Week 14 - Renal Flashcards
(116 cards)
1
Q
What are some of the functions of the kidney?
A
Metabolic waste excretion Endocrine functions Drug metabolism/excretion Control of solutes and fluid status Blood pressure control Acid/base balance
2
Q
What would be a normal amount of protein in the urine?
A
Less than 150mg of protein / 24h
3
Q
How would you measure urinary protein excretion?
A
24 hour urine collection: grams of protein/24hours (this is hard in clinical practice.)
So would normally do:
Protein:creatinine ratio (PCR) on morning spot sample(mg/mmol)
4
Q
How would you calculate the eGFR?
A
(urine creatinine concentration x urine volume)/plasma creatine concentration
5
Q
What GFR would be considered normal unless they had evidence of kidney disease?
A
≥60 ml/min/1.73m^2
6
Q
What is glomerulonephritis?
A
An inflammatory disease involving the glomerulus and the tubules.
7
Q
What are the three layers of the glomerular filtration barrier?
A
Endothelial cell Basement membrane Epithelial cells (podocytes)
8
Q
What are the 4 targets for injury in glomerulonephritis?
A
Podocytes, glomerular capilliaries, basement membrane, mesangial cells.
9
Q
How is glomerulonephritis diagnosed?
A
Kidney cortex biopsy
10
Q
What are the 3 features of nephrotic syndrome?
A
- Proteinuria - either 3.5g proteinuria/24 hours or PCR>300
- low serum albumin (<30)
- Oedema
11
Q
What are the potential complications of nephrotic syndrome?
A
Risk of venous thromboembolism
Increased risk of infection
12
Q
What are some secondary causes of glomerulonephritis?
A
Diabetes Drugs i.e. NSAIDs, bisphosphonates Rheum - RA, lupus, amyloid CV - Subacute bacterial endocarditis Respiratory - bronchiectasis, lung cancer, TB Hepatitis, HIV
13
Q
Which types of glomerulonephritis would fall under a more nephritic, nephrotic or rapidly progressive glomerulonephritis?
A
Rapidly progressive - IgA, lupus, vasculitis
Nephritic - IgA, lupus, post-infectious.
Nephrotic - minimal change, FSGS, membranous.
14
Q
What is the pathology behind IgA nephropathy? How does the clinical picture progress? How is it treated?
A
IgA depositions in the mesangial cells. 1. haematuria 2. hypertension 3. proteinuria 4. renal failure ACEi, ARBs then corticosteroids if still proteinuria
15
Q
How does membranous glomerulonephropathy present? What is it often secondary to? What antibodies are present in 70%?
A
Nephrotic syndrome
Malignancy, CTD, drugs.
Anti-phospholipiase A2 receptor antibody.
16
Q
How is membranous nephropathy treated?
A
Treat underlying disease
supportive non-immunological - ACEi, diuretics, statins
Specific immunotherapy i.e steroids, cyclosporin, rituximab, alkylating agents
17
Q
What age group is minimal change disease most common in? How does it present? What is the pathogenesis? What is it sometimes secondary to?
A
Children - 90% under 10
Nephrotic syndrome
T cell, cytokine mediated disease targeting the glomerular epithelial cell basement membrane.
URTI, malignancy.
18
Q
What is the treatment of minimal change disease?
A
High dose steroids - prednisolone.
19
Q
What are 3 causes of rapidly progressive glomerulonephritis?
A
ANCA vasculitis
Goodpasture’s syndrome
Lupus nephritis.
20
Q
What is the hallmark of diabetic nephropathy? What other diabetic complication is it usually associated with?
A
Proteinuria
Retinopathy
21
Q
What is the pathophysiology of diabetic nephropathy?
A
hyperglycaemia which leads to volume expansion which causes intraglomerular hypertension. This leads to hyperfiltration resulting in protein leaking through into the urine and ultimately, hypertension and renal failure.
22
Q
How do you prevent people developing diabetic nephropathy?
A
Tight glycaemic control, control blood pressure well with ACEi, ARBs and SGLT2 inhibitors.
23
Q
What is the pathogenesis of renovascular disease?
A
Progressive narrowing of renal arteries with atheroma.
Perfusion is reduced to 20%, GFR falls but tissue oxygenation maintained.
