Describe the structure of the glomerular filtration barrier
Constriction of afferent arteriole is controlled by SNS
Constriction of efferent arteriole is controlled by angiotensin II
Layers of filtration
Fenestrated capillary endothelium (endothelial cells covered by glycocalyx)
Negatively charged glomerular basement membrane
Foot processes of podocytes
> Wrap around capillaries and leave slits between them for blood to filter through
> Podocytes secrete the basement membrane
> . Filtration slits (slit diaphragm)
Describe how urea is processed and how its levels may change
Byproduct of amino acid metabolism in liver
Reabsorbed in inner medullary collecting ducts (passively)
Changes in urea
Diet
> High protein or GI bleed leads to high urea
Tissue breakdown e.g. corticosteroid
> High urea
Liver failure
> Lowers urea
Dehydration
> Passive reabsorption in proximal tubule - high urea
Explain why creatinine is used to measure renal function
Normal product of muscle metabolism
Provides good estimate of GFR because
> Daily production is constant
> (almost) fully filtered at the glomerulus
> Neither reabsorbed nor secreted (almost) in the tubule
Describe the limitations of eGFR
Only accurate in steady state and assumes average muscle mass
> Overestimation of function those with lower muscle mass e.g. amputees, para/quadriplegics, rheumatoid arthritis
eGFR not accurate >60ml/min and <18 years of age
Inverse relationship between GFR and serum creatinine leads to
> Slow recognition of loss of the first 70% of kidney function
> Surprise at the sudden rise in creatinine
Desribe the formulae used to calculate eGFR
Cockgroft and Gault formula for estimating creatinine clearance
> Attempts to correct for muscle mass
MDRD 4-variable formula for estimated GFR
> Based on serum creatinine, age, sex
eGFR < 60ml/min/1.73m2 or raised serum creatinine means reduced kidney function (adults)
CKD-EPI equation for patients with high levels of eGFR
Describe acute interstitial nephritis
May have raised eosinophil count and rash
- Haematuria, fever, oliguria
- Swelling, nausea, vomiting
Caused by autoimmune disorders, systemic disorders, infections, allergic reaction to antibiotics, anticonvulsants, diuretics…
Describe the staging of CKD
Stage 1:
Normal
GFR >90ml/min
Stage 2:
Early CKD
GFR 60-89ml/min
Stage 3:
Moderate CKD
GFR 30-59ml/min
Stage 4:
Severe CKD
GFR 15-29ml/min
Stage 5:
End-stage renal disease
GFR <15ml/min
Describe the measurement of urinary protein excretion
24h urine collection (g/24h)
Protein:creatinine ratio (PCR) on morning spot sample (mg/mmol)
Albumin:creatinine ratio (mg/mmol)
If excess proteinuria, the balance changes
30% other proteins
> Immunoglobulin
> Tamm Horsfall
70% albumin
Which cells and pathophysiological mechanisms are involved in glomerulonephritis?
Cells
- Parietal epithelial cells
- Podocytes
- Mesangial cells
- Endothelial cells
- Basement membrane
Pathophysiological mechanisms
- Antibodies, immune complexes, complement
- Cell-mediated mechanisms: cytokines, growth factors, proteinuria
- Metabolic / genetic / vascular causes
Describe the spectrum of presentations of glomerulonephritis
Incidental finding of urinary abnormalities +/- impaired kidney function
Visible haematuria
Synpharyngitic – sore throat and visible haematuria
Nephritic syndrome
Nephrotic syndrome
Acutely unwell with rapidly progressive glomerulonephritis
Describe nephrotic syndrome
Cause
> Damage to podocytes
> Scarring and deposits
Triad
> 3.5g proteinuria per 24h (urine PCR >300)
> Serum albumin <30
> Oedema
> (hyperlipidaemia)
Complications
> Venous thromboembolism
> Infection
Describe nephritic syndrome
More acute and inflammatory than nephrotic syndrome
Triad
> Hypertension
> Blood and protein in urine
> Declining kidney function (oliguria)
Berger’s disease (IgA nephropathy) is the most common cause of nephritic syndrome
Describe IgA nephropathy
Most common primary glomerular disease
> Precipitated by infection, can be synpharingitic
> May be secondary to HSP, cirrhosis, coeliac disease
Pathophysiology
> Abnormal overproduction of IgA1, IgA I/C
> Mesangial IgA, C3 deposition
> Mesangial proliferation
Clinical signs
> Haematuria
> Hypertension
> Proteinuria (varies with prognosis)
Complications
> End-stage renal failure (ESRF)
Treatment
> No specific therapy
> Antihypertensives
> ACE inhibitors
> SGLT2 inhibitors
Spectrum of disease
> Minor urinary abnormalities
> Hypertension
> Renal impairment and heavy proteinuria
> Rapidly progressive glomerulonephritis
Describe membranous glomerulonephritis
Presents with nephrotic syndrome
> Commonest primary cause
> Often chronic
Anti-phospholipase A2 receptor antibody – found in podocytes
IC in basement membrane / sub-epithelial space
Secondary causes
> Malignancy
> Connective tissue disease (CTD)
> Drugs
Variable natural history
> 1/3 spontaneously remit
> 1/3 progress to ESRF over 1-2 years
> 1/3 persistent proteinuria, maintain GFR
Treatment
> Treat underlying cause if secondary
> Supportive non-immunological
> ACEi
> Statin
> Diuretics
> Salt restriction
Specific immunotherapy
> Steroids
> Alkylating agents – cyclophosphamide
Alternative agents
> Rituximab: anti-CD20 MAb
> Cyclosporin
> Tacrolimus
Outcomes
> Complete or partial remission
> ESRD
> Relapse
> Death
Describe minimal change disease
Commonest form of glomerulonephritis in children
> 90% of GN <10 years, 20% of adults of all ages
Causes nephrotic syndrome
EM – foot process fusion
Causes
> Idiopathic
> Secondary to malignancy
Pathogenesis
> T cell and cytokine mediated
> Target podocytes, alter glomerular basement membrane charge
Clinical features
> Acute presentation
> May follow URTI
> GFR is normal or reduced due to intravascular depletion
> Rarely causes renal failure
> Not usually biopsied in children
Relapsing course – 50% will relapse
Treatment
> High dose steroids
> Prednisolone 1mg/kg for up to 8 weeks
Describe crescentic disease
Aka rapidly progressive GN
