renal Flashcards
(163 cards)
1
Q
NICE criteria for AKI
A
- rise in creatinine of >25micromol/L in 48hrs
- rise in creatinine of >50% in 7 days
- urine output of <0.5ml/kg/hour for >6hrs
2
Q
8 risk factors for AKI
A
- CKD
- HF
- DM
- liver disease
- older age (>65)
- cognitive impairment
- nephrotoxic medications - NSAIDs, ACE-i
- use of contrast medium i.e. CT
3
Q
categories for causes of AKI
A
pre-renal
renal
post-renal
4
Q
3 pre-renal causes of AKI
A
inadequate blood supply:
- dehydration
- hypotension
- heart failure
5
Q
3 renal causes of AKI
A
intrinsic disease:
- glomerulonephritis
- interstitial nephritis
- acute tubular necrosis
6
Q
4 post-renal causes of AKI
A
obstruction to urine outflow:
- kidney stones
- masses (cancers)
- ureter/urethral strictures
- enlarged prostate, prostate cancer
7
Q
investigations in AKI
A
urinalysis
US KUB
8
Q
urinalysis results and what they suggest
A
- leucocytes and nitrites suggest infection
- protein and blood suggest acute nephritis (or infection)
- glucose suggests diabetes
9
Q
treatment of AKI
A
treat underlying cause:
- fluid rehydration (pre-renal)
- stop nephrotoxic meds
- relieve obstruction (post-renal) e.g. insert catheter
10
Q
4 complications of AKI
A
- hyperkalaemia
- fluid overload, heart failure and pulmonary oedema
- metabolic acidosis
- uraemia -> encephalopathy, pericarditis
11
Q
6 causes of CKD
A
- diabetes
- hypertension
- age-related decline
- glomerulonephritis
- polycystic kidney disease
- medications: NSAIDs, PPIs, lithium
12
Q
5 risk factors for CKD
A
- older age
- hypertension
- diabetes
- smoking
- use of medicines which affect kidneys
13
Q
8 signs/symptoms of CKD
A
can be asymptomatic
- pruritis
- loss of appetite
- nausea
- oedema
- muscle cramps
- peripheral neuropathy
- pallor
- hypertension
14
Q
investigations to diagnose CKD
A
U&E - eGFR
measured twice, 3 months apart
15
Q
investigations for CKD
A
- eGFR (U&E)
- urine albumin:creatinine ratio >3mg/mmol
- haematuria (urine dip) 1+
- renal USS
16
Q
staging of CKD
A
G and A scores:
- G score based on eGFR
- A score based on Albumin:creatinine ration
17
Q
G score for CKD
A
G1 - eGFR >90 G2 - eGFR 60-89 G3a - eGFR 45-59 G3b - eGFR 30-44 G4 - eGFR 15-29 G5 - eGFR <15 (end-stage renal failure)
18
Q
A score for CKD
A
A1 - ACR <3mg/mmol
A2 - ACR 3-30mg/mmol
A3 - ACR >30mg/mmol
19
Q
diagnostic criteria for CKD
A
eGFR <60 or proteinuria
20
Q
5 complications of CKD
A
- anaemia
- renal bone disease
- cardiovascular disease
- peripheral neuropathy
- dialysis related problems
21
Q
4 criteria for specialist referral in CKD
A
- eGFR <30
- ACR >70mg/mmol
- accelerated progression: decrease in eGFR of 15 or 25% or 15ml/min in 1 year
- uncontrolled HTN despite 4+ antihypertensives
22
Q
4 main aims of CKD management
A
- slow progression
- reduce risk of CVD
- reduce risk of complications
- treat complications
23
Q
3 management approaches to slow progression of CKD
A
- optimise diabetic control
- optimise HTN control
- treat glomerulonephritis
24
Q
lifestyle modifications to reduce risk of complications from CKD
A
- exercise
- maintain healthy weight
- stop smoking
- dietary advice regarding: phosphate, sodium, potassium and water
25
which medication should be prescribed in CKD to prevent CVD
atorvastatin 20mg
26
4 complications of CKD and associated treatments
1. metabolic acidosis - oral sodium bicarbonate
2. anaemia - iron supplementation and erythropoietin
3. renal bone disease - vitamin D
4. end stage - dialysis or renal transplant
27
HTN treatment in CKD and when given
ACE-i (renoprotective)
- diabetes + ACR >3
- HTN + ACR >30
- anyone with ACR >70
28
aims of HTN tx in CKD
maintain BP <140/90 or <130/80 if ACR >70
29
monitoring necessary in HTN management in CKD
serum potassium
| ACE-i and CKD cause hyperkalaemia
30
pathophysiology of anaemia in CKD
healthy kidney cells produce erythropoietin which stimulates production of RBC
CKD = decreased kidney function = less RBC produced
31
why are blood transfusions not recommended for management of anaemia in CKD
can sensitise immune system (allosensitisation) so transplanted organs are more likely to be rejected
