
AKI
schistocytes on blood film
petechiae
lower abdominal pain
fatigue
typiclaly female
```
263
causes of TTP
```
post infection
pregnancy
drugs- ciclopsorin, OCP, penicillin, clopidogrel
tumours
SLE
HIV
```
264
inx findings for TTP
```
thrombocytopaenia
renal failure
anaemia
schistocytes
direct coomb's test will be negative
low ADAMTS13
```
265
management TTP
plasma exchange therapy and steroids
| capacuzimab
266
HUS haemolytic uraemic syndrome pathology
typical
-blood diarrhoea in children from E.coli toxin
shiga toxin causes endothelial damage which causes platelet activation and clumping
-activates GB3 receptors
-these then destroy red blood cells as they get damaged passing through- MAHA
atypical
-to do with complement dysregulation
chronic disease both children and adult
267
HUS presentation
```
anaemia
thrombocytopaenia
AKI
schistocytes
typical often children with bloody diarrhoea
```
268
other causes of HUS
pneumococcal infection
HIV
SLE
atypical
CTD
Drugs eg quinine, cytotoxic
malignancy
269
management HUS
typical
supportive only
dialysis if severe renal failure
in those with fhx atypical HUS may benefit from complement inhibitors
plasma exchange
ECULIZUMAB for atypical types
270
DIC management
haemostasis
| replace clotting factors
271
cholesterol emboli presentation
```
renal impairment
haematuria
proteinuria
sometimes eosinophilia
vasculitis
can be ischaemic toes
```
272
patient undergoes cardiac arteriiography then gets renal failure
suspect cholesterol emboli
273
myeloma and renal pathology
hypercalcaemia
| free light chains can be toxic to tubular cells and cause cast nephropathy and acute tubular necrosis
274
myeloma and renal presentations
1. cast nephropathy
2. fanconi syndrome- uric and phosphate ... all excreted
3. amyloidosis nephrotic
4. monoclonal immunoglobulin deposition disease
5. hypercalcaemia
275
3 main causes of amyloidosis
1. AL amyloid due to light chains eg from myeloma
2. ALL amyloid due to proteins in chronic infection or inflammation eg rheymatoid
3. diabetes amyloid
276
HIV nephropathy presentation
collapsing FSGS
Proteinuria, nephrotic, progressive renal imapirment
responds to HAART if treated early enough
277
sodium risks
up too fast= cerebral pontine myelinolysis
| low too fast= cerebral oedema
278
hypernatraemia causes
-reduced water intake eg coma, depression
-increased losses -hypovolaemic
increased loss via gut, skin, tract
-iatrogenic salt administration
-diabetes insipidus
279
features hypernatraemia
```
thirst
oliguria
concentrated urine
weakness
nausea
loss of appetitie
reduced cerebral function
```
280
inx findings hypernatraemia
increased plasma urea
281
management hypernatraemia
oral replacement
-water normal
-5% dextrose and .9% saline if severe
5% dextrose if mild
282
hypontaraemia causes
```
euvolaemic
SIADH
primary polydipsia
hypothyroidism
beer potomania
poor diet intake of sodium
```
hypervolaemic
excess water exceeds excess sodium
cardiac liver or renal failure
RAAS
```
hypovolaemic
large electrolyte losses
Addison
diuretic
vomiting
diarrhoea
GI
cerebral salt waste syndrome
```
283
clinical features of hyponatraemia
```
often asympatomatic
acute <48hrs
chronic >48hrs
oedema
confusion
drowsy
n and v
seizure
chovstek and trosseau
```
284
chronic hyponatraemia >48hrs
hypovolaemic give 0.9% saline
euvolaemic: fluid restrict, tolvaptan, vasopressin siadh
hypervolaemic: fluid and salt restrict,
285
acute hyponatraemia <48hrs rx
if also signs of cerebral oedema
| need to restore rapidly using hypertonic sodium chloride 1.8%
286
drugs causing hyponatraemia
```
thiazide
nsaid, antibiotics, PPI
SIADH drugs: antidp, antipsychotics, carbarmazepine, anti cancer, opioids, MDMA
Venlafaxine
MDMA
```
287
hyperkalaemia causes
```
increased intake
tissue breakdown- rhabdomyoloysis
hyperglycaemia and acidosis cause relase
addison
spironalactone
impaired excretion AKI and CKD
drugs
```
288
signs of hyperkalaemia
rare
asymptomatic
progressive muscle weakness
289
ECG changes hyperkalaemia
1. tented t waves
2. loss of p waves
3. wide QRS
4. sine waves
290
treatment hyperkalaemia
1. give IV calcium gluconate to stabilise the membrane
2.IV glucose and insulin
50ml 50% and 5units actrapid
3. salbutamol
4. sodium bicarbonate
5. IV fluids
6. dialysis
7. potassium biding resins -calcium resonium
8. loop diuretics
291
hypokalaemia causes
```
<3.5
loss of potassium from the GI tract eg vomiting
shift into cells eg insulin
endocrine eg hyperaldosteronism
drugs
decreased intake
increased excretion eg cushing
excessive liquorice
RTA
```
292
clinical features low K
asymptomatic
lethargy
muscle weakness
in chronic can get noctyria, polyuria, polydipsia
293
inx
ECG flatten and inversion t waves
| can often seem normal potassium as not measuring intracellular
294
management hypokalaemia
give KCL IV
rich diet
potassium bicarb if acidosis
295
hypercalacaemia ssymptoms
```
stones
bones
throans
psychiatric overtones
moans
```
296
management high calcium
```
IV 0.9% saline
IV bisphosphonates
steroids
calcitonin
calcimimetics
parathyroidectomy
```
