Med C - Renal Flashcards
(128 cards)
1
Q
What is AKI
A
Acute kidney injury (AKI) refers to a rapid drop in kidney function, diagnosed by measuring the serum creatinine. Acute kidney injury is most common in acutely unwell patients (e.g., infections or following surgery).
2
Q
What are the NICE guidelines (2019) criteria for diagnosing an acute kidney injury are:
A
- Rise in creatinine of more than 25 micromol/L in 48 hours
- Rise in creatinine of more than 50% in 7 days
- Urine output of less than 0.5 ml/kg/hour over at least 6 hours
3
Q
Risk factors that would predispose to developing acute kidney injury include
A
- Older age (e.g., above 65 years)
- Sepsis
- Chronic kidney disease
- Heart failure
- Diabetes
- Liver disease
- Cognitive impairment (leading to reduced fluid intake)
- Medications (e.g., NSAIDs, gentamicin, diuretics and ACE inhibitors)
- Radiocontrast agents (e.g., used during CT scans)
4
Q
Causes of AKI
A
TOM TIP: Whenever someone asks you the causes of renal impairment, start with, “the causes are** pre-renal, renal or post-renal**”. This will impress them and allow you to think through the causes more logically.
**Pre-renal **
- Dehydration
- Shock (e.g., sepsis or acute blood loss)
- Heart failure
**Renal **
- Acute tubular necrosis
- Glomerulonephritis
- Acute interstitial nephritis
- Haemolytic uraemic syndrome
- Rhabdomyolysis
**Post-renal **
- Kidney stones
- Tumours (e.g., retroperitoneal, bladder or prostate)
- Strictures of the ureters or urethra
- Benign prostatic hyperplasia (benign enlarged prostate)
- Neurogenic bladder
5
Q
What does pre renal, renal and post renal mean in AKI
A
- Pre-renal causes are the most common. Insufficient blood supply (hypoperfusion) to kidneys reduces the filtration of blood.
- Renal causes are due to intrinsic disease in the kidney.
- Post-renal causes involve obstruction to the outflow of urine away from the kidney, causing back-pressure into the kidney and reduced kidney function. This is called an obstructive uropathy.
6
Q
What is Acute Tubular Necrosis
A
Acute tubular necrosis refers to damage and death (necrosis) of the epithelial cells of the renal tubules. It is the most common intrinsic cause of acute kidney injury
7
Q
Acute Tubular Necrosis
Damage to the kidney cells occurs due to:
A
- Ischaemia due to hypoperfusion (e.g., dehydration, shock or heart failure)
- Nephrotoxins (e.g., gentamicin, radiocontrast agents or cisplatin)
8
Q
________ _______ _______ on urinalysis confirm acute tubular necrosis. _________ _____ epithelial cells may also be seen.
A
Muddy brown casts on urinalysis confirm acute tubular necrosis. Renal tubular epithelial cells may also be seen.
9
Q
Investigations for AKI
A
Urinalysis assesses for protein, blood, leucocytes, nitrites and glucose:
- Leucocytes and nitrites suggest infection
- Protein and blood suggest acute nephritis (but can be positive in infection)
- Glucose suggests diabetes
Ultrasound of the urinary tract assesses for obstruction when a post-renal cause is suspected.
10
Q
Acute kidney injury is often preventable by:
A
- Avoiding nephrotoxic medications where appropriate
- Ensuring adequate fluid intake (including IV fluids if oral intake is inadequate)
- Additional fluids before and after radiocontrast agents
11
Q
Treating an acute kidney injury involves reversing the underlying cause and supportive management, for example:
A
- IV fluids for dehydration and hypovolaemia
- Withhold medications that may worsen the condition (e.g., NSAIDs and ACE inhibitors)
- Withhold/adjust medications that may accumulate with reduced renal function (e.g., metformin and opiates)
- Relieve the obstruction in a post-renal AKI (e.g., insert a catheter in a patient with prostatic hyperplasia)
- Dialysis may be required in severe cases
- Input from a renal specialist
12
Q
TRUE OR FALSE
ACE inhibitors are bad in AKI
A
FALSE
Calling ACE inhibitors nephrotoxic is incorrect. ACE inhibitors should be stopped in an acute kidney injury, as they reduce the filtration pressure. However, ACE inhibitors have a protective effect on the kidneys long-term. They are offered to certain patients with hypertension, diabetes and chronic kidney disease to protect the kidneys from further damage.