Group of conditions which demonstrate glomerular crescents on kidney biopsy
Nephritic presentation
Kidney biopsy
> Crescent-shaped collection of fibrin and matrix in Bowman’s space
> Can break through into surrounding cortex
Course of disease
> Aggressive disease – progress to ESRF quickly
Causes
> ANCA vasculitis – MPO/PR3
> Goodpasture’s syndrome: anti-GBM
> Lupus nephritis
> Infection-associated
> HSP nephritis
Describe diabetic nephropathy
Glomerulus
> Kimmelstiel Wilson lesions - nodules characteristic of DM
> Thickened basement membrane
> Associated with proteinuria
Pathophysiology
> Hyperglycaemia
> Volume expansion
> Intra-glomerular hypertension
> Hyperfiltration
> Proteinuria
> Hypertension and renal failure
Natural course
> After 20 years of diabetes
> Associated with other complications such as retinopathy
> Always with proteinuria
» Microalbuminuria
» Proteinuria
» Rise in serum creatinine
Management
> Treat hypertension
» ACEi or ARB
» Low sodium diet
» Weight loss
» Exercise
> Improve blood glucose control
> Education – DAFNE course
> Drugs
» Insulin
» Oral hypoglycaemia drugs including SGLT2 inhibitors
>Technology
» Glucose sensors and pumps
Describe renal artery stenosis
Clinical diagnosis
> No angiogram/CT angiogram/ MRI
Angioplasty/stenting is rarely effective
Pathophysiology
> Progressive narrowing of renal arteries with atheroma
> Perfusion falls by 20%
> GFR falls but tissue oxygenation of cortex and medulla maintained
> RA stenosis
> Cortical hypoxia causes microvascular damage and activation of inflammatory and oxidative pathways
> Parenchymal inflammation and fibrosis progresses and becomes irreversible
> Restoration of blood flow provides no benefit
Management
> Medical
» BP control (avoid ACEi and ARBs)
» Statin
» If diabetic – good glycaemic control
> Lifestyle
> Smoking cessation
> Exercise
> Low sodium diet
> Angioplasty
> Rapidly deteriorating renal failure
> Uncontrolled BP on multiple agents
> Flash pulmonary oedema
Describe amyloidosis
Deposition of highly stable insoluble proteinous material (amyloid) in extracellular space (felt-like substance made of beta pleated sheets)
Amyloid deposits in liver, heart, kidneys, gut
8-10mm fibrils sticking to wall
Test – Congo Red stain
Apple green birefringence – pathognomic
Electron microscopy
> Amyloid fibrils 9-11nm cause mesangial expansion
AA amyloid
> Inflammatory diseases e.g. chronic pyogenic or granulomatous infections, familial mediterranean fever (FMF)
> Causes systemic amyloidosis
AL amyloid
> Immunological fragments from haematological condition e.g. myeloma
Treatment
> AA amyloid
» Optimise treatment for underlying condition
> AL amyloid
> Optimise treatment for underlying condition
Describe lupus nephritis
Pathophysiology
> Autoimmune disease: intravascular immune complex-mediated glomerular disease
> Auto-antibodies produced against dsDNA, nucleosomes, snRNPs (anti-dsDNA, anti-histone)
> Auto-antibodies attach to basement membrane
> Activate complement (consumes C4)
> Renal damage
Investigations
> ANCA
> Anti-GBM antibody
> ANA
> Complement – C3 & C4
> Anti-dsDNA antibodies
> Serum immunoglobulin
Kidney biopsy
Confirm diagnosis and stage disease
Poor prognosis
Treatment
Treat underlying disease
Immunosuppression
Steroids
MMF
Rituximab
Cyclophosphamide
Hydroxychloroquine
Describe lupus nephritis
Pathophysiology
> Autoimmune disease: intravascular immune complex-mediated glomerular disease
> Auto-antibodies produced against dsDNA, nucleosomes, snRNPs (anti-dsDNA, anti-histone)
> Auto-antibodies attach to basement membrane
> Activate complement (consumes C4)
> Renal damage
Investigations
> ANCA
> Anti-GBM antibody
> ANA
> Complement – C3 & C4
> Anti-dsDNA antibodies
> Serum immunoglobulin
Kidney biopsy
> Confirm diagnosis and stage disease
> Poor prognosis
Treatment
> Treat underlying disease
> Immunosuppression
> Steroids
> MMF
> Rituximab
> Cyclophosphamide
> Hydroxychloroquine
Describe myeloma renal disease
Cast nephropathy
Hypercalcaemia / dehydration
Amyloid
Light chain deposition disease
Acquired Fanconi syndrome (proximal tubule dysfunction)
Describe the inheritance and clinical presentation of Adult Polycystic Kidney Disease (ADPKD)
Autosomal dominant pattern of inheritance
PKD 1 gene mutation in chromosome 16
> More common and aggressive, reach ESRF before 50
> Codes for polycystin 1
PKD2 gene mutation in chromosome 4
> Less common, less aggressive, may never reach ESRF)
> Code for polycystin 2
Clinical presentation
> Incidental finding on USS
> Hypertension
> Impaired renal function
> Loin pain
> Haematuria
Cysts gradually enlarge, normal kidney tissue replaced
Kidney volumes increased and eGFR falls
Complications
> Cyst infection, cyst rupture, haematuria and pain
Extra-renal manifestations
> Intra-cranial aneurysms
> Hypertension, LVH, valve abnormalities e.g. mitral valve prolapse
> Liver cysts
> Bronchiectasis
> Diverticular disease and abdominal hernias (due to size and pressure effect of enlarged kidneys)
Describe the function of polycystins
Polycystins are located in renal tubular epithelia & liver and pancreas ducts
Overexpressed in cyst cells
Membrane proteins involved in intracellular calcium regulation
Mechanism of cyst formation poorly understood
Genetic testing not routine but increasing
Vasopressin drives cyst development
Describe the diagnosis and management of ADPKD
Diagnosis
- Family history
> Age 15-30: 2 unilateral or bilateral cysts
> Age 30-59: 2 cysts in each kidney
> Over age 60: 4 cysts in each kidney - No family history
> 10 or more cysts in both kidneys
> Renal enlargement
> Liver cysts - Ultrasound
> Differentiate between simple renal cysts - CT or MRI more sensitive
- Genetic testing
Management
> Supportive
> Early detection and management of blood pressure
> Treat complications
> Manage extra-renal associations
> Prepare for renal replacement therapy
Tolvaptan
> Vasopressor antagonist, acts at V2 receptor - counteracts vasopressin
> Delays onset of RRT by 4-5 years
