Nephrology Flashcards
(262 cards)
1
Q
List 3 functions of the kidney?
A
Primary role: maintain fluid and electrolyte homeostasis in response to blood pressure and hormones
- Metabolic waste excretion
- Endocrine functions
- Drug metabolism/excretion
- Control of solutes and fluid status
- BP control
- Acid/Base
2
Q
How do you measure kidney function?
A
Measure what is going out in urine or what’s left in the blood
- Metabolic waste excretion: urea, creatinine
- Endocrine fxn: Vit D, EPO, PTH
- Control of solutes and fluid status: sodium, potassium, fluid
3
Q
What is the role of the glomerulus?
A
- To filter blood
4
Q
What is the glomerular filtration barrier (GFB)?
A
- Semi-permeable membrane preventing the passage of a majority of proteins in urine
- Controls the glomerular filtration rate
- Glomerular basement membrane and podocytes make up the GFB
- Blood cells and large molecules (albumin, immunoglobulins) are not filtered due to size and charge barrier
- Electrolytes, amino acids and small molecules pass through Bowman’s space
5
Q
What controls blood flow through the glomerulus?
ie. describe what happens when a low blood volume is recognised
A
Reduced blood vol / low BP
- Baroreceptos stimulated causing juxtaglomerular cells to release renin causing angiotensin II production
- Angiotensin II: efferent arteriole vasoconstriction, inc. Na and water reabsorption and systemic vasoconstriction
- Sympathetic NS: systemic vasoconstriction
- Osmoreceptors of the hypothalamus cause ADH (from ant/ pituitary) to increase water retention and insert aquaporin channels in collecting duct
6
Q
What is the pathway for filtration/reabsorption etc at the nephron?
A
- Blood is filtered at the glomerulus which goes to tubules
- 99% is reabsorbed
- Small amount is secreted into the tubules
- What’s left in tubules exits via urine
- Tubules adjust filtrate content, with collecting ductules absorbing water
7
Q
In context of kidney function, which aspects of a dipstick are important?
A
- Presence of blood and protein
8
Q
How do you measure urinary protein excretion?
A
- 24hr urine collection: not routine as not standardised between patients
- Protein:Creatinine Ratio (PCR) on a morning spot sample (mg/mmol). Urine PCR (uPCR) of 100 is equivalent to 1g/day of protein in urine
- Albumin:Creatinine ratio (mg/mmol), measuring just albumin rather than all the protein in the urine
9
Q
What is proteinuria and what’s the pathology?
A
- Normal: less than 150mg/day (15% albumin, rest is other proteins)
- Protein: abnormal quantities of protein in urine, suggestive of kidney damage
- Damage to GFB: lose albumin into the urine
- When protein in the urine is pathological and due to glomerular dysfunction: 70% protein is albumin
- Urinalysis detects albumin
10
Q
What is haematuria and how is it caused?
A
Haematuria: presence of blood in the urine
- Non-visible haematuria: can be detected on dipstick and is caused by disruption of the GFB
- Visible haematuria: can come from anywhere in the urinary tract. More likely to come from kidney stones/malignancy/UTI rather than the glomerulus
11
Q
What makes a substance ideal to measure in urine?
What is the best substance to measure kidney function?
A
- Freely filtered at the glomerulus
- Not reabsorbed
- Not secreted
- Creatinine isn’t this straightforward but is the best marker
12
Q
What are the 3 most important measurements for determining kidney function?
A
- Urea
- Creatinine
- eGFR
13
Q
how is creatinine released into the blood and what affects it?
A
- From muscle breakdown
- Concentration affected by plasma volume
- Affected slightly by diet (high protein diet) or muscle building supplements
14
Q
When is urea released into the blood and how are levels affected?
What is the pathway in the nephron?
A
- Tissue breakdown product
- Diet: high protein or GI bleed
- Dehydration causes more passive reabsorption at proximal tubule, so urea is usually higher
- In liver failure, breakdown products aren’t processed as well so urea is lower
- Freely filtered at glomerulus but 40% is reabsorbed so less reliable in indicating kidney function
15
Q
Define renal clearance
A
Renal clearance = volume of plasma which would be cleared of the substance per unit time
- Expressed as ml/min
- Usually described as the glomerular filtration rate
16
Q
What information is needed to measure eGFR?
What units is it expressed in?
In what situation can it not be used?
What else needs taken into account?
A
MDRD*4 formula:
- Plasma creatinine concentration
- Age (need to be >16)
- Gender
- Race
- Units: ml/min/1.73m2
Not suitable in AKI (ie. not valid when kidney function is changing rapidly)
- eGFR assumes stable renal function
- Creatinine levels are related to muscle mass, so what’s normal for one patient may not be normal for another
17
Q
What are the stagings for chronic kidney disease with eGFR?
A
Stage 1: eGFR >90 with another abnormality*
Stage 2: eGFR 60-89 with another abnormality*
*patients with eGFR >60 should be regarded as normal unless other evidence of kidney disease eg. persistant haematuria or proteinuria
Only considered to have CKD if eGFR <60
Stage 3: eGFR 30-59 is CDK with moderate impairment
Stage 4: 15-29 is CDK with severe impairment
Stage 5: <15 is CKD with advanced impairment. Any patient on dialysis is considered stage 5.
18
Q
Define glomerulonephritis
What is a complication of glomerulonephritis?
A
Inflammatory disease involving the glomerulus and disruption of the glomerular filtration barrier
- It can develop into end-stage renal failure (ESRF)
19
Q
What cells are present in the glomerulus?
What are their roles?
What would damage of these cells lead to?
A
Parietal epithelial cell: lines Bowman’s capsule
- Damage is called a crescent lesion
Podocyte: sits on the outside of the glomerular membrane
- Has zipper-like foot processes
- Controls the charge and filtration barrier
- Damage: lose zipper effect and filtration barrier. Lots of protein will be present in urine
Mesangial cell: controls the matrix between the capillaries and produces mesangial matrix
- keeps the filter (GBM) free from debris
Endothelial cell: affected more often in systemic disease
20
Q
What are the targets for injury in glomerulonephritis?
What are the pathological mechanisms involved in glomerulonephritis
A
Targets: cells
- Parietal epithelial cells, podocytes, mesangial cells, endothelial cells
Pathological mechanisms
- Pre-formed antibodies that travel to the glomerulus and cause damage ie. form immune complexes or activate complement
- Cell-mediated mechanisms (cells infiltrate the kidney) eg. cytokines
- Metabolic e.g. diabetes, genetic, vascular disease (HTN)
21
Q
Many conditions are associated with glomerulonephritis. Give 3 examples
A
CV: SBE (subacute bacterial endocarditis)
Resp: lung cancer, TB
Infectious Disease: Hepatitis, HIV, chronic infection, Abx
Rheum: RA, lupud, amyloid, CT disease
Drugs: NSAIDs, bisphosphonates
Gastro: ALD, IBD, coeliac disease
Diabetes
Haem: myeloma, CLL, polycythaemia rubra vera (PRV)
22
Q
Label the diagram
A
23
Q
When do symptoms appear with kidney damage?
A
- When eGFR falls below 50%
- Creatinine only begins to rise when eGFR falls below 50%
24
Q
How do you approach a patient with suspected glomerulonephritis?
A
- Detailed medical and drug history (if symptoms, how long have they been present?)
- Basics: U&Es, dipstick for blood and to quantify proteinuria, check albumin, USS (1/2 kidneys)
- Glomerulonephritis screen: ANCA, ANA/dsDNA, RF, anti-GBM, immunoglobulins, virology (Hep B, C, HIV)
25
What is required for a clinical diagnosis of glomerulonephritis?
- Kidney biopsy of the **cortex** (where the glomeruli are found)
- Bleeding risk so avoid is possible
26
What is the spectrum of presentation for glomerulonephritidies?
- Incidental finding with urinary abnormalities +/- impaired kidney function
- Visible haematuria (usually lower urinary tract problem but could be glomerulus)
- Synpharyngitic: sore throat and coke-looking urine. This is classic of IgA nephropathy
- Nephritic syndrome (pt. often ends up in hospital): high BP, declining kidney function and blood and protein in urine
- Nephrotic syndrome (odematous patient): unwell with rapidly progressing GN
- Acutely unwell with rapidly progressive glomerulonephritis
27
How do you diagnose nephrotic syndrome?
What is the risk of nephrotic syndrome?
Triad:
- **Massive p****roteinuria:** 3.5g proteinuria per 24hr (ie. urine PCR \>300)
- **Hypoalbuminaemia:** Low serum albumin \<30 *liver tries to accomodate loss of albumin but usually unable to keep up*
- **Oedema**: ankles, puffy face, around the eyes. Due to salt and water retention and low serum albumin
- Usually see **hyperlipidaemia**
RIsk: loss of anticoagulants therefore risk of venous thromboembolism and inc. risk of infection
28
What are the classic causes of nephrotic syndrome?
- Minimal change disease
- Membranous glomerulonephritis
29
How do you diagnose nephritic syndrome?
- Hypertension
- Blood in urine (coke-coloured urine), sometimes protein
- Oliguria: production of abnormally small amounts of urine
- Usually caused by **inflammation** often involving the endothelium
30
Compare and contrast the mechanisms of nephritic and nephrotic syndrome
Nephrotic: oedema and injury to podocytes
Nephritic: inflammation
Nephrotic: altered architecture with scarring and matrix deposition
Nephritic: reactive cell proliferation, breaks in the GBM and Crescent formation
Nephrotic: always protein, sometimes blood
Nephritic: always blood, sometimes protein
31
What are the classic causes of nephritic syndrome?
