Wk14 - Nephrology/Urology Flashcards
(175 cards)
1
Q
Definition of AKI
A
“Decline of renal excretory function over hours or days …recognised by the rise in serum urea and creatinine”
RIFLE/AKI criteria
2
Q
What is oligouria classified as?
A
UO <3ml/kg/hr
3
Q
What system is used in hospital labs when trying to indicate change in creatinine that signifies AKI
A
AKI e-Alerts
4
Q
Stages of AKI (severity)
A
Using KDIFO:
Stage 1: Serum creatinine ≥1.5 and < 2.0 times AKI baseline or >=26.0 µmol/l increase above AKI baseline
Stage 2: Serum creatinine >=2.0 and < 3.0 times AKI baseline
Stage 3: Serum creatinine 3.0 times AKI baseline or >=354 µmol/l increase above AKI baseline
5
Q
Causes of AKI
A
Pre Renal = Circulatory Failure “Shock”
Hypotension
Hypovolaemia (burns, diarrhoea, haemorrhage etc)
Hypoperfusion (due to HF)
Hypoxia
Sepsis (vasodilation effective peprusion dec.)
Drugs, toxins
Renal = The cells of the kidney
- Glomerulonephritis (cause by SLE), acute tubular necrosis (most common), obstructive, acute tubulo-interstitial nephritis, vasculitis, atheroembolic rhabdomyolysis, drugs - Gentamicin
Post Renal = Obstruction: Calculi Tumours (ureter, bladder, prostate, cervix, ovarian) Lymph nodes (compression Prostate Etc.
6
Q
What is ATN
A
Acute tubular necrosis
Any pre-renal cause of AKI if severe/of sufficent duration
Usually reversible
~10-15% will never recover renal function
~A further 10-15% will have chronic renal impairment following ATN
7
Q
Causes of ATN
A
ATN is always due to under perfusion of the tubules and/or direct toxicity: Hypotension Sepsis Toxins Or often, all three
8
Q
Examples of toxins causing ATN
A
Exogenous:
Drugs (eg, NSAID’s gentamicin, ACEi)
Contrast
Poisons (eg, metals, antifreeze)
Endogenous: Myoglobin Haemoglobin Immunoglobins Calcium Urate
9
Q
Management of AKI
A
Acute or chronic?
Bloods – both urea and creatinine ↑
Potassium
Urine output (usually <400ml/day)
Clinical assessment of fluid status (BP, JVP, oedema, heart sounds)
Underlying diagnosis (history, exam, meds)
Treatment:
Immediate
Airway and Breathing
Circulation – shock - restore renal perfusion
–> hyperkalaemia
–> pulmonary oedema
Remove causes - drugs, sepsis
Exclude obstruction (with ultrasound) & consider ‘renal’ causes
are the pre-renal causes sufficient to account for ARF?
Ask for help: ICU or renal unit
10
Q
Diagnostic process for AKI - investigations
A
AKI or CKD?
History and exam (e.g. septic, rashes, haemoptysis, rhabomyolysis etc)
Drugs (prescribed, OTC, supplements, radio-contrast and abuse)
Urinalysis
Renal ultrasound
‘GN’ screen – ANCA, ANA, Immunoglobulins + EP, complement, aGBM, Urine Bence Jones protein
Others blood film, LDH, CK etc
Renal ultrasound to exclude obstruction:
Also gives info on size (CKD - small kidneys)
Loss of cortico-medullary differentiation suggests CKD
11
Q
Treatment of hyperkalaemia (with AKI) - causing arrhythmias (e.g. tachycardia)
A
Reduce absorption from gut – Calcium Resonium 15g 4x day orally (or enema)
Insulin 10-15units actrapid+ 50ml 50% dextrose moves potassium into cells (watch Blood Glucose)
Calcium gluconate 10ml 10% as cardiac membrane stabiliser
12
Q
Absolute and relative indications for dialysis
A
Absolute:
Refractory potassium ≥6.5 mmol/l
Refractory pulmonary oedema
Relative:
Acidosis (pH <7.1)
Uraemia (esp if urea >40) - pericarditis, encephalopathy
Toxins (lithium, ethylene glycol etc)
13
Q
Definition of CKD
A
CKD = kidney damage of GFR<60ml/min per 1.73m2 for 3 months or more
14
Q
How serum creatinine can be used to measure kidney function
A
Serum creatinine product of muscle metabolism.
Fairly constant production and constant serum levels
24h urine creatinine clearance – often inaccurate
Freely filtered but tubular secretion
Serum Creatinine is inversely proportional to GFR and also depends on muscle mass
Effect of muscle mass leas to:
Overestimation of function in women
Overestimation of function in the elderly
Overestimation in other low muscle mass groups e.g. amputees, para/quadriplegics, rheumatoid arthritis
15
Q
Problems with eGFR
A
Only validated in whites and African-Americans
Mean age 50 ie not validated in elderly
Values above 60ml/min not distinguishable so reported as eGFR >59ml/min
Drug dosing – doesn’t take weight into account
AKI – not valid
Pregnancy
16
Q
Classification of CKD
A
According to eGFR
Stage 1 - >90 2 - 60-89 3a - 45-59 3b - 30-44 4 - 15-29 5 - <15
17
Q
Proteinuria
A
Proteinuria suggests the filtration barrier has been damaged
Some protein in urine normal : <150mg/day
About 2/3 is albumin
Dipstick for albumin. Not very accurate
1+ : can see in fever, exercise, normals
24h collection gold standard but not used now in routine practice
PCR and ACR useful and correlate with 24h
Measures conc of urine (proteinuria) ‘against creatinine (to be able to compare it against a constant value)
18
Q
ACR and PCR (mg/mmol)
A
Normal ACR <2.5
Normal PCR <20
Albuminuria : ACR >30
ACR is about 2/3 of equivalent PCR result eg ACR 70 = PCR 100 = 24h urine protein 1g
Nephrotic range proteinuria : PCR >300 (3g/24h)
If heavy albuminuria use PCR to follow progress
19
Q
Aetiology of CKD
A
1) Diabetic nephropathy
2) Renovascular disease/ischaemic nephropathy (Look for asymmetric kidneys on scan)
3) Chronic glomerulonephritis
4) Reflux nephropathy/chronic pyelonephritis
5) ADPKD
6) Obstructive uropathy
20
Q
Symptoms of advanced CKD
A
Pruritus Nausea, anorexia, weight loss Fatigue Leg swelling Breathlessness Nocturia Joint/bone pain Confusion
21
Q
Signs of advanced CKD
A
Peripheral and pulmonary oedema Pericardial rub Rash/excoriation Hypertension Tachypnoea Cachexia Pallor &/or lemon yellow tinge
22
Q
CKD g
A
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 (RRT)
Renal replacement therapy
23
Q
Slowing progression of CKD
A
Aggressive BP control Good diabetic control Diet Smoking cessation Lowering cholesterol Treat acidosis
24
Q
ACEi/ARB in CKD
A
Reduction in eGFR of up to 25% in first few weeks is a good thing
Will get more of a reduction if critical reduced renal perfusion (volume depletion, sepsis, RAS)-
sick day rules
25
Anaemia in CKD
Common, particularly when eGFR <30
Iron absorption & utilisation suboptimal
Replace iron, B12, folate first if low
ESA eg Darbepoietin alfa 30microg every 2 weeks
Trigger usually Hb <100g/l
Target Hb 100-120g/l.