32
management of anaemia in CKD
'anaemia of chronic disease;
1. treat iron deficiency first (IV iron or oral iron)
2. exogenous erythropoietin
33
3 features of renal bone disease
1. osteomalacia (softening of bones)
2. osteoporosis (brittle bones)
3. osteosclerosis (hardening of bones)
34
x-ray changes in renal bone disease
- osteosclerosis (hardening) of both ends of vertebra = denser white appearance
- osteomalacia (softening) in centre of vertebra = less white appearance
35
pathophysiology of renal bone disease
- reduced phosphate excretion => high serum phosphate
- low active vit D => reduced calcium absorption from intestines and kidneys
- secondary hyperparathyroidism (PT glands react to low calcium and high phosphate by excreting more PTH) => increased osteoclast activity
36
why does osteomalacia occur in renal bone disease
increased turnover of bones without adequate calcium supply
37
why does osteosclerosis occur in renal bone disease
osteoblasts respond by increasing activity to match osteoclasts (due to secondary hyperparathyroidism)
new tissue is not properly mineralized due to low calcium
38
management of renal bone disease
- active forms of vitamin D (alfacalcidol, calcitriol)
- low phosphate diet
- bisphosphonates to treat osteoporosis
39
5 indications for acute dialysis and mnemonic
AEIOU
- Acidosis (severe, not responding to tx)
- Electrolyte abnormalities (severe and unresponsive hyperkalaemia)
- Intoxication (overdose of certain meds)
- Oedema (severe and unresponsive pulmonary oedema)
- Uraemia symptoms (seizure, reduced consciousness)
40
indications for long term dialysis
- end stage renal failure (CKD stage 5)
| - acute indications continuing long term
41
3 main options for long-term dialysis
1. continuous ambulatory peritoneal dialysis
2. automated peritoneal dialysis
3. haemodialysis
42
what is peritoneal dialysis
special dialysis solution added to the peritoneal cavity. ultrafiltration from blood to dialysis solution occurs through the peritoneal membrane (natural filtration membrane). leftover fluid with waste products filtered from blood then removed and clean dialysis fluid replaced and process repeats.
43
types of peritoneal dialysis
1. continuous ambulatory peritoneal dialysis
- dialysis solution in peritoneum at all times
- different regimes e.g. 2L fluid inserted and changed 4x day
2. automated dialysis
- dialysis occurs overnight
- machine continuously replaces fluid overnight, takes 8-10hrs
44
5 complications of peritoneal dialysis
1. bacterial peritonitis - infusion of glucose solution predisposes to bacterial growth
2. peritoneal sclerosis
3. ultrafiltration failure - starts to absorb dextrose in solution making filtration gradient less effective
4. weight gain - absorb carbohydrates in solution
5. psychosocial effect
45
what is haemodialysis
patients have blood filtered by haemodialysis machine e.g. 4hrs a day 3x week
need good access to blood supply
46
types of vascular access for haemodialysis
1. tunnelled cuffed catheter
| 2. AV fistula
47
what is a tunnelled cuffed catheter for dialysis
- tube inserted into subclavian or jugular vein with tip sitting in SVA or RA
- 2 lumens (enter/exit)
- Dacron cuff ring surrounding catheter promotes healing and adhesion to make more permanent and protect against infection
48
what is an AV fistula
- artificial connection between an artery and a vein
- bypasses capillary system allowing high pressure blood from artery into vein
- permanent, large, easy access to blood supply
49
3 typical sites for AV fistula (vessels)
- radio-cephalic
- brachio-cephalic
- brachio-basilic
50
complications of tunnelled cuffed catheter in haemodialysis
infection
| blood clots
51
time-frame for AV fistulas from formation to usage
requires surgical operation
| 4 week - 4 month maturation (needs to be made in advance of when dialysis is required)
52
signs to look for with AV fistula on examination
- skin integrity
- aneurysms
- palpable thrill
- stereotypical 'machinery murmur' on auscultation
53
6 complications of AV fistula
1. aneurysm
2. infection
3. thrombosis
