RENAL / UROLOGY - Clinical Flashcards
(271 cards)
1
Q
What is glomerulonephritis?
A
Inflammation of the glomeruli in the kidneys, which is a pathological process rather than a specific disease
2
Q
What are the features of nephritic syndrome?
A
A group of features that occur with nephritis:
- haematuria (can be microscopic or macroscopic)
- oliguria (production of abnormally small amount of urine)
- mild proteinuria (< 3g per 24hrs)
- fluid retention
3
Q
What is the underlying pathophysiology of nephrotic syndrome?
A
Nephrotic syndrome results from damage to the glomerular basement membrane and podocytes –> leading to increased permeability to proteins, causing proteinuria
- this results in hypoalbuminaemia and oedema due to reduced plasma oncotic pressure
4
Q
What are the three main features of nephrotic syndrome?
A
- Significant proteinuria (> 3g / 24hrs)
- Hypoalbuminaemia (< 30g/L)
- Peripheral oedema
5
Q
What is the most common cause of nephrotic syndrome in children?
A
Minimal change disease
- usually idiopathic and steroid-responsive
6
Q
2-5 year-old child with oedema, proteinuria, and low albumin.
What is the diagnosis?
A
Nephrotic syndrome (most likely minimal change syndrome)
7
Q
What are the top primary causes of nephrotic syndrome in adults?
A
- Membranous nephropathy
- Focal segmental glomerulosclerosis
8
Q
What secondary causes/systemic diseases can cause nephrotic syndrome?
A
- Henoch-Schönlein purpura (HSP)
- Diabetes mellitus
- SLE
- Amyloidosis
- Infection (e.g. HIV, hepatitis B and C)
- Membranoproliferative glomerulonephritis
- Drugs (NSAIDs, gold therapy)
9
Q
What is the most common cause of primary glomerulonephritis?
A
IgA nephropathy (Berger’s disease)
- typically presenting with haematuria in a patient in their 20s
10
Q
What is membranous nephropathy?
A
a cause of nephrotic syndrome due to immune complex deposits in the glomerular basement membrane (causing thickening and malfunctioning of the membrane and proteinuria as a result)
- often idiopathic, but can be secondary to malignancy, SLE, or NSAIDs
11
Q
What kidney condition presents 1–3 weeks after a streptococcal infection and often resolves fully?
+ give two examples of Strep. infections
A
Post-streptococcal glomerulonephritis
- Strep. infections –> eg. tonsillitis, impetigo
12
Q
What is rapidly progressive glomerulonephritis (or crescentic glomerulonephritis)?
A
a severe acute illness with glomerular crescentic histology, which generally responds well to treatment
13
Q
What is Goodpasture syndrome?
+ how does it usually present
A
- An autoimmune disease where anti-GBM (Anti-glomerular basement membrane) antibodies attack type IV collagen on the glomerulus and pulmonary basement membranes
- affects lungs (pulmonary haemorrhage) –> haemoptysis
AND - affects kidneys (glomerulonephritis) –> haematuria
.
Goodpasture (anti-GBM) syndrome typically presents with acute kidney failure (AKI) and haemoptysis
14
Q
What are the key antibody findings in glomerulonephritis-related conditions? (3)
A
- Anti-GBM antibodies - Goodpasture syndrome
- p-ANCA (or MPO antibodies) - microscopic polyangiitis
- c-ANCA (or PR3 antibodies) - granulomatosis with polyangiitis
15
Q
What systemic diseases can cause glomerulonephritis?
A
- Henoch-Schönlein purpura (HSP)
- Vasculitis (e.g. microscopic polyangiitis, granulomatosis with polyangiitis)
- Lupus nephritis (associated with SLE)
16
Q
What does histology show in IgA nephropathy (Berger’s disease)?
A
IgA deposits and mesangial proliferation
17
Q
What is the diagnostic test of choice in glomerulonephritis?
A
Renal biopsy - tissue is examined for glomerular inflammation, confirms diagnosis and assesses severity of damage
18
Q
What does histology show in membranous nephropathy?
A
IgG and complement deposits on the basement membrane
19
Q
What does histology show in rapidly progressive glomerulonephritis (or crescentic glomerulonephritis)?
A
glomerular crescents
20
Q
What initial investigations are performed when nephrotic syndrome is suspected?
A
- Urine dipstick: proteinuria and check for microscopic haematuria
- MSU to exclude urinary tract infection.
- Quantify proteinuria using an early morning urinary protein:creatinine ratio or albumin:creatinine ratio.
- FBC and coagulation screen
- Urea and electrolytes
21
Q
What is the management of glomerulonephritis?
A
- Supportive care - hypertension management, dialysis in severe disease
- Immunosuppression - eg. corticosteroids
22
Q
Name the causes of nephrotic syndrome, nephritic syndrome, and both
A
- Nephrotic syndrome is a problem with filtration - resulting in proteinuria
- Nephritic syndrome is inflammation of the glomeruli - leading to haematuria and reduced kidney function
23
Q
Why is there an increased risk of DVT, pulmonary embolism, and renal vein thrombosis in nephrotic syndrome?
A
due to loss of antithrombin III and plasminogen in the urine
- antithrombin III –> anticoagulant protein
- plasminogen – > breaks down fibrin blood clots
24
Q
Why is there an increased risk of infection in nephrotic syndrome?
A
due to loss of urinary immunoglobulins
25
How does nephrotic syndrome affect calcium levels?
can cause hypocalcaemia due to the loss of vitamin D and its binding protein in the urine
- vitamin D is essential for calcium absoprtion in the intestines
26
What defines acute kidney injury (AKI)?
Acute kidney injury (AKI) refers to a rapid drop in kidney function, diagnosed by measuring the serum creatinine
- AKI is most common in acutely unwell patients (eg. infections or following surgery)
27
What is the NICE criteria for diagnosing acute kidney injury (AKI)?
- Rise in creatinine of 26µmol/L or more in 48 hours
OR
- ≥ 50% rise in creatinine over 7 days
OR
- Fall in urine output to < 0.5ml/kg/hour for more than 6 hours in adults (8 hours in children)
OR
- ≥ 25% fall in eGFR in children / young adults in 7 days
28
What are some common risk factors for developing AKI?
- Older age (> 65 years)
- Emergency surgery (ie. increased risk of sepsis or hypovolemia)
- CKD (ie. if eGFR < 60)
- Diabetes
- Heart failure
- Liver disease
- Use of nephrotic drugs: NSAIDs, aminoglycosides (gentamicin), ACE inhibitors, diuretics)
29
How can AKI causes be classified?
AKI causes can be classified into three categories:
- Pre-renal - *due to insufficient blood supply (hypoperfusion) to kidneys, reduces the filtration of blood*
- Renal - *due to intrinsic disease in the kidney*
- Post-renal - *due to obstruction of urine outflow away from the kidney, causing back-pressure into the kidney and reduced kidney function (obstructive uropathy)*
30
Name some pre-renal causes of AKI
- Dehydration
- Shock - *septic shock, cardiogenic shock, hypovolaemic shock*
- Heart failure
- Renal artery stenosis/occlusion
31
Name some renal causes of AKI
- Acute tubular necrosis (most common)
- Glomerulonephritis
- Acute interstitial nephritis
- Haemolytic uraemic syndrome
- Rhabdomyolysis
32
Name some post-renal causes of AKI
- Kidney stones
- Tumours (e.g., retroperitoneal, bladder or prostate)
- Strictures of the ureters or urethra
- Benign prostatic hyperplasia (BPH)
- Neurogenic bladder -> *hydronephrosis damages kidneys*
33
What is the mechanism behind acute tubular necrosis (ATN)?
- caused by damage and death (necrosis) of the epithelial cells of the renal tubules
- this is due to ischaemia/hypoperfusion (eg. dehydration, shock, or heart failure) OR nephrotoxins (eg. gentamicin, radiocontrast agents, or cisplatin)
34
What finding on urinalysis confirms acute tubular necrosis?
Muddy brown casts
35
Is acute tubular necrosis permanent or reversible?