> Side-effects: hepatotoxicity, hypernatraemia
Describe Alport’s syndrome
Inherited progressive glomerular disease
Second most common inherited kidney disease
Caused by an inherited defect in type IV collagen (basement membrane) - found in ears, eyes and kidney
Usually X-linked - more severe presentation in males
Collagen IV abnormalities
> Alpha 3 gene mutation
> Alpha 4 gene (COL3A4) mutation
> Alpha 5 (COL3A5) mutation
Deafness and renal failure – can affect other organs including eyes
Presentation
> Asymptomatic persistent non-visible haematuria from early childhood
> Proteinuria, hypertension and progressive renal impairment
> ESRD – 90% on dialysis or transplanted by age 40
> Sensorineural hearing loss in late childhood
> Ocular defects
> Lens – anterior lenticonus
> Retina – bilateral white or yellow granulations
> Cornea – posterior polymorphous dystrophy, recurrent corneal erosion
Management
> Supportive – BP control
> Prepare for dialysis or transplant
Describe Fabry disease
Rare X-linked lysosomal storage disorder
Alpha galactosidase A deficiency resulting in accumulation of globotriaosylceramide (Gb3)
Also causes neuropathy, cardiac and skin features
GB3 accumulates in glomeruli, particularly in podocytes causing proteinuria and ESRF
> Pro-inflammatory and pro-fibrotic
Clinical presentation
> Intermittent episodes of burning pain in extremities
> Cutaneous vascular lesions – angiokeratomas
> Diminished perspiration
> Characteristic corneal and lenticular opacities
> Abdominal pain, nausea and/or diarrhoea
> Left ventricular hypertrophy
> Arrythmia
> Stroke
> CKD and proteinuria
Diagnosis
> Measure alpha-Gal A activity in leukocytes (unreliable in females)
> Renal biopsy
> Inclusion bodies of G3b aka zebra bodies
Management
> Enzyme replacement therapy; prevents progression to irreversible tissue damage
Describe the embryological development of the kidney
Pronephros
Mesonephros
Metanephros
Nephrogenesis commences in week 10
No new nephrons after 36 weeks
Approximately 1 million nephrons per kidney
GFR
> 120mls/min/1.73m2
> At birth: 40-65 mls/min/1.73m2
Describe the embryological development of the kidney
Pronephros
Mesonephros
Metanephros
Nephrogenesis commences in week 10
No new nephrons after 36 weeks
Approximately 1 million nephrons per kidney
GFR
> 120mls/min/1.73m2
> At birth: 40-65 mls/min/1.73m2
Describe renal hypodysplasia
Renal hypoplasia – reduction in number of nephrons but normal architecture
Renal dysplasia – malformed renal tissue
Renal hypodysplasia – congenital small kidneys with dysplastic features
Presentation
> Antenatal:US growth
> Neonate:
> Lung issues
> IUGR
> Acidosis
> Raised creatinine
> Children
> FTT
> Anorexia
> Vomiting
> Proteinuria
Management - supportive
Describe renal agenesis
Congenital absence of renal parenchymal tissue: metanephric stage
Male:female preponderance
Unilateral or bilateral (mostly sporadic)
Associated with increased risk of other anomalies
List renal cystic diseases
- Multicystic dysplastic kidney (MCDK)
- ADPKD
- ARPKD
Describe multicystic dysplastic kidney (MCDK)
Abdominal mass detected antenatally or neonatally
Involution: 35-65%
Risks
> Hypertension
> Malignancy
Which anomaly is associated with ARPKD?
Congenital hepatic fibrosis: subclinical to liver disease
> Portal hypertension
> Ascending cholangitis
Describe the childhood presentation of ADPKD and its associated anomalies
Presentation
> Haematuria
> Hypertension
> Flank pain
> UTIs
Associated anomalies
> Mitral valve prolapse
> Cerebral aneurysm
> AVM
> Hepatic / pancreatic cysts
> Colonic diverticula / hernia
Describe hydronephrosis and list its causes in children
Male preponderance
Bilateral in some cases
Associated with renal injury and renal impairment
Postnatal US – renal pelvic diameter >10mm
Causes
> Vesico-ureteric reflux
> Obstruction of urinary tract
Describe vesico-ureteric reflux
Describe obstruction of the urinary tract in children
Level of obstruction
- Pelvis/ureter (PUJ)
> Partial/total blockage of urine at ureter junction with kidney
> Males > females
Bilateral in some
> Antenatal diagnosis
> Abdominal mass, UTI, failure to thrive (FTT)
> Abdominal or flank pain
> Ureter
- Ureter/bladder (VUJ)
> Vesico-ureteric junction obstruction
> Functional or anatomical abnormality
> > Megaureter
> Primary: reflux / obstruction
> Secondary: bladder issues
> > Ureteric dilation >7mm
- Bladder
> Posterior urethral valves
» Most common obstructive uropathy
» Antenatal detection
» Investigations: US, MCUG
» Bilateral hydronephrosis; UTI
» Management – cystoscopy, ablation of valve
» Risk of CKD and bladder dysfunction - Urethra
Describe the staging of AKI
Decline of renal excretory function over hours or days
> Avoid eGFR – not reliable in AKI
> Serum creatinine more reliable
Severity of AKI – KDIGO
- Stage 1
> Serum creatinine >1.5 and <2x AKI baseline or >26 micromol/l increase above AKI baseline
- Stage 2
> Serum creatinine >2.0 and <3x AKI baseline - Stage 3
> Serum creatinine 3x AKI baseline or
> >354 micromol/l increase above AKI baseline
Oliguria
<1mL/kg/h in infants
<0.5mL/kg/h in children
<400-500mL/24h in adults
Describe the classification of the causes of AKI
Pre-renal
> Hypovolaemia + hypotension
> Reduced effective circulating volume
> Drugs
> Renal artery stenosis
Renal
> Glomerular
» Glomerulonephritis
> Tubular
> Ischaemic ATN
> Nephrotoxic ATN
> Myeloma cast nephropathy
> Tubulointerstitial
> Drugs
> Myeloma
> Sarcoid
Post-renal
> Renal papillary necrosis
> Kidney stones
> Retroperitoneal fibrosis
> Carcinoma of the cervix
> Prostatic hypertrophy/malignancy
> Urethral strictures
Describe the pre-renal causes of AKI
Hypotension
Hypovolaemia
> Blood loss
> Diarrhoea/vomiting
> Burns
Reduced effective circulating volume - hypoperfusion
> Cardiac failure
> Septic shock
> Cirrhosis
Hypoxia
Drugs
> ACEi
> NSAIDs
Toxins
Renal artery stenosis
Describe the renal causes of AKI
Large blood vessels
> Polyarthritis nodosa