Higher associated with adverse CV events
26
How are the kidneys associated with CKD
Secondary hyperparathyroidism:
27
CKD-MBD Treatment
Activated vitamin D : Alfacalcidol : start 0.25mcg
Occasionally Mg supplements
Phosphate binders : target phosphate 0.9-1.5 mmol/l
- Calcium based : calcium carbonate/acetate
- Non-calcium : sevelamer, lanthanum, aluminium
Calcimimetic : cinacalcet
Parathyroidectomy
28
Indications for dialysis
```
Medically resistant hyperkalaemia
Medically resistant pulmonary oedema
Medically resistant acidosis
Uraemic pericarditis
Uraemic encephalopathy
```
& specific drug overdoses
29
Signs of clinically uraemic patient
```
Anorexia
Vomiting
Itch
Restless legs
Weight loss
Metabolic taste
```
30
What level of GFR signifies you to start dialysis
Not a specific number
Generally eGFR between 5-10ml/min/1.73m2
(When GFR in single digits)
Assessed on an individual patient basis
31
What are the options for renal replacement
Haemodialysis - hospital or home
Peritoneal dialysis - predominantly home based, 2 variations - CAPD, APD
Renal transplant - 2 types - cadaveric or living transplant
32
2 aims of haemodialysis
Haemodialysis access
Removal of solutes – e.g. potassium, urea: DIFFUSION
Removal of fluid ‘ultrafiltration’ - pressure: HYDROSTATIC FILTRATION
Haemodialysis access:
TCVC (tunneled central venous catheter)
AV fistula
Graft
33
Practicalities of HD
Hospital or home based – hospital much more common
Standard: 4h, 3 times a week
Multiple other options – mainly home based:
- 6h 3 times a week
- Short daily dialysis
- Daily overnight
Home based treatment gives greater flexibility and empowerment but need carer, space and capital investment
34
Haemodialysis complications
```
‘Crash’ (acute hypotension)
Access problems (with fistula)
Cramps
Fatigue
Hypokalaemia
Blood loss
Dialysis disequilibrium
Air embolism
```
35
Describe the 2 types of peritoneal dialysis
Continuous cycling peritoneal dialysis is done with a machine at night on a daily basis.
Continuous ambulatory peritoneal dialysis is done on a daily basis. Patients manually exchange the peritoneal fluid
36
Practicalities of PD
Home based therapy
Better with some residual renal function
Different glucose concentrations of dialysate to provide more or less ultrafiltration
Dialysate contains other electrolytes like in HD
Gradual treatment – no good for AKI
Simple procedure once taught
Maintain independence
37
PD complications
Infection - peritonitis
Glucose load – development or worsening control of diabetes
Mechanical – hernia, diaphragmatic leak, dislodged catheter
Peritoneal membrane failure
Hypoalbuminaemia
Encapsulating peritoneal sclerosis
```
Some patients not suitable:
Grossly obese
Intra-abdominal adhesions
Frail
Home not suitable
```
38
Conservative care for kidneys
Increasingly frail and elderly population
Recognition that survival may be slightly better on RRT but quality may not
Symptom based management
39
Modality choice consideration for renal replacement
```
Lifestyle
Frailty
Vascular access
Time – travel to and from hospital
Carer
Physical – concurrent medical problems e.g. disseminated malignancy, severe dementia, severe psychiatric disease
```
40
Problems not helped by dialysis
Anaemia – need erythropoesis supplementing agents and iron
Renal bone disease – need phosphate binders and vitamin D
Neuropathy
Endocrine disturbances
41
Transplantation practicalities
Immunosuppressive medication for transplant patients
```
Cadaveric waiting list
- Kidney after brainstem death
- Kidney after cardiac death
Average wait on the list 3 years
Not all patients suitable for transplant
```
Immunosuppresion:
Cyclosporin (tacrolimus)
MPA
42
Pros and cons of transplantation of kidney
```
Pros
No dialysis
Better level of renal function
Can live much more independently
Better life expectancy
Fertility better
```
```
Cons
Immunosuppressive medication for duration of transplant
Increased cardiovascular risk
Increased infection
Post transplant diabetes
Skin malignancies and others
```
43
Lower urinary tract infection
| Upper
Lower - Cystitis
Upper - Pyelonephritis, renal abscess
44
Urosepsis
```
Urosepsis, complicated UTI:
Temp >38ºC
HR>90/min
RR>20/min
WBC >15.0 or <4.0
```
45
Those more affected with bacteriruia and RxF
Preschool age, girls > boys
Adults
Non- pregnant females,1-3%
Males, 0.1%
```
Other at risk groups:
Hospitalised
Catheterised
Diabetics
Anatomical abnormalities
Pregnant patients
```
46
Ascending UTI
Urethral colonisation
female>male
Multiplication in bladder
Ureteric involvement
47
Descending UTI
Blood-born infections
| Involvement of renal parenchyma
48
Clinical features of UTI
```
Suprapubic discomfort
Dysuria
Urgency
Frequency
Cloudy, blood stained, smelly urine
Low-grade fever
Sepsis
```
Failure to thrive, jaundice; in neonates
Abdominal pain and vomiting in children
Nocturia, incontinence, confusion in the elderly
49
Common organisms causing UTI
```
Gram negative bacilli
E.coli
Klebsiella sp.
Proteus sp.
Pesudomonas sp.,...
```
```
Gram positive bacteria
Streptococcus sp.
- Enterococcus sp.
- S. agalactiae (Group B streptococcus)
Staphylococcus sp. (S.saprophyticus, S.aureus (S.aureus usually with presence of a catheter
)),…
```
Anaerobes (uncommon)
(Candida sp.)