RA stenosis progresses to 70% and cortical hypoxia causes microvascular damage and activation of inflammatory and oxidative processes.
Parenchymal inflammation and fibrosis progress and become irreversible, restoration of blood flow provides no benefit.
24
Q
How is renal artery stenosis managed?
A
Blood pressure control (not ACEi/ARB)
Glycaemic control if diabetic.
Smoking cessation, exercise, low sodium diet.
Angioplasty if rapidly deteriorating renal failure.
25
What is the pathophysiology of lupus nephritis?
Auto-antibodies produced against dsDNA or nucleosomes.
Form intravascular immune complexes or attach to GBM.
Activate complement (low C4)
Renal damage
26
What is the treatment of lupus nephritis?
Immunosuppression - steroids, MMF, cyclophosphamide, rituximab.
27
What is the diagnosis of lupus nephritis?
Autoantibodies and renal biopsy.
28
What is cystitis? What is its presenting features?
```
Infection of the bladder.
Dysuria (pain passing urine)
Frequency
Urgency
Suprapubic pain
Haematuria
```
29
What is pyelonephritis? What are its presenting features?
```
All of the features for cystitis...PLUS
Fever >38 degrees
Chills/rigors
Flank pain
Costo-vertebral angle tenderness
Nausea and vomiting
```
30
What are the risk factors for developing UTI?
```
Infancy - boys and girls under 1
Abnormal urinary tract - congenital or other.
Females
Bladder dysfunction/incomplete emptying
Foreign body i.e. catheters, stones
Diabetes mellitus
Renal transplant
Immunosuppression
```
31
How is urinary tract infection diagnosed?
Urinalysis - positive for leucocyte esterase and nitrite.
Microscopy/flow cytometry to detect pus cells and bacteria.
Urine culture
32
What are the most common bacteria that causes UTI?
E-coli - 90%
Klebsiella
Proteus (kidney stones)
33
What should be done in ALL children under three when clinical suspicion of a UTI?
Urine culture
34
What is the management of UTI in children?
Prompt identification - test urine if infant/child presents with urinary symptoms or unexplained fever >38 degrees.
Begin empirical antibiotics while awaiting culture and sensitivities. Oral antibiotic unless severely ill, vomiting or under 6 months.
35
What IV and oral antibiotics would be used in UTI?
IV - cefriaxone or gentamicin
| Oral - co-amoxiclav, nitrofurantoin, trimethoprin, cephalosporin, quinolone.
36
What imaging modalities are used when investigating UTI?
Ultrasound
MCUG (micturating cystourethrogram)
Nuclear medicine imaging - DMSA, MAG3 indirect cystogram, MAG3 diuesis renogram.
37
What is vesico-ureteric reflux (VUR)? What does it predispose you to?
Retrograde passage of urine from the bladder into the upper urinary tract.
Recurrent UTIs
38
What is the management of VUR?
Antibiotic prophylaxis for high grade VUR (grade III-V) until toilet trained by day.
If this failed (i.e. recurrent febrile UTI, new scarring)
STING procedure
Open ureteric re-implantation
Circumcision
39
What are some of the causes of bladder outlet obstruction?
Posterior urethral valve
Prostatic hypertrophy
Functional neuropathy
Prune belly syndrome
40
What is the inheritance pattern of adult polycystic kidney disease?
Autosomal dominant
41
What two genes commonly cause polycystic kidney disease? What is the result of these mutations?
PKD1
PKD2
Overexpression of polycystins in the renal tubular epithelium forming cysts.
42
What is the natural history of adult polycystic kidney disease?
Cysts gradually enlarge and kidney volume increases. There is some compensation and then eGFR falls, usually 10 years before kidneys fail.
43
How is APKD diagnosed?
Ultrasound scan
CT or MRI scan more sensitive.
Genetic test
44
What are the clincial consequences of APKD?
```
End stage renal disease
Cyst accidents - bleeding, infection, rupture
Hypertension
Intracranial aneurysms
Mitral valve prolapse
Aortic incompetence
Colonic diverticular disease
Liver/pancreas cysts
Hernias
```
45
What is the management of polycystic kidney disease?
Supportive management
Early detection and management of blood pressure
Treat complications
Manage extra-renal associations
Renal replacement therapy i.e. transplant, dialysis
46
What can be used to treat APKD?