Glomeruli and small blood vessels
> Glomerulonephritis
> Vasculitis
Tubular
> Ischaemic acute tubular necrosis (ATN)
> > Unresolved pre-renal causes:
> hypoperfusion or direct toxicity
> Hypotension
> Sepsis
Toxins
Exogenous
> Drugs
> NSAIDS, gentamicin, ACEi
> Contrast
> Poisons (metals, antifreeze)
Endogenous
> Myoglobin (rhabdomyolysis)
> Haemoglobin
> Immunoglobulins (myeloma)
> Calcium
> Urate
Nephrotoxic ATN
> Toxins (ethylene glycol, lithium), contrast, gentamicin
> Myeloma cast nephropathy
Tubulointerstitial
> Acute tubulointerstitial nephritis
> Rhabdomyolysis
> Drugs
> Myeloma
> Sarcoid
Describe post-renal causes of AKI
Describe glomerular haemodynamic regulation
Hypovolaemia leads to a fall in glomerular filtration pressure
Prostaglandins dilate afferent arteriole to increase flow as MAP falls towards 80 mmHg
> Blocked by NSAIDs
Efferent arteriole can vasoconstrict, increasing glomerular pressure
> Blocked by ACEi
Describe the investigations used in AKI
Acute or chronic
Bloods – both urea and creatinine elevated
Potassium must be controlled as it can cause heart problems
> <6.0 is abnormal but no immediate concern
6.0-6.4 risk of arrhythmia
>6.5 is a medical emergency
Urine output
Clinical assessment of fluid status
> BP, JVP, oedema, heart sounds
Underlying diagnosis – history, exam, meds
Briefly summarise the treatment of AKI
- Circulation - restore renal perfusion
- Treat hyperkalaemia
- Treat pulmonary oedema if present
- Remove causes: drugs, sepsis…
- Exclude obstruction and consider renal causes
- Refer to ICU or renal unit
Describe the treatment of hyperkalaemia
Protect the heart
> IV calcium gluconate 10ml 10% as cardiac membrane stabiliser
Drive K+ into cells
> Insulin 10-15 units actrapid + 50ml dextrose – moves potassium into cells
> If raised potassium and low bicarb, supplementation of bicarb – IV NaBicarb 1.26%
> Beta agonists – nebulised salbutamol
Remove K+ from body
> Acute
> > Haemodialysis
> Refractory potassium >6.5 mmol/l
> Refractory pulmonary oedema
> May be considered for
» Acidosis (pH < 7.1)
» Uraemia (pericarditis, encephalopathy)
» Toxins (lithium, ethylene glycol…)
> > Loop diuretic - furosemide
> Long-term
> Reduce absorption from gut – calcium resonium 15g/day orally or enema
Describe the recovery from ATN
Polyuric phase 48-72h
Up to 6L urine/day
Often subsequent low K, Ca, Mg
Tubules fail to concentrate urine
Define CKD and list causes
Kidney damage or GFR <60ml/min per 1.73m2 for 3 months or more
Aetiology
- Diabetic nephropathy
- Glomerular sclerosis
- Nodular lesions
- Proteinuria and deterioration of renal function
- Renovascular disease / ischaemic nephropathy
- Chronic glomerulonephritis
- Membranous glomerulonephritis
- IgA nephropathy
- Reflux nephropathy / chronic pyelonephritis
- ADPKD
- Obstructive uropathy
Describe symptoms of CKD
- Pruritus
- Nausea, anorexia, weight loss
- Fatigue
- Leg swelling
- Breathlessness
- Nocturia
- Joint/bone pain
- Confusion
Advanced CKD
- Peripheral and pulmonary oedema
- Pericardial rub
- Rash/excoriation
- Hypertension
- Tachypnoea
- Cachexia
- Pallor & lemon yellow tinge
Describe the treatment for anaemia as a consequence of renal failure
eGFR <30
Iron absorption and utilisation are suboptimal
Replace iron, B12 and folate if low
Treatment
> ESA (erythropoiesis stimulating agent) e.g. darbepoietin alfa 30 micrograms every 2 weeks
> Trigger usually Hb < 100g/L
> Target Hb is 100-120g/L
Describe the pathophysiology and treatment of secondary hyperparathyroidism due to renal failure
Reduced 1-alpha hydroxylation of 25-hydroxycholecalciferol - low vitamin D, low calcium
Reduced phosphate excretion - high phosphate
High PTH – can lead to osteitis fibrosa cystica, left ventricular hypertrophy…
Treatment
> Activated vitamin D: alfacalcidol
> Mg supplements
> Phosphate binders
> Calcium-based: calcium carbonate/acetate
> Non-calcium: sevelamer, lanthanum, aluminium
> Calcimimetic: cinacalcet
> Parathyroidectomy
Describe the management of CKD
Slowing progression
> Aggressive BP control - ACEi/ARB
Good diabetic control
Diet
Smoking cessation
Lowering cholesterol
Treating acidosis
Renal replacement therapy (RRT)
> Conservative care
> Home-based therapies
> > Home haemodialysis
> > > Most start with eGFR 6-8ml/min
> > > Side-effects
> Weight loss and persistent nausea
> Persistent hyperkalaemia
> Acidosis
> Severe hyperphosphataemia
> Pruritus
> Problematic fluid overload
> > Peritoneal dialysis
> Hospital-based therapies
> Hospital haemodialysis
> Self-care unit
> Transplant
List the indications for renal replacement therapy
Medically resistant hyperkalaemia
Medically resistant pulmonary oedema
Medically resistant acidosis
Uraemic pericarditis
Uraemic encephalopathy
List the symptoms a clinically uraemic patient would experience
Anorexia
Vomiting
Itch
Restless legs
Weight loss
Metallic taste
Describe the mechanisms behind haemodialysis
> Hospital or home
Daily or nocturnal
Mechanism
> Blood is removed using a blood pump
> Passed through arterial circuit into dialysis filter
> Blood flows countercurrent to dialysis fluid
> Dialysis fluid is lower in concentration of solutes such as potassium, phosphate…
> Removal of solutes from blood e.g. potassium, urea occurs via diffusion down a concentration gradient
> Removal of fluid or “ultrafiltration” occurs through hydrostatic filtration
> Filtration removes fluid and dialysate is discarded
> Passes through dialysis filter into an air detector and back into patient
> Continuous loop for 4 hours
Access
> AVF access
> Arteriovenous fistula – connection between artery and vein
If veins not suitable for procedure, graft can be used
> TCVC (tunneled central venous catheter)
Describe peritoneal dialysis
CAPD (continuous ambulatory peritoneal dialysis) or APD (automated peritoneal dialysis)
Daily or nocturnal
Describe the process of kidney transplantation
Donor kidney placed in right or left iliac fossa
Ureter is shorter
Stent placed from donor kidney to bladder, removed a few weeks after transplantation