13
Q
Complication of AKI
A
- Fluid overload, heart failure and pulmonary oedema
- Hyperkalaemia
- Metabolic acidosis
- Uraemia (high urea), which can lead to encephalopathy and pericarditis
14
Q
What is CKD
A
Chronic kidney disease (CKD) describes a chronic reduction in kidney function sustained over three months. It tends to be permanent and progressive.
15
Q
Kidney function naturally declines with age. Factors that can speed up the decline and cause CKD include:
A
- Diabetes
- Hypertension
- Medications (e.g., NSAIDs or lithium)
- Glomerulonephritis
- Polycystic kidney disease
16
Q
Most patients with CKD are asymptomatic. Signs and symptoms as the renal function worsens may be non-specific:
A
- Fatigue
- Pallor (due to anaemia)
- Foamy urine (proteinuria)
- Nausea
- Loss of appetite
- Pruritus (itching)
- Oedema
- Hypertension
- Peripheral neuropathy
17
Q
Investigations for CKD
A
- (eGFR)
- Proteinuria with a urine albumin:creatinine ratio (ACR).
- Haematuria with a urine dipstick or microscopy.
- Renal ultrasound helps identify obstructions
- Blood pressure (for hypertension)
- HbA1c (for diabetes)
- Lipid profile (for hypercholesterolaemia)
18
Q
The __ ______ is based on the eGFR. The A score is based on the ___________ _______ ratio.
A
The G score is based on the eGFR. The A score is based on the albumin:creatinine ratio.
19
Q
CKD
A diagnosis can be made when there are consistent results over three months of either:
A
- Estimated glomerular filtration rate (eGFR) is sustained below 60 mL/min/1.73 m2
- Urine albumin:creatinine ratio (ACR) is sustained above 3 mg/mmol
20
Q
Whar is Accelerated progression in CKD
A
Accelerated progression is a sustained decline in the eGFR within one year of either 25% or 15 mL/min/1.73 m2.
21
Q
Complications of CKD
A
- Anaemia
- Renal bone disease
- Cardiovascular disease
- Peripheral neuropathy
- End-stage kidney disease
- Dialysis-related complications
22
Q
The _______ ______ ______ _______ can be used to estimate the 5-year risk of kidney failure requiring dialysis.
A
The Kidney Failure Risk Equation can be used to estimate the 5-year risk of kidney failure requiring dialysis.
23
Q
The NICE clinical knowledge summaries (May 2023) suggest referral to a renal specialist when
A
- eGFR less than 30 mL/min/1.73 m2
- Urine ACR more than 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
24
Q
CKD
Treating the underlying cause involves:
A
- Optimising diabetic control
- Optimising hypertension control
- Reducing or avoiding nephrotoxic drugs (where appropriate)
- Treating glomerulonephritis (where this is the cause)
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BP targets for people with CKD
The blood pressure target is less than 130/80 in patients under 80 with CKD and an ACR above 70 mg/mmol.
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Medications that help slow CKD disease progression are:
* ACE inhibitors (or angiotensin II receptor blockers)
* SGLT-2 inhibitors (specifically dapagliflozin)
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Reducing the risk of CKD complications involves:
* Exercise, maintain a healthy weight and avoid smoking
* **Atorvastatin** 20mg for primary prevention of cardiovascular disease (in all patients with CKD)
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Management of CKD complications involves:
* Oral **sodium bicarbonate** to treat **metabolic acidosis**
* **Iron** and **erythropoietin** to treat **anaemia**
* **Vitamin D, low phosphate diet** and **phosphate binders** to treat renal bone disease
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Management of end-stage renal disease involves:
* Special dietary advice
* Dialysis
* Renal transplant
30
ACE inhibitors are offered to all CKD patients with:
* Diabetes plus a urine ACR above 3 mg/mmol
* Hypertension plus a urine ACR above 30 mg/mmol
* All patients with a urine ACR above 70 mg/mmol
The **serum potassium** needs close monitoring, as both CKD and ACE inhibitors can cause **hyperkalaemia**.