- The epithelial cells can regenerate, making acute tubular necrosis reversible
- Recovery usually takes 1-3 weeks
36
What is the hallmark of acute interstitial nephritis (AIN)?
characterised by acute inflammation of the kidney interstitium, it is caused by an immune reaction associated with:
- drugs (eg. NSAIDs or antibiotics)
- infections (eg. E.coli or HIV)
- autoimmune conditions (eg. sarcoidosis or SLE)
.
Other features that can accompany the AKI are: *rash, fever, flank pain, eosinophilia*
- eosinophilia is a sign of a hypersensitivity reaction, typically to medications, which triggers a cell-mediated immune response (T cells) that leads to inflammation and eosinophil infiltration into the kidney
37
How is AKI investigated?
1. Urinalysis:
- leucocytes and nitrites --> *infection*
- protein and blood --> *acute nephritis or infection*
- glucose --> *diabetes*
.
2. Ultrasound of urinary tract --> *assess for obstruction when a post-renal cause is suspected*
.
38
What measures can be taken to try and prevent acute kidney injury (AKI)?
- avoiding nephrotoxic medications
- ensuring adequate fluid intake (IV fluids if oral intake is inadequate)
- additional fluids before and after radiocontrast agents
39
What is the management approach for AKI?
Treat underlying cause of AKI and provide supportive management:
- IV fluids - *for dehydration and hypovolaemia*
- Withhold medications that may worsen the condition (eg. NSAIDs, ACE inhibitors)
- Withhold/adjust medications that may accumulate with reduced renal function (eg. metformin, opiates) - *many medications are excreted by the kidneys*
- Relieve the obstruction in a post-renal AKI - *eg. insert catheter for prostatic hyperplasia*
- Dialysis - *if severe*
40
Are ACE inhibitors nephrotoxic?
NO
- ACE inhibitors should be stopped in an AKI as they reduce the filtration pressure
- However, ACE-i have a protective effect on the kidneys long-term --> *offered to patients with hypertension, diabetes, and CKD to protect the kidneys from further damage*
41
What complications are associated with AKI?
- Fluid overload, heart failure and pulmonary oedema - *due to inability to effectively excrete excess water and salt, resulting in fluid accumulation in the body*
- Hyperkalaemia - *kidneys are filtering less fluid and therefore less K+ is being excreted in the urine*
- Metabolic acidosis - *reduced ability to excrete acids and regenerate bicarbonate*
- Uraemia (high urea) - *due to less filtering of waste products (urea) --> can lead to encephalopathy and pericarditis*
42
What is chronic kidney disease (CKD)?
a chronic reduction in kidney function sustained over three months - *it tends to be permanent and progressive*
43
Kidney function naturally declines with age, name some factors/conditions that can speed up the decline and cause CKD.
- Diabetes - *High blood sugar levels damage the tiny blood vessels and filtration units (glomeruli) in the kidneys, leading to diabetic nephropathy and impaired kidney function*
- Hypertension - *damages the blood vessels in the kidneys, reducing blood flow and impairing their ability to filter waste and fluid*
- Medications (e.g. NSAIDs or lithium) - *toxic to kidneys*
- Glomerulonephritis - *inflammation of glomeruli, leading to damage and impaired function*
- Polycystic kidney disease - *leads to impaired kidney function*
44
What are some signs and symptoms of CKD?
Most patients with CKD are asymptomatic, signs and symptoms as renal function worsens may be non-specific:
.
- Fatigue
- Pallor (due to anaemia)
- Foamy urine (proteinuria)
- Nausea
- Loss of appetite
- Pruritus (itching)
- Oedema
- Hypertension
- Peripheral neuropathy
45
How is CKD investigated?
- eGFR --> estimates GFR (rate at which fluid is filtered from the blood into Bowman's capsule) based on serum creatinine, age, and gender
- Urine albumin:creatinine ratio (ACR) --> quantifies proteinuria
- Haematuria --> urine dipstick or microscopy (macroscopic/microscopic)
- Renal ultrasound --> assesses for obstruction (eg. kidney stones or tumours) and polycystic kidney disease
.
Other tests to identify risk factors:
- Blood pressure (hypertension)
- HbA1c (diabetes)
- Lipid profile (hypercholesterolemia)
46
What criteria confirm a CKD diagnosis?
Consistent results over 3 months of either:
- eGFR < 60 mL/min/1.73 m²
- Urine ACR > 3 mg/mmol
47
CKD can be staged using the G score and the A score.
(G score --> *based on the eGFR*)
(A score --> *based on the albumin:creatinine ratio*)
Fill in the blanks for the stages of CKD.
48
What are complications of CKD?
- Anaemia - *due to decreased EPO production*
- Renal bone disease - *due to imbalances of calcium and phosphate*
- Cardiovascular disease - *due to uraemic toxins (atherosclerosis) and hypertension*
- Peripheral neuropathy - *kidneys fail to properly filter waste products from the blood, these toxins accumulate and directly damage the peripheral nerves*
- End-stage kidney disease
- Dialysis-related complications
48
What is considered accelerated progression in CKD?
a sustained decline in the eGFR within one year of either 25% or 15 mL/min/1.73 m2
49
What is the kidney failure risk equation?
can be used to estimate the 5-year risk of kidney failure requiring dialysis
50
When should a CKD patient be referred to a renal specialist?
- eGFR <30 mL/min/1.73 m2
- Urine ACR >70 mg/mmol
- Accelerated progression (a decrease in eGFR of 25% or 15 mL/min/1.73 m2 within 12 months)
- 5-year risk of requiring dialysis over 5%
- Uncontrolled hypertension despite four or more antihypertensives
51
How is CKD managed?
Treat underlying causes:
- optimise diabetic control
- optimise hypertension control
- reduce/avoid nephrotoxic drugs (where appropriate)
- treat glomerulonephritis (where it is the cause)
.
- Blood pressure target - *< 130/80 (if pt is under 80yrs old and has an ACR >70 mg/mmol)*
.
Medications to help slow disease progression:
- ACE inhibitors (or angiotensin II receptor blockers)
- SGLT-2 inhibitors (dapagliflozin)
52
How can CKD complications be reduced?
- Lifestyle: Exercise, healthy weight, no smoking
- Atorvastatin 20mg - *for cardiovascular prevention*
- Oral sodium bicarbonate - *to treat metabolic acidosis*
- Iron + erythropoietin -*for anaemia*
- Vitamin D + low phosphate diet + phosphate binders - *to treat renal bone disease*
53
What are the treatment options for end-stage renal disease?
- Special dietary advice - *limiting foods high in sodium, potassium, phosphorus, and fluid intake, while ensuring adequate protein from high-quality sources*
- Dialysis
- Renal transplant
54
When are ACE inhibitors used in CKD?
ACE-i offered to all pts with:
- Diabetes + urine ACR > 3 mg/mmol
- Hypertension + urine ACR > 30 mg/mmol
- All patients with urine ACR > 70 mg/mmol
55
Which electrolyte needs to be monitored in patients with CKD on ACE inhibitors?
Potassium - *both CKD and ACE-i can cause hyperkalemia --> cardiac arrhythmias*
56
When is dapagliflozin (SGLT-2 inhibitor) used in CKD?
Offered to pts with:
- diabetes + urine ACR >30 mg/mmol
.
Considered for pts with:
- diabetes + urine ACR 3-30 mg/mmol
- non-diabetics with an ACR of 22.6 mg/mmol or above
57
Why does CKD cause anaemia?
- Healthy kidneys produce erythropoietin (EPO) --> *a hormone that stimulates production of RBCs*
- CKD results in lower EPO and less RBCs --> *normocytic normochromic anaemia*
58
What is the treatment of anaemia in CKD?
- Erythropoiesis-stumlating agents (eg. recombinant human erythropoietin)
- Iron deficiency should be treated before using erythropoietin --> *IV iron is usually given*
.
(pts with CKD often have poor iron absorption from oral supplements due to impaired gut function, this is why IV iron is given)
.
(note: avoid blood transfusions due to risk of allosensitization, increasing the risk of future transplant rejection)
59
What is renal bone disease (CKD-MBD)?
Renal bone disease is aka. chronic kidney disease-mineral and bone disorder (CKD-MBD), it involves:
- high serum phosphate - *reduced excretion*
- low vitamin D activity - *kidney disease reduces activation*
- low serum calcium - *due to reduced vitamin D*
- secondary hyperparathyroidism - *high PTH stimulates osteoclasts*
60
Explain why there is low vitamin D and low calcium in CKD.