Native kidneys are left in body unless causing infection
List the disadvantages of dialysis
Fatigue
Fluid restriction
Restricted diet – potassium, phosphate
Women are infertile
Reduced life expectancy
Describe contraindications for transplant
Reduced life expectancy
> Older age
> Comorbidity
Surgical contraindications
> No bladder
> Calcified blood vessels
Medical contraindications
> Hypertension
> Hypotension
> Diseases that will recur in the transplant
Describe the pathogenesis of transplant rejection
> Body recognises cell surface proteins as “non-self”
Blood group or HLA incompatibility
Pathogenesis of transplant rejection
> Foreign antigenic peptide recognised and bound by APC
> APC presents foreign antigenic peptide to T cell receptor and binds
> T cell activated, produces IL-2
> Leads to cascade of events and results in activation of T and B cells, as well as antibody production
Cell-mediated rejection
> Interstitial inflammation and tubulitis
> Treated with steroids
> Diagnosis – biopsy
> Does not present with proteinuria
Antibody-mediated rejection
> Endothelial swelling, glomerulitis and peritubular capillaritis
> Donor specific antibodies
> May present with proteinuria
Describe the immunosuppressive agents used after transplantation
Basiliximab
> Chimeric mouse-human monoclonal antibody directed against IL-2 receptor
Tacrolimus
> Calcineurin inhibitor
Mycophenolate mofetil
> Inhibitor of inosine-5’-monophosphate dehydrogenase – depletes guanosine nucleotides in T and B lymphocytes, inhibits proliferation
Steroids
Describe the complications associated with immunosuppression
Rejection
Infection
Common organisms in common sites
> Chest infection
> Skin/wound infections
> Urine infection
Re-activation infections
> CMV disease – pneumonitis, colitis, hepatitis, renal disease
> BK nephropathy
Uncommon organisms
> Pneumocystis jirovecii
Malignancy
> Kaposi sarcoma
> Skin: non-melanoma, non-epithelial; melanoma
> Non-Hodgkin & Hodgkin lymphoma
> Lung
> Kidney
> Colon and rectum
> Pancreas
Define bacteriuria, giving risk factors and management plan
Bacteria in urine
Asymptomatic
Affects preschool age (girls > boys), adults (females > boys)
Other risk factors
> Urinary catheterisation
> Diabetes
> Anatomical abnormalities of urinary tract
> Pregnancy
Management
> Treat asymptomatic bacteriuria only in
> Preschool children
> Pregnancy
> Renal transplant
> Immunocompromised
> Treatment in other asymptomatic patients not indicated
Describe the causes of UTI
> 95% caused by single organism
> Gram negative bacilli
> E. coli
> Klebsiella species
> Proteus species
> Pseudomonas species
> Gram positive bacteria
> Streptococcus species
» Enterococcus species
» S. Agalactiae (Group B streptococcus)
> > Staphylococcus species
> S. saprophyticus
> S. aureus
> Candida species
> Fungal balls
> Renal / peri-nephric abscesses
> Anaerobes
> Associated with bladder malignancies
Multiple organisms in
> Long-term catheteres
> Recurrent infections
> Structural / neurological abnormalities
Multi-drug resistant organisms
> Anatomical/neurological abnormalities
> Frequent infections
> Multiple antibiotic courses
> Prophylactic antibiotic use
List the clinical features of a UTI
Suprapubic discomfort
Dysuria
Urgency
Frequency
Cloudy, blood-stained, smelly urine
Low-grade fever
Sepsis
Failure to thrive or jaundice in neonates
Abdominal pain and vomiting in children
Nocturia, incontinence and delirium in the elderly
Describe the management of UTIs
Non-pregnant women
> First presentation, culture not mandatory
> Dipstick – high false positive rate
> Check previous culture results
Empirical antibiotic
> Amoxicillin, trimethoprim, nitrofurantoin
> Pivmecillinam, fosfomycin
No response to treatment
> Urine culture
> Change antibiotic
Children and men
> Send urine for every presentation
> Treat appropriately (empirical > targeted)
Pregnancy
> Send urine and treat each episode
> Check previous sensitivities > Amoxicillin and cefalexin relatively safe
> Avoid trimethoprim 1st trimester; avoid nitrofurantoin near term
Recurrent UTI
> Send sample from each episode
> Encourage hydration, urge-initiated and post-coital voiding
> Urology investigation
> Intravaginal/ oral oestrogen
> Antibiotic therapy as per symptoms
Catheter-associated UTI
> Colonisation common
> Biofilm production by bacteria
> Send CSU
> Start antibiotic – initially empirical based on previous microbiology
> Drug resistant and polymicrobial infections
> Remove / replace catheter
Describe the symptoms of acute pyelonephritis as well as its management
Upper urinary tract infection
> Moderate to severe infection
> Flank pain +/- systemic infection
> Enlarged kidney
> Abscesses on surface of kidney (severe)
Management
> Urine
> Blood culture
> Imaging
Community
> Co-amoxiclav
> Ciprofloxacin
> Trimethoprim
Hospital
> IV antibiotics
> Amoxicillin / vancomycin
> Gentamicin / aztreonam / temocillin
> Uncomplicated pyelonephritis
7 day antibiotic course
Complicated pyelonephritis
> At least 2 weeks of antibiotics +/- radiological/surgical intervention (drainage of abscesses)
Describe the complications of pyelonephritis
Renal abscess
> Complication of pyelonephritis – similar symptoms
> Positive urine and blood culture
> Usually gram negative bacilli
Can become life-threatening
> Emphysematous pyelonephritis
> Bubblewrap appearance
> Poor response to antibiotic therapy alone
Perinephric abscess
> Uncommon
> Often from haematogenous spread
> Common organisms
» Gram negative bacilli – E. coli, proteus species
» Gram positive cocci – S. aureus, streptococci
» Candida species
> Symptoms
> Similar to pyelonephritis
> Localised signs, local invasion
> Investigations
> Urine and blood cultures usually positive
> Pyuria +/- bacterial growth
> Poor response to antibiotic therapy – surgical management
Describe acute bacterial prostatitis, including causes, signs and symptoms, complications, investigations and management