50
Investigation of UTI
```
Non-pregnant women:
1st presentation, culture not mandatory
Dipstick, high false positive rate
Check previous culture results
Antibiotic 3-7/7
No response to treatment
Urine culture
Change antibiotic
Children and men
Send urine for each and every presentation
Treat appropriately
```
51
UTI in pregnancy - Tx
Common
Send urine sample with each presentation
Treat for 7-10 days
- Amoxicillin and cefalexin relatively safe
- Avoid Trimethoprim in 1st trimester
- Avoid Nitrofurantoin near term
May need hospital admission for IVs if severe
Can develop into pyelonephritis (~30%) - causes risk of bacteraemia and sepsis
52
Classification of recurrent UTI & Tx
```
≥2 episodes in six months
≥3 episodes/year
(Microbiological confirmed)
Mostly women
Send sample with each episode
Encourage hydration
Encourage urge initiated and post coital voiding
Intravaginal/oral oestrogen
Urology investigation
```
```
Self administered single dose/short course therapy
Single dose post coital abx
Prophylactic antibiotics
If simple measures fail
Ideally six months
Trimethoprim
Nitrofurantoin (Can cause pulmonary fibrosis)
Associated risk with long term use
Development of antimicrobial resistance
```
53
Catheter associated UTI - a complicated UTI
```
Millions of catheter insertions/year
Colonisation common - Treatment not required
Infection (HAI, 35%)
- Disturbance of the flushing system
- Colonisation of the urinary catheter
- Biofilm production by bacteria
```
Likely organisms
Patient’s flora
Healthcare environment
54
Complications of catheters
```
CAUTI
Obstruction-hydronephrosis
Chronic renal inflammation
Urinary tract stones
Long term risk of bladder cancer
```
55
Prevention of catheter infections
```
Catheterise only if necessary
Remove when no longer needed “
“Forgotten catheter”
Remove/replace if causing infection
Catheter care (bundles)
Hand hygiene
```
56
Tx of CAUTI
```
Check recent /previous microbiology
Start empirical antibiotics
Remove catheter if not needed
Replace catheter under antibiotic cover
Historically Gentamicin/ Ciprofloxacin
Poor Gram positive cover
Increase in resistant GNB- treatment failure
May need to use broad spectrum antibiotics
```
57
Features of acute pyelonephritis
```
Upper urinary tract infection
Moderate to severe infection
Ascending infection involving pelvis of kidney
Enlarged kidney
Abscesses on surface of kidney
```
58
Management of acute pyelonephritis
Check previous/recent microbiology results (might be on wrong antibiotics)
Send urine +/- blood culture+/- imaging
Community: Co-amoxiclav/ Ciprofloxacin/ /Trimethoprim (NICE guideline)
Options may be limited
Allergy
Drug interaction
Antimicrobial resistance
Uncomplicated pyelonephritis, 7-14/7 antibiotic
Complicated pyelonephritis, ≥ 14/7 therapy
+/- radiological/surgical intervention
Even under right antibiotic likely to be pyrexial
59
What is a complication of pyelonephritis
Renal abscess
| Perinephrtic abscess
60
Renal abscess
```
Complication of pyelonephritis
Similar symptoms to pyelonephritis
Usually positive urine and blood culture
Gram negative bacilli, likely organisms
Can become life-threatening
- Emphysematous pyelonephritis
- Urgent urology review
- High mortality rate
Poor response to antibiotics
```
61
Perinephric abscess
Complication of pyelonephritis
```
Uncommon
Risk factors
- Untreated LUTI, anatomical abnormalities
- Renal calculi
- Bacteraemia, haematogenous spread
```
Common organisms:
Gram negative bacilli, E.coli, Proteus sp.
Gram positive cocci, S.aureus, Streptococci
Candida sp.
```
Symptoms
- Similar to pyelonephritis
- Localised signs/symptoms
Usually positive blood cultures
Pyuria +/- bacterial growth
Treat empirically as complicated UTI
Poor response to antibiotic therapy
Surgical management
```
62
Management of complicated UTIs
```
FBC, U+Es, CRP
Urine sample
Urethral, CSU, Suprapubic, Nephrostomy
Blood culture if pyrexia or hypothermic
Renal ultrasound
CT KUB
Antibiotic therapy14/7 or more
PO Amoxicillin, Trimethoprim, Nitrofurantoin
Pivmecillinam, Fosfomycin
(Co-amoxiclav, Ciprofloxacin, Cefalexin)
- Look out for penicillin allergy
```
63
Reasons for pyuria with no bacteria
```
Previous/recent antibiotic
Tumour
Calculi
Urethritis (check for Chlamydia)
Tuberculosis
```
64
Features of acute bacterial prostatitis - likely organisms
```
Male UTI
Localised infection
Usually spontaneous
May follow urethral instrumentation
Fever, perineal/ back pain, UTI, urinary retention
Diffuse oedema, micro abscesses
```
Likely organisms:
Gram negative bacilli, e.g. E.coli, Proteus sp.
S.aureus (MSSA, MRSA)
N.gonorrhoea (less common)
65
Investigations for acute bacterial prostatitis
```
Urine culture, usually positive
Blood culture
Trans-rectal U/S
CT/ MRI
Obtaining prostatic secretions NOT advisable
```
66
Complications of acute bacterial prostatitis & Abx management
```
Complications:
Prostatic abscess
Spontaneous rupture
Urethra, rectum
Epididymitis
Pyelonephritis
Systemic sepsis
```
Antibiotic management:
Check recent/previous microbiology
Ciprofloxacin/ Ofloxacin (no streptococcus cover)
D/W microbiology in systemic infections
67
Features of chronic prostatitis
```
Rarely associated with acute prostatitis
May follow Chlamydia urethritis
Recurrent UTIs
Diagnosis difficult
Relapse common
Most asymptomatic
```
Symptoms:
Perineal discomfort/ back pain
+/- low grade fever
UTI symptoms
Common organisms:
Gram negative bacilli, e.g. E.coli, Proteus sp.
Enterococcus sp.
S.aureus (MSAA, MRSA)
68
Features of epididymitis
Inflammatory reaction of the epididymis
Relatively common
Aetiology:
Ascending infection from urethra
Urtheral instrumentation
Symptoms:
Pain, fever, swelling, penile discharge
Symptoms of UTI/urethritis
69
Common organisms causing epididymitis
GNB (e.g. enterobacteriaece), enterococci, staphylococci
TB in high risk areas and individuals
In sexually active men - rule out Chlamydia and N.gonorrhoea (urethritis)
70
Features of orchitis
```
Inflammation of one or both testicles
Testicular pain and swelling
Dysuria
FEver
Penile discharge
```
Aetiology:
Usually mumps
Bacterial - complication of epidiymitis
Bacterial orchitis:
Acutely unwell
Rule out sexually transmitted bacteria
Intravenous antibiotics - as per complicated UTI
71
Features of bacterial orchitis
Testicular infarction
| Abscess formation
72
Features of Fournier's gangrene
| Inc risk factors
Form of necrotising fasciitis
Usually >50 yrs of age
Rapid onset and spreading of infection
Systemic sepsis
```
Risk factors:
UTI
Complications of IBD
Trauma
Recent surgery
```
73
Common pathogens causing Fournier's gangrene
Mixed infections, mainly GNB (e.g. enterobacteriacae) and anaerobes
