Med C - Renal

Question 1

What is AKI

Answer 1

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).

Question 2

What are the NICE guidelines (2019) criteria for diagnosing an acute kidney injury are:

Answer 2

• 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

Question 3

Risk factors that would predispose to developing acute kidney injury include

Answer 3

• 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)

Question 4

Causes of AKI

Answer 4

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

Question 5

What does pre renal, renal and post renal mean in AKI

Answer 5

• 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.

Question 6

What is Acute Tubular Necrosis

Answer 6

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

Question 7

Acute Tubular Necrosis
Damage to the kidney cells occurs due to:

Answer 7

• Ischaemia due to hypoperfusion (e.g., dehydration, shock or heart failure)
• Nephrotoxins (e.g., gentamicin, radiocontrast agents or cisplatin)

Question 8

________ _______ _______ on urinalysis confirm acute tubular necrosis. _________ _____ epithelial cells may also be seen.

Answer 8

Muddy brown casts on urinalysis confirm acute tubular necrosis. Renal tubular epithelial cells may also be seen.

Question 9

Investigations for AKI

Answer 9

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.

Question 10

Acute kidney injury is often preventable by:

Answer 10

• Avoiding nephrotoxic medications where appropriate
• Ensuring adequate fluid intake (including IV fluids if oral intake is inadequate)
• Additional fluids before and after radiocontrast agents

Question 11

Treating an acute kidney injury involves reversing the underlying cause and supportive management, for example:

Answer 11

• 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

Question 12

TRUE OR FALSE
ACE inhibitors are bad in AKI

Answer 12

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.

Question 13

Complication of AKI

Answer 13

• Fluid overload, heart failure and pulmonary oedema
• Hyperkalaemia
• Metabolic acidosis
• Uraemia (high urea), which can lead to encephalopathy and pericarditis

Question 14

What is CKD

Answer 14

Chronic kidney disease (CKD) describes a chronic reduction in kidney function sustained over three months. It tends to be permanent and progressive.

Question 15

Kidney function naturally declines with age. Factors that can speed up the decline and cause CKD include:

Answer 15

• Diabetes
• Hypertension
• Medications (e.g., NSAIDs or lithium)
• Glomerulonephritis
• Polycystic kidney disease

Question 16

Most patients with CKD are asymptomatic. Signs and symptoms as the renal function worsens may be non-specific:

Answer 16

• Fatigue
• Pallor (due to anaemia)
• Foamy urine (proteinuria)
• Nausea
• Loss of appetite
• Pruritus (itching)
• Oedema
• Hypertension
• Peripheral neuropathy

Question 17

Investigations for CKD

Answer 17

• (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)

Question 18

The __ ______ is based on the eGFR. The A score is based on the ___________ _______ ratio.

Answer 18

The G score is based on the eGFR. The A score is based on the albumin:creatinine ratio.

Question 19

CKD

A diagnosis can be made when there are consistent results over three months of either:

Answer 19

• 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

Question 20

Whar is Accelerated progression in CKD

Answer 20

Accelerated progression is a sustained decline in the eGFR within one year of either 25% or 15 mL/min/1.73 m2.

Question 21

Complications of CKD

Answer 21

• Anaemia
• Renal bone disease
• Cardiovascular disease
• Peripheral neuropathy
• End-stage kidney disease
• Dialysis-related complications

Question 22

The _______ ______ ______ _______ can be used to estimate the 5-year risk of kidney failure requiring dialysis.

Answer 22

The Kidney Failure Risk Equation can be used to estimate the 5-year risk of kidney failure requiring dialysis.

Question 23

The NICE clinical knowledge summaries (May 2023) suggest referral to a renal specialist when

Answer 23

• 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

Question 24

CKD
Treating the underlying cause involves:

Answer 24

• Optimising diabetic control
• Optimising hypertension control
• Reducing or avoiding nephrotoxic drugs (where appropriate)
• Treating glomerulonephritis (where this is the cause)

Question 25

BP targets for people with CKD

Answer 25

The blood pressure target is less than 130/80 in patients under 80 with CKD and an ACR above 70 mg/mmol.