31
Which SGLT-2 Inhibitor is offered to CKD patients with Diabetes and a urine ACR above 30 mg/mmol
Dapagliflozin
32
Dapagliflozin is considered for patients with:
Dapagliflozin is considered for patients with:
* Diabetes plus a urine ACR or 3-30 mg/mmol
* Non-diabetics with an ACR of 22.6 mg/mmol or above
33
What is erythropoietin
a hormone that stimulates the production of red blood cells
34
CKD results in lower erythropoietin and a drop in red blood cell production. What disease does this cause?
CKD results in lower erythropoietin and a drop in red blood cell production.
It causes a** normocytic (normal sized) normochromic (normal colour) anaemia**.
35
Anaemia in Chronic Kidney Disease can be treated with?
**erythropoiesis-stimulating** agents, such as recombinant human erythropoietin. Blood transfusions can sensitise the immune system (allosensitization), increasing the risk of future transplant rejection.
BUT treat iron deficiency first
36
Renal bone disease is also known as chronic kidney disease-mineral and bone disorder (CKD-MBD). It involves:
* High serum phosphate
* Low vitamin D activity
* Low serum calcium
37
Reduced phosphate excretion by diseased kidneys results in ______ _____ _______
Reduced phosphate excretion by diseased kidneys results in **high serum phosphate. **
38
WHat is renal dialysis?
Dialysis is a method for performing the filtration tasks of the kidneys artificially. It is used in patients with **end-stage renal failure or complications of acute kidney injury**. It involves removing excess fluid, solutes and waste products.
39
What are the indications for renal dialysis
The **“AEIOU”** mnemonic can be used for the indications for short-term dialysis:
* A – Acidosis (severe and not responding to treatment)
* E – Electrolyte abnormalities (particularly treatment-resistant hyperkalaemia)
* I – Intoxication (overdose of certain medications)
* O – Oedema (severe and unresponsive pulmonary oedema)
* U – Uraemia symptoms such as seizures or reduced consciousness
* End-stage renal failure (CKD stage 5) is the main indication for long-term dialysis.
40
There are two options for dialysis in patients requiring it long-term:
Haemodialysis
Peritoneal dialysis
41
What is haemodialysis?
With haemodialysis, patients have their blood filtered by a **haemodialysis machine**. Regimes can vary, but a typical regime might be 4 hours a day, three days per week.
Blood is taken out of the body, passed through the dialysis machine, and pumped back into the body. The blood passes along a series of **semipermeable membranes** inside the dialysis machine. Solutes filter out of the blood, across the membrane and into a fluid called dialysate. The **concentration gradient** between the blood and the dialysate fluid causes water and solutes to diffuse out of the blood and across the membrane. **Anticoagulation** with **citrate** or **heparin** is necessary to prevent blood clotting in the machine and during the process.
42
Haemodialysis requires good access to an abundant blood supply. Two tubes are needed, one to remove the blood and one to put the blood back in. The options for longer-term access are:
Tunnelled cuffed catheter
Arteriovenous fistula
43
What are Tunnelled Cuffed Catheter
A tunnelled cuffed catheter is a tube inserted 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 (usually red) and one for blood entering the body (usually blue). They can stay long-term and be used for regular haemodialysis.
44
A ________ cuff surrounds the Tunnelled Cuffed catheter. The cuff promotes healing and adhesion of tissue, making the catheter more permanent and providing a barrier to infection.
A **Dacron** cuff surrounds the catheter. The cuff promotes healing and adhesion of tissue, making the catheter more permanent and providing a barrier to infection
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What is the main complications of Tunnelled Cuffed Catheter
The main complications are infection and blood clots within the catheter.