- Healthy kidneys metabolise vitamin D into its active form - *25-hydroxyvitamin D into 1,25-dihydroxyvitamin D (calcitriol)*
- Active vitamin D is essential in calcium absorption in the intestines and reabsorption in the kidneys, it is also responsible for regulating bone turnover and promoting bone reabsorption to increase the serum calcium lvl
- CKD leads to less vitamin D activity and low serum calcium as a result
61
Explain why there is secondary hyperparathyroidism in CKD.
- parathyroid glands react to low serum calcium and high serum phosphate by excreting more PTH --> *causing secondary hyperparathyroidism*
- PTH stimulates osteoclast activity, increasing calcium absorption from bone
62
What are the bone changes seen in CKD-MBD? (3)
- Osteomalacia - *due to increased bone turnover without adequate calcium supply*
- Osteosclerosis - *osteoblasts respond by increasing their activity to match the osteoclasts, creating new tissue in the bone (but due to the low calcium level, this new bone is not properly mineralised)*
- Rugger jersey spine (characteristic finding on a spinal x-ray) - *involves sclerosis of both ends of each vertebral body (denser white) and osteomalacia in the centre of the vertebral body (less white)*
.
(rugger jersey spine --> *the name refers to the stripes found on a rugby shirt*)
63
What is dialysis?
Dialysis is an artificial method of performing kidney filtration, removing excess fluid, solutes, and waste products
- it is used in pts with end-stage renal failure or complications of AKI
63
How is renal bone disease managed?
- Low phosphate diet
- Phosphate binders
- Active forms of vitamin D (alfacalcidol and calcitriol)
- Ensuring adequate calcium intake
.
- if osteoporosis present --> *bisphosphonates*
64
What are some indications for short-term dialysis?
- the “AEIOU” mnemonic can be used
- A – Acidosis (severe and not responding to treatment)
- E – Electrolyte abnormalities (especially treatment-resistant hyperkalaemia)
- I – Intoxication (overdose of certain medications)
- O – Oedema (severe, resistant pulmonary oedema)
- U – Uraemia symptoms - *such as seizures or reduced GCS*
65
What is the main indication for long-term dialysis?
End-stage renal failure (CKD stage 5)
66
What are the two types of long-term dialysis?
- Haemodialysis
- Peritoneal dialysis
67
How does haemodialysis work?
- Pts have their blood filtered by a haemodialysis machine
- Blood is removed out of the body, passed through the dialysis machine, filtered using semipermeable membranes, and then returned to the body
.
- Solutes filter out of blood, across membrane, and into a fluid called dialysate
- the conc. gradient between the blood and the dialysate fluid causes water and solutes to diffuse out of the blood and across the membrane
.
(a typical regime might be 4 hrs a day, 3 days a week)
68
What medication is necessary for a patient to take when having dialysis?
Anticoagulation - *with citrate or heparin*
- to prevent blood clotting in the machine/process
69
What are the main vascular access options for haemodialysis?
- Tunnelled cuffed catheter
- Arteriovenous (AV) fistula
70
Where is a tunnelled cuffed catheter inserted and what is it?
- into the subclavian or jugular vein with a tip in the superior vena cava or right atrium
- it has two lumens - *one for blood exiting the body (red) and one for blood entering the body (blue)*
- a Dacron cuff surrounds the catheter --> *promotes healing and adhesion of tissue, making the catheter more permanent and provides a barrier to infection*
.
(can stay long-term and be used for regular haemodialysis)
71
What are the main complications of a tunneled cuffed catheter?
- infection
- blood clots (thrombosis) within the catheter
72
What is an AV (arteriovenous) fistula?
- A surgically created connection between an artery and a vein to provide high-flow vascular access (bypasses the capillary system)
- provides a permanent, large, easy-access blood vessel with high-pressure arterial blood flow
- a maturation period of 4-16 weeks is needed after the surgical operation before it can be used
73
Where can AV fistulas be created?
- Radiocephalic fistula (wrist) --> *radial artery to cephalic vein*
- Brachiocephalic fistula (antecubital fossa) --> *brachial artery to cephalic vein*
- Brachiobasilic fistula (upper arm) --> *less common and a more complex operation*
74
What are the key examination findings of an AV fistula?
- Palpable thrill (a fine vibration felt over the anastomosis)
- “machinery murmur” on auscultation
.
- Skin integrity
- Aneurysms
75
What are complications of AV fistulas?
- Aneurysm
- Infection
- Thrombosis
- Stenosis
- STEAL syndrome
- High-output heart failure
76
What is STEAL syndrome?
A potential complication of AV fistulas
- occurs when there is ischaemia in the limb due to blood being diverted away from the limb it was supposed to supply - *AV fistula "steals" blood from the rest of the limb*
77
What is high-output heart failure?
A potential complication of AV fistulas
- caused by excessive blood return to the heart, increasing the preload (how full heart is before it pumps) --> *leads to hypertrophy of heart muscle and heart as a result heart failure*
78
Should you take blood from an AV fistula?
NEVER take blood from a fistula, this is a lifeline for the pt, providing dialysis access
- if it gets damaged, it will set the pt back massively
79
How does peritoneal dialysis work?
- uses the peritoneal membrane to filter the blood
- a special dialysis solution is added to the peritoneal cavity - *ultrafiltration occurs from the blood, across the peritoneal membrane, into the dialysis solution*
- the dialysis solution is replaced, taking away the waste products that have been filtered out of the blood
.
involves a Tenckhoff catheter - *a plastic tube inserted into the peritoneal cavity, with one end on the outside*
80
What are the two main types of peritoneal dialysis?
- Continuous ambulatory peritoneal dialysis (CAPD) --> *dialysis solution is always in the peritoneal cavity (various regimes for changing the solution - eg. 2 litres of solution replaced 4 times daily)*
- Automated peritoneal dialysis --> *a machine continuously replaces the dialysis fluid for 8-10 hrs overnight*
81
What are complications of peritoneal dialysis?
- Bacterial peritonitis (most serious) - *infections in the high-sugar environment are common and serious*
- Peritoneal sclerosis - *thickening/scarring of peritoneal membrane*
- Ultrafiltration failure - *the dextrose is absorbed, reducing the filtration gradient, making ultrafiltration less effective*
- Weight gain - *due to glucose absorption from the dialysate*
- Psychosocial burden
82
What is a renal transplant + how does it compare to dialysis?
- A renal transplant is the surgical transplantation of a kidney into a patient with end-stage renal failure
- it typically adds 10 years to life and significantly improves QOL compared to dialysis
83
How are donor kidneys matched to recipients + does a perfect match have to be achieved?
- Patient and donor kidneys are matched based on the human leukocyte antigen (HLA) type A, B and C on chromosome 6
- they do not have to match fully, but a closer match reduces rejection risk and improves outcomes
83
What can be done to prepare a recipient for a less well-matched donor kidney?
Desensitisation therapy can be used to reduce the recipient’s immune response to the donor HLA
- removes harmful antibodies from the blood to allow patients to receive a kidney from a donor - *eg. plasmapheresis, IVIg, rituximab*
84
In a renal transplant, what happens to the patient's original kidneys?
original kidneys are left in place
85
In a renal transplant, where is the donor kidney placed + how is the donor kidney connected?
- the donor kidney is placed anteriorly in the abdomen - *can usually be palpated in the iliac fossa area*
.
- donor kidney blood vessels are connected (anastomosed) with the pelvic vessels (usually external iliac vessels)
- the ureter of the donor kidney is anastomosed directly with the bladder
86
What is the typical incision shape in renal transplant surgery?
A "hockey stick" incision - *leading to a "hockey stick" scar*
87
After a renal transplant surgery, when does the new kidney start functioning?
Immediately
87
What medication is given following a renal transplant surgery to prevent acute rejection?
2 doses of Basiliximab - *monoclonal antibody targeting the IL-2 receptor on T-cells*
88
What type of medication is required for life-long use after transplantation?
Life-long immunosuppression - *to reduce risk of transplant rejection*
89
Following a renal transplant surgery, what are common immunosuppressant options?