Question 26

Medications that help slow CKD disease progression are:

Answer 26

* ACE inhibitors (or angiotensin II receptor blockers) * SGLT-2 inhibitors (specifically dapagliflozin)

Question 27

Reducing the risk of CKD complications involves:

Answer 27

* Exercise, maintain a healthy weight and avoid smoking * **Atorvastatin** 20mg for primary prevention of cardiovascular disease (in all patients with CKD)

Question 28

Management of CKD complications involves:

Answer 28

* 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

Question 29

Management of end-stage renal disease involves:

Answer 29

* Special dietary advice * Dialysis * Renal transplant

Question 30

ACE inhibitors are offered to all CKD patients with:

Answer 30

* 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**.

Question 31

Which SGLT-2 Inhibitor is offered to CKD patients with Diabetes and a urine ACR above 30 mg/mmol

Answer 31

Dapagliflozin

Question 32

Dapagliflozin is considered for patients with:

Answer 32

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

Question 33

What is erythropoietin

Answer 33

a hormone that stimulates the production of red blood cells

Question 34

CKD results in lower erythropoietin and a drop in red blood cell production. What disease does this cause?

Answer 34

CKD results in lower erythropoietin and a drop in red blood cell production. It causes a** normocytic (normal sized) normochromic (normal colour) anaemia**.

Question 35

Anaemia in Chronic Kidney Disease can be treated with?

Answer 35

**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

Question 36

Renal bone disease is also known as chronic kidney disease-mineral and bone disorder (CKD-MBD). It involves:

Answer 36

* High serum phosphate * Low vitamin D activity * Low serum calcium

Question 37

Reduced phosphate excretion by diseased kidneys results in ______ _____ _______

Answer 37

Reduced phosphate excretion by diseased kidneys results in **high serum phosphate. **

Question 38

WHat is renal dialysis?

Answer 38

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.

Question 39

What are the indications for renal dialysis

Answer 39

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.

Question 40

There are two options for dialysis in patients requiring it long-term:

Answer 40

Haemodialysis Peritoneal dialysis

Question 41

What is haemodialysis?

Answer 41

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.

Question 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:

Answer 42

Tunnelled cuffed catheter Arteriovenous fistula

Question 43

What are Tunnelled Cuffed Catheter

Answer 43

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.

Question 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.

Answer 44

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

Question 45

# ``` ``` What is the main complications of Tunnelled Cuffed Catheter

Answer 45

The main complications are infection and blood clots within the catheter.

Question 46

What is Arteriovenous Fistula

Answer 46

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.

Question 47

What are types of Arteriovenous Fistula

Answer 47

* 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)

Question 48

AV fistula features to examine in an OSCE are:

Answer 48

* Skin integrity * Aneurysms * Palpable thrill (a fine vibration felt over the anastomosis) * A **“machinery murmur”** on auscultation over the fistula

Question 49

Complications of AV fistula include:

Answer 49

Aneurysm Infection Thrombosis Stenosis STEAL syndrome High-output heart failure

Question 50

What is STEAL syndrome

Answer 50

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.

Question 51

What is High-output heart failur

Answer 51

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.

Question 52

Do you take blood from a pt with a fistula

Answer 52

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.

Question 53

What is Peritoneal Dialysis

Answer 53

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.

Question 54

What type of catheter is used for peritoneal dialysis?

Answer 54

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.

Question 55

What is Continuous ambulatory peritoneal dialysis (CAPD)

Answer 55

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.

Question 56

What is Automated dialysis

Answer 56

Automated dialysis is the alternative. A machine continuously replaces the dialysis fluid for 8-10 hours overnigh

Question 57

Complications of peritoneal dialysis include:

Answer 57

* **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**

Question 58

What is a renal transplant

Answer 58

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

Question 59

What is donor matching

Answer 59

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.

Question 60

How does the renal transplant proedure work?

Answer 60

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.**

Question 61

Which monoclonal antibody is given to the patient after renal transplant surgery and why?

Answer 61

**Basiliximab** is a monoclonal antibody targeting the interleukin-2 receptor on T-cells. Two doses are given after surgery to prevent **acute rejection.**

Question 62

Patients require life-long immunosuppression to reduce the risk of transplant rejection. There are various options and combinations of:

Answer 62

Tacrolimus Mycophenolate Ciclosporin Azathioprine Prednisolone

Question 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?