46
What is Arteriovenous Fistula
An AV fistula is an artificial connection between an artery and a vein. It bypasses the capillary system and allows blood to flow under high pressure from the artery directly into the vein. This provides a permanent, large, easy-access blood vessel with high-pressure arterial blood flow. Creating an A-V fistula requires a surgical operation and a maturation period of 4-16 weeks before it can be used.
47
What are types of Arteriovenous Fistula
* Radiocephalic fistula at the wrist (radial artery to cephalic vein)
* Brachiocephalic fistula at the antecubital fossa (brachial artery to cephalic vein)
* Brachiobasilic fistula at the upper arm (less common and a more complex operation)
48
AV fistula features to examine in an OSCE are:
* Skin integrity
* Aneurysms
* Palpable thrill (a fine vibration felt over the anastomosis)
* A **“machinery murmur”** on auscultation over the fistula
49
Complications of AV fistula include:
Aneurysm
Infection
Thrombosis
Stenosis
STEAL syndrome
High-output heart failure
50
What is STEAL syndrome
occurs when there is inadequate blood flow to the limb distal to the fistula. The AV fistula “steals” blood from the rest of the limb. Blood is diverted away from the part of the limb it was supposed to supply, leading to ischaemia. Instead, it flows through the fistula and into the venous system.
51
What is High-output heart failur
is caused by blood flowing quickly from the arterial to the venous system through an A-V fistula. There is a rapid return of blood to the heart, increasing the pre-load (how full the heart is before it pumps). This leads to hypertrophy of the heart muscle and heart failure.
52
Do you take blood from a pt with a fistula
no
NEVER take blood from a fistula! This is a lifeline for the patient, providing dialysis access. If it gets damaged, it will set them back massively.
53
What is Peritoneal Dialysis
Peritoneal dialysis uses the **peritoneal membrane** to filter the blood. A special dialysis solution containing dextrose 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 filtered out of the blood.
54
What type of catheter is used for peritoneal dialysis?
Peritoneal dialysis involves a **Tenckhoff catheter.** This plastic tube is inserted into the peritoneal cavity, with one end on the outside, allowing access to the peritoneal cavity to insert and remove the dialysis solution.
55
What is Continuous ambulatory peritoneal dialysis (CAPD)
Continuous ambulatory peritoneal dialysis (CAPD) is where dialysis solution is always in the peritoneal cavity. There are various regimes for changing the solution. For example, two litres of solution replaced four times daily.
56
What is Automated dialysis
Automated dialysis is the alternative. A machine continuously replaces the dialysis fluid for 8-10 hours overnigh
57
Complications of peritoneal dialysis include:
* **Bacterial peritonitis** (infections in the high-sugar environment are common and serious)
* **Peritoneal sclerosis** (thickening and scarring of the peritoneal membrane)
* **Ultrafiltration failure** (the dextrose is absorbed, reducing the filtration gradient, making ultrafiltration less effective)
* **Weight gain** (due to absorption of the dextrose)
* **Psychosocial implications**
58
What is a renal transplant
A renal transplant is where a kidney is transplanted into a patient with end-stage renal failure. It typically adds ten years to life compared to just using dialysis and significantly improves quality of life
59
What is donor matching
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 the closer the match, the less likely there is organ rejection and the better the outcomes. Recipients can receive treatment to desensitise them to the donor HLA in preparation for a transplant from a living donor.
60
How does the renal transplant proedure work?
The patient’s kidneys are left in place. The donor kidney blood vessels are connected **(anastomosed)** with the pelvic vessels, usually the **external iliac vessels**. The ureter of the donor kidney is anastomosed directly with the bladder. The donor kidney is placed anteriorly in the abdomen and can usually be palpated in the iliac fossa area. A “**hockey stick”** incision is typically used, and there will be a **“hockey stick” scar.**
61
Which monoclonal antibody is given to the patient after renal transplant surgery and why?
**Basiliximab** is a monoclonal antibody targeting the interleukin-2 receptor on T-cells. Two doses are given after surgery to prevent **acute rejection.**
62
Patients require life-long immunosuppression to reduce the risk of transplant rejection. There are various options and combinations of:
Tacrolimus
Mycophenolate
Ciclosporin
Azathioprine
Prednisolone
63
When examining a patient with a renal transplant, you can look particularly clever by looking for the side effects of particular immunosuppressant medications.