- Tacrolimus
- Mycophenolate
- Ciclosporin
- Azathioprine
- Prednisolone
90
What skin changes can immunosuppressants cause?
- Seborrhoeic warts
- Skin cancer (especially SCC)
- Scars from skin cancer removal
91
92
What oral side effect is caused by ciclosporin?
Gum hypertrophy
92
What are complications directly related to a renal transplant?
- Transplant rejection (hyperacute, acute or chronic)
- Transplant failure
- Electrolyte imbalances
93
What endocrine effects are caused by steroids?
Cushingoid features (e.g. moon face, weight gain, skin thinning)
94
Following a renal transplant patients have to receive life-long immunosuppression, what are complications related to immunosuppressants?
- Ischaemic heart disease
- Type 2 diabetes (steroids)
- Increased risk of infections (including unusual pathogens)
- Non-Hodgkin lymphoma
- Skin cancer (particularly SCC)
95
Name the 3 unusual infections associated with immunosuppressants.
- Pneumocystis jiroveci pneumonia (PCP/PJP)
- Cytomegalovirus (CMV)
- Tuberculosis (TB)
96
What is renal tubular acidosis (RTA)?
A group of disorders causing metabolic acidosis due to pathology in the renal tubules, which balance H+ and HCO3– ions between the blood and urine to maintain a normal pH
97
How many types of renal tubular acidosis are there?
Four, but type 3 is rare and unlikely to be tested
- type 4 is the most common
98
99
What is the pathophysiology of Type 1 renal tubular acidosis (or distal RTA)?
Distal tubule cannot excrete H+ --> H+ retention in blood --> metabolic acidosis
.
Results in:
- High urinary pH (>6) --> *due to absence of H+ in urine*
- Metabolic acidosis --> *due to retained H+ ions in blood*
- Hypokalaemia --> *due to failure of hydrogen and potassium exchange (H+/K+ ATPase)*
100
What are the causes of Type 1 renal tubular acidosis (RTA)?
- Genetic - *there are both autosomal dominant/recessive forms*
- Autoimmune diseases - *SLE, Sjögren’s, PBC*
- Hyperthyroidism - *due to increased metabolic rate --> can lead to increased bone resorption, resulting in hypercalciuria which can damage the kidney tubules*
- Sickle cell disease - *due to sickled RBCs causing obstruction*
- Marfan’s syndrome
101
What are the clinical features of Type 1 renal tubular acidosis (RTA)?
- Failure to thrive in children
- Recurrent UTIs (due to alkaline urine)
- Bone disease (rickets/osteomalacia)
- Muscle weakness
- Arrhythmias (due to hypokalaemia)
102
What is the treatment for Type 1 renal tubular acidosis (RTA)?
Oral bicarbonate - *to correct acidosis and electrolyte imbalances*
103
What is the pathophysiology of Type 2 renal tubular acidosis (or proximal RTA)?
Proximal tubule cannot reabsorb HCO3- from the urine to the blood --> excessive HCO3- is excreted in the urine
.
Results in:
- High urinary pH (>6) - *due to excess bicarbonate lost in urine*
- Metabolic acidosis - *due to inadequate bicarbonate in blood*
- Hypokalaemia - *due to urinary loss of K+ along with HCO3-*
104
What are the key causes of Type 2 renal tubular acidosis (RTA)?
- Genetic (autosomal dominant/recessive)
- Multiple myeloma
- Fanconi’s syndrome
104
What is the treatment for Type 2 renal tubular acidosis (RTA)?
Oral bicarbonate replacement
105
What is the pathophysiology of Type 4 renal tubular acidosis (or hyperkalaemic RTA)?
Reduced aldosterone or aldosterone resistance --> decreased Na+ reabsorption and decreased K+ and H+ excretion
(aldosterone stimulates Na+ reabsoprtion and K+ and H+ ion excretion in the distal tubules)
.
Results in:
- Metabolic acidosis - *due to retained H+ ions in blood*
- Hyperkalaemia - *due to retained K+ in blood*
- Low urinary pH - *due to reduced ammonia production in response to hyperkalaemia*
.
(Normally, ammonia is produced in the distal tubules to balance the excretion of H+ ions, ammonia is a base and buffers the H+ ions, preventing the urine from becoming too acidotic --> *hyperkalaemia suppresses ammonia production, therefore the urine becomes acidotic*)
106
What are the causes of Type 4 renal tubular acidosis (RTA)?
- Adrenal insufficiency
- Diabetic nephropathy
- Medications (e.g. ACE inhibitors, spironolactone or eplerenone)
106
What is the management for Type 4 renal tubular acidosis (RTA)?
- Treat underlying cause
- Fludrocortisone (mineralcorticoid) - *for aldosterone deficiency*
- Oral bicarbonate and treatment of hyperkalemia may also be required
107
What is haemolytic uraemic syndrome (HUS) + what commonly triggers it?
- A condition involving thrombosis in small blood vessels - *usually triggered by Shiga toxins from E. coli O157 or Shigella*
- most often affects children following an episode of gastroenteritis (E.coli 0157 and Shigella cause gastroenteritis)
108
How do antibiotics and anti-motility agents (eg. loperamide), used to treat gastroenteritis caused by either E. coli or Shigella, affect HUS risk?
They increase the risk of HUS - *slow down gut motility, allowing more toxins to be absorbed into the bloodstream*
109
What is the classic triad of HUS?
- Microangiopathic haemolytic anaemia
- Acute kidney injury (AKI)
- Thrombocytopenia (low platelets)
110
Why does thrombocytopenia occur in HUS?
Platelets are consumed in the formation of thrombi in small blood vessels
111
How does HUS cause acute kidney injury (AKI)?
Thrombi and damaged RBCs disrupt blood flow in the kidneys
112
What is the first symptom of HUS?
Diarrhoea, which becomes bloody within 3 days
112
What is microangiopathic haemolytic anaemia (MAHA)?
Destruction of RBCs (haemolysis) due to pathology in the small vessels (microangiopathy) - *thrombi partially obstruct the small blood vessels and churn the RBCs as they pass through*
113
When do HUS symptoms typically develop after diarrhoea onset + what are the features of HUS?
Features of HUS develop around a week after the onset of diarrhoea:
- Fever
- Abdominal pain
- Lethargy
- Pallor
- Oliguria (reduced urine output)
- Haematuria
- Hypertension
- Bruising
- Jaundice (due to haemolysis)
- Confusion
114
What test is used to confirm the causative organism in HUS?
Stool culture
115
Why is HUS a medical emergency?
It can cause severe anaemia, kidney failure, and multi-organ complications
116
What is the mainstay of HUS management?
Supportive care, including:
- IV fluids - *for hypovolaemia*
- Blood transfusions - *for severe anaemia*
- Management of hypertension
- Haemodialysis - *for severe renal failure*
117
What is the prognosis of HUS?
It is self-limiting, and most patients recover fully with good supportive care
118
What is rhabdomyolysis?
A condition where skeletal muscle breaks down, muscle cells (myocytes) undergo cell death (apoptosis), releasing the following into the blood:
- myoglobin
- potassium
- phosphate
- creatine kinase
119
Which breakdown product in rhabdomyolysis is the most immediately dangerous?
Potassium - *hyperkalaemia can cause cardiac arrhythmias and cardiac arrest*
120
Why does rhabdomyolysis cause acute kidney injury (AKI)?
Myoglobin (in particular) is toxic to the kidneys in high concentrations, and impaired renal function leads to further accumulation of breakdown products in the blood
121
Other than hyperkalaemia complications and AKI, what are two other serious complications of rhabdomyolysis?
- Compartment syndrome - *when muscle swelling from rhabdomyolysis occurs within a closed fascial compartment, it can increase pressure, compromising blood flow to the affected area and causing tissue damage*
- DIC - *the released muscle breakdown products can trigger a cascade of clotting events, leading to widespread blood clots that can consume clotting factors, resulting in bleeding complications associated with DIC*
122
Name some causes of rhabdomyolysis
Anything that causes significant damage to muscle cells:
- Prolonged immobility - *particularly frail patients who fall and spend time on the floor before being found*
- Extremely rigorous exercise - *beyond the person’s fitness level (e.g., endurance events or CrossFit)*
- Crush injuries
- Seizures
- Statins
123
What are some signs/symptoms of rhabdomyolysis?