- Crescentic GN
- Vasculitis
- Post-infectious
- IgA (usually presents with nephritis but can present as nephrotic)
32
What is IgA nephropathy?
What is the aetiology?
- IgA deposition in the mesangial cells
- The most common GN type in adults
Aetiology
- Secondary to infection: synpharyngitic IgA nephropathy until proven otherwise (sore throat and coke-coloured urine)
- Secondary to coeliac disease, cirrhosis, HSP (IgA vasculitis)
- IgA vasculitis: purpuric spots on extensor surfaces and protein in urine
-
33
What is the pathophysiology of IgA nephropathy?
What is the clinical presentation?
What is the treatment?
- Abnormal/Over-production of IgA immune complexes that deposit in the mesangium
- Mesangium responds bu proliferating, disrupting the GFB
Presentation
- Haematuria, usually HTN, proteinuria
- 1/3 progress to ESRF
Treatment
- Antihypertensive therapy ie. BP control (ideally \<125/75)
- ACEi (Ramipril) or ARB
34
What is membranous glomerulonephritis?
What are the causes?
- Damage to podocytes and glomerular basement membrane due to deposits
Causes
- Idiopathic
- 10% due to underlying disease
- 70% have an antibody (anti-phospholipase A2 receptor antibody Anti-PLA2R) that binds to receptors on podocytes and causes dysfunction ie. immune complexes found in basement membrane
35
How does membranous glomerularnephritis present?
What is the natural history?
Presentation: nephrotic syndrome
- Oedema, inc. risk of infection and clots
- Fatigue
Natural history
- 1/3 spontaneous remission
- 1/3 progress to ENRF over 1-2yrs
- 1/3 persistent to proteinuria, maintain GFR
36
How is membranous glomerulonephritis treated?
- If secondary: treat underlying disease e.g. stop NSAIDs
**ACEi/ARB**, statin, diuretics
- BP control is **essential,** to \<125/75
- Anything blocking RAAS will affect both BP and GMB to reduce proteinuria
Specific immunotherapy (if still deteriorating)
- Steroids along with alkylating agents for 6 months
- Rituximab
37
What age bracket is minimal change disease most common?
What is it's pathogenesis?
What's seen with a microscope?
- Commonest form of GN seen in children
- 90% of GN \<10yrs is Minimal Change Disease I therefore don't need to biopsy
Pathogenesis: disorder of the T cell that targets podocytes
- Damage to the GFB
Light microscope: normal glomerulus, no sign of inflammation or proliferation
Electron microscope: **podocytes fused together and lose of finger-like processes (characteristic of MCD I)**
38
What causes MCD and how does it present?
Cause: idiopathic
- Can be seen 2o to malignancy
Presentation: nephrotic syndrome
- MCD I: rapid presentation
- MCD II: acute presentation (overnight), 50% will relapse
39
How is minimal change disease treated?
Children: prednisolone (high dose corticosteroid) for 8 weeks
Adult: ACEi/ARB or diuretics
40
What is the mainstay for treatment of glomerulonephritis?
ACEi (ramipril)/ARB or statin or diuretics
- Ie. **BP control \<125.75mmHg**
41
What primary causes of nephrotic syndrome are prevalent in different age categories?
Children: Minimal Change Disease (MCD)
- \<45: Minimal change
45-65: Focal Segmental Glomerular Sclerosis (FSGS)
\>65: Membranous GN
42
What is the pathology of Focal Segmental Glomerular Sclerosis (FSGS)?
What is the aetiology?
How does it present?
Pathology:
- Focal: only some glomeruli are affected
Segmental: only part of each glomerulus
Aetiology:
- Idiopathic or systemic disease
Presentation:
- Nephrotic syndrome
- 50% progress to ESRF
43
What are cresentic/rapidly progressing glomerulonephritidies?
What is the pathology?
How does the disease progress?
- A group a conditions demonstrating glomerular crescents on kidney biopsy
- Glomerular crescents = defined as 2+ layers of proliferating cells in Bowman's space
- Presence of active proliferative disease
- Inside the glomerulus looks normal but the Bowman's capsule has expanded out due to inflammatory cells, necrosis and ECM
Aggressive disease therefore will progress to ESRF
- Needs urgent treatment
- When crescents heal, the whole glomerulus scleroses and dies
44
Describe some common causes of Crescentic GN
**ANCA Vasculitis**
- Systemic disease, patient usually has other symptoms e.g. rash, joint paint, deaf, neuropathy
- ANCA positive
**Goodpasture's syndrome**
- Autoimmune condition with anti-GBM antibodies
- Glomerulus and lungs are affected
- Symptoms: haematuria and haemoptysis
- Treatment: steroids
**Lupus Nephritis**
- ANA +ve, anti-dsDNA +ve, anti-histone +ve
**HSP Nephritis**
- ANA positive
45
What are the embryological stages of the kidney?
When is urine produced?
How much kidney function is developed by the 3rd trimester?
Pronephros: appears in the 4th week of development and regresses by end of week 4
Mesonephros: regresses by end of 2nd month
Metanephros: appears in week 5 and becomes functional around the 12th week. This is the definitive kidney
Urine production starts at week 10
Only 60% of kidney function (ie. 60% of glomeruli) by 3rd trimester
46
What is the most common cause of ESRF in children?
Congenital anomalies
- 50% of congenital problems lead to CKD needing renal replacement therapy (RRT)
47
# Define renal agenesis
What stage of embryogenesis does this occur?
What is the prognosis?
- Congenital **absence** of renal parenchymal tissue, with less glomerli
- Occurs in the metanephric stage
Prognosis
- Bilateral: not compatible with life
- Unilateral: good prognosis
48
What is the most common congenital abnormality that progresses to ESRF?
- Renal hypodysplasia
49
What is renal hypodysplasia?
**Renal hypodysplasia:** **congenitally small kidneys with dysplastic features**
- Can be accompanied by a cystic component
- Renal hypoplasia: reduction in the number of nephrons but normal architecture
- Renal dysplasia: malformed renal tissue
50
How would a patient with renal hypodysplasia present?
How is renal hypodysplasia managed?
Presentation:
- Antenatal US: reduced kidney growth, reduction in amniotic fluid
- Neonate: lung issues (need ventilated), intrauterine growth restrictions, acidosis, raised creatinine
Children: failure to thrive (FTT), anorexia, vomiting, proteinuria
Management: supportive
51
What is MCDK?
How would multi-cystic dysplastic kidney (MCDK) present?
What are the risks of MCDK?
- Large low-functioning kidney with multiple fluid-filled cysts, which may get smaller over time causing the kidney to shrink
- 50% involute (shrink): monitoring is required
Presentation
- Mainly antenatal detection on US
- Neonate: abdominal mass
- Usually unilateral (unaffected kidney does all the work), rarely bilateral (incompatible with life)
Risks
- Non-functioning kidney
- Malignancy
- HTN
52
What is the main risk factor for renal disease in infancy?
- Male
53
# Define hydronephrosis
What is hydronephrosis associated with?
What modality is it usually discovered on?
Definition: distension of the kidney with urine, caused by obstruction to urinary outflow
- Associated with renal injury and impairment
- Usually unilateral (60-80%)
- Commonly seen on ultrasound (enlarged renal pelvis w/ diameter \>10mm)
54
What are the causes of hydronephrosis?
- Vesico-ureteric reflux
- Obstruction in urinary tract
55
# Define obstruction (in relation to hydronephrosis)
What are the levels of obstruction in the urinary tract?
Def: impedence to urinary flow which causes progressive damage
Levels of obstruction:
- Pelvic-Ureteric Junction (PUJ)
- Ureter
- Vesico-ureteric junction (VUJ)
- Bladder
- Urethra
56
How is PUJ obstruction diagnosed?
What is the effect of PUJ obstruction?
Effect: partial or total urine blockage at ureter junction
- usually unilateral
Diagnosis:
- Antenatal diagnosis (US)
- Neonate: abdominal mass (enlarged renal pelvis), UTI, FTT
- Children: abdominal/flank pain
57
What is vesico-ureteric junction obstruction?
What causes it?
What are the effects?
- Functional/Anatomical abnormality at vesico-ureteric junction, causing obstruction of urinary flow
Causes:
- Primary: reflex or obstruciton
- Secondary: bladder issues
Effect: develop a megaureter
- Ureteric dilatation \>7mm (\>1cm is significant)
58
What are posterior urethral valves?
How would they present?
What is the diagnosis, management and outcome?
- They are **obstructive** membranes that develop in the urethra, close to the bladder
- **Only** seen in boys
Presentation: UTI (bilateral hydronephrosis)
Diagnosis: US
Management: cystoscopy
Outcomes: 1/3 normal renal function, 1/3 with bladder problems and incontinence, 1/3 with ESRF
59
# Define vesico-ureteric reflux
What are the consequences?
How is it diagnosed?
How is it graded?
Def: retrograde passage of urine from the bladder into the upper urinary tract
Consequences: can lead to scarring, HTN, ESRF
Diagnosis: MCUG (Micturating Cystourethrogram)
Graded I-V
- Grade I&II: reflux into ureters
- Grade I-III: usually resolve spontaneously
- Grade IV&V: need intervention
60
Define pyelonephritis
Bacterial infection of the kidneys causing inflammation
- Aka UTI (urinary tract infection)
61
How does pyelonephritis present?
- More common in girls (unless \<3 months)
Upper tract pyelonephritis:
- Pyrexia, vomiting, systemic upset, abdominal pain
- More likely to cause kidney damage
Lower tract pyelonephritis:
- Dysuria, frequency, haematuria, wetting
- Similar to adult clinical presentation
62
What is the commonest caustive organism of pyelonephritis?
E. Coli
63
How do you diagnose pyelonephritis?