74
Investigation and Tx of Fournier's gangrene
Blood cultures
Urine
Tissue/pus
Surgical debridement 1st line management
Broad spectrum/combination antibiotics initially e.g. Pip-tazobactam + Gentamicin + Metronidazole +/- Clindamycin
75
Describe the function of the kidney
Primary role of kidneys is to maintain fluid and electrolyte homeostasis in response to blood pressure and hormones
Metabolic waste excretion (urea, creatinine)
Control of solutes and fluid status (sodium, potassium, fluid)
Blood pressure control
Endocrine functions (vitamin D, EPO, PTH)
Drug metabolism/excretion
Acid/base
76
Structure of glomerular filtration barrier
Podocyte foot processes
| Capillary with fenestrated endothelium
77
Measuring urianry protein excretion
24 hour urine collection (grams/24hr)
Protein:Creatinine ratio (PCR) on monitoring spot sample (mg/mmol)
Albumin:creatinine (mg/mmol)
78
Detecting haematuria
Can be blood detectable on dipstick (non-visible haematuria)
Visible haematuria - can come from anywhere in the urinary tract (kidneys, stones, infection, malignancy, cysts, inflammation
79
Renal clearance of a substance =
volume of plasma which would be cleared of the substance per unit of time
Usually described as GFR
80
Glomerulonephritis - targets for injury
```
Of glomerulus:
m=Meangial cells
Basement membrane
Glomerular cpaillaries
Podocytes
```
81
Features of glomerulonephritis
```
Inflammatory disease involving the glomerulus and tubules - categorised by biopsy findings
Rare
Variable natural history
May be primary or secondary (e.g. SLE)
Few specific treatments
```
82
Secondary causes of glomerulonephritis
```
Haem - myeloma, CLL
CV - SBE
Rheum - RA, lupus, amyloid
ID - hepatitis, HIV, malaria, antibiotics
Resp - bronchiectasis, lung cancer, TB
Drugs - NSAIDs, bisphosphonates, heroin
Gastro - ALD, IBD, coeliac disease
```
83
What is required for clinical diagnosis of glomerulonephritis
Kidney biopsy
Biopsy of kidney cortex examined under:
- Light microscopy (glomerular and tubular structure)
- Immunofluorescnce (looking for Ig and complement)
- Electron microscopy (glomerular basement membrane and deposits)
84
Glomerulonephritis will present with
- Proteinuria
- Hypertension
- Haematuria
- Renal impairment
- Nephrotic syndrome
○ Heavy proteinuria and reduced serum albumin
○ Oedema and hyperlipidaemia (inc triglycerides)
- Rapidly progressing glomerulonephritis (RPGN)
○ This is a condition which can go from normal functioning kidneys to end stage renal failure in weeks
○ Associated with an underlying disease such as polyarteritis, lupus or idiopathic
85
Name the types of glomerulonephritis
- Post-infectious GN
- IgA nephropathy
- Membranous GN
- Minimal change disease
- RPGN/ Crescentric GN
86
GN:
| IgA nephropathy - mesangial disease
The most primary glomerular disease
Precipitated by infection
May be secondary to HSP, cirrhosis, coeliac disease
```
Abnormal/overproduction of IgA
Mesangial proliferation
Haematuria
Hypertension
Proetinuria
```
About 1/3rd progress to ESRF
Antihypertensive Rx, ACEi
87
Features of membranous GN
A disease of adults
Presents with nephrotic syndrome - commonest primary cause, often chronic
Can be secondary to malignancy, CTD, drugs
Anti-phospholipase A2 receptor antibody in 70%
Ic in basement membrane/sub-epithelial space
Tx:
Treat underlying disease if secondary
Supportive non-immunological - ACEi, statin, diuretics, salt restriction
Specific immunotherapy - steroids, alkylating agents (cyclophosphamide), cyclosporin, alternative agents - rituximab, anti-CD20 MAb
Outcomes - complete remission, partial remission, ESRD, relapse, death
88
Minimal change disease I
The commonest form of GN in children
Causes nephrotic syndrome
EM - foot process fusion
Idiopathic but may be secondary to malignancy
Pathogeneis - T cell, cytokine mediated
Targets glomerular epithelial cell, GBM charge
89
Minimal change disease II
Acute presentation - may follow URTI
GFR - normal, or reduced due to intravascular depletion
VEry rarely causes renal failure
Relapsing course
Tx:
High dose steroids, Prednisolone 1mg/kg for up to 8 weeks
90
Features of Crescentic GN/ rapidly progressive GN
Group of conditions which demonstrate crescents on kidney biopsy
Aggresive - progresses to ESRF
```
Common causes:
ANCA vasculitis
Goodpasture's syndrome (anti-GBM)
Lupus nephritis
Infeciton associated
HSP nephritis
```
91
Investigations for glomerulonephritis
Medical and drug (including recreational) history
Basics - UEs, dip urine for blood, quantify proetinuria, check albumin, check USS
```
Glomerulonephritis screen:
HbA1c - diabetic neuropathy
ANCA/anti-GBM - vasculitis
ANA/PLA2R/virology - Membranous
Complement/ANA/dsDNA - Lupus
Complement/Virology (hep B, C, HIV)/RF - MPGN, FSGS
```
92
Examples of systemic disease associated with renal dysfunction
```
DM
Atheromatous vasucular disease
Amyloidosis
Myeloma
SLE
RA
Streptococcus
Salmonella
Hep A, B, C
HIV
TB
```
93
How do systemic disease manifest in the kidneys?
```
AKI
CKD
Nephritic syndrome
Proteinuria
Nephrotic syndrome
```
94
How DM affects the kidneys
```
Hyperglycaemia -->
Volume expansion -->
Intra-glomerular hypertension -->
Hyperfiltration -->
Proteinuria -->
Hypertension and renal failure
```
95
Clinical presentation of diabetic nephropathy
- Proteinuria - give ACEi
- Hypertension
- Renal failure - progressive
- Associated with other complications also
96
Histology of diabetic nephropathy
- Thickening of glomerular basement membrane
- Nodular glomerulosclerosis
- Known as kimmelsteil-Wilson kidney
97
Pathogenesis of renovascular disease
Progressive narrowing of renal arteries
Perfusion falls by 30%
GFR falls but tissue oxyfgenation of cortex and medulla maintained
RA stenosis progresses to 70%
Cortical hypoxia causes microvascualr damage and activation of inflammatory and oxidative pathways
Parenchymal inflammation and fibrosis progress and becomes irreversible
Restoration of blood flow provides no benefit
98
Management of renal artery stenosis
Medical:
BP control (not ACEi or ARB)
Stain
If diabetic, good glycaemic control
Lifestyle:
Smoking cessation
Exercise
(low sodium diet)
Angioplasty:
Rapidly deteriorating renal failure
Uncontrolled inc. BP on multiple agents
Flash pulmonary oedema
Treat the underlying condition
99
Amyloidosis - features
Deposition of highly stable insoluble proteinous material in extracellular space (felt-like substance made of beta-pleated sheets)
Kidney, heart , liver, gut
Specific ultrastructural features (8-10nm fibrils)
High affinity for the constituents of the capillary wall
100
Two classes of amyloidosis
AA = systemic amyloidosis (inflammation/infection)