4. stenosis
5. STEAL syndrome
6. high output heart failure
54
what is STEAL syndrome
inadequate blood supply to limb distal of AV fistula - fistula 'STEALs' blood from distal limb causing distal ischaemia
55
how does AV fistula cause high output cardiac failure
blood flows very quickly from arterial to venous system
rapid return of blood to the heart which increases pre-load to the heart which leads to hypertrophy of heart muscle and heart failure
56
how are patients and donors matched for kidney transplant
based on human leucocyte antigen (HLA) type A, B and C on chromosome 6
57
kidney transplant procedure
patients own kidneys left in place
donor kidneys blood vessels connected with patients pelvic vessels (external iliac)
donor ureter anastomosed directly with patients bladder
donor kidney placed anterior in abdomen and can be palpated in iliac fossa
58
typical scar for kidney transplant
'hockey stick scar'
59
immunosuppressant regime after kidney transplant
tacrolimus
mycophenolate
prednisolone
can also use: cyclosporine, sirolimus, azathioprine
60
transplant-related complications from kidney transplant
- transplant rejection
- transplant failure
- electrolyte imbalance
61
immunosuppressant-related complications from kidney transplant
- ischaemic heart disease
- T2DM
- infection risk
- unusual infections: PCP, PJP, CMV, TB
- non-Hodgkin lymphoma
- skin cancer (SCC)
62
definition of nephritis
generic term: inflammation of the kidneys
| not a diagnosis
63
what is nephritic syndrome
group of symptoms not a diagnosis
fit a clinical picture of having kidney inflammation
does not give diagnosis or underlying cause
64
features of nephritic syndrome
- haematuria (microscopic or macroscopic)
- oliguria (reduced UO)
- proteinuria (<3g in 24hrs)
- fluid retention
65
criteria for nephrotic syndrome
1. peripheral oedema
2. proteinuria >3g in 24hrs
3. serum albumin <25g/L
4. hypercholesterolaemia
66
what is glomerulonephritis
umbrella term for conditions which cause inflammation of or around glomerulus and nephron
many conditions described as glomerulonephritis
67
definition of interstitial nephritis
inflammation of the space between cells and tubules (interstitium) within the kidney
68
specific diagnoses within interstitial nephritis
1. acute interstitial nephritis
| 2. chronic tubulointerstitial nephritis
69
definition of glomerulosclerosis
pathological process of scarring of tissue in glomerulus
| not a diagnosis itself
70
causes of glomerulosclerosis
- any type of glomerulonephritis
- obstructive uropathy (blockage of urine outflow)
- focal segmental glomerulosclerosis
71
8 types of glomerulonephritis
1. minimal change disease
2. focal segmental glomerulosclerosis
3. membranous glomerulonephritis
4. IgA nephropathy (mesangioproliferative glomerulonephritis, Berger's disease)
5. post-strep glomerulonephritis
6. mesangiocapillary glomerulonephritis
7. rapidly progressive glomerulonephritis
8. Goodpasture syndrome
72
basic treatment approach for most types of glomerulonephritis
immunosuppression (steroids)
| blood pressure control by inhibiting RAS: ACE-i or ARBs
73
common presentation of nephrotic syndrome
oedema
| may notice frothy urine (proteinuria)
74
most common cause of nephrotic syndrome in children vs adults
```
children = minimal change disease
adults = focal segmental glomerulosclerosis
```
75
complications of nephrotic syndrome
predisposes you to:
- thrombosis
- HTN
- high cholesterol
76
histology of IgA nephropathy (Berger's)
IgA deposits and glomerular mesangial proliferation
77
what is meant by primary glomerulonephritis and what i the most common cause
```
not caused by another disease
IgA nephropathy (Berger's)
```
78
peak age of presentation of IgA nephropathy (Berger's)
20s
79
which is the overall most common cause of glomerulonephritis
membranous glomerulonephritis
80
peak age of presentation of membranous glomerulonephritis
20s and 60s (2 peaks)
81
histology of membranous glomerulonephritis
IgG and complement deposits on basement membrane
82
aetiology of membranous glomerulonephritis
```
70% idiopathic
secondary to:
- malignancy