What are the complications of pyelonephritis?
Urine sample
- Need proper urine collection
- Significant bacteriuria: \>105 colony forming units (CFU)/ml
Investigations
- US, MCUG (\<1yr), nuclear medicine (if questioning obstruction)
Complications
- Scarring, HTN, ESRF
64
What is the epidemiology of diabetic nephropathy
30-40% diabetes develop kidney problems (usually T2DM)
- 26% of people starting RRT (ie. dialysis or transplant) are diabetic
65
Describe the pathophysiology of diabetic nephropathy
Structural changes of the glomerulus:
- inc. number of mesangial cells
- thickening of the glomerular basement membrane
- mesangial matrix expansion
- fusion of foot processes
Progression:
hyperglycaemia → volume expansion → intra-glomerular hypertension → hyperfiltration → proteinuria → hypertension and renal failure
- Often takes 5-10 years for microalbuminuria to occur
66
What is the clinical presentation for diabetic nephropathy
Early on: may be asymptomatic
Later:
- worsening BP control
- proteinuria
- peripheral oedema (ankles, feet, hands)
- inc. frequency
- confusion / difficulty concentrating
- SOB, nausea, loss of appetite, persistent itch, fatigue
67
Describe the histology of diabetic nephropathy
Pathognominic hyaline material containing nodules (excess mesangial matrix) in glomerular capillary loops
68
What are 3 complications of diabetic nephropathy
anaemia
bone and mineral metabolism
retinopathy
neuropathy
69
What is the management for reducing diabetic nephropathy and it's progression to needing dialysis
- tight glycaemic control
- BP control
- SGLT-2 inhibitors
70
What is the pathophysiology of renovascular disease?
- progressive narrowing of the renal arteries with atheroma (degradation of the walls due to fatty deposits)
- perfusion through kidney falls by 20%: GFR falls but tissue oxygenation of cortex and medulla are maintained
- a hypoxic medulla can be compensated for
- RA stenosis progresses to 70%: if it becomes so hypoxic, the compensation is overwhelmed and the medulla becomes ischaemic and dysfunction develops
- cortical hypoxia causes microvascular damage and activation of inflammatory and oxidative pathways
- Parenchymal inflammation and fibrosis progress and become irreversible. Restoration of blood flow provides no benefit
71
At what stage do symptoms develop with renal artery stenosis and list 3
Symptoms usually develop after advanced stage
- hypertension with sudden onset or worsens without explanation
- hypertension that begins \<30yrs or \>50yrs
As RA stenosis develops..
- HTN that's difficult to maintain
- Bruit over the kidneys
- Proteinuria
- worsening kidney function with HTN treatment
- fluid overload and oedema
- treatment resistant HF
72
What is the aim of treatment for RA stenosis
Give 2 medical and lifestyle and one surgical management option(s) for renal artery stenosis
- when would the surgical option be considered?
Aim: *Treat underlying systemic disease and always control BP as it will always affect kidney function*
Medical:
- BP control (not ACEi/ARB, think verapamil or amlodipine or bisoprolol)
- Statin: lower cholesterol
- If diabetic, tight glycaemic control
- Stop ACEi, and avoid it and ARBs in future
Lifestyle
- smoking cessation, exercise, low Na diet
Surgical: angioplasty
- rapidly deteriorating renal failure
- uncontrolled inc. BP on multiple agents
- flash pulmonary oedema
73
A 42yr old male attends medical receiving unit
PC: leg swelling
HPC: normal ECG, albumin low, BP 105/65mmHg
Urinalysis: uPCR 742
PMH: 20yr hostory of ulcerative colitis
Comment on any significant results
What are the differentials and what investigations are needed to confirm/exclude these differentials
Low albumin
- either losing albumin in urine or failure to make albumin (liver disease - no evidence in this case)
uPCR 742 = excreting about 7.5g/day ie. proteinuria - nephrotic syndrome
Nephrotic syndrome on background of colitis
Differentials: diabetic nephropathy, lupus nephritis, virual infections (HBV, HCV, HIV), amyloidosis, myeloma
Investiagtions:
- Bloods: glucose (diabetes), ANA (lupus nephritis), viral infection screen, protein electrophroesis (myeloma - looking for light chains), kidney biopsy (amyloidosis)
74
# Define amyloidosis
What are the primary organs that are affected?
A group of diseases that result from the abnormal deposition of a highly stable insoluble proteineous material, amyloid, in the extracellular space
- Amyloid is made of beta-pleated sheets
- mainly found in the kidneys, heart, liver, gut
75
How is amyloidosis diagnosed?
For the kidney: biopsy
- Light microscope with Congo red stain: apple green birefringence
- Electron microscope: Amyloid fibrils causing mesangial expansion
76
What are the two classes of amyloidosis and what conditions are they associated with
AA: systemic amyloidosis
- inflammation/infection
- more widely seen in TB and IBD
AL: immunoglobulin fragments
- haematological conditions eg. myeloma
77
How are the two classes of amyloidosis treated?
AA amyloid: treat underlying cause of infection or inflammation
AL amyloid: treat the underlying haematological condition
78
What is protein in the urine associated with
GLOMERULI disease
- if no protein: damage to another part of the kidney other than the glomerulus
79
36yr old attends the rheumatology ward
Investigations: SCrumol/l 200 (70 in Jan)
- Urinalysis P4+ and B3+, uPCR 400 and albumin 29
- Presents with butterfly rash, hair loss, Ryanoids', some arthritis associated
Comment on noteworthy values
What are the differentials and what investigations are needed to confirm/exclude these differentials
SCr elevated: kidney dysfunction and rapidly progressing
Urinalysis: haematuria and proteinuria
Nephritic syndrome: rapidly progressing, haematuria and proteinuria
Differentials:
- Crescentric nephritis: ANCA vasculitis, Goodpasture's, HSP nephritis, Lupus nephritis
- IgA nephropathy
Investigations: antibodies: ANCA (ANCA vasculitis), anti-GBM (Goodpasture's), ANA (HSP/lupus), anti-dsDNA and anti-histone (lupus nephritis)
- check C4 (low in SLE)
80
# Define systemic lupus erythematous
What is the pathology of this ocndition?
A chronic inflammatory condition caused by an autoimmune disease
- It's a immune complex mediated glomerular disease
Pathology:
- multiple autoantibodies directed against DNA (anti-dsDNA), histones (anti-histone), snRNPs, translational machinery, nucleus (ANA)
81
Describe the pathophysiology of systemic lupus erythematous (SLE)
- auto-antibodies produced against dsDNA or nucleosomes (anti-histone)
- form intravascular immune complexes or attach to GBM
- activate complement, resulting in a low C4
- renal damage
82
How is systemic lupus erythematous diagnosed and treated?
Diagnosis: kidney iopsy
Treatment: immunosuppression ie. **steroids**
83
What genes are involved in the development of adult polycystic kidney disease?
PKD 1 gene mutation (chromosome 16) - 85%
- Typical rapid progression with ESRD \<50yrs
PKD 2 gene mutation (chromosome 4) - 15%
- Slower progression, may never reach ESRD
84
Define autosomal dominant polycystic kidney disease (ADPKD)
- the most common form of polycystic kidney disease characterised by the progressive development of innumerable kidney cysts, causing HTN, renal pain and renal insufficiency
- usually mutations of PKD 1 gene on chromosome 16, less often PKD 2 gene on chromosome 4
85
Define autosomal recessive polycystic kidney disease (ADPKD)
- early onset disorder characterised by the presence of innumerable kidney cysts and enlarged kidneys that can usually be detected via ultrasound before birth or in the neonatal period
- mutated gene found on chromosome 6
86
What are the roles of the PKD 1 and 2 genes?
They code for polycystin 1 and 2
- membranr proteins found all over (kidneys, brain, bone, heart)
- located in the renal tubular epithelial
- involved in intracellular calcium regulation
Overexpressed in cyst cells
87
Describe the progression of ADPKD
Cysts gradually enlarge causing pressure, and the normal kidney tissue starts getting replaced
- Kidney volume increased and eGFR falls
- cyst infection, rupture, haematuria and pain
- extra-renal manifestations explained as polycystin proteins are found systemically
Hepatic cysts: originate from bile ducts, so can enlarge and cause enlargement of the liver but **will not cause liver failure**
88
Describe the presentation of ADPKD at different ages
Antenatal: antenatal US
Childhood: haematuria, flank pain, HTN, UTIs, renal US findings
Adult (usual presentation):
- HTN, impaired renal function, loin pain, haematuria, UTIs, renal US findings
Family associated
89
Describe the presentation of ARPKD at different ages
Antenatal: US or oligohydramnios (deficiency of amniotic fluid)
Infancy:
- large palpable renal mass, resp. distress, renal failure, HTN, hyponatraemia
Childhood:
- Renal failure, HTN
90
Describe the histpathology and associated anomalies of ARPKD
Histopathology:
- Cystic dilatations of collecting tubules with flattening of the epithelium that runs perpendicular to the renal capsule
Associated anomalies:
- congenital hepatic fibrosis → portal HTN → ascending cholangitis
91
Compare the prognosis of ADPKD and ARPKD
ADPKD:
- progression of ESRF in adulthood, 50% by 60yrs
ARPKD:
- 20-30% mortality in neonate period
- 5yr survival: 70-88%
- Progression to ESRF \>50% (often \>15yrs)
92
List 3 extra-renal manifestations associated with polycystic kidney disease (PKD)
Heart: mitral valve prolapse, AV malformation
Brain: cerebral aneurysm
GI: hepatic/pancreatic cysts, colonic diverticula, colonic hernia
93
How is polycystic kidney disease managed?