- treat the underlying source of inflammation/infection
AL = immunoglobulin fragments from haematological condition e.g. myeloma
- treat the underlying haematological condition
101
Features of SLE
Autoimmune disease
Imune complex mediated glomerular disease
Feamle>> Male
Genetic predisposition an environmental trigger
102
Pathophysiology of lupus nephritis
Auto-antibodies produced against dsDNA or nucleosomes (anti-dsDNA, anti-histone)
Form intravscular immune complexes or attach to GBM
Activate complement (low C4)
Renal damage
103
Diagnose and treatment of SLE (lupus nephritis)
Renal biopsy to confirm diagnosis and stage disease
Tx:
Immunosuppression - steroids/MMF/cyclophosphamide/rituximab
104
What is a cyst
Sac like structure containing fluid
In the kidneys, these arise from the tubules
Casue problems by compressing other structures, replacing useful tissue, becoming infected, bleeding, pain
105
Features of adult polycystic kidney disease
Autosomal dominant
Commonest inherited kidney disorder
PKD 1 gene mutation - Ch 16 (most common)
PKD 2 gene mutation - Ch4
106
PKD1 and PKD2 gene mutations
Genes code for polycystin 1 and 2
Polycystins are loacated in renal tubular epithelia (and liver and pancrreas ducts)
Overexpressed in cyst cells
Membrane proteins involved in intracellular regulation
Mechanism of cyst formation poorly understood
Genetic testing not routine but is increasing
107
Natural history of APKD
Cysts gradually enlarge
Kidney volume increases
Some compensation
eGFR falls, usually 10y before kidney fails
108
Diagnosis of APKD
Ultrasound
CT or MRI more sensitive
109
APKD clinical consequences
Renal complications:
- 50% risk ESRD by 50y, (seen earlier in PKD1; PKD ~75)
```
Other complications:
Hypertension
Intracranial aneurysms
Mitral valve prolpase
Aortic incompetence
Colonic diverticular disease
Liver/pancreas cysts
Hernia
```
110
Management of APKD
```
Management is supportive
Early detection and management of blood pressure
Treat complications
Manage extra-renal associations
Renal replacement therapy
```
Tolvaptan treatment:
- Vasopressin V2 receptor antagonist
- Shown to slow progression of disease, delaying failure by ~3 years
- SE - hepatotoxicity, hypernatraemia
- Very expensive
111
Examples of other inherited renal disease
Alports syndrome (x-linked) - deafness and renal failure; Collagen 4 abnormalities; Haematuria, proteinuria and ESRF
Fabry's disease (X-linked) - Alpha galactosidase A deficiency resulting in accumulation of Gb3 (esp in podocytes) --> proteinuria and ESRF, neuropathy, cardiac and skin (angiokeratoma) features
Diagnosis - measure alpha-Gal A in leukocytes; Renal biopsy - inclusion bodies of G3b
Management - enzyme replacement therapy
112
Presenting features of pyelonpehritis
```
Pyelonephritis - infection of the kidney
the above PLUS
fever (>38ºC)
chills/rigors
flank pain
costo-vertebral angle tenderness
nausea/vomiting
```
113
UTI risk factors
```
Infancy - boys and girls under 1 year
Abnormal urinary tract - congenital or other abnormalities
Females
Anatomy
Sexual intercourse
Pregnancy
Bladder dysfunction/incomplete emptying
Constipation (‘dysfunctional elimination syndrome’)
Neurogenic bladder
Prostate enlargement in men
‘Foreign' body
catheters
stones
Diabetes mellitus
glycosuria promotes bacterial growth
Renal transplant
Immunosuppression
```
114
Distinguishing features between upper lower UTI in children
```
Upper tract:
Fever
Lethargy
General malaise
Vomiting
Loin pain
```
```
Lower tract:
Non-specific abdo pain
Urgency
Frequency
Wetting
Frank haematuria
```
115
Diagnosis of UTI
Multistix (leucocyte esterase + nitrite)
- Useful for child >3 years
- Positive LE & nitrite → UTI in 90%
- Negative for LE & nitrite → No UTI
- False negatives in < 3 years old
Microscopy/flow cytometry
- Flow cytometry negative for pus cells and bacteria → No UTI
Urine culture
In all children <3 years if clinical suspicion
- Obtain urine before starting antibiotics
- “Clean catch”; supra pubic aspiration; catheter specimen
116
Renal scarring in response to UTI risk factors
```
Age
High grade VUR
Anatomical obstruction
Dysfunctional voiding
Frequent episodes of APN
Therapeutic delay
Bacterial virulence factors
Host response
Low birth weight
Prenatal dysplasia
```
117
Congenital abnormalities of kidney and urinary tract (CAKUT)
Vesico-Ureteric Reflux (VUR)
Obstruction of urinary drainage tracts
Both may be associated with congenital renal dysplasia
118
Role of antenatal renal US
Antenatal alerts - ultrasound
Dilated drainage tract
Renal parenchyma – ‘bright kidneys’
Oligohydramnios
```
Post-natal confirmation
Ultrasound
MCUG
NM studies
DMSA
MAG-3
```
119
Features of CAKUT - VUR
Vesico-ureteric reflux (VUR)
retrograde passage of urine from the bladder into the upper urinary tract
Most common urologic finding in children,
- approximately 1 percent of newborns
- 30 - 40%of young children with UTI
Presentation:
Antenatal hydro-uretero-nephrosis
UTI & Pyelonephritis
VUR in 30-40%
UTI + VUR then 30% ‘renal scarring’
Much damage due to VUR is prenatal = dysplasia
120
Management of VUR and UTI
Medical
Antibiotic prophylaxis for high grade VUR (III-V) until toilet trained by day
Surgical
- Done when medical management hasn't worked, having recurrent febrile UTI or when there is new scarring
- ‘STING’ procedure
- Open ureteric re-implantation
- Role of circumcision
121
Types of bladder outlet obstruction
Posterior Urethral Valve
- Commonest congenital cause in male infants
Prostatic Hypertrophy
- Commonest acquired cause in world
```
Functional obstruction:
Neurogenic Bladder
- Spina Bifida
- Sacral agenesis
- Spinal Dysraphism
- Transverse Myelitis
- Trauma
Prune Belly Syndrome
```
122
Presentation and management of posterior urethral valve (a cause of bladder obstruction)
```
Presentation
- Antenatal hydronephrosis
- Urinary tract infection
- Poor urinary stream
- Renal dysfunction
Valve leaflets or circumferential diaphragm
```
Management
- Valve resection
- Antibiotic prophylaxis
- CKD care
123
Presentation of PUJO (Pelvi-ureteric junction obstruction)
Commonest cause of hydronephrosis in children
Frequently noted on antenatal ultrasound
Abdominal mass; pain; haematuria; UTI.
124
Presentation of VUJO (Vesico-ureteric junction obstruction)
Anatomical narrowing v. functional obstruction
| Antenatal dilatation; UTI; Abdominal mass; pain; haematuria.
125
Management of PUJO
Observant
- USS and DMSA; MAG 3 diuresis renogram
Surgical
- Pyeloplasty
126
Why do stones form?
Abnormal urine
Urinary obstruction
Urinary infection
127
Risk factors for prostate cancer
Age:
85% diagnosed in over 65yrs old
Microscopic foci 30% 50yo and 70% >80yo.
