Wk14 - Nephrology/Urology Flashcards
Definition of AKI
“Decline of renal excretory function over hours or days …recognised by the rise in serum urea and creatinine”
RIFLE/AKI criteria
What is oligouria classified as?
UO <3ml/kg/hr
What system is used in hospital labs when trying to indicate change in creatinine that signifies AKI
AKI e-Alerts
Stages of AKI (severity)
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
Causes of AKI
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.
What is ATN
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
Causes of ATN
ATN is always due to under perfusion of the tubules and/or direct toxicity: Hypotension Sepsis Toxins Or often, all three
Examples of toxins causing ATN
Exogenous:
Drugs (eg, NSAID’s gentamicin, ACEi)
Contrast
Poisons (eg, metals, antifreeze)
Endogenous: Myoglobin Haemoglobin Immunoglobins Calcium Urate
Management of AKI
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
Diagnostic process for AKI - investigations
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
Treatment of hyperkalaemia (with AKI) - causing arrhythmias (e.g. tachycardia)
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
Absolute and relative indications for dialysis
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)
Definition of CKD
CKD = kidney damage of GFR<60ml/min per 1.73m2 for 3 months or more
How serum creatinine can be used to measure kidney function
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
Problems with eGFR
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
Classification of CKD
According to eGFR
Stage 1 - >90 2 - 60-89 3a - 45-59 3b - 30-44 4 - 15-29 5 - <15
Proteinuria
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)
ACR and PCR (mg/mmol)
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
Aetiology of CKD
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
Symptoms of advanced CKD
Pruritus Nausea, anorexia, weight loss Fatigue Leg swelling Breathlessness Nocturia Joint/bone pain Confusion
Signs of advanced CKD
Peripheral and pulmonary oedema Pericardial rub Rash/excoriation Hypertension Tachypnoea Cachexia Pallor &/or lemon yellow tinge
CKD g
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
Slowing progression of CKD
Aggressive BP control Good diabetic control Diet Smoking cessation Lowering cholesterol Treat acidosis
ACEi/ARB in CKD
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
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
How are the kidneys associated with CKD
Secondary hyperparathyroidism:
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
Indications for dialysis
Medically resistant hyperkalaemia Medically resistant pulmonary oedema Medically resistant acidosis Uraemic pericarditis Uraemic encephalopathy
& specific drug overdoses
Signs of clinically uraemic patient
Anorexia Vomiting Itch Restless legs Weight loss Metabolic taste
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
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
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
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
Haemodialysis complications
‘Crash’ (acute hypotension) Access problems (with fistula) Cramps Fatigue Hypokalaemia Blood loss Dialysis disequilibrium Air embolism
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
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
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
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
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
Problems not helped by dialysis
Anaemia – need erythropoesis supplementing agents and iron
Renal bone disease – need phosphate binders and vitamin D
Neuropathy
Endocrine disturbances
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
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
Lower urinary tract infection
Upper
Lower - Cystitis
Upper - Pyelonephritis, renal abscess
Urosepsis
Urosepsis, complicated UTI: Temp >38ºC HR>90/min RR>20/min WBC >15.0 or <4.0
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
Ascending UTI
Urethral colonisation
female>male
Multiplication in bladder
Ureteric involvement
Descending UTI
Blood-born infections
Involvement of renal parenchyma
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
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.)
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
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
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
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
Complications of catheters
CAUTI Obstruction-hydronephrosis Chronic renal inflammation Urinary tract stones Long term risk of bladder cancer
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
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
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
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
What is a complication of pyelonephritis
Renal abscess
Perinephrtic abscess
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
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
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 allergyReasons for pyuria with no bacteria
Previous/recent antibiotic Tumour Calculi Urethritis (check for Chlamydia) Tuberculosis
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)
Investigations for acute bacterial prostatitis
Urine culture, usually positive Blood culture Trans-rectal U/S CT/ MRI Obtaining prostatic secretions NOT advisable
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
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)
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
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)
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
Features of bacterial orchitis
Testicular infarction
Abscess formation
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
Common pathogens causing Fournier’s gangrene
Mixed infections, mainly GNB (e.g. enterobacteriacae) and anaerobes
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
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
Structure of glomerular filtration barrier
Podocyte foot processes
Capillary with fenestrated endothelium
Measuring urianry protein excretion
24 hour urine collection (grams/24hr)
Protein:Creatinine ratio (PCR) on monitoring spot sample (mg/mmol)
Albumin:creatinine (mg/mmol)
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
Renal clearance of a substance =
volume of plasma which would be cleared of the substance per unit of time
Usually described as GFR
Glomerulonephritis - targets for injury
Of glomerulus: m=Meangial cells Basement membrane Glomerular cpaillaries Podocytes
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
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
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)
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
Name the types of glomerulonephritis
- Post-infectious GN
- IgA nephropathy
- Membranous GN
- Minimal change disease
- RPGN/ Crescentric GN
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
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
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
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
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
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
Examples of systemic disease associated with renal dysfunction
DM Atheromatous vasucular disease Amyloidosis Myeloma SLE RA Streptococcus Salmonella Hep A, B, C HIV TB
How do systemic disease manifest in the kidneys?