Usually spontaneous; may follow urethral instrumentation
Signs and symptoms
> Diffuse oedema
> Microabscesses
> Perineal / back pain
> UTI symptoms
> Urinary retention
> Pyrexia
Complications
> Prostatic abscess
> Spontaneous rupture – urethra, rectum
> Epididymitis
> Ascending infection
> Systemic sepsis
Investigations
> Urine and blood culture
> Transrectal US
> CT/MRI
> Do not obtain prostatic secretions
Likely organisms
> Gram negative bacilli – E. coli, proteus species
> S. aureus – MSSA, MRSA
> Neisseria gonnorhoea
Management
> Empirically ciprofloxacin / ofloxacin
Describe chronic prostatitis
Rarely associated with acute prostatitis
> May follow Chlamydia urethritis
Signs and symptoms
> Recurrent UTI symptoms
> Perineal discomfort
> Back pain
> Low grade fever
Relapse common
Common organisms
> Gram negative bacilli – E. coli, proteus species
> Enterococcus species
> S. aureus – MSSA, MRSA
Describe epidiymitis
Inflammatory reaction of the epididymis
Cause
> Ascending infection from urethra
> Urethral instrumentation
Symptoms
> Symptoms of UTI / urethritis
> Pain
> Fever
> Swelling
> Penile discharge
Common organisms
> GNB, enterococci, staphylococci
> TB in high risk areas and individuals
> Rule out Chlamydia and N. gonorrhoea in sexually active men
Describe orchitis, including aetiology & signs and symptoms
Inflammation of one or both testicles
Signs and symptoms
> Testicular pain and swelling
> Dysuria
> Fever
> Penile discharge
Aetiology
> Usually viral – mumps
> Bacterial
> Pyogenic
> Complication of epididymitis
> IV antibiotics as per complicated UTI + surgical drainage
Complications
> Testicular infarction
> Abscess formation
Describe Fournier’s gangrene including risk factors, investigations and management
Form of necrotising fasciitis
Usually >50 years of age
Rapid onset and spreading infection
Systemic sepsis
Risk factors
> UTI
> Complications of IBD
> Trauma
> Recent surgery
Common organisms
> Mixed infections – mainly GNB and anaerobes
Investigations
> Blood cultures
> Urine
> Tissue / pus
Management
> Surgical debridement
> Broad spectrum / combination antibiotics
> Piperacillin-tazobactam + gentamicin + metronidazole +/- clindamycin
Describe the risk factors for prostate cancer
Age >65
Familial and genetic risk factors
> Especially first degree relatives
> Abnormalities on chromosomes 1q, 8p and Xp
> BRCA2 gene mutations
> PTEN and TP53 TSGs mutations
Hormones
Racial factors - increased risk in black population
Geographic variation - highest incidence in westernised nations
What are the signs and symptoms of prostate cancer
Often asymptomatic
Painful or slow micturition
Urinary tract infection
Haematuria – blood in urine
Urinary retention – may cause anuria, uraemia
Lymphoedema
Describe the metastatic complications of prostate cancer
Bone pain – most common symptom of metastases
Renal failure – ureteric obstruction
> Anorexia
> Weight loss
> Raised creatinine
> Stent or nephrostomy
Spinal cord compression
> Urological emergency – urgent MRI
> Severe pain
> Off legs
> Retention
> Constipation
> Radiotherapy v spinal decompression surgery
Describe PSA and how it changes throughout life
PSA is a 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
> Tends to rise with age
Depends on prostate size
Is influenced by inflammation and infection
Describe the diagnosis and screening of prostate cancer
Digital rectal examination
PSA – prostate specific antigen
TRUS (trans-rectal ultrasound) – guided needle biopsy
Describe the pathophysiology and grading of prostate cancer
Majority is primary adenocarcinoma
Usually arises in peripheral zone of prostate
Gleason grading
6 – well-differentiated, 25% likelihood of local progression
7– moderately differentiated, 50% likelihood of local progression
> 7 – poorly differentiated, 75% likelihood of local progression
Describe the staging and treatment of prostate cancer
TNM classification
> T1 – within prostate
> T2 – felt on DRE
> T3 – cancer invades wall into seminal vesicles
> T4 – cancer invades adjacent organ i.e. bladder, bowel, pelvic floor
Localised prostate cancer
> Watchful waiting
> Active surveillance
> Radiotherapy (with or without LHRH analogue)
> External beam
> Conformal
> Brachytherapy
> Radical prostatectomy
Cryotherapy / HIFU
TURP if symptomatic
Advanced prostate cancer
> Androgen ablation therapy
> Medical castration – LHRH analogue
> Surgical castration – orchidectomy
Chemotherapy
TURP for relief of symptoms (transurethral resection of the prostate)
Radiotherapy
List risk factors for bladder cancer
Age >50
Race – more common in Caucasians
Environmental carcinogens
Chronic inflammation
> Stones
> Infection – schistosomiasis
> Long-term catheters
Drugs – phenacitin, cyclophosphamide
Pelvic radiotherapy
Occupation
Smoking – especially from 4-ABP and naphythylamines
Describe the presentation and investigations used in bladder cancer
Presentation / diagnosis
> Classically painless frank haematuria
Investigations
> Cystoscopy
> Renal US
> CT KUB
List the different types of bladder cancer
Transitional cell carcinoma (90%)
> Superficial – 75%
> Invasive – 25%
Squamous carcinoma (5%)
Adenocarcinoma (2%)
Other secondaries
Muscle invasive bladder cancer is highly aggressive
Describe the treatment of bladder cancer
> Diagnosed at flexible cystoscopy
Urgent TURBT (trans-urethral resection of bladder tumour)
CT IVU
Bimanual examination carried out at TURBT
Intravesical mitomycin reduces risk of recurrence
Low-grade superficial TCC
> Flexible check cystoscopy 3 months
> 30% chance of recurrence
> Course of 6 weekly mitomycin treatment given for persistent Ta tumours
High-grade non-muscle-invasive bladder cancer (HG NMIBC)
> 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 if treatment fails
MIBC
> Requires radical therapy
> Radical cystectomy or radiotherapy
> Bladder and prostate/uterus removed
> Urine diverted into an ileal conduit or rarely an orthotopic neobladder
> Neo-adjuvant chemotherapy