Familial and genetic factors:
Abnormalities on chromosomes - 1q, 8p and Xp
PTEN and TP53 - TSGs
Hormones
Racial factors: african american 1.6 x risk of white american
Geographic variations: highest incidence in westernized nations, least in Asia and Far East. US migrants from Japan and Asia 20x increase
128
Signs and symptoms of prostate cancer
```
Local (66%) and locally advanced (27%)
symptoms:
OFTEN ASYMPTOMATIC (PSA)
Painful or slow micturition
Urinary tract infection
Haematuria - blood in urine
Urinary retention (may cause anuria, uraemia)
Lymphoedema
Metastastic (7%)
Bone pain - most common symptom of metastases
Renal failure- ureteric obstruction
```
Raised PSA level - on suspicion or screening
129
Diagnosis and screening of prostate cancer
DRE - digital rectal examination
PSA - prostate-specific antigen
TRUS - guided needle biopsy
130
Pathology of prostate cancer
Majority is primary adenocarcinoma
Usually arises in peripheral zone of prostate
Gleason grading
131
Staging of prostate cancer
TNM classification includes:
Clinical tumour staging (T)
Lymph node involvement (N)
Metastases (M)
132
Prostate specific antigen (PSA)
Serine protease (33kD) secreted into seminal fluid
Responsible for liquefaction of seminal coagulation. Efficiently hydrolyses semenogelins causing release of sperm.
Small proportion leaks into circulation
Tissue not Tumour specific
Tends to rise with age
Depends on prostate size
Other influences (eg inflammation, infection)
133
Tx options for localised prostate cancer
```
Watchful waiting
Active Surveillance
Radiotherapy (with or without LHRH analogue)
external beam
conformal
brachytherapy
Radical prostatectomy
Cryotherapy/HIFU
TURP if symptomatic
```
134
Metastatic complications of prostate cancer
```
Spinal cord compression:
Urological emergency
Severe pain
Off legs
Retention
Constipation
Urgent MRI
Radiotherapy vs spinal decompression surgery
```
Ureteric obstruction:
Anorexia, weight loss, raised creat
To nephrostomize or not and then to stent or not
Temporary measure will not improve cancer progression
135
Treatment options for advanced prostate cancer
Androgen ablation therapy - medical castration (LHRH analogue) or surgical castration (orchidectomy)
Chemotherapy
TURP for relief of symptoms
Radiotherapy
136
What gender is more commonly affected in bladder cancerr
MAles
Male:Females 2.5:1
More common in elderly
137
Risk factors of bladder cancer
Age – rare <50yrs, most common 80th decade
Race- more common in caucasians
Environmental Carcinogens
Chronic inflammation- stones, infection (schistosamiasis), long term catheters
Drugs- phenacitin, cyclophosphamide
Pelvic radiotherapy
Occupation .
Smoking accounts for 30-50% of all bladder cancers - risk only returns to normal after smoking cessation of 20 years
138
Presentation and diagnosis of bladder cancer
Classically painless frank haematuria
25% serious cause for this in over 65s
All should have cystoscopy, renal USS/KUB
Cystoscopy is mandatory
Some present with microscopic haematuria (5% serious causes)
139
Pathology of bladder cancer
```
Transitional cell carcinoma is the most common histological type of bladder cancer - 90% (Superficial 75%
and Invasive 25%)
Squamous carcinoma – 5%
Adenocarcinoma – 2%
Other secondaries
```
140
Grading of bladder cancer
Grade 1 – well differentiated – good prognosis
Grade 2 – moderately differentiated
Grade 3 – poorly differentiated
Least common
Most likely to progress to invasive disease
Carcinoma in situ
141
Treatment of bladder cancer
Diagnosed at flexible cystoscopy
Urgent TURBT (trans-urethral resection of bladder tumour) booked
CT IVU (5% chance upper tract involvement)
Bimanual examination carried out at TURBT
Intravesical mitomycin reduces risk of recurrence
142
Stages of bladder cancer
```
Low grade
superficial
High grade superficial
Muscle invasive
Metastatic TCC
```
143
Tx of low grade superficial bladder cancer
LOW risk of progression (10%)
Flexible check cystoscopy 3 months
30% chance recurrence
Course of 6 weekly mitomycin treatments given for persistent Ta tumours
144
Tx of high grade superficial bladder cancer
80% recurrence risk
50% chance of progressing to muscle invasive disease
Do early check cystoscopy and rebiopsy
Treat with intravesical BCG immunotherapy – effective in 50%
Course of 6 weekly instillations then further cystoscopy/biopsy
Cystectomy of treatment fails
145
Tx of muscle invasive bladder cancer
```
Require radical therapy
radical cystectomy or radiotherapy
Both equally effective (?)
Radiotherapy poor if multifocal disease or widespread CIS
Neo-adjuvant chemotherapy
```
146
Radical cystectomy
Bladder and prostate/uterus removed
Urine diverted into an ileal conduit or (rarely) an orthotopic neobladder
Complex surgery
Mortality 2%
Sometimes required after radiotherapy failure “salvage cystectomy”
147
Tx of metastatic bladder cancer
```
Often pulmonary
Treat with chemotherapy
Classic M-VAC
Methotrexate, vinblastine, doxorubicin, cisplatin
Highly toxic
Gemicitobine/Docetaxel
```
148
What gender is more commonly affected with renal cancer
Male: Female 2:1
149
Risk factors of renal cancer
```
Smoking (RR 1.4-3.0)
Obesity (RR 1.5-3.0)
Hypertension
Acquired renal cystic disease (RR 4)
Haemodialysis
```
Genetics- VHL (vhl), HPRCC (Met), HLRCC (FH), Birt-Hogg-Dube (FLNC), Tuberous sclerosis (TS)
150
Presentation of renal cancer
```
80% incidental
<25% systemic symptoms-
Night sweats
Fever
Fatigue
Weight loss
Haemoptysis
10% classic triad- mass, pain, haematuria
Varicocele
Lower limb oedema
Paraneoplastic syndrome
```
Paraneoplastic syndromes:
- Polycythaemia:(3-10%) from increased erythropoetin production
- Hypercalcaemia:(3-13%) either from a PTH-like substance, or from osteolytic hypercalcaemia
- Hypertension:(Up to 40%) renin secretion
- Deranged LFT’s:Stauffer’s syndrome, from hepatotoxic tumour products
- Rarely produces ACTH (Cushing’s syndrome), enteroglucagon (protein enteropathy), prolactin (galactorrhoea), insulin (hypoglycaemia) and gonadotropins.
151
Diagnosis and investigation of renal cancer
Initial diagnosis:
Usually on USS
FBC, UE, LFT, CRP, bone profile, LDH
CT kidneys +/- MRI RV
Renal Biopsy
CT Chest
152
Histology of renal cancer
Conventional or clear cell (80%)- vascular, granular and clear (lipids)
Papillary (10%)- solid and 40% multi-focal
Chromophobe (5%)- large polygonal
Collecting duct- rare
Medullary cell- rare
153
Treatment of renal cancer
Large Renal Mass
Radical Nephrectomy
If no absolute indication for NSS
Radical Nephrectomy
Removal of kidney and Gerota’s fascia. Sparing adrenal gland.