AKI CKD Nephritic syndrome Proteinuria Nephrotic syndrome
How DM affects the kidneys
Hyperglycaemia --> Volume expansion --> Intra-glomerular hypertension --> Hyperfiltration --> Proteinuria --> Hypertension and renal failure
Clinical presentation of diabetic nephropathy
- Proteinuria - give ACEi
- Hypertension
- Renal failure - progressive
- Associated with other complications also
Histology of diabetic nephropathy
- Thickening of glomerular basement membrane
- Nodular glomerulosclerosis
- Known as kimmelsteil-Wilson kidney
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
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
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
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
Features of SLE
Autoimmune disease
Imune complex mediated glomerular disease
Feamle» Male
Genetic predisposition an environmental trigger
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
Diagnose and treatment of SLE (lupus nephritis)
Renal biopsy to confirm diagnosis and stage disease
Tx:
Immunosuppression - steroids/MMF/cyclophosphamide/rituximab
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
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
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
Natural history of APKD
Cysts gradually enlarge
Kidney volume increases
Some compensation
eGFR falls, usually 10y before kidney fails
Diagnosis of APKD
Ultrasound
CT or MRI more sensitive
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
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
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
Presenting features of pyelonpehritis
Pyelonephritis - infection of the kidney the above PLUS fever (>38ºC) chills/rigors flank pain costo-vertebral angle tenderness nausea/vomiting
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
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
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
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
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
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
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
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
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
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
Presentation of PUJO (Pelvi-ureteric junction obstruction)
Commonest cause of hydronephrosis in children
Frequently noted on antenatal ultrasound
Abdominal mass; pain; haematuria; UTI.
Presentation of VUJO (Vesico-ureteric junction obstruction)
Anatomical narrowing v. functional obstruction
Antenatal dilatation; UTI; Abdominal mass; pain; haematuria.
Management of PUJO
Observant
- USS and DMSA; MAG 3 diuresis renogram
Surgical
- Pyeloplasty
Why do stones form?
Abnormal urine
Urinary obstruction
Urinary infection
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
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
Diagnosis and screening of prostate cancer
DRE - digital rectal examination
PSA - prostate-specific antigen
TRUS - guided needle biopsy
Pathology of prostate cancer
Majority is primary adenocarcinoma
Usually arises in peripheral zone of prostate
Gleason grading
Staging of prostate cancer
TNM classification includes:
Clinical tumour staging (T)
Lymph node involvement (N)
Metastases (M)
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)
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
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
Treatment options for advanced prostate cancer
Androgen ablation therapy - medical castration (LHRH analogue) or surgical castration (orchidectomy)
Chemotherapy
TURP for relief of symptoms
Radiotherapy
What gender is more commonly affected in bladder cancerr
MAles
Male:Females 2.5:1
More common in elderly
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
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)
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
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
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
Stages of bladder cancer
Low grade superficial High grade superficial Muscle invasive Metastatic TCC
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
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
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
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”
Tx of metastatic bladder cancer
Often pulmonary Treat with chemotherapy Classic M-VAC Methotrexate, vinblastine, doxorubicin, cisplatin Highly toxic Gemicitobine/Docetaxel
What gender is more commonly affected with renal cancer
Male: Female 2:1
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)
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.
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
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
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
Risk factors of testicular cancer
Age 20-45yo
Cryptorchidism
HIV
Caucasian population
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
Classification of testicular cancer
Germ cell tumours (most common) - Seminoma, teratoma, mixed, yolk sac
Stromal tumours (10% malignant) - leydig, sertoli
Other - lymphoma, metastasis
Treatment of testicular cancer
Radical Orchidectomy
Chemotherapy
Para-aortic nodal radiotherapy
Retroperitoneal Lymph Node Dissection
Features of penile cancer
Rare
Associated with HPV infection and smoking
Premalignant lesions: chronic changes
Even rarer in males circumcised at birth
Tx of penile cancer
Circumcision Topical treatment CO2/5FU Penectomy +/- reconstruction Lymphadenopathy Chemo-radiotherapy
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
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)
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
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
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
CBL emphasised GN screen - go over this
-
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)
Histology/cytology of IgA nephropathy
Proliferation of mesangial cell matrix and hypercellularity with IgA deposits in mesangium on immunofluorescence.
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
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
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
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
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
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
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
List 5 possible causes of haematuria
Glomerulonephritis IgA nephropathy UTI (lower) Prostate cancer Bladder cancer Renal cancer