Metastatic disease
> Often pulmonary
> Treat with chemotherapy
> Classic M-VAC
» Methotrexate
» Vinblastine
» Doxorubicin
» Cisplatin
> Gemicitobine / docetaxel
Describe the types of renal cell carcinoma and associated risk factors
85% of all renal tumours
Others
> Transitional cell carcinoma
> Sarcoma
> Metastases
Risk factors
> Smoking
> Obesity
> Hypertension
> Acquired renal cystic disease
> Haemodialysis
Genetics
> VHL (Von Hippel Lindau)
> HPRCC – hereditary papillary renal carcinoma
> HLRCC – hereditary leiomyomatosis and renal cell cancer
> Birt-Hogg-Dube
> Tuberous sclerosis
Describe the presentation of renal cell carcinoma
Incidental
Systemic symptoms
> Night sweats
> Fever
> Fatigue
> Weight loss
> Haemoptysis
Classic triad
> Mass
> Pain
> Haematuria
> Varicocoele
> Lower limb oedema
> Paraneoplastic syndrome
> Polycythaemia due to increased EPO
> Hypercalcaemia due to PTHrP or from osteolytic hypercalcaemia
> Hypertension due to renin secretion
> Deranged LFTs – Stauffer’s syndrome – due to hepatotoxic tumour products
Describe the histology and staging of renal cell carcinoma
Histology
> Clear cell (80%)
» Vascular, granular and clear (lipids)
> Papillary
Chromophobe – large polygonal
Collecting duct – rare
Medullary cell – rare
Staging - TNM staging
> T3a – invasion into renal vein
> T3B – IVC below diaphragm
> T3c – IVC above diaphragm
> T4 – beyond Gerota’s and adrenal gland
Describe the treatment of renal cell carcinoma
Radical nephrectomy (includes Gerota’s fascia, spares adrenal gland)
> Large renal mass
> If no absolute indication for nephron-sparing surgery (NSS)
Indications for NSS
> Single kidney
> CKD
> CV risk factors
> pT1a tumours
Small renal mass
> Biopsy
> Treatment
> > NSS
> Partial nephrectomy
> Cryotherapy
> > Radical nephrectomy
> > Surveillance
> Metastatic disease - tyrosine kinase inhibitors
Describe the risk factors and presentation of testicular cancer
Most common solid cancer in younger men (20-45)
Most curable cancer
Risk factors
> Age 20-45
> Cryptorchidism
> HIV
> Caucasian population
Clinical presentation
> Painless lump
Describe the investigations and classification of testicular cancer
Scrotal ultrasound
Tumour markers
> Alpha-fetoprotein – teratomas and yolk sac tumours
> Beta hCG – teratoma, seminoma
> LDH – seminoma
Classification
> Germ cell tumours
> Seminoma
> Teratoma
> Mixed
> Yolk sac
Stromal tumours
> Leydig
> Sertoli
Other
> Lymphoma
> Metastasis
Describe the treatment of testicular cancer
Radical orchidectomy
Chemotherapy
Para-aortic nodal radiotherapy
Retroperitoneal lymph node dissection
Describe penile cancer and its treatment
Rare
Associated with HPV infection (16, 18, 21) and smoking
Premalignant lesions – chronic changes
Even rarer in males circumcised at birth
Treatment
> Circumcision
> Topical treatment CO2/5FU
> Penectomy +/- reconstruction
> Lymphadenectomy
> Chemo-radiotherapy
Describe the position, size and surrounding fascia of the kidneys
Paired retroperitoneal organs (T12-L3))
Right lies lower than left; normally 10-12cm in length, 5-7cm wide and 3cm thick
Surrounded by Gerota’s fascia
Clinically important
> For PCNL (percutaneous nephrolithotomy)
> Upper pole more posterior and medial
> Medial surface more anterior
> Gerota’s fascia deficient inferiorly
> Often where haemorrhage or haematoma can appear after trauma
Describe the anatomy of the ureters including layers and physiological narrowings
25-30cm long, 4-5mm calibre
3 segments
> Proximal: PUJ-pelvic brim
> Mid: segment over sacral bone
> Distal: lower sacral border to UO
4 layers
> Urothelial mucosa
> Lamina propria
> Muscular layer
> Adventitial layer
3 physiological narrowings
> Pelviureteric junction (PUJ)
> Ureters cross iliac vessels at pelvic brim (midureter)
> Vesicoureteric junction (VUJ)
> Ureter joins bladder
Describe the risk factors for urolithiasis
Intrinsic
> Sex (male:female 2:1)
> Testosterone increases production of oxalate
> Females produce more citrate (productive)
> Age: peak 20-50 years
> Family history
> More common in Caucasian, Asian
> Familial renal tubular acidosis
> Cystinuria
> Comorbid factors
Extrinsic
> Fluid intake
> Diet
> High animal protein
» High oxalate, low pH, low citrate
> High salt – hypercalciuria
>Low calcium diets
> Sedentary lifestyle
> High incidence in hot climates
> Country of residence
Describe the different types of kidney stones
Calcium oxalate stones most common
> Radio-opaque: seen on X-ray
Uric acid
> Form due to chronic dehydration
> Increased risk with gout, genetic tendency, diet with excess protein
Calcium phosphate + calcium oxalate
Pure calcium phosphate
> Rare
> May be seen in renal tubular acidosis
Struvite
> Seen in UTIs
> Consist of magnesium, ammonium and phosphate
> Require aggressive treatment of UTI
Cysteine
> Rare, predominantly associated with cysteinuria (genetically inherited condition)
Xanthine
> Enzyme deficiency causes buildup of xanthine deposits
Silica
> Rare
> Caused by medications or herbal supplements
Describe the pathogenesis of urolithiasis
Undersaturated
Supersaturated but stable – metastable
Supersaturated with spontaneous precipitation – unstable
Saturation product
> level at which no more solute will dissolve in a solution without a change in pH, temperature
Formation product – level at which spontaneous formation occurs
Free particle model of stone formation
> Crystals growing and agglomerating
> Critical particle trapped in tubule
Fixed particle model of stone formation
> Crystals growing and agglomerating
> Particle adheres to a damaged site on the tubule wall and other crystals agglomerate with it
Describe the presentation of kidney stones
Incidental
Pain
> Colic
> Radiates from loin to groin
> In males can be testicular or penile pain
> Cannot settle
> Unable to stay still
Haematuria
> Visible or non-visible
Sepsis/infection
> Unknown source until imaged
DDX
> AAA
> Appendicitis
> Gynae pathology
Describe the investigations used for kidney stones