```
Small Renal Mass
1. Biopsy
2. Treatment
Nephron sparing surgery
Partial Nephrectomy
Cryotherapy
Radical Nephrectomy
Surveillance
```
Indications for NSS
single kidney
CKD
CV risk factors
pT1a tumours
Tyrosine Kinase Inhibitors for metastatic disease
154
Risk factors of testicular cancer
Age 20-45yo
Cryptorchidism
HIV
Caucasian population
155
Clinical features of testicular cancer
Majority present as painless lump
May be noticed after incidental trauma
```
Investigation:
Scrotal ultrasound
Tumour markers:
Alpha-fetoprotein (50-70% Teratoms and Yolk Sac Tumours)
Beta hCG (40% Teratoma, 15% Seminoma)
LDH (10-20% Seminoma)
```
Regular Testicular Self Examination advised
156
Classification of testicular cancer
Germ cell tumours (most common) - Seminoma, teratoma, mixed, yolk sac
Stromal tumours (10% malignant) - leydig, sertoli
Other - lymphoma, metastasis
157
Treatment of testicular cancer
Radical Orchidectomy
Chemotherapy
Para-aortic nodal radiotherapy
Retroperitoneal Lymph Node Dissection
158
Features of penile cancer
Rare
Associated with HPV infection and smoking
Premalignant lesions: chronic changes
Even rarer in males circumcised at birth
159
Tx of penile cancer
```
Circumcision
Topical treatment CO2/5FU
Penectomy +/- reconstruction
Lymphadenopathy
Chemo-radiotherapy
```
160
Child presents with swelling around eyes (bilateral periorbital swelling) and swollen ankles (pitting oedema). Urine appears 'bubbly'.
No other abnormalities found on examination of CVS, RS, abdomen or CNS.
What is the likely diagnosis?
Straightforward presentation of nephrotic syndrome in a previously fit child (Confirm by looking for proteinuria and low serum albumin).
The diagnosis of minimal change nephropathy is so likely that renal US, and later renal biopsy, are performed only if there is an atypical feature on intial investigation
161
Definition of nephrotic syndrome
3.5g proteinuria per 24h (urine PCR >300mg/mmol)
Serum albumin <30g/l
Oedema
```
Triad of:
Proteinuria
Hypoalbumin
Oedema
(often there is hyperlipidaemia)
```
162
Management of minimal change nephropathy (in a child)
High dose oral steroid (prednisolone)
Continue steroid until urinalysis negative for protein for 2 weeks then taper dose down over weeks
If no response to steroid within 4 weeks consider biopsy if not already performed
163
50y female presents with ankle swelling, No chest pain or palpitations. No cough. No blood seen in urine. No dysuria. No diurnal urinary frequency, but nocturia once per night for 4 weeks. Some nasal stuffiness. No skin rash.
Hypertensive on therapy for 5 years (found at routine insurance medical examination, can’t remember if urine tested then).
DH: Irbesartan and amlodipine. No over-the-counter medications. No known allergies
Systems enquiry: Weight increased by 5 kg in past month.
Minimal generalised joint stiffness for a few minutes each morning.
Examination:
. BP146/92. JVP 2cm. Apex beat not displaced. No thrills or heaves. Heart sounds normal, with grade 1/6 ejection systolic murmur heard only at the left sternal edge. Pitting oedema to knees, symmetrical.
Adult npehrotic syndrome. Diagnosis is membranous nephropathy
164
Management of membranous glomerulonephritis
Treat oedema: Salt and fluid restriction, diuretics
Consider secondary causes
Start ACEi / ARB to target BP 130/80mmHg
Consider statin therapy and anticoagulation
Observe for 6 months - ?spontaneous remission (resolution of proteinuria, normalisation of serum albumin)
If no spontaneous remission consider immunosuppressive therapy
165
CBL emphasised GN screen - go over this
-
166
Teenage male presents with:
Last night urine appeared to be “all blood”. Urine still “dark” colour this morning.
No loin pain or dysuria. No nocturia or diurnal frequency.
Dark urine for a few days after episode of tonsillitis 6 months ago, but no frank blood in urine then
Flushed. T 37.5. Fauces inflamed with purulent exudate. No cervical lymphadenopathy
CVS, RS, abdominal and CNS examination all unremarkable. BP 132/74
Urine: inspection - frank haematuria
: Urine Protein:Creatinine ratio 456mg/mmol
immunoglobulins (IgA 6.4g/l (0.8-4.0))
Throat swab: Strep pyogenes
Other results all normal
Diagnosis?
Acute glomerulonephritis - IgA nephropathy.
Loin pain and haematuria after resp tract infection in young patients more often now reflects IgA nephropathy than classical post-streptococcal glomerulonephritis.
In this case, the short time between the resp symptoms and the development of haematuria, the high IgA level, normal complement levels and negative ASO titre all point to IgA nephropathy.
Timing of haematuria doesn’t fit with post-infectious glomerulonephritis (requires a latent period)
167
Histology/cytology of IgA nephropathy
Proliferation of mesangial cell matrix and hypercellularity with IgA deposits in mesangium on immunofluorescence.
168
70y female presents with:
Nausea, breathlessness and coughing up blood
Gradual but progressive tiredness. Breathless when walking 50 yards and, over past week, when lying in bed. Ankle swelling for 2 weeks. Feeling sick and unable to eat for 5 days, but has not vomited. Cough for 3 days. Last night coughed up blood. Has passed only a few drops of urine today. Urine volume has fallen over the past few days, when she says she has drunk less fluid than usual because of nausea
Retired cleaner. Smokes 10 cigarettes/day (20/day till 10 years ago). Alcohol only at weddings
Systematic enquiry: No chest pain or palpitation. Morning cough throughout winter, but no previous haemoptysis. Weight loss approx 1 stone over past 2 months.
Thin, pale, breathless at rest (respiratory rate 20/min). Mucous membranes pale. No finger clubbing
JVP 2cm. BP 143/67mmHg. Apex beat not displaced. Heart sounds normal with no added sounds. Pitting oedema at ankles.
Sats 94% on 35% oxygen. Trachea central. Expansion symmetrical. Percussion note resonant. Air entry good to all areas. Breath sounds vesicular with widespread coarse inspiratory crepitations.
Active crescent obliterating Bowman’s space and compressing glomerular tuft
Differential diagnosis?
Diagnosis?
Management?
Differential - malignancy, heart failure, TB, nephropathy, vascultitis
Diagnosis:
Rapidly progressive glomerulonephritis secondary to ANCA-associated vasculitis (AAV)
cANCA PR3 antibody positive – GranulomatosIs with polyangiitis
The presentation of acute golumeronephritis is a medical emergency. The falling urine volume and rising serum creatinine indicate irreversible destruction of glomeruli, asspcoated with glomerular crescents on renal biopsy. With strong clinical suspicison of a rapidly progressive glomerulonephritis and the risk of life-threatening haemoptysis, the patient should start cortciosteroid therapy before the results of renal biopsy and anti-GBM testing are available.
Management:
High dose steroids, oral cyclophosphamide and plasma exchange (based on renal function and pulmonary involvement)
May require haemodialysis
169
Signs and symptoms of granulomatosis with polyangiitis
Oral cavity: ulceratinos throughout oral mucosa
Eye: pseudotumours, conjuctivitis
Nose - stuffiness, nose bleeds
Heart - pericarditis
Kidneys - glomerulonephritis
Granulomas and patchy necrosis in blood vessels
Skin - nodules on elbow, purpura
Lungs - cavities, bleeds, lung infiltrates
Positive anti-neutrophil cytoplasm test
170
```
Young male (24) presents with painful right arm and leg.