- rheumatoid disorders
- drugs e.g. NSAIDs
```
83
presentation of post-strep glomerulonephritis
<30yo
- presents 1-3 weeks after strep infection e.g. tonsillitis, impetigo
- nephritic syndrome (haematuria, oliguria)
84
pathophysiology of Goodpasture syndrome
anti-GBM (glomerular basement membrane) antibodies attack glomerulus and pulmonary basement membranes
causes glomerulonephritis and pulmonary haemorrhage
85
example presentation of Goodpasture syndrome
patient presenting with acute kidney failure and haemoptysis
(antibodies attack glomerular and pulmonary basement membranes)
86
histology of rapidly progressive glomerulonephritis
crescentic glomerulonephritis
87
presentation of rapidly progressive glomerulonephritis
very acute illness and sick patients but responds well to tx (immunosuppression)
88
aetiology of rapidly progressive glomerulonephritis
often secondary to Goodpasture syndrome
89
6 medications which are usually safe to continue in AKI
1. paracetamol
2. warfarin
3. statins
4. aspirin (75mg OD)
5. clopidogrel
6. beta-blockers
90
5 medications which should be stopped in AKI
1. NSAIDs (except aspirin if 75mg OD)
2. aminoglycosides
3. ACE-i
4. ARBs
5. diuretics
91
3 medications which may need to be stopped in AKI as increased risk of toxicity
1. metformin
2. lithium
3. digoxin
92
what is the most common cause of glomerular pathology and CKD in the UK
diabetic nephropathy
93
pathophysiology of diabetic nephropathy
chronic high glucose levels passing through glomerulus causes scarring = glomerulosclerosis
94
features of diabetic nephropathy
- glomerulosclerosis
| - proteinuria (damage to glomerulus allowing protein to be filtered)
95
management of diabetic nephropathy
optimizing blood sugar and blood pressure
| ACE-i tx of choice - should be started in diabetic nephropathy even with normal BP
96
presentation of acute interstitial nephritis
- AKI
- HTN
- hypersensitivity features: rash, fever, eosinophilia
97
aetiology of acute interstitial nephritis
hypersensitivity reaction to drugs (NSAIDs, abx) or infection
presents with hypersensitivity features: rash, fever, eosinophilia
98
treatment of acute interstitial nephritis
treat underlying cause i.e. infection, stop medications
| steroids to reduce inflammation and improve recovery
99
aetiology of chronic tubulointerstitial nephritis
chronic inflammation of the tubules and interstitium
| underlying disease: autoimmune, infectious, iatrogenic, granulomatous
100
presentation of chronic tubulointerstitial nephritis
presents with CKD
101
management of chronic tubulointerstitial nephritis
treat underlying cause
| steroids
102
definition of acute tubular necrosis
damage and death of the epithelial cells of the renal tubules
most common cause of AKI
103
causes of acute tubular necrosis
```
ischaemia:
- shock
- sepsis
- dehydration
direct toxin damage:
- radiology contrast dye
- gentamycin
- NSAIDs
```
104
prognosis of acute tubular necrosis
epithelial cells have the ability to regenerate therefore ATN is reversible
takes 7-21 days to recover
105
urinalysis findings in acute tubular necrosis
**'muddy brown casts'**
| renal tubular epithelial cells
106
treatment of acute tubular necrosis
same as mx of AKI:
- supportive
- IV fluids
- stop nephrotoxic meds
- treat complications
107
definition of renal tubular acidosis
metabolic acidosis due to pathology in the tubules of the kidney
108
pathophysiology of renal tubular acidosis
tubules are responsible for balancing hydrogen and bicarb ions between blood and urine and maintaining normal pH therefore disruption to tubular function can cause disturbance to pH
109
4 types of renal tubular acidosis and key facts
- type 1 = distal tubule pathology meaning DCT is unable to excrete hydrogen ions
- type 2 = proximal tubule pathology meaning PCT is unable to resorb bicarb
- type 3 = combination of type 1 and 2 (rare)
- type 4 = MOST COMMON, reduced aldosterone
110
7 causes of type 1 renal tubular acidosis
1. genetic (autosomal dominant and recessive forms)
2. SLE
3. Sjogren's
4. primary biliary cirrhosis
5. hyperthyroidism
6. sickle cell anaemia