- **Supportive**
- Early detection and BP management
- Treat complications
- Manage extra-renal associations
- Prepare for renal replacement therapy (RRT): dialysis or kidney transplant
For ADPKD: Tolvaptan (only in CKD that's stage II/II at start of treatment and evidence of rapidly progressing kidney disease)
94
Define acute kidney injury
A sudden decline in renal function over hours or days, recognised by the rise in serum urea and creatinine
95
What are the diagnostic classifications of AKI and list three causes of each
**Pre-renal failure:** Due to circulatory failure ie. shock
- occurs secondary to renal hypoperfusion
1. hypovolaemia and hypotension eg. diarrhoea, dehydration, haemorrhage, burns
2. Reduced effective circulatory volume eg. septic shock, cardiac failure, cirrhosis
3. drugs eg. NSAIDs and ACEi together
4. renal artery stenosis
**Renal failure:** due to an injury/failure of the cells of the kidney
1. glomerular: glomerulonephritis and other glomerular pathology
2. Tubulointersitial: ischaemic and nephrotoxic acute tubular necrosis (ATN) caused by pre-renal failure, drugs, myeloma, sarcoid
3. Vascular: renal artery stenosis causing structural abnormalities
**post-renal failure:** due to obstruction
- renal papillary necrosis, kidney stones
- retroperitoneal fibrosis
- carcinoma of the cervix, prostatic hypertrophy/maligancy
- urethral strictures
96
How does septic shock affect the kidneys?
Causes systemic vasodilation which reduces renal perfusion pressure and leads to hypoperfusion
97
How does the combination of NSAIDs and ACEi induce vascular changes that could lead to renal failure?
NSAIDs: vasoconstrict the afferent glomerular arteriole
ACEi: vasodilate the efferent glomerular arteriole
98
How does hypoperfusion of the kidneys lead to renal failure?
hypoperfusion results in ischaemia of the renal parenchyma
- if this lasts, intrinsic damage may occur and acute tubular necrosis will develop
99
Explain the development of intrinsic renal failure
3 categories: glomerular, tubulointerstitial and vascular
Pre-renal failure can cause intrinsic renal failure due to lack of blood supply to the kidney parenchyma
Tubulointerstitial causes:
- due to damage of the parenchyma which leads to scarring and fibrosis
- most common is acute tubular necrosis (ATN)
- always occurs due to prolonged renal hypoperfusion (pre-renal) and / or direct toxicity
100
List 3 symptoms of acute kidney injury
Non-specific
- nausea or vomiting
- diarrhoea
- dehydration
- oligouria
- confusion, drowsiness
- irregular heart beat (due to hyperkalaemia)
101
What can acute kidney injury result in?
Decline in renal function can result in dysregulation of
- fluid balance
- acid-base homeostasis
- electrolytes
102
List the classification systems used for AKI and their stages
What measurements are used for their classification
RIFLE: Risk, Injury, Failure, Loss, ESRD
- sCr / GFR and urine output
AKIN: Stages 1-3
- sCr and urine output
KDIGO: Stages 1-3
- sCr and urine output
103
What are the stages involved in the RIFLE classification of AKI
Risk:
- inc. sCr x1.5 or GFR dec. by \>25%
- UO \<0.5ml/kg/hr for 6hrs
Injury:
- inc. sCr x2.0 or GFR dec. by \>50%
- UO \<0.5ml/kg/hr for 12hrs
Failure:
- inc. sCr x3.0 or GFR dec. by \>75% or Cr \>4mg/dl with acute rise \>0.5mg/dl
- UO \<0.3ml/kg/hr for 24hrs or anuria for 12hours
Loss:
- persistant acute renal failure = complete loss of renal function for \>4 weeks
ESRD: End stage renal disease
104
What are the stages involved in AKIN?
Stage 1:
- sCr inc. x1.5 or \>0.3mg/dl
- UO \<0.5mg/kg/hr x6hrs
Stage 2:
- sCr inc. x2.0
- UO \<0.5mg/kg/hr x12hrs
Stage 3:
- sCr inc. x3.0 or \>4mg/dl with acute rise of \>0.5mg/dl
- UO \<0.3ml/kg/hr x24hrs or anuria x12hrs
105
Where are patients on renal replacement therapy placed on the AKIN classification?
Stage 3
106
What are the criteria to warrent an AKI e-alert?
What are AKI e-alerts used for?
Used in hospitals to highlight when creatinine has changed to indicate underlying AKI
Criteria:
Serum creatinine 1.5x higher than median of all creatinine values of 8-365 days ago
Serum creatinine 1.5x higher than the lowest creatinine within the last 7 days
Serum creatinine \>26 umol/l than the lowest creatinine within 48hrs
107
What is the KDIGO classification based on and what's involved in each stage
Based on:
- absolute sCr rise in 38hrs
- sCr inc. 1.5x baseline in last 7 days
- UO \<0.5ml/kg/hr for 6hours
Stage 1:
- sCr \>26umol/l (48hours) or \>1.5-1.9x inc. in 7 days
- UO \<0.5ml/kg/hr for 6 hours
Stage 2:
- sCr \>2.0-2.9x inc. in 7 days
- UO \<0.5ml/kg/hr for 12 hours
Stage 3:
- sCr \>354 umol/l or 3x reference or if on RRT
- UO \<0.3ml/kg/hr for 24hrs or anuria for 12hrs
108
Define oliguria
urine output \<1ml/kg/h in infants and \<0m5ml/kg/h in children and \<400ml-500ml/24h in adults
109
Describe the pathophysiology of acute kidney injury
- largely dependent on cause
- common link: reduction in GFR
- as the pressure within the afferent arteriole falls and approaches 80mmHg, prostglandins dilate the arteriole to inc. flow through the vessel
- NSAIDs prevent this from occuring
- ACEi dilate the efferent arteriole thus decreasing glomerular pressure
110
How is acute kidney injury diagnosed?
Need for urgent action \> making final diagnosis
Determination of acute or chronic kidney injury dependent on timeline
Bloods: raised urea and creatinine
Potassium: severe hyperkalaemia (K \>6.5mmol/l) is a common complication of AKI
Urine output: \<400ml/day (oliguria in adults)
Fluid assessment:
- raised JVP and oedema: fluid overload
- BP and heart sounds
Consider **sepsis** and **medications** (ie. underlying causes)
**Perform urinalysis (protein/blood) and renal USS**
GN screening for glomerulonephritis cause: bloods (ANA, anti-GBM, ANA, Ig, complement)
Renal USS to exclude obstruction
- Loss of cortico-medullar differentiation suggests CKD as well as smaller kidneys
111
How is acute kidney injury treated?
ABCDE protocol
May need emergency correction of:
- Circulatory shock: hypovolaemia, hypotension, shock and hyperkalaemia. Restore renal perfusion
- Remove causes and correct them quickly: eg. drugs or sepsis
- Exlude obstruction and consider renal causes
112
What is the main complication of AKI
Hyperkalaemia = serum potassium \>5.5mmol/l
Mild: 5.5-5.9mmol.l
Moderate: 6-6.4mmol/l - risk of arrythmias and should be treated
Severe: \>6.5mmol/l - **medical emergency**
113
How is hyperkalaemia treated?
1. Reduce absorption from the gut
- calcium resonium
2. Drive K back into cells
- insulin and dextrose
3. Portect heart by stabilising cardiac membrane
- calcium gluconate
114
What are the absolute indications for needing dialysis
In which scenarios would dialysis be adviced but not necessary
Absolutely:
1. Refractory severe hyperkalaemia (\>6.5mmol/l)
2. Refractory pulmonary oedema
refractory: uncontrolled/resistant
Beneficial:
1. acidosis ie. pH \<7.1
2. Uraemia esp. if urea \>40 or pericarditis
115
Define chronic kidney disease
The presence of kidney damage or reduced kidney function for 3 or more months, suggested by a reduction to a GFR \<60ml/min/1.73m2
116
What pathological markers can be used to characterise CKD?
- albuminuria
- radiological abnormalities (polycystic kidneys)
- evidence of kidney pathology
117
What problems arise as kidney function begins to fall in CKD
Dysregulation of
- fluid balance
- acid/base homeostasis
- electrolyte balance
- calcium/phosphate handling (secondary hyperparathyroidism)
118
What is the relationship between serum creatinine and the glomerular filtration rate
What is the main association with creatinine and why
- sCr is inversely proportionate to GFR
- creatinine is strongly dependent on muscle mass as it is a product of muscle metabolism (breakdown)
119
What are the two downfalls for using serum creatinine as a marker for kidney function?
An **exponential relationship exists** leading to inaccuracies:
- loss of the first 70% of renal function is not recognised quickly enough (lag time)
- late renal referral - may encounter sudden, sharp rise in creatinine
Due to the effects of muscle mass:
- renal function tends to be over-estimated in women, elderly and amputees who all have a lower muscle mass
120
What is the formula to calculate eGFR and what's involved?
MDRD 4 formula
- age, gender, race, serum creatinine
121
List 3 situations where eGFR cannot be used and one other downfall
- Not validated in the elderly
- Not useful in AKI
- Not useful for pregnancy
- Only validated for white and African-American populations
Downfall: not distinguishable above 60ml/min/1.73m2
122
What markers are involved in the classification of CKD?
eGFR: stages 1-5
ACR (albumin creatinine ratio)
these are used in combination to work out a provisional prognosis for a patient
A1: normal (male \<2.5; female \<3.5)
A2: microalbuminura (male 2.2-25; female 3.5-35)
A3: macroalbuminuria (male \>25; female \>35)
123
What is a normal amount of protein excretion per day in urine
\<150mg per day
124
What protein is measured on a dipstick for proteinuria?