Tolvaptan - vasopressin V2 receptor antagonist to slow cyst formation.
47
What is the inheritance pattern of Alport's syndrome? What protein is abnormal? What does alport's syndrome cause?
X-linked
Collagen 4 - affects glomerular basement membrane
Deafness and renal failure
48
What are the clinical consequences of alport's syndrome?
Microscopic haematuria, proteinuria and ESRF
90% on dialysis or transplant by age 40.
Sensorineural hearing loss late childhood
49
What is the inheritance pattern of fabry's disease? What enzyme is deficient and what does this lead to? What other issues does it cause?
X linked
Alpha galactosidase A resulting in Gb3 accumulation in glomeruli and podocytes. Progression to ESRF.
Also causes neuropathy, cardiac and skin features.
50
What is the diagnosis and management of fabry's disease?
Diagnosis: measure alpha-gal A activity in leukocytes. Renal biopsy.
Management: enzyme replacement therapy.
51
Give a definition of acute kidney injury.
AKI: decline of renal excretory function over hours or days, recognised by the rise in serum urea or creatinine.
52
What are the three main classification of causes of AKI?
Pre-renal - circulatory failure
Renal - problem with the cells of the kidney
post renal - obstruction
53
What are some pre-renal causes of AKI?
```
Hypotension
Hypovolaemia (D&V, burns, haemorrhage)
Hypoperfusion
Hypoxia
Sepsis
Drugs, toxins
```
54
What are some of the renal causes of AKI?
Glomerulonephritis, drugs i.e. gentamicin.
| Tubulo-interstitial nephritis, rhabdomyolysis
55
What are some of the post renal causes of AKI?
Renal papillary necosis, kidney stones, tumours (can be extrinsic), prostatic hypertrophy, urethral strictures, lymph node compression.
56
What is the most common cause of intrinsic AKI?
Acute tubular necrosis.
57
What is the cause of acute tubular necrosis?
ATN is always due to underperfusion of the tubules and/or direct toxicity:
- hypotension
- sepsis
- toxins
- or often, all three
58
What exogenous and endogenous toxins can cause ATN?
Exogenous - drugs i.e. NSAIDs, gentamicin, ACEi. Contrast, poisins e.g. metals, antifreeze.
Endogenous - myoglobin, haemoglobin, immunoglobulins, calcium, urate.
59
What is the treatment of AKI?
Airway and breathing
Circulation - shock - restore renal perfusion - treat hyperkalaemia and pulmonary oedema.
Remove causes - drugs, sepsis
Exclude obstruction and consider renal causes - ultrasound.
Ask for help: ICU or renal unit.
60
How is hyperkalaemia treated?
Calcium resonium to reduce absorption from the gut.
Insulin + dextrose to move K into cells.
Calcium gluconate as cardiac membrane stabiliser.
61
What are the indications for dialysis?
```
Refractory potassium ≥6.5 mmol/l
Refractory pulmonary Oedema.
Acidosis - pH <7.1
Uraemia (esp if urea >40) - pericarditis, encephalopathy
Toxins (lithium, ethylene glycol.)
```
62
What is the definition of chronic kidney disease?
Kidney damage or GFR<60ml/min per 1.73m^2 for 3 months or more.
63
What is the aetiology of CKD?
Diabetic nephropathy
Renovascular disease/ischaemic nephropathy
Chronic glomerulonephritis
Reflux nephropathy/chronic pyelonephritis
Adult polycystic kidney disease
Obstructive uropathy
64
What are the symptoms of advanced CKD?
```
Pruritis
Nausea, anoerxia, weight loss
Fatigue
Leg swelling
Breathlessness
Nocturia
Joint/bone pain
Confusion
```
65
What are the signs of advanced CKD?
```
Peripheral and pulmonary oedema
Pericardial rub
Rash/excoriation
Hypertension
Tachypnoea
Cachexia
Pallor &/or lemon yellow tinge
```
66
What are the general principles of managing CKD?
Targeted screening for CKD
Interventions to slow the rate of progression of CKD and reduce cardiovascular risk
Medicines to replace impaired individual functions of the kidney
Advanced planning for future renal replacement therapy
Renal replacement therapy
67
How do you slow the progression of CKD?