- Muscle pain
- Muscle weakness
- Muscle swelling
- Reduced urine output (oliguria)
- Red-brown urine (myoglobinuria)
- Fatigue
- Nausea and vomiting
- Confusion (particularly in frail patients)
124
What is the key blood test for diagnosing rhabdomyolysis?
Creatine kinase (CK)
- it is normally <150 U/L, in rhabdomyolysis it can be 1000-100,000 U/L
(typically rises in the first 12 hrs, then remains elevated for 1-3 days, then gradually falls)
125
How are creatinine kinase (CK) levels associated with kidney function in rhabdomyolysis?
the higher the CK, the greater the risk of kidney injury
126
What is myoglobinuria, and how is it detected?
- Myoglobin in urine - *causing red-brown discoloration*
- a urine dipstick will be positive for blood
127
Why are urea and electrolytes (U&E) important in rhabdomyolysis?
To assess for acute kidney injury and hyperkalaemia
127
Why is an ECG used in rhabdomyolysis?
To monitor for cardiac arrhythmias due to hyperkalaemia
128
What is the main treatment for rhabdomyolysis?
- IV fluids to correct hypovolaemia and encourage filtration of the breakdown products
- Treat hyperkalemia - *to prevent cardiac arrhythmias and cardiac arrest*
129
What is the main complication of hyperkalaemia?
Cardiac arrhythmias - *such as ventricular fibrillation, which can lead to cardiac arrest*
130
131
What conditions can cause hyperkalaemia?
- Acute kidney injury (AKI)
- CKD (stage 4 or 5)
- Rhabdomyolysis
- Adrenal insufficiency
- Tumour lysis syndrome
132
What medications can cause hyperkalaemia?
- Aldosterone antagonists (e.g., spironolactone and eplerenone)
- ACE inhibitors (e.g., ramipril)
- Angiotensin II receptor blockers (e.g., candesartan)
- NSAIDs (e.g., naproxen)
133
What is pseudohyperkalaemia?
- A falsely elevated potassium level due to haemolysis (rupture of blood cells) during blood sampling
- *lab might notice some haemolysis and request a repeat sample*
134
What are the key ECG changes in hyperkalaemia?
- Tall peaked T-waves
- Flattening or absence of P waves
- Prolonged PR interval
- Broad QRS complexes
134
When does hyperkalaemia require urgent treatment?
If serum potassium is >6.5 mmol/L or if there are ECG changes
135
What is the first-line emergency treatment for hyperkalemia??
+
What additional treatments can help lower serum potassium?
1. IV calcium gluconate - *stabilises the cardiac muscle cells and reduces the risk of arrhythmias*
2. Insulin and dextrose infusion - *insulin drives potassium into cells and dextrose prevents hypoglycaemia while on insulin*
3. Nebulised salbutamol - *temporarily drives potassium into cells*
.
additional options for lowering potassium:
- Oral calcium resonium - *reduces potassium absorption in the GI tract (slow and causes constipation)*
- Sodium bicarbonate (in acidotic patients on renal advice) - *drives potassium into cells as it corrects the acidosis*
- Haemodialysis - *may be required in severe or persistent cases*
135
How is mild hyperkalaemia (below 6.5 mmol/L without ECG changes) managed?
By treating the underlying cause, for example:
- treating AKI and stopping causative medications (e.g. spironolactone, ACE inhibitors)
136
What is polycystic kidney disease?
A genetic condition where healthy kidney tissue is replaced with multiple fluid-filled cysts, leading to renal failure
- the enlarged kidneys may be palpable on examination of the abdomen
137
What are the two types of polycystic kidney disease?
- Autosomal dominant polycystic kidney disease (ADPKD) - *more common*
- Autosomal recessive polycystic kidney disease (ARPKD) - *rarer and more severe*
138
What genes are affected in Autosomal dominant polycystic kidney disease (ADPKD)?
- PKD1 gene on chromosome 16 (85% of cases)
- PKD2 gene on chromosome 4 (15% of cases)
.
(PKHD = *polycystic kidney and hepatic disease*)
139
What are the extra-renal manifestations of Autosomal dominant polycystic kidney disease (ADPKD)?
- Cerebral aneurysms
- Hepatic, splenic, pancreatic, ovarian and prostatic cysts
- Mitral regurgitation
- Colonic diverticula
140
What are the complications of Autosomal dominant polycystic kidney disease (ADPKD)?
- Chronic loin/flank pain
- Hypertension
- Gross haematuria - *can occur with cyst rupture (usually resolves within a few days)*
- Recurrent urinary tract infections
- Renal stones
- End-stage renal failure - *occurs at a mean age of 50 years*
141
What gene mutation causes Autosomal recessive polycystic kidney disease (ARPKD)?
PKHD1 gene on chromosome 6
.
(PKHD = *polycystic kidney and hepatic disease*)
142
How is Autosomal recessive polycystic kidney disease (ARPKD) often detected prenatally?
Antenatal scans show oligohydramnios (low amniotic fluid volume due to reduced fetal urine output)
143
What does oligohydramnios lead to in Autosomal recessive polycystic kidney disease (ARPKD)?
Pulmonary hypoplasia (underdevelopment of the fetal lungs) --> respiratory failure shortly after birth
144
What early complications are seen in Autosomal recessive polycystic kidney disease (ARPKD)?
- Respiratory failure at birth (due to pulmonary hypoplasia)
- Haemodialysis required within first few days of life
- Dysmorphic features - *underdeveloped ear cartilage, low-set ears, flat nasal bridge)
- End-stage renal failure usually occurs before reaching adulthood
145
What investigations are used to diagnose polycystic kidney disease (PKD)?
Ultrasound and genetic testing
146
What medication can slow cyst development and renal failure in Autosomal dominant polycystic kidney disease (ADPKD)?
Tolvaptan (vasopressin receptor antagonist)
147
What are key management steps for PKD?
- Antihypertensives (e.g., ACE inhibitors) - *for hypertension *
- Analgesia - *for acute pain*
- Antibiotics - *for infections (e.g., UTIs or cyst infections)*
- Drainage of symptomatic cysts - *aspiration or surgery*
- Dialysis - *for end-stage renal failure*
- Renal transplant - *for end-stage renal failure*
148
What lifestyle advice should be given to PKD patients?
- Genetic counselling
- Avoiding contact sports due to the risk of cyst rupture
- Avoiding NSAIDs and anticoagulants
149
How are cerebral aneurysms screened in Autosomal dominant polycystic kidney disease (ADPKD)?
MR angiography (MRA)
150
What is obstructive uropathy?
a blockage preventing urine flow through the ureters, bladder and urethra
151
What are the key structures of the urinary tract?
- Kidneys
- Ureters
- Bladder (with the detrusor muscle)
- Urethra
- Internal urethral sphincter (smooth muscle under autonomic control)
- Prostate (in males)
- External urethral sphincter (skeletal muscle under voluntary control)
152
What are the basic anatomical structures of the kidney?
- Cortex
- Medulla
- Pyramids and columns
- Major and minor calyx (pleural: calyces)
- Renal pelvis
- Pelviureteric junction (PUJ)
- Ureter
153
What happens proximal to the obstruction in obstructive uropathy?
There is back-pressure in the urinary system --> *urine backs up, causing swelling of the affected structures (e.g. hydronephrosis if the kidney is involved)*
.
(eg. obstruction at the opening of the ureters in the bladder, from a bladder tumour, will result in swelling of the ureter and kidney on that side)
154
What is vesicoureteral reflux (VUR)?
urine refluxing from the bladder back into the ureters
155
What type of acute kidney injury (AKI) does obstructive uropathy cause?
Post-renal AKI (due to urinary outflow obstruction)
155
How does post-renal AKI differ from pre-renal and renal AKI?
- Pre-renal AKI - *caused by hypoperfusion of kidneys (e.g., dehydration, sepsis, acute blood loss)*
- Renal AKI - *refers to intrinsic kidney damage (e.g., glomerulonephritis, nephrotoxic medications)*
- Post-renal AKI - *urinary outflow obstruction (e.g. kidney stones, prostate enlargement)*
156
How does upper urinary tract obstruction (e.g., ureteric blockage) present?