Albumin
125
How is proteinuria quantified?
Concentration of urine changes based on hydration status, therefore need to test urine conc. against something that's excreted independently of urine conc. - urine creatinine concentration
ie. uPCR: urine protein creatinine ratio
126
What are the normal ACR and PCR values?
How can ACR be converted into PCR?
Albumin:Creatinine Ratio (ACR) - normal ACR \<2.5
Protein:creatinine ratio (PCR) - normal PCR \<20
Conversion: ACR = 2/3 of PCR
ie. ACR 70 = PCR 100 = 1g protein excreted /24hrs
127
Define proteinuria
The presence of excess levels of protein in the urine
PCR \>300 ie. 3g protein excreted / day
128
Describe the pathophysiology of CKD
As we age, there is a progressive loss in renal mass and structural changes occur resulting in a decline in renal function
- Irrespective of cause, CKD leads to progressive loss of nephrons and a subseuqent reduction in GFR
129
List 3 causes of Chronic Kidney Disease (CDK)
Majority are secondary to diabetes, HTN and glomerulopathies
- Diabetic nephropathy
- Renovascular disease/Ischaemic nephropathy eg. artery occlusion, venous thrombosis
- Chronic glomerulonephritis: membranous or IgA nephropathy
- Reflux nephropathy or chronic pyelonephritis
- Adult polycystic kidney disease
- obstructive uropathy: hydronephrosis
130
How can diabetic nephropathy cause CKD?
- glycosuria damages the glomerular filtration barrier
- small vessel damage in the glomerulus
- develop nodular lesions
131
How can renovascular disease cause CKD?
- Naorriwng or blockage of renal vasculature usually stemming from artery occulsion, venour thrombosis or renal atheroembolism
- Glomerulus gets eroded and you get local sclerosis of the vessels
132
How can reflux nephropathy lead to CKD
- urinary reflux from the bladder causes scarring of the renal tissue
- bladder contracts and urine goes back up ureters
- if consistant efflux of urine, it will present with an inflammatory response
- this can happen over time and scar the tissues
133
Which part of the kidney is damaged in APKD
The parenchyma
134
List 3 symptoms and 3 signs of CDK
Early stage CKD: usually asymptomatic
Advanced CKD: non-specific features ie. when eGFR falls beow 45ml/min
Symptoms of advanced CKD:
- pruritus/itch
- nausea, anorexia, weight-loss, fatigue
- SOB/breathlessness
- leg swelling, bone/joint pain
- nocturia (impaired ability to concentrate urine)
- confusion
Signs of advanced stage CKD
- peripheral and pulmonary oedema
- pericardial rub
- rash, pallor and/or yellow tinge
- HTN, tachypnoea
- cachexia (muscle weakness/wasting)
135
Describe the management for CKD
3-fold: renal protection; complications; RRT
- there are interventions to slow progression of CKD and may reduce cardiovascular risk
- dialysis shown to slow progression of CKD and drop in eGFR
Renoprotection
- Agressive BP control (ACEi/ARB)
- Diabetic control, improve diet, stok smoking
- Improve lipid profile, treat acidosis
RRT: 4 domains
1. Transplant
2. Home haemodialysis
3. Hospital based therapies (haemodialysis or self-care unit)
4. Conservative care
136
List and explain the development of two complications of CKD
Anaemia
- normocytic-normochromic anaemia
- occurs when eGFR falls below 30
- due to reduction of EPO production (stimulates BM to produce more RBCs)
- can also occur due to suboptimal iron absorption and utilisation
Mineral Bone Disorders
- Reduction of Vitamin D
- Vit. D needed for cellular Ca uptake, and with CKD there's reduced Vit D production
- So intracellular Ca falls leading to stimulationg of parathyroid gland to inc. PTH production
- Inc. PTH production inc. bone turnover leading to metabolic deposition of calcium in other body parts, mostly blood vessels
- Secondary hyperparathyroidism may occur due to abnormal handling of calcium and phosphate
- once eGFR \<30: hypocalaemia, hyperphosphatemia and hyperparathyroidism occur leading to bone pathology
137
What is the treatment for bone mineral disorders due to CKD
manage the underlying conditions:
Hypocalcaemia: supplement with calcitriol
Hyperphosphataemia: restrict diet and give phosphate binders
- Calcium based treatments: calcium carbonate/acetate
Hyperparathyroidism: calcimimetics or surgery
138
List 4 functions of the kidney
Water and waste
- Regulates total body water
- waste excretion eg. urea and creatinine
- regulate electrolyte balance
- regulate acid-base
Hormonal
- mineral metabolism
- renin production
- EPO production
- glucose metabolism
139
List the indications for starting renal replacement therapy
- Medically resistant severe hyperkalaemia (\>6.5)
- Medically resistant pulmonary oedema
- Medically resistant acidosis
- Urinemic pericarditis
- Uraemic encephalopathy
Some drugs are only cleared by dialysis and therefore dialysus is used alongside normal kidney function in acute reatment of certain drug overdoses
140
Define uraemia
Raised levels of urea and nitrogenous waste products in serum
- Uraemia manifests as uraemic syndrome (renal failure) and can affect several body systems
141
List 3 symptoms of uraemia
- itch
- vomiting
- anorexia, weight-loss
- restless leg
- metallic taste
142
What is the importance of GFR when deciding on RRT?
What is the timing of RRT based on?
There is no absolute rule nor absolute threshold with regards to a GFR at which it is appropriate/adviced to initiate GFR
- RRT should be considered on a patient-by-patient basis
- Generally start RRT when GFR falls to 5-10ml/min/1.73m2
- Most start with RRT at a GFR of 7-8ml/min
**Timing is symptom based with no absolute threshold**
143
What are the three main options for a patient requiring RRT?
- Haemodialysis
- Peritoneal dialysis
- Renal transplant
144
In what setting would haemodialysis be done and how long does it take?
Setting: either home or hospital (more common)
- can e either daily or nocturnal
Timing: usually a 4-hour procedure 3x week
- Can be 6hrs 3x a week, short daily or daily overnight
145
What are the aims of haemodialysis
Aims:
1. Removal of solutes eg. urea, potassium, creatinine via **diffusion**
2. Removal of fluid via ultrafiltration - **hydrostatic pressure filtration**
146
Describe the process of haemodialysis
- Blood removed from body and pumped through the dialysis machine in one direction
- dialysis fluid (purified water with added ions - dialysate) is pumped through in the opposite direction (counter-current flow)
- Blood and dialysis fluid are separated by a semi-permeable membrane
- **Diffusion:** Urea, creatinine and waste products diffuse down conc. gradient
- **Hydrostatic pressure Filtration:** drives fluid and solute through the membrane from blood into dialysate
NB heparin is needed in the machine to prevent blood clotting
- An air detected and bubble trap are placed on the line taking blood back to the blood to prevent air-emboli
147
Where are the access points on the body for haemdialysis?
AVF (Arteriovenous Fistula)
- Gold standard
- the connection between artery and vein
- increases blood flow through the vein leading to inc. venous diameter and becomes stronger
- the vein can now withstand repeated needle insertions and provides good flow without collapsing
- rate of infection and thromboembolic event is low
TCVC (tunelled central venous catheter)
- required central line access
- doesn't last as long as AVF but more prone to complications and infections
- lines are wide bore and have red and blue cap for the venous and arterial vessels
AV graft
- if veins aren't good enough to form a fistula, and a tube is attached to the artery
148
List 3 complications of haemodialysis
- May go into shock due to acute hypotension
- May be problems with vascular access eg. infection, thromboembolic events, fatigue, blood loss
- Cramps
- Hypokalaemia (over dialysed)
- Air embolism
- Blood loss
- Dialysis disequilibrium: rapid shift in urea leads to rapid shift in cerebral water flow and can cause cerebral oedema
149
List three advantages and three disadvantages of using haemodialysis
Pros:
- can be used even when no kidney function left
- replaces many functions of the normal kidney
- quicker than peritoneal dialysis
Cons:
- massive impact on QoL and not definitive
- Expensive
- Preferable to be hospital-based
150
In what setting would peritoneal dialysis be used?
What are the procedures used for peritoneal dialysis?
Setting: allows for home-based therapy
Procedures:
- can be daily or nocturnal
- continuous ambulatory peritoneal dialysis
- automated peritoneal dialysis: machine will filter blood as they sleep and don't need to carry it around during the day
151
Describe the process of peritoneal dialysis
The exchange occurs between the peritoneal capillary blood and dialysis fluid (dialysate) which is put into the peritoneal cavity
- 2l of glucose rich (K depleted) dialysate is used
- blood should be high in K and low in glucose
- gradual in nature therefore not appropriate for AKI
- glucose conc. can be changed to alter rate of ultrafiltration
- need some residual renal function (not good options if no/minimal kidney function)
Two mechanisms:
1. **Osmotic fitration (ultrafiltration)**: movement of water and small solutes due to presence of glucose in dialysate inc. osmolarity
2. **Diffusion** down the conc. gradient: urea, creatinine and electrolytes cross into the fluid from blood down the conc. gradient
- the longer the dialysate remains within the peritoneal cavity, the smaller the gradient becomes and the lower the rate of diffusion
152
List 3 complications of peritoneal dialysis
- infection of peritoneum may occur (peritonitis)
- glucose load may impact existing or lead to development of diabetes
- can inc. risk of hernias, diaphragmatic leaks or other mechanical issues
- hyperalbuminaemia
153
List 3 advantages and 3 disadvantages of peritoneal dialysis
Pros:
- Maintains independence and less impact on QoL
- Needs to be taight
- Can be altered/controlled to a degree
Cons:
- Requires some residual kidney function
- Infection risk
- Not suitable for obese or frail patients or those with intra-abdominal adhesions
154
List 3 practicalities of peritoneal dialysis
- home-based therapy
- better with some residual kidney function
- gradual treatment: no good for AKI
- different glucose concs. of dialysate to provide more or less ultrafiltration
- maintain independence
- simple procedure once taught
155
What patients wouldn't be suitable for peritoneal dialysis?