```
Aggressive BP control
Good diabetic control
Diet
Smoking cessation
Lowering cholesterol
Treat acidosis
```
68
Which would be the drugs of choice to reduce hypertension in CKD?
ACEi or ARB
69
How do we treat CKD-MBD (mineral and bone disorder)?
```
Activated vitamin D
Occasional Mg supplements
Phosphate binders
Calcimimetic: cinacalet
Occasionally parathyroidectomy
```
70
What options are there for renal replacement therapy?
Transplant, conservative care, haemodialysis (home or hospital)
71
What would be the indications for renal replacement therapy?
```
Medically resistant hyperkalaemia
Medically resistant pulmonary oedema
Medically resistant acidosis
Uraemic pericarditis
Uraemic encephalopathy
Specific drug overdoses
```
72
What are some of the symptoms of clinical uraemia?
Anorexia, vomiting, itch, restless legs, weight loss, metallic taste.
73
What GFR level would you start someone renal replacement therapy?
No absolute rule. Generally eGFR between 5-10ml/min/1.73m^2.
| Assessed on an individual patient basis.
74
What are the three options for renal replacement therapy?
Haemodialysis
Peritoneal dialysis
Renal transplant
75
What are the two aims of haemodialysis?
Removal of solutes i.e. urea, potassium via diffusion.
| Removal of fluid via hydrostatic filtration.
76
What are the different methods of getting haemodialysis access?
Creating an arteriovenous fistula, central venous catheter, arteriovenous graft.
77
What are the potential complications of haemodialysis?
```
Crash - acute hypotension
Access problems
Cramps
Fatigue
Hypokalaemia
Blood loss
Dialysis disequilibrium
Air embolism
```
78
What are the principles of peritoneal dialysis?
Osmotic filtration to remove fluid, diffusion to remove solutes.
79
What are the benefits of peritoneal dialysis?
Home based therapy.
Simple to do once taught
Can maintain independence.
80
What are the potential complications of peritoneal dialysis?
Infection - peritonitis
Glucose load can result in developing or worsening diabetes.
Peritoneal membrane failure.
Mechanical - hernia, diaphragmatic leak, dislodged catheter.
Hypoalbuminaemia
Encapsulating peritoneal sclerosis.
81
What do you need to give patient's who are on dialysis?
EPO injections
| Phosphate binders and vitamin D
82
What are the pros and cons to renal transplantation?
Pros - no dialysis, better renal function, can live more independently, better life expectancy, fertility better.
Cons - immunosuppressive medication, increased CV risk, increased infection, post transplant diabetes, skin and other malignancies.
83
In what patients should you treat asymptomatic bacteriuria?
Pre-school children
Pregnancy
Renal transplant
Immunocompromised
84
What are the common organisms that cause UTI?
Majority gram negative bacilli:
- E Coli
- Klebsiella
- Proteus
- Pseudomonas
85
What gram positive can cause UTI?
Streptococcus - enterococcus, group B strep
| Staphylococcus - aureas (associated with catheter).
86
What would you do for a first presentation of UTI in non-pregnant women?
```
Dipstick urine (high false +ve)
Check previous culture results, antibiotics for 3-7 days.
If no response to treatment:
Urine culture
Change antibiotic
```
87
What would you do for a first presentation of UTI in children and men?
Send urine away for culture, treat appropriately.
88
What would you do for a presentation of UTI in pregnancy? What antibiotics would you avoid?
Send urine for culture every time.
Treat for 7-10 days
Amoxicillin and cefalexin relatively safe.
Avoid trimethoprin in 1st trimester and nitrofurantoin near term.
89
What are the treatment options for recurrent UTI?
Self administered single dose/short course therapy.
Single dose post coital abx.
Prophylactic antibiotics
- if all measures fail, ideally 6 months of trimethoprim, nitrofurantoin (PF)
90
What is the management of acute pyelonephritis?
Check previous/recent microbiology results.
Send urine +/- blood culture +/- imaging
Community: co-amoxiclav/ciprofloxacin/trimethoprim
Hospital: often broad spectrum antibiotics +/- radiological/surgical infection
91
What is the management of complicated UTI?