7. Marfan's
111
presentation of type 1 renal tubular acidosis
- failure to thrive in children
- hyperventilation (respiratory compensation)
- CKD
- bone disease (osteomalacia)
112
biochemistry results in type 1 renal tubular acidosis
- hypokalaemia
- metabolic acidosis
- high urine pH (>6)
113
treatment of type 1 renal tubular acidosis
oral bicarb
114
main cause of type 2 renal tubular acidosis
Fanconi's syndrome
115
biochemistry results in type 2 renal tubular acidosis
- hypokalaemia
- metabolic acidosis
- high urinary pH (>6)
116
treatment for type 2 renal tubular acidosis
oral bicarb
117
3 causes of type 4 renal tubular acidosis
reduced aldosterone due to:
- adrenal insufficiency
- drugs: ACE-i, spironolactone
- systemic conditions: SLE, DM, HIV
118
biochemistry results in type 4 renal tubular acidosis
- hyperkalaemia
- high chloride
- metabolic acidosis
- low urinary pH
119
management of type 4 renal tubular acidosis
fludrocortisone
| sodium bicarb + tx of hyperkalaemia may be required
120
exchange of substances in the PCT
secreted:
- creatinine
- drugs
- H+
reabsorbed:
- sodium, chloride, potassium
- glucose
- amino acids
- urea
- bicarb
- water
121
exchange of substances in the descending limb of the LOH
water is reabsorbed
122
exchange of substances in the ascending limb of the LOH
reabsorption of sodium, chloride and potassium
123
exchange of substances in the DCT
secreted:
- H+
- potassium
reabsorbed:
- sodium, chloride, calcium, magnesium
- bicarb
124
exchange of substances in the CD
reabsorption of sodium, chloride, urea and water
125
definition of haemolytic uraemic syndrome
thrombosis in the small blood vessels throughout the body usually triggered by bacterial toxin called shiga toxin
126
triad of biochemical signs in haemolytic uraemic syndrome
1. haemolytic anaemia
2. AKI
3. low platelet count (thrombocytopaenia)
127
pathophysiology of haemolytic uraemic syndrome
- formation of clots consumes platelets = thrombocytopaenia
- clots within small vessels chop up RBCs as they pass through = haemolytic anaemia
- blood flow through kidney affected by clots = AKI
128
aetiology of haemolytic uraemic syndrome
toxin called the shiga toxin which is produced by:
- e. coli 0157
- shigella
129
which medicines increase the risk of haemolytic uraemic syndrome
- antibiotics
| - antimotility meds such as loperamide (tx gastroenteritis)
130
presentation/disease course of haemolytic uraemic syndrome
e. coli causes brief gastroenteritis with blood diarrhoea then 5 days after display symptoms of HUS
131
symptoms of HUS
- reduced urine output
- haematuria or dark brown urine
- abdo pain
- lethargy, irritability
- confusion
- HTN
- bruising
132
management of HUS
self-limiting with supportive management
- antihypertensives
- blood transfusions
- dialysis
133
definition of rhabdomyolysis
skeletal muscle breaks down and releases breakdown products into the blood
usually triggered by events causing muscles to break down such as extreme under- or over- use or trauma
134
pathophysiology of rhabdomyolysis
myocytes undergo apoptosis (cell death) resulting in the release of:
- myoglobin (myoglobinaemia)
- potassium (hyperkalaemia)
- phosphate
- creatine kinase
135
complications of rhabdomyolysis
- potassium = cardiac arrhythmias e.g. VF => cardiac arrest
- myoglobin is nephrotoxic => AKI
- AKI causes breakdown products to further accumulate in the blood
136
4 causes of rhabdomyolysis
1. prolonged immobility
2. extreme rigorous exercise
3. crush injuries
4. seizures
137
5 signs/symptoms of rhabdomyolysis
1. muscle aches and pains
2. oedema
3. fatigue
4. confusion (especially in the elderly)
5. red-brown urine
138
investigations in rhabdomyolysis
- creatine kinase (CK) in 100,000s
- urine dipstick positive for blood (myoglobinuria which gives red-brown appearance)
- U&E for AKI and hyperkalaemia
- ECG to assess for effects of hyperkalaemia
139
management of rhabdomyolysis
- IV fluids to encourage filtration of breakdown products
- consider IV sodium bicarb
- consider IV mannitol to increase GFR and reduce oedema
- treat complications especially hyperkalaemia
140