What are they?
* Immunosuppressants cause seborrhoeic warts and skin cancers (look for scars from skin cancer removal)
* Tacrolimus causes a tremor
* Cyclosporine causes gum hypertrophy
* Steroids cause features of Cushing’s syndrome
64
Complications relating to the renal transplant:
* Transplant rejection (hyperacute, acute or chronic)
* Transplant failure
* Electrolyte imbalances
65
Complications related to immunosuppressants:
* Ischaemic heart disease
* Type 2 diabetes (steroids)
* Infections are more likely, more severe and may involve unusual pathogens
* Non-Hodgkin lymphoma
* Skin cancer (particularly squamous cell carcinoma)
66
Unusual infections can occur secondary to immunosuppressant medication, such as:
* Pneumocystis jiroveci pneumonia (PCP/PJP)
* Cytomegalovirus (CMV)
* Tuberculosis (TB)
67
What is Glomerulonephritis
Glomerulonephritis refers to inflammation of the glomeruli in the kidneys. The glomerulus is the first part of the nephron. It filters fluid out of the capillaries and into the renal tubule.
Glomerulonephritis describes the pathology that occurs in various diseases rather than being a disease. Treatment is targeted at the underlying cause and often involves supportive care and immunosuppression (e.g., corticosteroids).
68
Nephritic syndrome refers to a group of features that occur with nephritis which are:
* **Haematuria** (blood in the urine), which can be microscopic (not visible) or macroscopic (visible)
* **Oliguria** (significantly reduced urine output)
* **Proteinuria** (protein in the urine), but less than 3g per 24 hours (higher protein suggests nephrotic syndrome)
* **Fluid retention**
69
Whay is nephrotic syndrome
Nephrotic syndrome occurs when the** basement membrane** in the glomerulus becomes **highly permeable**, resulting in significant **proteinuria**. It refers to a group of features without specifying the underlying cause. It involves:
* **Proteinuria **(more than 3g per 24 hours)
* **Low serum albumin** (less than 25g per litre)
* **Peripheral oedema**
* **Hypercholesterolaemia**
70
Other presentation s of Nephrotic syndrome
Nephrotic syndrome presents with **oedema.** Patients might notice **frothy urine** due to the high protein content. Nephrotic syndrome predisposes patients to **thrombosis**, **hypertension** and** high cholesterol.**
71
The most common cause of nephrotic syndrome in children is ______ _____ _______. This is usually:
Idiopathic (no identified cause)
Treated successfully with steroids
The most common cause of nephrotic syndrome in children is **minimal change disease**. This is usually:
Idiopathic (no identified cause)
Treated successfully with steroids
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The top causes of nephrotic syndrome in adults are:
* Membranous nephropathy
* Focal segmental glomerulosclerosis
73
Other causes of nephrotic syndrome include:
Membranoproliferative glomerulonephritis
Henoch-Schönlein purpura (HSP)
Diabetes
Infection (e.g., HIV)
74
Minimal change disease comes up fairly frequently in exams as the most common cause of nephrotic syndrome in children. If you spot a 2 – 5 year old child with oedema, proteinuria and low albumin, you may be asked about the underlying cause. The answer is likely to be __________ ________.