- Grossly obese
- Frail
- Intra-abdominal adhesions
156
In what situation in conservative care used in RRT?
- Symptom based management
- With an increasingly frail and elderly population, the survival on RRT may only be marginally greater but with a much reduced quality of life
- reserved for the older population
157
List 3 factors taken into consideration to decide the type of RRT that should be used for a patient
- frailty
- ability to gain vascular access
- time constraints (time to travel to/from hospital)
- physical - concurrent medical problems eg. severe dementia, psychiatric disease, disseminated malignancy
- patient lifestyle and wishes ie. patient choice
- need someone living with patient at home for home-based therapies
158
How much GFR can dialysis provide?
only around 10ml/min GFR, nowhere near as good as a transplant
159
Explain how kidney transplants can be acquired
Cadaveric transplant
- there's a waiting list for patients who can receive a kidney from a registered donor following brainstem death or cardiac death
- average wait: 3 years
Live donor kidneys
- best success
- altruistic donor - an individual who donates one of their kidneys
NB not all patients are suitable for a transplant as surgery is demanding and requires immunosuppressant **lifelong** to prevent organ rejection
160
What immunosuppression can be offered after a kidney transplant?
Immunosuppression is given following the procedure **lifelong**
- Tacrolimus: inhibits IL-2 thus effectively blocking proliferation of T-cells
- Mycophenolate: blocks nucleosynthesis of B and T cells
- Methotrexate: inhibits DNA production
Given to prevent organ rejection
161
List 3 advantages and 3 disadvantages of a renal transplant
Pros:
- no need for dialysis
- better renal fucntion
- longer independent living
- increased life expentancy
- improved fertility
Cons:
- lifelong immunosuppression
- inc. CVS risk
- increased infection risk
- post-transplant diabetes may occur
- skin malignancy associations
162
What is the class, indication and action of methotrexate
Class: immunosuppressant
Indication
- Post-transplantation immunosuppression
- Inflammatory bowel disease
- Renal vasculitis
- Paediatric leukaemia
Action:
- disrupts DNA synthesis
- blocks the action of the enzyme dihydrofolate needed for DNA production
163
Define bacteruria
The presence of bacteria in the urine in the absence of symptoms
164
List 3 groups in which bacteruria is common
- girls \> boys
- pre-school age
- adult males
- non-pregnant females
165
List 3 high-risk groups of bacteruiria
- hospitalised patients
- catheterised patients
- diabetics
- patients with structural abnormalities
- immunocompromised patients
- pregnant patients
166
How is bacteruria managed?
Asymptomatic bacteriuria should only be treated in the following:
- pre-school children
- pregnant women (can escalate to pyelonephritis)
- those who have undergone a renal transplant
- immunocompromised
Treatment in other asymptomatic patients is *not* indicated
167
Outline the classification of urinary tract infections
Ascending:
- urethral colonisation
- more common in females
- bacteria multiply in the bladder and ureters are involved
Descending:
- aka 'haematogenous'
- often blood-borne infections (blood filters through the kidney)
- usually an abnormal causative organism
- involed renal parenchyma
168
List a gram negative and 3 gram positive organisms that commonly cause urinary tract infections (UTIs)
Gram -ve Bacilli
- E. Coli
Gram +ve
- Streptococcus sp.
- Enterococcus sp.
- Staphylococcus sp. (S. aureus, s. saprophyticus)
* - S. saureus found more often in UTIs of catheterised patients*
169
Outline the clinical features seen with a UTI
Outline the additional features seen in neonates, children and the elderly with a UTI
- suprapubic discomfort
- dysuria
- urinary frequency
- cloudly, blood stained, smelly urine
- low grade fever (potentially complicated)
- features of SIRS or sepsis (complicated)
Neonates: failure to thrive and jaundice
Children: abdominal pain and vomiting
Elderly: nocturia, incontinence, confusion
170
In what situations would the following most likely occur:
Multiple-organism infections
Multi-drug resistant organisms
Multi-organism infections:
- long-term catheterisation
- long term infection
- structural and neurological abnormalities
Multi-drug resistant organisms:
- abnormalities
- frequent infections
- courses of prophylactic antibiotics
171
Outline the investigations and treatment for a uncomplicated suspected UTI in non-pregnant women
1st presentation: culture not mandatory
- Dipstick (high false positive rate)
- check previous culture results (multi-resistant organism will change treated)
- trimethoprim for 3-7 days
- hydrate, rest, paracetamol (analgesics)
No response to treatment:
- urine culture and change abx
172
Outline the investigations and treatment needed for a suspected uncomplicated UTI in children and men
- send urine samples for culture with each presentation and treat accordingly
173
Outline the investigations and treatment for a suspected UTI in pregnant women
Send urine culture with each presentation
Treat with abx for 7-10 days
- amoxicillin and cefalexin are fairly safe
Avoid:
- Trimethoprim in 1st trimester (teratogenic)
- Nitrofuratonin near term
Hospital admission may be neccessary for IV abx if infection is severe: progression pyelonephritis occurs in around 30% cases
174
# Define a recurrent UTI
Who are mostly affected and why?
occurance of more than two episodes in 6 months or more than 3 episodes in a year
- mostly affects women due to shorter urethra
175
Outline the management for recurrent UTIs
- abx may be given as a short-course therapy or single doses given as a post-coital dose
- abx prophylaxis is given when simple measures fail and usually involve trimethoprim and nitrofuratoin ideally for 6 months
- *NB risk of antibiotic resistance*
176
What is a complicated UTI?
Upper UTIs which are associated with systemic signs and symptoms and/or catheter associated infection (CAUTI)
177
How can catheter-associated UTIs develop and what are the likely causative organisms?
Development due to the disturbance of:
- the flushing-system
- colonisation of urinary catheters
- production of biofilm by the bacteria
Likely causative organisms:
- patient's flora
- healthcare environment
178
Outline three complications of catheter use
- catheter associated UTI (CAUTI)
- obstruction leading to hydronephrosis than can progress into (chronic) renal inflammation
- urinary tract stones
- long-term risk of bladder cancer
179
Outline the prevention strategies for catheter associated UTIs
- only catheterise when necessary (do not catheterise if urine can be produced and measured without catheter)
- promptly remove catheters when no longer needed
- continually assess the need for a catheter
- signs of infection, remove catheter immediately
- catheter bundle care
180
Outline the management for cstheter associated UTIs
empirical antiboitics
- check previous microbiology results
- remove catheter if needed
- replace catheter: ensure catheters are changed under abx cover (gentamicin or ciprofloxacin)
- broad spec abx
181
Differentiate upper and lower urinary tract infections
upper UTI: ureters and kidney
lower UTI: involves bladder and urethra
182
Define acute pyelonephritis
moderate to severe upper UTI which is ascending and involves the renal pelvis
- acute inflammation of the kidney
183
Outline the clincal and morphological features of acute pyelonephritis
Clinical: UTI symptoms
Morphologically:
- kidney enlargement with possible abscess formation on the surface
- US changes
- hydronephrosis can contribute
184
How is acute pyelonephritis diagnosed and managed
Diagnosis:
- check previous microbiology
- request urine samples +/- blood culture +/- imaging (US)
Management:
community prescription of co-amoxiclav / ciprofloxacillin / trimethoprim
hospital prescription: usually broad spec abx
- uncomplicated pyelonephritis: 7-14 days
- complicated pyelonephritis: \>14 days
185
Outline the main complication of acute pyelonephritis
What are the outcomes of this complication?
Renal abscess
- clinical features similar to acute pyelonephritis
- positive urine and blood cultures
- usually due to Gram -ve bacilli
Outcome:
- life-threatening with a poor response to antibiotics
186
Outline the investigations that are needed for patients with suspected complicated UTIs
Bloods:
- FBC, U&Es, CRP
- Blooc cultures who are pyrexial or hypothermic
Urine sample (microscopy and culture)
Imaging:
- renal ultrasound
- CT kidneys, ureters, bladder
187
How are the following results with urine microscopy interpreted?
Epithelial cells
Bacteria with no WBCs
Bacteria with WBCs but no catheter
bacteria with WBCs with catheter
epithelial cells: contamination
bacteria with no WBCs: contamination
bacteria with WBCs but no catheter: infection
bacteria with WBCs with catheter: assess clinically
188
If a urine sample is continually negative in a patient but presenting with UTI complaint, what diagnoses would need investigated?