History and examination
Bloods
> U&Es, CRP, FBC
Urine
> Dipstick
MSSU
> Calcium
> Urate
> Sodium nitroprusside – cystine
Stone analysis
Imaging
> Gold standard – CT KUB
» Stone diameter
» Skin to stone distance
> Ultrasound
> Especially young females
> X-ray
> Better for follow-up of known radioopaque stone
Describe the treatment of
Analgesia
> NSAIDs – reduce pain due to reduced glomerular filtration, renal pressure and ureteric peristalsis
Tamsulosin
> Alpha blocker which blocks muscle contraction
> Relaxes ureter and encourages stone passage
Surgical options
> Ureteroscopy and basket
> Ureteroscopy and fragmentation
> FURS – flexible ureteroscopy
> ESWL – extracorporeal shockwave lithotripsy
> PCNL – percutaneous nephrolithotomy
Evidence of sepsis
> Retrograde ureteric stent
> Inserted by urology under anaesthetic
> Connects bladder to kidney
> Nephrostomy
> Inserted percutaneously by interventional radiology in an antegrade fashion
Describe ESWL
Produces a shockwave
> Electrohydraulic
> Electromagnetic
> Piezoelectric
Direct effect
> Shearing
> Spalling
Cavitation effect
> Shockwave in fluid causes a microbubble
> Dissolved gas in fluid around bubble expands into bubble
> Bubble collapses
> Microjets enter stone causing fragmentation
Describe staghorn calculi and how they are formed
Branched stones that fill all or a part of the renal pelvis and branch into several or all of the calyces
Most often composed of struvite
> Bacteria produce urease, breaks down urea into ammonia
> Causes alkalinisation of urine and formation of magnesium ammonium phosphate crystals
Describe percutaneous nephrolithotomy (PCNL)
Creates a percutaneous tract from skin to kidney
Able to clear larger volumes of stone e.g. struvite
Increased risk as it is an invasive procedure
Describe the fluid compartments of the body
Intracellular
> 2/3 of fluid
> Composition: potassium
Extracellular
> 1/3 of fluid
> Composition
> > Interstitium: sodium, chloride
> > Plasma (intravascular)
Describe third space losses and risks associated with osmolar problems
Third space losses
> More fluid in extracellular compartment than there should be
e.g. low albumin in intravascular space – fluid taken into interstitium
> Interstitial space becomes overexpanded
Risk of osmolar problems
> Cerebral oedema
> Acute hyponatraemia
> Osmotic demyelination syndrome
> Sodium corrected too quickly
Describe signs and symptoms associated with fluid depletion and fluid overload
Relevant history
> Fluid depletion – diuretics, abnormal losses
> Fluid overload - heart failure, renal failure
Symptoms
> Fluid depletion – postural hypotension, thirst, dry mouth
> Fluid overload – breathlessness, swollen ankles
Signs
> Fluid depletion – reduced skin turgor, CRT >2 secs, tachycardia
> Fluid overload – hypertension, increased JVP, 3rd heart sound, pulmonary oedema
Lab tests
> Fluid depletion - U&Es, especially high urea
> Fluid overload – serum albumin
Describe the NICE guidelines’s 5 R’s
Resuscitation
> Restore circulation to vital organs following loss of intravascular volume
Clinical signs of hypovolaemia
> Hypotension
> Tachycardia
> Peripherally cool
> CRT > 2 secs
> NEWS > 5
Passive leg raising suggests fluid responsiveness
Fluid bolus, usually saline or Hartmann’s
Routine maintenance
> Patients not drinking / unable to drink / having to fast for over 8-12h
> Calculate requirement based on
> Projected losses
> Intake e.g. IV drug volumes / NG feed
Replacement
> Treat deficits or ongoing losses not needed urgently for resus
Redistribution
Reassessment
> Daily U&Es and fluid balance
> Consider daily bicarbonate or magnesium if abnormal GI or renal losses
Describe the different types of IV fluids
Crystalloids
> Saline (various, 0.9% is standard)
> Distributes between extracellular compartments
> Dextrose (various, 5% is standard)
> goes straight into intracellular compartments
> Balanced solutions e.g. Hartmann’s or Ringer’s lactate
> Distributes between extracellular compartments
> Sodium bicarbonate (1.26%) - expert advice only
Colloids
> E.g. Gelofusion or starch-based fluid
> Stay in intravascular space
Blood products
> Packed red cells
> Platelets or fresh frozen plasma (clotting factors)
> Human albumin solution
Describe the KDIGO criteria for AKI
Severity of AKI – KDIGO
Stage 1
> Serum creatinine >1.5 and <2x AKI baseline or >26 micromol/l increase above AKI baseline
Stage 2
> Serum creatinine >2.0 and <3x AKI baseline
Stage 3
> Serum creatinine 3x AKI baseline or >354 micromol/l increase above AKI baseline
State why peritoneal dialysis can cause hyperglycaemia
The dialysate contains dextrose.
Absorbing some of the dialysate might cause the consumption of hundreds of extra calories daily, leading to hyperglycaemia and weight gain.
Discuss why nephrotic syndrome can increase risk of DVT
Antithrombin II deficiency can be inherited or acquired.
The patient has nephrotic syndrome, which is associated with a loss of antithrombin III from the kidneys resulting in an acquired deficiency and a hypercoagulable state and thus puts this patient at risk of the development of deep vein thrombosis.
Discuss presentation and management of renal carcinoma
Painless flank mass, haematuria, and paraneoplastic features including hypertension, polycythaemia, hypercalcaemia, and Cushing’s syndrome
Localised renal cancer (that is 7 cm or larger) is definitively treated with a radical nephrectomy. Adjuvant treatment does not help completely resected disease
List characteristics of Wegener granulomatosis
elevated serum creatinine level
sinusitis
hematuria
pleural effusions
positive result of antineutrophil cytoplasmic antibody test
What bacteria infection is commonly associated with peritoneal dialysis
staphylococcus epidermis
State the difference in onset after respiratory infection in PSGN and IgA nephropathy
IgA nephropathy would occur a few days after the respiratory infection rather than weeks.
State the first line analgesia in renal colic
IM diclofena