Minimal change disease comes up fairly frequently in exams as the most common cause of nephrotic syndrome in children. If you spot a 2 – 5 year old child with oedema, proteinuria and low albumin, you may be asked about the underlying cause. The answer is likely to be **nephrotic syndrome.**
75
What are the different types of Glomerulonephritis
* Membranous nephropathy
* Membranous nephropathy
* Membranoproliferative glomerulonephritis
* Post-streptococcal glomerulonephritis
* Rapidly progressive glomerulonephritis
* Goodpasture syndrome
76
Systemic diseases that can cause glomerulonephritis include:
* Henoch-Schönlein purpura (HSP)
* Vasculitis (e.g., microscopic polyangiitis or granulomatosis with polyangiitis)
* Lupus nephritis (associated with systemic lupus erythematosus)
77
If you come across a patient in your exams with significant acute kidney injury and haemoptysis, the top conditions to consider can be differentiated based on the antibodies:
* Anti-GBM antibodies –
* p-ANCA (or MPO antibodies) –
* c-ANCA (or PR3 antibodies) –
If you come across a patient in your exams with significant acute kidney injury and haemoptysis, the top conditions to consider can be differentiated based on the antibodies:
* Anti-GBM antibodies – **Goodpasture syndrome**
* p-ANCA (or MPO antibodies) – **microscopic polyangiitis**
* c-ANCA (or PR3 antibodies) – **granulomatosis with polyangiitis**
78
How does a typical pt present with IgA nephropathy?
The typical patient is in their 20s presenting with haematuria. Histology shows **IgA deposits** and **mesangial proliferation**. The **mesangial cells** are found in the centre of the glomerulus and help support the capillaries (as well as performing other functions).
79
What is Membranous nephropathy
Membranous nephropathy involves deposits of immune complexes in the glomerular basement membrane, causing thickening and malfunctioning of the membrane and proteinuria. Histology shows IgG and complement deposits on the basement membrane. It is a key cause of nephrotic syndrome in adults. The majority (around 70%) are idiopathic. It can be secondary to malignancy, systemic lupus erythematosus or drugs (e.g. NSAID
80
Membranoproliferative glomerulonephritis (or mesangiocapillary glomerulonephritis) typically affects patients under ____. It involves ______ ______ deposits and __________ _______.
Membranoproliferative glomerulonephritis (or mesangiocapillary glomerulonephritis) typically affects patients under 30. It involves **immune complex** deposits and **mesangial proliferation**.
81
Typical presentation of a Post-streptococcal glomerulonephritis pt
tends to affect patients under 30. It presents 1-3 weeks after a streptococcal infection (e.g., tonsillitis or impetigo). Patients usually make a full recovery.
82
Typical presentation of apt with Rapidly progressive glomerulonephritis
presents with an acute severe illness but tends to respond well to treatment. Histology shows **glomerular crescents**.
83
Typical presentationo fpt with Goodpasture syndrome is also known as anti-glomerular basement membrane (anti-GBM)
The typical presentation is a patient in their 20s or 60s with **acute kidney failure** and **haemoptysis** (coughing up blood).
84
Diagnosis of glomerulonephritis
Diagnosis may require a renal biopsy for histology.
85
Management of Glmerulonephritis
A renal specialist will guide treatment, which depends on the underlying cause. It may involve:
* Supportive care (e.g., hypertension management and dialysis in severe disease)
* Immunosuppression (e.g., corticosteroids)
86
What is Renal tubular acidosis
Renal tubular acidosis (RTA) involves metabolic acidosis due to pathology in the tubules of the kidneys. The tubules balance hydrogen (H+) and bicarbonate ions (HCO3–) between the blood and urine to maintain a normal pH. There are four types of renal tubular acidosis, with different pathophysiology
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Which RTA are worth remembering and how
Remembering types 1 and 4 for your exams (type 4 is the most common). Both involve inadequate hydrogen excretion in the distal tubules. In type 1, there is hypokalaemia. In type 4, there is hyperkalaemia.
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What is Type 1 Renal Tubular Acidosis
Type 1 RTA (or distal RTA) occurs when the distal tubule cannot excrete hydrogen ions
90
Type 1 RTA results in
* High urinary pH (above 6) due to the absence of hydrogen ions
* Metabolic acidosis, due to retained hydrogen ions in the blood
* Hypokalaemia, due to failure of the hydrogen and potassium exchange (H+/K+ ATPase)
91
Type 1 RTA presents with
* Failure to thrive in children
* Recurrent UTIs (due to alkaline urine)
* Bone disease (rickets or osteomalacia)
* Muscle weakness
* Arrhythmias (due to hypokalaemia)
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Treatment for RTA Type 1
Treatment is with oral **bicarbonate**, which corrects the acidosis and electrolyte imbalances.