Gonorrhoea and chlamydia
189
List 3 causes of pyruia with no bacteria
Pyruia = pus in the urine
- recent/recent abx
- tumour
- calculi
- urethritis (check for chlamydia)
- TB
190
Outline the antibiotic options for uncomplicated UTIs
prescription of **oral:**
- trimethoprim
- amoxicillin
- nitrofuratoin
- co-amoxiclav, ciprofloxacin, cefalexin
191
Outline the antibiotic options for a complicated UTI
treated with **IV therapy**
- amoxicillin or vancomycin
- Gentamicin (require monitoring)
192
What are the recommendations for the following antibiotics in a UTI:
Amoxicillin
Co-amoxiclav
Ciprofloxacin
Trimethoprim
Nitrofuratoin
Gentamicin
Vancomycin
Amoxicillin: some gram -ves and strep
Co-amoxiclav: inc. gram -ve cover, some anaerobes and strep
Ciprofloxacin: gram negatives
Trimethoprim and Nitrofuratoin: both gram +ves and -ves
- used in uncomplicated UTIs
Gentamicin: Gram -ves and most staph
Vancomycin: Gram +ves only, includes MRSA
193
What antibiotics would be recommended for the following
Strep
Staph
Gram -ves
Gram +ves
uncomplicated UTIs
MRSA
Strep: amoxicillin, co-amoxiclav
Staph: Gentamicin, Vancomycin
Gram -ves: Ciprofloxacin, Gentamicin, trimethoprim, nitrofuratoin
Gram +ves: amoxicillin, vancomycin, trimethoprim, nitrofuratoin
uncomplicated UTIs: trimethoprim, nitrofuratoin
MRSA: vancomycin
194
# Define acute bacterial prostatitis
List 3 aetiologies
# Define: often spontaneous, localised infection and inflammation of the prostate gland, which may be secondary to urethral instrumentation
Aetiology:
- gram -ve bacilli eg. E. coli
- S. aureus (MRSA, MSSA)
- N. gonorrhoea
195
Outline the clinical presentation of acute bacterial prostatitis
- Fever
- Perineal and back pain
- UTIs, urinary retention
- Diffuse oedema
- Micro-abscesses
196
Outline the diagnosis and management for acute bacterial prostatitis
Diagnosis:
- urine cultures usually +ve
- blood cultures
- trans-rectal US: prostatic enlargement
- DT/MRI: prostatic enlargement
Management:
- Check previous microbiology results
- Abx: ciprofloxacin
197
List 3 complications with acute bacterial prostatitis
- Prostatic abscesses
- Spontaneous rupture of urethra/rectum
- Epididymitis
- Pyelonephritis
- Sepsis
198
List 3 aetiologies of chronic prostatitis
Outline the clinical presentation
- often secondary to chlamydia urethritis
- Gram -ve bacilli (E. coli)
- Enterococci
- S. aureus (MSSA, MRSA)
Presentation:
- asymptomatic, perineal discomfort or back pain with low-grade fever
199
List 3 risk factors for prostate cancer
age (\>65yrs)
genetics: Hereditary Prostate Cancer 1 gene (HPC1) or BRCA2
familial: 2x risk if 1st degree relative diagnosed \<60yrs
environment: UV light
sexual activity from a young age
hormones: *the normal function of the prostate gland is regulated by testosterone and DHT. Higher incidence of PC associated with elevated 5-alpha reductase (converts testosterone to DHT)*
200
Outline the pathology of prostate cancers
Majority of malignant cancers of the prostate are **primary adenocarcinomas** which usually arise in the peripheral zone of the gland
201
Outline the local and metastatic clinical presentations of prostate cancer
Local:
- asymptomatic
- painful or slow miturition, urinary retention, UTI
- haematuria
- lymphadenopathy
Metastatic:
- Bone pain
- Renal failure (ureteric obstruction)
- *Fatigue, weight loss etc.*
202
Outline the investigations to diagnose prostate cancer
PSA (Prostate Specific Antigen)
- not very specific (also elevated with an enlarged prostate (occurs with age), prostatitis, UTI)
- PSA is a serine protease secreted into seminal fluid and causes the release of sperm
DRE (Digital Rectal Examination)
- Palpation of the prostate: should have a smooth surface with two, equal and palpable hemispheres
MRI
True Biopsy
- biopsy taken trans-rectally under US guidance
203
Outline how prostate cancers are graded and stages
Grading: Gleason Score
- sum of two prominent Gleason Grades seen histologically within a sample
- \<4: histologically characteristics are well differentiated, unlikely to progress locally
- 5-7: moderately differentiated, 50% likelihood of local progression
- \>7: poorly differentiated with 75% likelihood of local progression
Staging: TNM (Tumour-Nodes-Metastases)
204
Outline the management for early/localised prostate cancer
Watchful waiting
Active surveillance: regular DRE, PSA, MRI and biopsy
Radiotherapy:
- external beam radiotherapy
- brachytherapy: radioactive seeds put inside the prostate
- Radiotherapy usually alongside hormone therapy: LHRH therapy (causes initial testosterone surge but anti-androgens given to stop this)
Radial prostatectomy:
- removal of all or part of the prostate
- can be done robotically
205
OUtline the management for advanced prostate cancer
Androgen ablation
Medical castration (orchiectomy): removal of the testes
Hormone therapy (LHRH / GnRH agonists)
Chemotherapy
TURP (transurethral resection of the prostate) for symptomatic relief
Radiotherapy
206
Outline two complications of metastatic prostatic cancer and the clinical presentation they would elicit
Spinal cord compression
- severe pain, retention and constipation
- urgent MRI and intervention
- radiotherapy and/or spinal decompression surgery
Ureteric Obstruction
- Anorexia, weight loss, raised creatinine
207
Outline the epidemiology of bladder cancer
More common in males
Incidence increases with age
208
Identify 3 risk factors of bladder cancer
- Age (increased age)
- Causacian
- Environmental carcinogens
- Chronic inflammation (causes: renal stones, infection, long-term catheterisation)
- pelvic radiotherapy
- smoking
209
What cancer types are most commonly seen in the bladder?
- transitional cell carcinoma (90%)
- squamous carcinoma
- adenocarcinoma
210
Outline the clinical presentation of cancer of the bladder
**painless frank haematuria**
- some may present with microscopic haematuria
211
Outline the investigations for a case of suspected bladder cancer
Diagnosis: need flexible cystoscopy (can visualise inside of the bladder with a camera)
- Also can do renal ultrasound
212
Outline the staging and grading for bladder cancer
Staging
- NMIBC: non-muscle invasive bladder cancer
- MIBC: muscle invasive bladder cancer
Grading
- dependent on the grade of inflammation
- Grade 1: well differentiated
- Grade 2: moderately differentiated
- Grade 3: poorly differentiated
213
How is bladder carcinoma in-situ staged?
Based on degree of invasion through the bladder wall
T1: confined by lamina propria
T4a: through bladder wall and invading prostate
214
Outline the management for bladder cancer following flexible cystoscopy
Surgical:
- trans-urethral resection of bladder tumour (TURBT)
Medical:
- Mitomycin C: chemotherapy, targets DNA synthesis
- Immunotherapy: induction and maintenance
- radial cystectomy: removal of the bladder +/- prostate/uterus, with urine being directed into an ileal conduit or neobladder
215
What is the main cancer type seen in renal cancer?
renal cell carcinoma
- conventional or clear cell tumour
216
Identify 3 risk factors for renal cell carcinoma
- smoking
- obesity
- HTN
- acquired renal cystic disease
- genetics
- haemodialysis
217
Outline the clinical features seen with renal carcinoma
80% - incidental finding (asymptomatic)
Non-specific features:
- weight loss, night sweats, fever, fatigue
Classic Kidney Cancer triad:
**- mass, pain, haematuria**
Small maj can present with:
- oedema of the left leg
- paraneoplastic syndrome
- varicocele (more common of the left due to the angle at which the left testicular vein enters the left renal vein)
218
# Define paraneoplastic syndromes
Outline it's common presentation
Def: set of signs or symptoms in the body caused by underlying cancer but not due to local presence of cancer cells
Common presentation:
- HTN: due to renin secretion
- Hypercalcaemia: due to PTH secretion or osteolytic hypercalaemia
- Polycythaemia: inc. EPO production
Abnormal LFTs
Rarer:
- CTH (Cushing's syndrome), prolactin (galactorrhoea), insulin (hypoglycaemia)
219
how is renal carcinoma diagnosed?
initial diagnosis: US
bloods:
- fbc, U&E, lft, crp, ldh
CT of Kidneys and MRI
220
Outline how renal carcinomas are staged
- staging based on the size of tumour and extent of invasion
T1a: \<4cm
T1b: 4-7cm
T2: \>7cm
T3a: extends to renal vein
T3b: extends into IVC below diaphragm
T4: extends to IVC above diaphragm
T4: extends beyond adrenal gland
221
Outline the management for renal carcinoma
Dependent on tumour stage and patient preference
**Radical Nephrectomy**
- removal of kidney + gerota's fascia (encapsulates kidneys and adrenal glands)
- indication: large renal mass
**Nephron Sparing Surgery**
- resection-type surgery in which only part of the kidney is removed
**Tyrosine Kinase Inhibitors**
- metastatic disease treatment
- inhibits angiogenesis
- indications: small renal mass, single kidney, patient has CKD, CV risk factors, stage is only T1
-
222
Identify 3 risk factors for testicular cancer
- age: 20-40yrs
- cryptorchidism
- HIV infection
- Caucasian
223
Outline the cell types commonly seen in testicular cancers
Germ cell tumours
- Teratomas, seminomas
Stromal tumours
- Leydig cell tumours, Sertoli cell tumours
Others:
- lymphoma, metastases
224
Outline the clinical presentation and investigations for testicular cancer
Presentation: painless lump
Diagnosis:
- Scrotal US
- tumour markers: AFP (alpha fetoprotein), beta-HCG, LDH
- CT staging
225
Outline the management for testicular cancer
Radical orchidectomy
Chemotherapy
it's important to check lymph nodes and if necessary:
- para-aortic nodal radiotherapy
- retroperitoneal lymph node dissection
226
What are the treatment options for a patient with kidney failure (eGFR 7-10ml)
- renal dialysis: haemodialysis peritoneal dialysis
- renal transplant
- conservative care
227
Identify three disadvantages of renal dialysis
- always exhausted
- fluid restriction
- diet restriction (K and phosphate restrictions)
- women are infertile
228
Identify three indications for renal transplant
- increased life expectancy
- improved quality of life
- less time in hospital
- Cost saving
229
identify 3 contra-indications for a renal transplant
reduced life expectancy:
- older age
- co-morbidities
- unlikely to survive 5 years post-transplant
surgical contra-indications:
- calcified blood vessels
- bladder removed
medical contraindications
- hypertension / hypotension
- disease that will recur in the transplanted kidney
230
What is the challenge of a renal transplant?