Answer 63

* 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

Question 64

Complications relating to the renal transplant:

Answer 64

* Transplant rejection (hyperacute, acute or chronic) * Transplant failure * Electrolyte imbalances

Question 65

Complications related to immunosuppressants:

Answer 65

* 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)

Question 66

Unusual infections can occur secondary to immunosuppressant medication, such as:

Answer 66

* Pneumocystis jiroveci pneumonia (PCP/PJP) * Cytomegalovirus (CMV) * Tuberculosis (TB)

Question 67

What is Glomerulonephritis

Answer 67

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).

Question 68

Nephritic syndrome refers to a group of features that occur with nephritis which are:

Answer 68

* **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**

Question 69

Whay is nephrotic syndrome

Answer 69

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**

Question 70

Other presentation s of Nephrotic syndrome

Answer 70

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.**

Question 71

The most common cause of nephrotic syndrome in children is ______ _____ _______. This is usually: Idiopathic (no identified cause) Treated successfully with steroids

Answer 71

The most common cause of nephrotic syndrome in children is **minimal change disease**. This is usually: Idiopathic (no identified cause) Treated successfully with steroids

Question 72

The top causes of nephrotic syndrome in adults are:

Answer 72

* Membranous nephropathy * Focal segmental glomerulosclerosis

Question 73

Other causes of nephrotic syndrome include:

Answer 73

Membranoproliferative glomerulonephritis Henoch-Schönlein purpura (HSP) Diabetes Infection (e.g., HIV)

Question 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 __________ ________.

Answer 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 **nephrotic syndrome.**

Question 75

What are the different types of Glomerulonephritis

Answer 75

* Membranous nephropathy * Membranous nephropathy * Membranoproliferative glomerulonephritis * Post-streptococcal glomerulonephritis * Rapidly progressive glomerulonephritis * Goodpasture syndrome

Question 76

Systemic diseases that can cause glomerulonephritis include:

Answer 76

* Henoch-Schönlein purpura (HSP) * Vasculitis (e.g., microscopic polyangiitis or granulomatosis with polyangiitis) * Lupus nephritis (associated with systemic lupus erythematosus)

Question 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) –

Answer 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 – **Goodpasture syndrome** * p-ANCA (or MPO antibodies) – **microscopic polyangiitis** * c-ANCA (or PR3 antibodies) – **granulomatosis with polyangiitis**

Question 78

How does a typical pt present with IgA nephropathy?

Answer 78

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).

Question 79

What is Membranous nephropathy

Answer 79

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

Question 80

Membranoproliferative glomerulonephritis (or mesangiocapillary glomerulonephritis) typically affects patients under ____. It involves ______ ______ deposits and __________ _______.

Answer 80

Membranoproliferative glomerulonephritis (or mesangiocapillary glomerulonephritis) typically affects patients under 30. It involves **immune complex** deposits and **mesangial proliferation**.

Question 81

Typical presentation of a Post-streptococcal glomerulonephritis pt

Answer 81

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.

Question 82

Typical presentation of apt with Rapidly progressive glomerulonephritis

Answer 82

presents with an acute severe illness but tends to respond well to treatment. Histology shows **glomerular crescents**.

Question 83

Typical presentationo fpt with Goodpasture syndrome is also known as anti-glomerular basement membrane (anti-GBM)

Answer 83

The typical presentation is a patient in their 20s or 60s with **acute kidney failure** and **haemoptysis** (coughing up blood).

Question 84

Diagnosis of glomerulonephritis

Answer 84

Diagnosis may require a renal biopsy for histology.

Question 85

Management of Glmerulonephritis

Answer 85

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)

Question 86

What is Renal tubular acidosis

Answer 86

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

Question 87

Answer 87

Question 88

Which RTA are worth remembering and how

Answer 88

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.

Question 89

What is Type 1 Renal Tubular Acidosis

Answer 89

Type 1 RTA (or distal RTA) occurs when the distal tubule cannot excrete hydrogen ions

Question 90

Type 1 RTA results in

Answer 90

* 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)

Question 91

Type 1 RTA presents with

Answer 91

* Failure to thrive in children * Recurrent UTIs (due to alkaline urine) * Bone disease (rickets or osteomalacia) * Muscle weakness * Arrhythmias (due to hypokalaemia)

Question 92

Treatment for RTA Type 1

Answer 92

Treatment is with oral **bicarbonate**, which corrects the acidosis and electrolyte imbalances.