- Loin to groin or flank pain on the affected side - *due to stretching and irritation of ureter and kidney*
- Reduced or no urine output
- Non-specific systemic symptoms, such as vomiting
- Impaired renal function on blood tests (i.e. raised creatinine)
157
How does lower urinary tract obstruction (e.g., bladder/urethral blockage) present?
- Difficulty or inability to pass urine - *e.g. poor flow, difficulty initiating urination, or terminal dribbling*
- Urinary retention, with an increasingly full bladder
- Impaired renal function on blood tests (i.e. raised creatinine)
158
What imaging is useful in diagnosing obstructive uropathy?
Ultrasound of kidneys, ureters, and bladder
159
Anatomically, where are the lower part of the kidneys?
At the renal angle (or costovertebral angle) - *angle formed by the twelfth rib and vertebral column at the back*
160
What are common causes of upper urinary tract obstruction?
- Kidney stones
- Tumours pressing on the ureters
- Ureter strictures - *due to scar tissue narrowing the tube*
- Retroperitoneal fibrosis - *the development of scar tissue in the retroperitoneal space*
- Bladder cancer - *blocking the ureteral openings to the bladder*
- Ureterocele - *ballooning of the most distal portion of the ureter (usually congenital)*
161
What are common causes of lower urinary tract obstruction?
- Benign prostatic hyperplasia (benign enlarged prostate)
- Prostate cancer
- Bladder cancer (blocking the neck of the bladder)
- Urethral strictures (due to scar tissue)
- Neurogenic bladder
162
What is neurogenic bladder?
Dysfunction of the bladder and urethral sphincters due to nerve damage
- can result in overactivity or interactivity in the detrusor muscle of the bladder and the sphincter muscles of the urethra
163
What are key causes of neurogenic bladder?
- Multiple sclerosis
- Diabetes
- Stroke
- Parkinson’s disease
- Brain or spinal cord injury
- Spina bifida
164
What complications can result from neurogenic bladder?
- Urge incontinence
- Increased bladder pressure
- Obstructive uropathy
165
What is the main principle of obstructive uropathy management?
Remove or bypass the obstruction
166
How is upper urinary tract obstruction (eg. ureteral stone) bypassed?
Nephrostomy - *involves inserting a thin tube through the skin at the back, through the kidney and into the ureter --> this tube allows urine to drain out of the body, into a bag*
167
How is lower urinary tract obstruction (e.g., a urethral stricture or prostatic hyperplasia) bypassed?
- Urethral catheter - *tube inserted via the urethra into the bladder*
- Suprapubic catheter - *tube inserted through the lower abdomen, directly into the bladder*
168
What are complications of obstructive uropathy?
- Pain
- Acute kidney injury (post-renal AKI)
- Chronic kidney disease
- Infection - *due to bacteria tracking up urinary tract into areas of stagnated urine*
- Hydronephrosis
- Urinary retention and bladder distention
- Overflow incontinence of urine
169
What is hydronephrosis?
Swelling of the renal pelvis and calyces - *occurs due to obstruction of urinary tract, leading to back-pressure into the kidneys*
170
What is idiopathic hydronephrosis + what is the treatment?
Narrowing at the pelviureteric junction (PUJ) - *site where renal pelvis becomes the ureter*
- may be congenital or acquired
.
- Treatment --> pyeloplasty (operation to correct the narrowing and restructure the renal pelvis)
171
What are common features of hydronephrosis?
- Vague renal angle pain
- Palpable kidney mass (may be seen on ultrasound, CT, or IV urogram - *x-ray with IV contrast collecting in the urinary tract*)
172
What are treatment options for hydronephrosis?
1. Treat the underlying cause
2. Pressure can be relieved with either:
- Percutaneous nephrostomy - *drains urine via a tube through the skin and kidney into the ureter*
- Antegrade ureteric stent - *stent inserted via the kidney into the ureter*
173
What is the purpose of a urinary catheter?
A urinary catheter is inserted into the bladder to passively drain urine into a catheter bag
174
How is a long-term urinary catheter kept in place?
a balloon on the end of the catheter bladder is inflated inside the bladder with sterile water (usually 10mls), preventing it from falling out
175
What are the main indications for urinary catheterisation?
- Urinary retention - *due to a lower urinary tract obstruction (e.g., enlarged prostate)*
- Neurogenic bladder - *e.g. intermittent self-catheterisation in multiple sclerosis*
- Surgery - *during and after*
- Output monitoring in acutely unwell patients - *e.g. sepsis or intensive care*
- Bladder irrigation - *e.g. to wash out blood clots in the bladder*
- Delivery of medications - *e.g. chemotherapy to treat bladder cancer*
176
A bladder scanner can be used to measure the volume of urine in the bladder. What post-void residual volume (measured after pt attempts to empty their bladder) on a bladder scan indicates the need for catheterisation?
More than 500mls of urine post-void suggests urinary retention requiring catheterisation
177
A common presentation requiring catheterisation is an older man presenting acutely with urinary retention due to an enlarged prostate. What is the typical management for this?
- Insert a catheter
- Start tamsulosin (alpha-blocker)
.
(tamsulosin relaxes the muscles around the bladder and prostate gland)
178
What is the key side effect of tamsulosin?
Postural hypotension - *leading to dizziness on standing or falls*
179
Types of catheters describe each:
- Intermittent catheters
- Foley catheter (two-way catheter)
- Coudé tip catheter
- Three-way catheter
- Suprapubic catheters
- Intermittent catheters - *a simple catheter used to drain urine and then immediately removed*
- Foley catheter (two-way catheter) - *the 'standard' two-way catheter with an inflatable balloon to hold it in place*
- Coudé tip catheter - *a catheter with a curved tip designed to navigate past obstructions, such as an enlarged prostate*
- Three-way catheter - *has three tubes for balloon inflation, irrigation, and urine drainage (commonly used for bladder irrigation)*
- Suprapubic catheters - *A catheter inserted through the abdominal wall into the bladder (just above pubic symphysis), held in place by a balloon, and typically used for long-term catheterisation*
180
How does a catheter increase the risk of urinary tract infection (UTI)?
Bacteria can colonise the catheter, with infection risk increasing the longer it remains in place
180
The most common catheter type seen on wards is the Foley catheter (two-way catheter). It might not be possible to insert a Foley catheter into a man with acute urinary incontinence due to an enlarged prostate, if the Foley catheter fails, what catheter would be worth trying next?
Coudé tip catheter - *slightly curved tip can make bypassing an obstruction much easier*
181
What is a trial without a catheter (TWOC) and how is TWOC assessed?
- TWOC - *a process where a urethral catheter is removed to assess if the patient can urinate independently*
.
- After the catheter is removed, the urine output is monitored, and a bladder scanner is used to check residual volume in the bladder (urinary retention)*
.
(if a pt fails TWOC twice, then another catheter is reinserted)
182
How should a urine sample be obtained from a catheter?
(eg. to check for a catheter-associated urinary tract infection)
A sample of urine should be taken directly from the catheter or sample port using an aseptic technique (not from the catheter bag as this may be contaminated)
183
When should antibiotics be given for bacteriuria (bacteria in urine) in catheterised patients + what is the duration of antibiotics?
Only if the patient has symptoms of a UTI - *7 days of antibiotics, with IV therapy considered for severe cases*
184
Other than giving antibiotics, what additional step should be taken when treating a symptomatic catheter-associated UTI?
The catheter should be changed as soon as possible (but not delaying antibiotics)
185
What is a lower urinary tract infection (UTI)?
A bacterial infection of the bladder, causing cystitis (inflammation of the bladder)
186
What condition can occur if infection from a lower UTI spreads up to the kidneys?
Pyelonephritis
187
Why are UTIs more common in women?
Women have a shorter urethra, allowing bacteria easier access to the bladder
188
What is the primary bacterial source for UTIs + what factors can contribute to UTI development?
Faecal bacteria - *primarily E. coli (normal intestinal bacteria), which can travel from the anus to the urethral opening*
.
Factors that can contribute to UTI development:
- sexual activity - *spreading of bacteria around perineum*
- poor hygiene or incontinence
- urinary catheters - *catheter-assocaited UTIs tend to be more severe*
189
What are the symptoms of a lower urinary tract infection?