What treatment is given to avoid this?
The immune system recognises foreign cells and proteins
- it responds to destroy foreign tissue through complex amplification pathways
- evolved to deal with infection and malignancy
Therefore, the immun system will attack the new kidney which could lead to organ rejection
- Therefore immunosuppression is needed to prevent rejection
231
What causes rejection of an organ in organ transplant?
- Recognising cell proteins as non-self
- Blood group incompatibility
- HLA compatibility
- T cell mediated and antibody mediated rejection
232
What immunosuppression treatment is given following a renal transplant and outline what each drug does?
- Basiliximab: monoclonal antibody directed against IL-2 receptor
- Tacrolimus: calcineurin inhibitor
- Mycophenolate mofetil: depletes guanosine nucleotides in T and B lymphocytes and inhibits proliferation
+/- steroids
233
Outline the 3 major complications of organ transplantation
Rejection
- cell mediated rejection: interstitial inflammation and tubulitis. Often easily treated with steroids if caught early
- antibody-mediated rejection: endothelial swelling, glomerulitis and peritubular capillaries. Difficult to treat, usually inc. immunosuppression
Infection
- Chest infection, skin wound infection, UTI
Malignancy
- melanoma, non-Hodgkin's lymphoma, Hodgkin's lymphoma
- treatment: reduce immunosuppression +/- rituximab or chemotherapy
234
identify 3 diseases that would indicate need for renal dialysis over transplant
- renovascular disease
- T2 diabetic nephropathy
- vasculitis
- obstructive uropathy
235
Identify 3 conditions that would indicate need for renal transplant rather than dialysis
- adult polycystic kidney disease
- glomerulonephritis
- reflux nephropathy
- T1 diabetic nephropathy
236
What two sources are there for renal transplants?
Deceased donors
- Following brainstem death
- Need good kidney function
- Average wait time: 2-3 years
Living donors:
- friend, family altruistic donor
237
Identify three advantages of getting a renal transplant from a living donor rather than a deceased donor
To be a living donor, what matches must be made with the patient?
- pre-emptive transplantation
- better kidneys
- better outcomes and longer kidney survival
Donor:
- must be fit and healthy
- have excellent kidney function
- blood and HLA compatible
238
List the segments of the ureters at which renal stones are most likely to get trapped
Narrowed segments of ureter:
- Proximal: pelviureteric junction
- Mid: pelvic brim (segment over the sacral bone)
- Distal: uretero-vesical junction
239
List the layers of the ureter wall
- Urothelial mucosa
- Lamina propria
- Muscular layer
- Adventitial layer
240
Identify 3 intrinsic and 3 extrinsic risk factors for developing kidney stones
Intrinsic:
- Age: 20-50yrs
- Gender: men (males have a higher oxalate production and females have higher urinary citrate (stops stone formation)
- Caucasians
- Familial renal tubular acidosis
- Cystinuria
- Co-morbidity
Extrinsic:
- Low fluid intake
- Diet and lifestyle
- More likely in summer (higher urinary concentrations, lower pH, sunlight and Vit D - inc. calcium with inc. Vit D levels)
- Hot climates
- Sedentary (occupation, exercise etc.)
241
What is the clinical importance of the content of kidney stones?
- If patients are presenting as an emergency, it doesn't matter what type of stone it is, immediately want to treat the patient eg. sepsis, AKI, pain
- Content of stone is useful as it influences management
eg. urate stones can be managed with medication, ESWL is unlikely to be successful for calcium oxalate dihydrate which are much harder stones
242
Identify the main renal stone morphologies
Calcium Stones (80%):
- Calcium oxalate monohydrate
- Calcium oxalate dihydrate
Infection stones:
- Struvite (Mg-ammonium-phosphate)
Uric acid stones
Cystine (genetic)
Xanthine stones
243
Outline the mechanism for development of calcium-oxalate monohydrate and dihydrate renal stones
*Ca-oxalate stones are the most common renal stones*
Calcium-Oxalate Monohydrate:
- Due to excess of oxalate
- Oxalate commonly found in fruit, vegetables, nuts and chocolate
Calcium-Oxalate Dihydrate:
- Calcium driven
244
Outline the mechanism for development of Struvite stones
aka. magnesium-ammonium-phosphate stones
- infection driven
- staghorn calculi that grow quickly and become quite large
- Staghorn calculi: branched stones that fill part or all of the renal pelvis and branch into several or all calyces
245
Outline the mechanism for development of uric acid stones
- metabolic syndromes
- these form due to chronic dehydration
- the risk of development increases in those with gout, a genetic tendency or a high protein diet
246
Outline the mechanism of development of cystine stones
genetic - runs in families
- inherited disorders that cause the kidneys to excrete certain types of amino acids
247
Outline the mechanism of development of xanthine renal stones
- enzyme deficiency that causes build-up of xanthine deposits
248
Identify the three accepted mechanisms that lead to formation of renal stones
1. Abnormal urine
2. Urinary obstruction
3. Urinary infection
249
Identify the causes of abnormal urine can lead to the formation of renal stones
Normal urine is understanderated, but if the composition of urine changes making it abnormal, stone formation becomes more likely
Too much salt
Abnormalities of blood
- Elevated calcium eg. underlying hyperparathyroidism
- Metabolic syndrome causing elevated uric acid levels
Abnormal urine
- Hypercalciruia, Hyperoxaluria
Dehydration (insufficient intake or excess output)
250
Identify levels of factors and inhibitors that affect stone formation
Low levels can predispose to stone formation
- low urine volume
- pH, citrate, magnesium
- Lack of inhibitors: citric acid, magnesium, pyrophosphate, glycoproteins
Inc. in certain substances promote stone formation
- high uric acid, calcium, oxalate
251
Identify the causes of urinary obstruction that can lead to formation of renal stones
Congenital
- abnormalities preventing normal outflow of urine through the ureters into the bladder
- medullary sponge kidney
- uretourocele
- pelvico-urinary junction obstruction
Acquired
- ureteric strictures
- anastomotic strictures
252
Outline the causes of urinary infection that can lead to formation of renal stones
Organisms that produce urease are linked to urinary stone formation
Proteus mirabilis
- Gram -ve, anaerobic rod
- forms characteristic bullseye patterns
- splits urea into ammonium and raises the pH of urine
Struvite
- magnesium ammonium phosphate precipitates in alkaline urine to form stones which means infection with proteus can potentiate the formation of stones
253
Outline the clinical presentation of kidney stones
- can be asymptomatic and found incidentally on imaging
Typical presentation:
- colicky pain which radiates from loin to groin without settling
- the patient may be unable to sit still, constantly moving
- Haematuria (frank or microscopic)
- UTI or sepsis with no known cause (confirmed with imaging)
254
What initial investigations are needed for a patient with suspected kidney stones
History and Examination
Bloods: U&Es, CRP, FBC
Urine: urinalysis (blood and infection) and cultures
Biochemistry:
- First stone: U&Es, Ca, urate, stone analysis
- Recurrent stone: U&E, Ca, urate, venous bicard, two sets of 24hr urine analysis
Imaging:
- CT KUB (CT of kidneys, ureters and bladder): gold standard
- US
- X-Ray KUB: cannot detect uric acid stones
255
What are the advantages of CT KUB scan for a renal stone?
- suggests the fluoroscopic appearance of a stone, which determines whether it can be targeted with extra-corporeal shock wave lithrotripsy (ESWL)
- stone diameter
- skin to stone distance: if \>10cm, can consider EWSL
- lower radiation dose
256
Identidy the management options for kidney stones and what affects management
- Observation: small and asymptomatic stones
- Medical therapy: involves dissolution therapy
- Non-invasive
- Invasive
Affecting management plan: size of stones
- \<4mm: 75% chance of passing passively
- \<7cm: 25% chance of passing if proximal, 35% chance if mid, 64% chance if distal
257
Describe the medical treatment used for kidney stones
For acute pain: NSAIDs or opiates
- NSAIDs: reduce pain as they reduce GFR, reduce renal pressure and ureteric peristalsis
- Medical Expulsive Therapy: alpha-blocker, only used for large, distal stones
258
Identify the surgical options for renal stones
Dependent on size and location
**Ureteroscopy**
- ureteric or renal stones \<2cm
- Ureteroscopy and basket
- Ureteroscopy and fragmentation
- FURS: flexible ureteroscopy
**ESWL: extracorporeal shockwave lithrotripsy**
- proximal ureteric stones of \<10mm or \<20mm renal stones (location dependent)
**PCNL: percutaneous stent or nephrostomy**
- Stones \>2cm that are within the kidney
- Used for staghorn calculi
**Nephrostomy**
- laparoscopic or open surgery
- suitable for *huge* stones in non-functioning kidneys
- required reconstruction afterwards
259
Identify three situations in which admission to hospital with renal stones would be required
- Uncontrollable pain
- Fever or signs of sepsis
- Solitary kidney with a ureteric stone
- Bilateral ureteric stones
- Renal failure caused by an obstructing stone
260
Outline the emergency presentation of kidney stones
**Pain**
- worst pain ever (worse than labour)
- typical loin pain which radiates to the groin
\**Watch for AAA - similar presentation*
261
What are the differentials for the clinical presentation of pain ('worst pain ever'), typically in the loin that radiates to the groin
- Kidney stone
- Appendicitis
- Ovarian cysts / gynaecological pathology
262