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What is RTA type 4
Type 4 RTA (or hyperkalaemic RTA) is caused by reduced aldosterone. Aldosterone stimulates sodium reabsorption and potassium and hydrogen ion excretion in the distal tubules. Low aldosterone or impaired aldosterone function leads to insufficient potassium and hydrogen ion excretion.
94
RTA type 4 results in
The results are:
* Metabolic acidosis, due to retained hydrogen ions in the blood
* Hyperkalaemia, due to retained potassium in the blood
* Low urinary pH due to reduced ammonia production in response to hyperkalaemia
95
Management for RTA 4
Management is targeted at the underlying cause. Fludrocortisone (a mineralocorticoid steroid) may be used in aldosterone deficiency. Oral bicarbonate and treatment of hyperkalaemia may also be required.
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What is Haemolytic uraemic syndrome
Haemolytic uraemic syndrome (HUS) involves **thrombosis** in **small blood vessels** throughout the body, usually triggered by **Shiga toxins** from either **E. coli O157 o**r **Shigella**
It most often affects children following an episode of gastroenteritis. Antibiotics and anti-motility medication (e.g., loperamide) used to treat gastroenteritis caused by E. coli O157 or Shigella increase the risk of HUS
97
HUS leads to the classic triad of:
* Microangiopathic haemolytic anaemia
* Acute kidney injury
* Thrombocytopenia (low platelets)
98
The formation of blood clots consumes platelets, leading to ______________
thrombocytopenia
99
What is Microangiopathic haemolytic anaemia (MAHA)
involves the destruction of red blood cells (haemolysis) due to pathology in the small vessels (microangiopathy). Tiny blood clots (thrombi) partially obstruct the small blood vessels and churn the red blood cells as they pass through, causing them to rupture.
100
Presentation of Haemolytic Uraemic Syndrome
E. coli O157 and Shigella cause gastroenteritis. Diarrhoea is the first symptom, which turns bloody within 3 days. Around a week after the onset of diarrhoea, the features of HUS develop:
* Fever
* Abdominal pain
* Lethargy
* Pallor
* Reduced urine output (oliguria)
* Haematuria
* Hypertension
* Bruising
* Jaundice (due to haemolysis)
* Confusion
101
Management of Haemolytic Uraemic Syndrome
Stool culture is used to establish the causative organism.
HUS is a **medical emergency** and requires **hospital admission** and **supportive management** with treatment of:
* Hypovolaemia (e.g., IV fluids)
* Hypertension
* Severe anaemia (e.g., blood transfusions)
* Severe renal failure (e.g., haemodialysis)
It is self-limiting, and most patients fully recover with good supportive car
102
What is Rhabdomyolysis
Rhabdomyolysis involves skeletal muscle breaking down and releasing various chemicals into the blood. Muscle cells (myocytes) undergo cell death (apoptosis), releasing:
* Myoglobin
* Potassium
* Phosphate
* Creatine kinase
103
What is the most dangerous breakdown product in rhabdomyolysis?
Potassium is the most immediately dangerous breakdown product. Hyperkalaemia can cause cardiac arrhythmias and cardiac arrest.
104
What is a serious complication of rhabdomyolysis?
These breakdown products can cause **acute kidney injury**. Myoglobin, in particular, is toxic in high concentrations. Impaired renal function results in further accumulation of these substances in the blood.
Other complications include compartment syndrome and disseminated intravascular coagulation.
105
Causes of rhabdomyolysis
Anything that causes significant damage to muscle cells can cause rhabdomyolysis. For example:
* 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
106
Investigations for rhabdomyolysis
**Creatine kinase (CK) **is the crucial diagnostic blood test for rhabdomyolysis. It is normally less than around 150 U/L. In rhabdomyolysis, it can be 1,000-100,000 U/L.
**Myoglobinuria** refers to myoglobin in the urine. It gives urine a red-brown colour. A urine dipstick will be positive for blood.