- Dysuria (pain/burning when passing urine)
- Suprapubic pain or discomfort
- Increased frequency and urgency
- Incontinence
- Haematuria
- Cloudy or foul-smelling urine
- Older patients --> *may present with confusion only*
190
What does the presence of nitrites on a urine dipstick indicate + why?
UTI - *suggests bacteria in urine*
- gram-negative bacteria (eg. E. coli) break down nitrates (normal waste product in urine), into nitrites
190
It is important to distinguish between patients with a lower urinary tract infection and those with pyelonephritis. What features suggest pyelonephritis rather than a lower UTI?
- Fever
- Loin/back pain
- Nausea/vomiting
- Renal angle tenderness O/E
191
What does leukocyte esterase indicate on a urine dipstick?
Indicates presence of WBCs (leukocytes) --> *suggesting infection (UTI) or inflammation*
.
(note: it is normal to have a small number of leukocytes in the urine, but a significant increase indicates infection/inflammation)
192
When should a UTI be treated based on dipstick results?
- Nitrites present --> *treat as a UTI*
- Nitrites + leukocytes/haematuria --> *likely UTI, treat*
- Only leukocytes --> *do not treat unless clinically indicated*
.
(note: nitrites are a better indication of infection than leukocytes)
192
How does haematuria present on a urine dipstick?
- Microscopic haematuria - *blood detected on dipstick but not visible*
- Macroscopic haematuria - *blood visibly present in urine*
.
(haematuria is a common sign of infection, but can also indicate bladder cancer or nephritis)
193
Not all patients with an uncomplicated UTI require an MSU. When is a midstream urine (MSU) sample required for microscopy, culture, and sensitivity (MC&S)?
- Pregnant patients
- Patients with recurrent UTIs
- Atypical symptoms
- No symptom improvement with antibiotics
194
What is the most common cause of UTIs?
Escherichia coli (E. coli) - *a gram-negative, anaerobic rod (part of the normal lower intestinal microbiome)*
.
(it is found in faeces and can easily spread to the bladder)
195
Other than E. coli, name other bacterial causes of UTIs.
- Klebsiella pneumoniae (gram-negative anaerobic rod)
- Enterococcus
- Pseudomonas aeruginosa
- Staphylococcus saprophyticus
- Candida albicans (fungal)
196
What are the first-line antibiotics for a lower UTI in the community?
- Trimethoprim (often associated with high rates of bacterial resistance)
- Nitrofurantoin (avoided if eGFR <45)
.
alternatives:
- pivmecillinam
- amoxicillin
- cefalexin
197
Duration of antibiotic treatment for lower UTIs:
- 3 days -->
- 5-10 days -->
- 7 days -->
- 3 days --> *for simple lower urinary tract infections in women*
- 5-10 days --> *for immunosuppressed women, abnormal anatomy or impaired kidney function*
- 7 days --> *for men, pregnant women or catheter-related UTIs*
198
Why are UTIs concerning in pregnancy?
They increase the risk of pyelonephritis, premature rupture of membranes, and pre-term labour
199
What is the management of a UTI in pregnancy?
- 7 days of antibiotics
- MSU sample for microscopy, culture, and sensitivity
.
Antibiotic options:
- Nitrofurantoin (avoid in the third trimester)
- Amoxicillin (only after sensitivities are known)
- Cefalexin
200
Why should nitrofurantoin be avoided in the third trimester of pregnancy?
risk of neonatal haemolysis (destruction of the neonatal red blood cells)
201
Why should trimethoprim be avoided in early pregnancy (first trimester)?
It is a folate antagonist, increasing the risk of neural tube defects (eg. spina bifida)
- folate is essential in early pregnancy for normal development of the fetus
202
What is pyelonephritis?
Inflammation of the kidney due to bacterial infection, affecting the renal pelvis (join between kidney and ureter) and parenchyma (tissue)
203
What are the risk factors for pyelonephritis?
- Female sex
- Structural urological abnormalities
- Vesico-ureteric reflux - *urine refluxing from the bladder to the ureters (usually in children)*
- Diabetes
204
What is the most common cause of pyelonephritis?
Escherichia coli (E. coli) – a gram-negative, anaerobic rod found in faeces - *most common cause of lower UTI, which then spreads to cause an upper UTI*
205
How does pyelonephritis typically present?
Similar presentation to lower UTIs (dysuria, suprapubic discomfort, increased frequency) plus the triad of:
- Fever
- Loin/back pain (unilateral or bilateral)
- Nausea/vomiting
.
patients may also have:
- Systemic illness
- Loss of appetite
- Haematuria
- Renal angle tenderness O/E
206
What findings are expected on a urine dipstick in pyelonephritis?
Signs of infection - *nitrites, leukocytes and blood*
207
Why is a midstream urine (MSU) sample important in the investigation of pyelonephritis?
MSU (for microscopy, culture and sensitivity testing) is essential to establish the causative organism
(note: sample should ideally be collected before starting antibiotics)
208
What blood test abnormalities are seen in pyelonephritis?
- raised white blood cells
- raised inflammatory markers - *i.e. CRP*
209
When/why is imaging considered for pyelonephritis?
to rule out kidney stones or renal abscesses (using ultrasound or CT scan)
210
When should a patient with pyelonephritis be referred to the hospital?
- Features of sepsis
- Not safe to manage in the community
211
What are the first-line antibiotics when treating pyelonephritis in the community?
7-10 days of:
- Cefalexin
- Co-amoxiclav (if culture results are available)
- Trimethoprim (if culture results are available)
- Ciprofloxacin (consider risk of tendon damage & lower seizure threshold)
212
Patients with pyelonephritis who are admitted to hospital require the sepsis 6, what is the sepsis 6?
Take 3 - *3 tests*:
- Blood lactate level
- Blood cultures
- Urine output monitoring - *catheterise*
.
Give 3 - *3 treatments*:
- Oxygen (94-98%, or 88-92% in COPD)
- IV broad-spectrum antibiotics (per local guidelines)
- IV fluids
213
If you are treating a patient for pyelonephritis and they are not responding to treatment or they have severe symptoms, what two things should be considered?
- Renal abscess
- Kidney stone obstructing the ureter --> *causing pyelonephritis*
214
What is chronic pyelonephritis?
Recurrent kidney infections leading to renal scarring and chronic kidney disease (CKD), potentially progressing to end-stage renal failure
215
What imaging is used in recurrent pyelonephritis to assess kidney damage?
Dimercaptosuccinic acid (DMSA) scans - *involve injecting radiolabeled DMSA, which builds up in healthy kidney tissue*
- when imaged using gamma cameras, it indicates scarring or damage in areas that do not take up the DMSA
216
What are the alternative names for renal stones/kidney stones?
Renal calculi, urolithiasis, nephrolithiasis
217
Where do renal stones form?
In the renal pelvis, where urine collects before travelling down the ureters
- they can get stuck at any point along the ureters, but commonly at the vesico-uteric junction
218
What are the two key complications of kidney stones?
- Obstruction leading to acute kidney injury (AKI)
- Infection with obstructive pyelonephritis
218
What is the most common type of kidney stone?
Calcium-based stones (~80% of cases)
.
There are 2 types of calcium stones:
- Calcium oxalate (more common)
- Calcium phosphate
219
What are key risk factors for calcium collecting into a stone (renal calculi formation)?
Having a raised serum calcium (hypercalcaemia) and a low urine output
219
Other than calcium-based kidney stones, name 3 other types of kidney stones
- Uric acid stones - *not visible on X-ray*
- Struvite stones - *produced by bacteria --> associated with infection*
- Cystine stones - *associated with cystinuria (an autosomal recessive disease)*
220
What is a staghorn calculus + what type of stone most commonly forms a staghorn calculus?
A large stone shaped like the renal pelvis (resembling stag antlers) - *body sits in the renal pelvis with horns extending into the renal calyces*
.
Struvite stones - *often associated with recurrent upper urinary tract infections*
(the bacteria can hydrolysed the urea in urine to ammonia, creating the solid struvite)
221
What is the typical presenting symptom of symptomatic kidney stones + what are some other possible symptoms?