```
FBC, U&Es, CRP
Urine sample
Blood culture if pyrexia or hypothermic
Renal ultrasound
CT KUB
Antibiotic therapy for two weeks or more.
```
92
What could cause pyuria with no bacteria?
```
Previous/recent antibiotic
Tumour
Calculi
Urethritis (check for chlamydia)
TB
```
93
What would be the antibiotic therapy used for complicated UTI?
Usually IV therapy - amoxicillin/vancomycin
| Gentamicin/aztreonam/temocillin
94
What are the clinical features of acute bacterial prostatitis?
Fever, perineal/back pain, UTI, urinary retention.
| Diffuse oedema, microabscesses.
95
How would investigate acute bacterial prostatitis?
Urine culture, usually positive
Blood culture
Trans-rectal U/S
CT/MRI
96
What are the potential complications of acute bacterial peritonitis?
```
Prostatic abscess
Spontaneous rupture - urethra, rectum
Epipidymitis
Pyelonephritis
Systemic sepsis
```
97
What antibiotic therapy is commonly used for Acute bacterial prostatitis?
Ciprofloxacin
98
What is epididymitis? What is the aetiology? What are the symptoms?
```
Inflammatory reaction of the epididymis
Ascending infection from the urethra
Urethral instrumentation
Pain, fever, swelling, penile discharge
Symptoms of UTI/urethritis
```
99
What organisms commonly cause epididymitis?
Gram negatives i.e. enterococci, staphylococci
TB
Chlamydia, N.gonorrhoea
100
What is orchiditis and its symptoms?
Inflammation of one or both testicles.
Testicular pain and swelling, dysuria, fever, penile discharge.
Usually viral - i.e. mumps
101
What are the potential complications of bacterial orchiditis?
Testicular infarction
| Abscess formation
102
What is fournier's gangrene? What are the risk factors?
Form of necrotising fasciitis of the genital region due to infection.
Risk factors: UTI, complications of IBU, trauma, recent surgery.
103
What are the common pathogens that cause fournier's gangrene? What investigations would you do?
Gram negatives and anaerobes.
Blood cultures, urine, tissue/pus.
Surgical debridement + broad spectrum antibiotics i.e. gentamicin, metronidazole, clindamycin.
104
What are the three broad causes of stone formation in the urinary tract?
Abnormal urine
Urinary obstruction
Urinary infection
105
What can cause too much salt in the urine, causing stones?
Hypercalciuria - i.e. through hyperparathyroidism, sarcoid
Too much acid - metabolic syndrome
Renal tubular acidosis
Hyperoxaliuria
106
What can cause not enough water in the urine, causing stones?
Not drinking enough water
107
What 4 substances act as stone inhibitors? Which
Citrate, magnesium, pyrophosphate, glycoproteins.
108
What factors encourage stone formation?
Low volume, low pH, low citrate, low magnesium.
| High uric acid, high calcium, high oxalate.
109
List some congenital and acquired causes of urinary obstruction?
Congenital - medullary sponge kidney, PUJ obstruction, mega ureter, urterocele.
Acquired - ureteric stricture, anastomotic stricture.
110
What type of urinary infection causes stones to form?
Urease producing organisms i.e. proteus mirablis
111
Name 3 different types of stones?
Calcium stones i.e. calcium oxalate, calcium phosphate
Infection stones - struvite (proteus)
Uric acid stone
112
What different ways can stones present?
Incidental finding on imaging.
Pain - colic, radiates from loin to groin, cannot settle, unable to stay still.
Haematuria
UTI or Sepsis
113
What initial investigations would you do for stones?
History and examination
Bloods FBC, U&E, CRP
Urine examination and dipstick
Imaging - CT KUB gold standard
114
How are stones managed?
If they are small or asymptomatic - observation
Medical therapy - dissolution therapy
Non-invasive therapy
Invasive therapy
115
What medical therapies can be used to treat stones that are causing acute pain?
Analgesics - i.e. NSAIDs
| Medical expulsive therapy i.e. tamsulosin
116
What are the surgical options for stones?
```
ESWL
Rigid ureteroscopy and fragmentation/basket extraction
FURS - flexible ureteroscopy
Percutaneous nephrolithotomy
Emergency stent or nephrostomy
Laparoscopic or open surgery
```