main complications of hyperkalaemia
cardiac arrhythmias such as ventricular fibrillation which can lead to cardiac arrest
141
5 causes of hyperkalaemia (not medications)
1. AKI
2. CKD
3. rhabdomyolysis
4. adrenal insufficiency
5. tumour lysis syndrome
142
5 medications that can cause hyperkalaemia
1. aldosterone antagonists (spironolactone and eplerenone)
2. ACE-i
3. ARBs
4. NSAIDs
5. potassium supplements
143
what to consider with hyperkalaemia found on U&E
could be falsely elevated due to haemolysis during blood sampling
144
ECG changes in hyperkalaemia
1. tall peaked T waves
2. flattening or absence of P waves
3. broad QRS
VF
145
levels of hyperkalaemia and associated management approach
- potassium <6mmol/L and otherwise stable renal function = no urgent tx required, change in diet and meds
- potassium >6mmol/L and ECG changes = urgent tx
- potassium >6.5mmol/L regardless of ECG = urgent tx
146
mainstay of treatment for hyperkalaemia
1. insulin and dextrose infusion - drives carbohydrates into cells and takes potassium with it, reducing blood potassium
2. IV calcium gluconate - stabilises cardiac myocytes reducing risk of arrhythmias
147
5 other options for tx of hyperkalaemia
1. nebulised salbutamol - drives K into cells
2. IV fluids - increase urine output
3. oral calcium resonium - draws K into stool
4. sodium bicarb - drives K into cells as acidosis corrected
5. dialysis if severe/persistent
148
definition of polycystic kidney disease
genetic condition where kidneys develop multiple fluid-filled cysts
kidney function significantly impaired
149
extra-renal findings associated with polycystic kidney disease
- hepatic, splenic, pancreatic, ovarian and prostatic cysts
- berry (cerebral) aneurysms
- cardiac valve disease (MR)
- colonic diverticula
- aortic root dilation
150
genetics of polycystic kidney disease
```
autosomal dominant and autosomal recessive types
(AD > AR)
autosomal dominant genes:
- PKD-1 on chromosome 16
- PKD-2 on chromosome 4
```
151
6 complications of polycystic kidney disease
1. chronic loin pain
2. hypertension
3. CVD
4. gross haematuria
5. renal stones
6. end-stage renal failure
152
common presentation of autosomal recessive polycystic kidney disease
often presents during pregnancy with oligohydramnios as foetus doesn't produce enough urine
leads to underdevelopment of lungs => respiratory failure shortly after birth
153
features of children with AR polycystic kidney disease
dysmorphic features such as underdeveloped ear cartilage, low set ears, flat nasal bridge
may require dialysis within first few days of life
usually have end-stage renal failure before reaching adulthood
154
management of autosomal dominant polycystic kidney disease
tolvaptan (vasopressin receptor antagonist) to slow development of cysts and progression of renal failure
155
management of complications of PKD
- antihypertensives
- analgesia for renal colic (stones or cysts)
- abx for infections, drainage of infected cysts
- dialysis or transplant for end-stage RF
156
general management approaches and lifestyle modifications for PKD
- genetic counselling
- no contact sports (rupture)
- no anti-inflammatory meds or anticoagulants
- regular US, U&E, BP
- MR angiogram to diagnose intracranial aneurysms in symptomatic/FHx
157
definition of renal papillary necrosis
coagulative necrosis of the renal papillae
158
5 causes of renal papillary necrosis
- severe acute pyelonephritis
- diabetic nephropathy
- obstructive nephropathy
- analgesic nephropathy e.g. NSAIDs
- sickle cell anaemia
159
features of renal papillary necrosis
- visible haematuria
- loin pain
- proteinuria
160
genetics of Alport syndrome
x-linked dominant condition
| defect in gene coding for type IV collagen
161
definition of Alport syndrome
genetic condition leading to defects in glomerular-basement membrane
162
features of Alport syndrome
- microscopic haematuria
- progressive renal failure
- bilateral sensorineural hearing loss
- retinitis pigmentosa
163
renal biopsy findings in Alport syndrome
splitting of lamina densa seen on electron microscopy giving 'basket-weave' appearance