Renal colic --> *unilateral, excruiating, colicky loin-to-groin pain*
(colicky - *fluctuating in severity as the stone moves and settles*)
.
other possible symptoms:
- Haematuria
- Nausea or vomiting
- Reduced urine output
- Symptoms of sepsis (if infection is present)
222
What urine dipstick findings are expected in kidney stones?
Haematuria (blood in urine)
- note: a normal urine dipstick does not exclude stones
- urine dipsticks are also helpful to exclude infection
223
What blood tests should be done in suspected kidney stones?
- Serum calcium - *to check for hypercalcaemia*
- Inflammatory markers - *if infection is suspected*
- Renal function tests
224
Which imaging is first line for diagnosing kidney stones?
Non-contrast CT KUB (Kidneys, Ureters, Bladder) - *should be performed within 24hrs of presentation*
225
Other than a non-contrast CT KUB, what imaging alternatives exist for kidney stones?
- abdominal x-ray - *detects calcium-based stones, but not uric acid stones*
- ultrasound KUB - *less effective at identifying kidney stones, but is helpful in pregnant women and children*
226
Why is stone analysis important when investigating kidney stones?
Helps determine the stone type, which can help establish the cause, and reduce the risk of recurrence
227
Symptoms of hypercalcaemia (4)
“renal stones, painful bones, abdominal groans and psychiatric moans”
228
3 causes of hypercalcaemia to remember
- calcium supplementation
- hyperparathyroidism
- cancer (e.g., myeloma, breast or lung cancer)
229
What is the first-line analgesic for kidney stone pain + give an alternative if contraindicated
1. NSAIDs - *intramuscular diclofenac*
2. IV paracetamol - *alternative if NSAIDs are contraindicated*
.
(note: opiates are not effective for pain management in kidney stones, so are not used)
230
In the management of kidney stones, other than pain relief, what additional medications can be given?
- antiemetics - *eg. metoclopramide, prochlorperazine, cyclizine*
- antibiotics - *if infection is present*
- Tamsulosin (alpha-blocker) - *can help aid spontaneous passage of stones*
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When is watchful waiting appropriate for kidney stones?
- Stones <5mm --> *good chance they will pass spontaneously*
- Some 5-10mm stones, depending on patient factors - *can take several weeks for stone to pass*
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When is surgical intervention required for kidney stones?
- Stones ≥10mm
- Stones that do not pass spontaneously
- Complete obstruction or infection
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There are multiple surgical interventions for kidney stones, describe each of the following:
- Extracorporeal shock wave lithotripsy (ESWL) -->
- Ureteroscopy and laser lithotripsy -->
- Percutaneous nephrolithotomy (PCNL) -->
- Open surgery --> rarely used
- Extracorporeal shock wave lithotripsy (ESWL) --> *external machine generates shock waves which break stones into smaller pieces to make easier to pass (performed under x-ray guidance)*
- Ureteroscopy and laser lithotripsy --> *endoscopic camera inserted via urethra, bladder, and into ureter - laser breaks stones into smaller pieces to make easier to pass*
- Percutaneous nephrolithotomy (PCNL) --> *nephroscope inserted through the back into the kidney to assess ureter, stones then broken into smaller pieces and removed, nephrostomy tube may be left in place after to help drain kidney (performed under general anaesthetic, used for larger/complex stones)*
- Open surgery --> *rarely used, only for large, complex stones that cannot be removed by other means*
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What lifestyle changes reduce the risk of kidney stones?
- Increase oral fluid intake - *2.5 – 3 litres per day*
- Add fresh lemon juice to water - *citric acid binds to urinary calcium reducing the formation of stones*
- Avoid carbonated drinks - *cola drinks contain phosphoric acid, which promotes calcium oxalate formation*
- Reduce dietary salt intake - *less than 6g per day*
- Maintain a normal calcium intake - *low dietary calcium might increase the risk of kidney stones*
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What dietary advice is specific for different stone types?
- calcium stones -->
- uric acid stones -->
- calcium stones --> *reduce the intake of oxalate-rich foods (e.g., spinach, beetroot, nuts, rhubarb and black tea)*
- uric acid stones --> *reduce the intake of purine-rich foods (e.g., kidney, liver, anchovies, sardines and spinach)*
.
(another common recommendation is to limit dietary protein intake)
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What medications help reduce kidney stone recurrence? (2)
- Potassium citrate - *in patients with calcium oxalate stones and raised urinary calcium*
- Thiazide diuretics (e.g., indapamide) - *in patients with calcium oxalate stones and raised urinary calcium*
236
What is the most common type of kidney tumour?
Renal cell carcinoma (RCC)
237
Where does renal cell carcinoma arise from?
adenocarcinoma that arises from the renal tubules
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What is the classic triad of presentation in renal cell carcinoma (RCC)?
- Haematuria
- Flank pain
- Palpable mass
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What are the three most common subtypes of renal cell adenocarcinoma?
- Clear cell (80%)
- Papillary (15%)
- Chromophobe (5%)
240
What is the most common type of kidney tumour that affects children under 5 years old?
Wilms' tumour (or nephroblastoma)
241
Name six key risk factors for renal cell carcinoma.
- Smoking
- Obesity
- Hypertension
- End-stage renal failure
- Von Hippel-Lindau Disease
- Tuberous sclerosis
242
Renal cell carcinoma can be asymptomatic, but what are the possible symptoms of renal cell carcinoma?
- Haematuria
- Vague loin pain
- Non-specific cancer symptoms (weight loss, fatigue, anorexia, night sweats)
- Palpable renal mass
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What does NICE recommend for a two-week wait referral for suspected RCC?
Patients aged over 45 with unexplained visible haematuria, either:
- without a UTI
- persisting after UTI treatment
244
Where does renal cell carcinoma tend to spread first?
Tissues around kidney (within Gerota's fascia), then to the renal vein and to the inferior vena cava (IVC)
245
What is a classic radiological feature of metastatic spread of renal cell carcinoma (RCC) in the lungs?
Cannonball metastases (well-defined circular opacities on chest X-ray)
.
*(cannonball mets can also appear with choriocarcinoma (cancer in placenta), and sometimes prostate, bladder, and endometrial cancer)*
246
What are four paraneoplastic syndromes associated with renal cell carcinoma (RCC)?
- Polycythaemia - *due to unregulated secretion of erythropoietin*
- Hypercalcaemia - *due to tumour secretion of PTH-related protein*
- Hypertension - *due to increased renin secretion, polycythaemia and/or physical compression*
- Stauffer’s syndrome - *abnormal LFTs (raised ALT, AST, ALP, and bilirubin) without liver metastasis*
247
In renal cell carcinoma, other than due to tumour secretion of PTH-related protein, what other condition can cause hypercalcemia?
Bony metastases
248
What imaging modality is used to stage RCC?
CT thorax, abdomen, and pelvis
249
What staging system is commonly used for RCC?
TNM staging system:
- Tumour (size of tumour) - *T1 (small) to T4 (largest)*
- Node (no. nearby lymph nodes that contain cancer) - *N0 means no lymph nodes contain cancer, N3 means many lymph nodes contain cancer*
- Metastasis - *M0 means cancer hasn't spread, M1 means cancer has spread*
250
Describe the number staging system for RCC (stage 1-4)
- Stage 1: tumour < 7cm, confined to kidney
- Stage 2: tumour > 7cm, confined to kidney
- Stage 3: local spread to nearby tissues or veins, but not beyond Gerota’s fascia
- Stage 4: spread beyond Gerota’s fascia, including metastasis
251
Surgical removal of the tumour is the first-line treatment for renal cell carcinoma (RCC), what are the two surgical options available?
- Partial nephrectomy - *removal of part of the kidney*
- Radical nephrectomy - *removal of entire kidney, surrounding tissue, lymph nodes, and possibly the adrenal gland*
252
For a patient with renal cell carcinoma who is unsuitable for surgery, what other options are available?
Less invasive procedures:
- Arterial embolisation - *cutting off blood supply to the affected kidney*
- Percutaneous cryotherapy - *injecting liquid nitrogen to freeze/kill tumour cells*
- Radiofrequency ablation - *electrical current (via needle in tumour) destroys tumour cells*
.
(note: chemo and radiotherapy can be used for RCC, but not as effective compared to surgery)
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