**Urea and electrolytes (U&E)** are required for acute kidney injury and hyperkalaemia.
**ECGs** are used to assess and monitor the heart’s response to hyperkalaemia.
107
Signs and 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)
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Management of Rhabdomyolysis
**Intravenous fluids** are the mainstay of treatment to correct hypovolaemia and encourage filtration of the breakdown products. Treatment of complications, particularly **hyperkalaemia**, is also essential.
Additional options that are debatable and have associated risks include:
* Intravenous sodium bicarbonate (to increase urinary pH and reduce the toxic effects of myoglobinuria)
* Intravenous mannitol (to increase urine output and reduce oedema)
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The main complication of hyperkalaemia is _________ _________, such as _________ _________ which can lead to cardiac arrest.
The main complication of hyperkalaemia is **cardiac arrhythmias**, such as **ventricular fibrillation**, which can lead to cardiac arrest.
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Conditions that can cause hyperkalaemia include:
* Acute kidney injury
* Chronic kidney disease (stage 4 or 5)
* Rhabdomyolysis
* Adrenal insufficiency
* Tumour lysis syndrome
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Medications that can cause hyperkalaemia include:
* Aldosterone antagonists (e.g., spironolactone and eplerenone)
* ACE inhibitors (e.g., ramipril)
* Angiotensin II receptor blockers (e.g., candesartan)
* NSAIDs (e.g., naproxen)
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ECG Changes for hyperkalaemia?
* Tall peaked T-waves
* Flattening or absence of P waves
* Prolonged PR interval
* Broad QRS complexes
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Management of serum potassium below** 6.5 mmol/L without ECG changes** is aimed at
at the underlying cause, for example, treating acute kidney injury and stopping medications (e.g., spironolactone or ACE inhibitors).
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Patients require urgent treatment for hyperkalaemia if they have either:
* ECG changes
* Serum potassium above 6.5 mmol/L
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The mainstay of treatment for hyperkalaemia is with
insulin and dextrose infusion and IV calcium gluconate:
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Other options for lowering the serum potassium are
* Nebulised salbutamol temporarily drives potassium into cells
* Oral calcium resonium reduces potassium absorption in the GI tract (this is 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
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What is Polycystic kidney disease
Polycystic kidney disease is a genetic condition where the healthy kidney tissue is replaced with many fluid-filled cysts. The enlarged kidneys may be palpable on examination of the abdomen. It leads to renal failure
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There is an autosomal dominant and an autosomal recessive type of PKD. Which one is more common
autosomal dominant type is more common.
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The affected genes in autosomal dominant polycystic kidney disease (ADPKD) are:
PKD1 gene on chromosome 16 (85% of cases)
PKD2 gene on chromosome 4 (15% of cases)
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Extra-renal manifestations of ADPKD include:
Cerebral aneurysms
Hepatic, splenic, pancreatic, ovarian and prostatic cysts
Mitral regurgitation
Colonic diverticula
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Complications of ADPKD include
* 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
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What is Autosomal Recessive Polycystic Kidney Disease
Autosomal recessive polycystic kidney disease (ARPKD) is caused by a mutation in the polycystic kidney and hepatic disease 1 (PKHD1) gene on chromosome 6. It is more rare and severe than ADPKD. It is often picked up on antenatal scans with oligohydramnios (reduced amniotic fluid volume due to reduced urine output)
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Diagnosis of PKD
Ultrasound and genetic testing are used for diagnosis.
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how is tolvaptan used in PKD
Tolvaptan (a vasopressin receptor antagonist) can slow the development of cysts and the progression of renal failure in autosomal dominant polycystic kidney disease. This requires specific criteria and specialist monitoring.
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Management for PKD may involve:
* Antihypertensives for hypertension (e.g., ACE inhibitors)
* Analgesia for acute pain
* Antibiotics for infections (e.g., UTIs or cyst infections)
* Drainage of symptomatic can be performed by aspiration or surgery
* Dialysis for end-stage renal failure
* Renal transplant for end-stage renal failure
Other management steps include:
* Genetic counselling
* Avoiding contact sports due to the risk of cyst rupture
* Avoiding NSAIDs and anticoagulants
* MR angiography (MRA) can be used to screen for cerebral aneurysms