Fouund lying at home next to radiator, his clothes soaked in urine and covered in faeces. Mother last spoke to him 3 days ago and thought he was fine. Now that he's awake he says he can't move his right arm or leg, which are sore and swollen.
```
```
Ex-IV drug user, prescribed methadone.
Jaundice 1 year ago with liver problem.
DHx - methadone, sodium valporate
20 cigarettes a day
70 units alcohol/week
```
Reduced skin turgor and tongue dry.
Pulse 104/min
BP 84/52
CRT >5 seconds
R limb swollen, tender, grade 1 power (red). Tendon reflexes absent on R, R plantar withdrawal.
Urine - inspection - chocolate-brown
Dipstick analysis - blood ++++
Myoglobinuria - with false positive dipstick haematuria
He is hyperkalaemic
Diagnosis?
Management
Acute kidney injury - Rhabdomyolysis
Has several RxF - drugs, local heat, and a history suggesting of seizures. The risk of AKI is increased by dehydration
```
Management:
Manage his hyperkaelamia
Rehydrate
Probably acute haemodialysis
Refer to orthopedics for consideration of muscle compartment syndrome
Screen for sepsis
```
171
Tx of hyperkalaemia (cbl)
Protect the heart --> IV calcium
Drive K+ into cells --> Insulin/dextrose beta agonists, sodium bicarbonate
Remove K+ from the body --> Dialysis resonium
172
```
Elderly women (82) - not passing urine.
Admitted to surgical ward 5 days ago with 2 day H/O left iliac fossa pain and fever. Presumptive diagnosis at that time diverticular abscess, confirmed on CT scan of abdomen and pelvis. Given antibiotics (including gentamicin). Fever settled but now has not passed urine for 24 hours. Serum creatinine was 157micromols/l on the day of admission and 268micromols/l 2 days later
```
Metformin, gliclazide, amlodipine, bisoprolol, ramipril, warfarin, aspirin, omeprazole, simvastatin, diclofenac
Over-the-counter paracetamol if joints sore. No known allergies.
```
Multimorbid patient with polypharmacy
Risk factors for AKI:
Age
Baseline renal function? Likely impaired
Diabetes
Sepsis
Drugs: Gentamicin, ramipril, diclofenac
Intravenous contrast administration
```
Obese, pale, breathless (respiratory rate 24/min
HR 96/min, irregularly irregular. BP 84/50. JVP not visible. Apex beat impalpable. Apical heart rate 154/min. Heart sounds poorly audible but normal. Ejection systolic murmur (grade 2/6) heard maximally in aortic area, radiating to neck. Pitting sacral oedema
RS: Reduced air entry to both lung bases.
Abdomen: Mild tenderness in left iliac fossa. No rigidity or guarding
Investigations?
Diagnosis?
Management?
```
Investigations:
Urine
FBC
Serum biochemistry – renal function, CRP, liver function, bone profile
Serum gentamicin level
ECG
CXR
Renal ultrasound
```
Diagnosis:
Acute kidney injury - multifactorial
Management:
Resuscitation, including correction of hypotension - fluid resuscitation; inotropes difficult with tachyarrhythmia
Correction of hyperkalaemia
Treat sepsis
Withdrawal of potentially nephrotoxic drugs
Consideration of haemodialysis
173
34y female presents with tiredness.
Tired for “years” but worse over past 6 months. Last menstruated 2 months ago – periods always irregular. Denies possibility of pregnancy. Morning nausea for 3 weeks. “Rotten taste” in mouth. No vomiting. Poor appetite, loss of normal taste sensation, has lost 2 stone in past 3 months
PMH:
Childhood bedwetting till age 8
Lifelong urinary tract infections, attended hospital clinic in childhood but stopped attending in teens
High blood pressure and urinary tract infections during her only pregnancy (aged 22), has not had blood pressure checked for “years”
Son attends paediatric clinic because of urine infections
Nocturia, twice per night since childhood, but 3 or 4 times recently. Increasing urinary frequency
Thin, with obvious weight loss. No rashes or joint abnormalities
CVS: P68/min, regular, normal volume and character. BP 104/68
Urine: dipstick urinalysis: protein++, no haematuria, no glycosuria
```
Renal function:
Na 130 (135-145 mmol/l)
K 3.4 (3.5-5.0 mmol/l)
HCO3 14 (22-26 mmol/l)
Urea 32 (2.5-6.5 mmol/l)
Creat 876 (40-130 umol/l)
eGFR 5ml/min/1.73m2
Urine PCR 67mg/mmol
```
Diagnosis?
Management?
Chronic kidney disease - Reflux nephropathy
Management:
Overall diagnosis likely chronic pyelonephritis associated with reflux nephropathy
Investigate and treat secondary metabolic abnormalities
Anaemia: Correct haematinic deficiencies, ?ESA
Acidosis: Oral sodium bicarbonate
Hyperparathyroidism: Manage phosphate, replace vitamin D
Prepare for renal replacement therapy
174
56y female presents with Abdominal pain and diarrhoea
HPC: Abdominal pain for 1 week, increasing in frequency and intensity. Episodes now every day, lasting for up to 4 hours. Colicky in nature. At times generalised, but worst in the right iliac fossa. No exacerbating or relieving factors; pain unresponsive to paracetamol and peppermint water. Diarrhoea 6 times a day for last 2 weeks, including overnight, no blood in stools. No vomiting, but nausea and loss of appetite. 3kg weight loss over past 3 weeks.
Hypertension – diagnosed at antenatal clinic 1977
Adult polycystic kidney disease – diagnosed during pregnancy 1981
Cerebral haemorrhage 1990 (aneurysm clipped)
Renal failure – started peritoneal dialysis 2007
Living donor renal transplant from sister 2009 – excellent kidney function
Post-transplant diabetes 2010
No TB, jaundice, asthma, epilepsy. BCG aged 13.
Prednisolone, tacrolimus, mycophenolate mofetil, atenolol, amlodipine, insulin
No over-the-counter medications. Allergic to penicillin (rash)
```
Pale. Temperature 37.9⁰C
CVS, RS, CNS: no abnormality detected
Investigations?
Diagnosis?
Management?
```
Investigations:
FBC
Serum biochemistry – renal function, bone profile, liver function, including lactate dehydrogenase (LDH), CRP
Stool culture and blood cultures
Virology testing
Consider abdominal imaging e.g. CT abdomen and pelvis
Diagnosis:
Renal transplant recipient on immunosuppression with abdominal pain, diarrhoea, pyrexia and weight loss
Shows opportunistic infections and tumours associated with immunosuppressive therapy for transplantation.
Management:
Minimise immunosuppression
Specific anti-viral therapy (ganciclovir or valganciclovir)
If renal function doesn’t normalise consider transplant biopsy
175
List 5 possible causes of haematuria
```
Glomerulonephritis
IgA nephropathy
UTI (lower)
Prostate cancer
Bladder cancer
Renal cancer
```