Question 93

What is RTA type 4

Answer 93

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.

Question 94

RTA type 4 results in

Answer 94

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

Question 95

Management for RTA 4

Answer 95

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.

Question 96

What is Haemolytic uraemic syndrome

Answer 96

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

Question 97

HUS leads to the classic triad of:

Answer 97

* Microangiopathic haemolytic anaemia * Acute kidney injury * Thrombocytopenia (low platelets)

Question 98

The formation of blood clots consumes platelets, leading to ______________

Answer 98

thrombocytopenia

Question 99

What is Microangiopathic haemolytic anaemia (MAHA)

Answer 99

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.

Question 100

Presentation of Haemolytic Uraemic Syndrome

Answer 100

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

Question 101

Management of Haemolytic Uraemic Syndrome

Answer 101

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

Question 102

What is Rhabdomyolysis

Answer 102

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

Question 103

What is the most dangerous breakdown product in rhabdomyolysis?

Answer 103

Potassium is the most immediately dangerous breakdown product. Hyperkalaemia can cause cardiac arrhythmias and cardiac arrest.

Question 104

What is a serious complication of rhabdomyolysis?

Answer 104

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.

Question 105

Causes of rhabdomyolysis

Answer 105

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

Question 106

Investigations for rhabdomyolysis

Answer 106

**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.

Question 107

Signs and Symptoms of rhabdomyolysis

Answer 107

Muscle pain Muscle weakness Muscle swelling Reduced urine output (oliguria) Red-brown urine (myoglobinuria) Fatigue Nausea and vomiting Confusion (particularly in frail patients)

Question 108

Management of Rhabdomyolysis

Answer 108

**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)

Question 109

The main complication of hyperkalaemia is _________ _________, such as _________ _________ which can lead to cardiac arrest.

Answer 109

The main complication of hyperkalaemia is **cardiac arrhythmias**, such as **ventricular fibrillation**, which can lead to cardiac arrest.

Question 110

Conditions that can cause hyperkalaemia include:

Answer 110

* Acute kidney injury * Chronic kidney disease (stage 4 or 5) * Rhabdomyolysis * Adrenal insufficiency * Tumour lysis syndrome

Question 112

Medications that can cause hyperkalaemia include:

Answer 112

* Aldosterone antagonists (e.g., spironolactone and eplerenone) * ACE inhibitors (e.g., ramipril) * Angiotensin II receptor blockers (e.g., candesartan) * NSAIDs (e.g., naproxen)

Question 113

ECG Changes for hyperkalaemia?

Answer 113

* Tall peaked T-waves * Flattening or absence of P waves * Prolonged PR interval * Broad QRS complexes

Question 114

Management of serum potassium below** 6.5 mmol/L without ECG changes** is aimed at

Answer 114

at the underlying cause, for example, treating acute kidney injury and stopping medications (e.g., spironolactone or ACE inhibitors).

Question 115

Patients require urgent treatment for hyperkalaemia if they have either:

Answer 115

* ECG changes * Serum potassium above 6.5 mmol/L

Question 116

The mainstay of treatment for hyperkalaemia is with

Answer 116

insulin and dextrose infusion and IV calcium gluconate:

Question 117

Other options for lowering the serum potassium are

Answer 117

* 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

Question 118

What is Polycystic kidney disease

Answer 118

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

Question 119

There is an autosomal dominant and an autosomal recessive type of PKD. Which one is more common

Answer 119

autosomal dominant type is more common.

Question 120

The affected genes in autosomal dominant polycystic kidney disease (ADPKD) are:

Answer 120

PKD1 gene on chromosome 16 (85% of cases) PKD2 gene on chromosome 4 (15% of cases)

Question 121

Extra-renal manifestations of ADPKD include:

Answer 121

Cerebral aneurysms Hepatic, splenic, pancreatic, ovarian and prostatic cysts Mitral regurgitation Colonic diverticula

Question 122

Complications of ADPKD include

Answer 122

* 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

Question 123

What is Autosomal Recessive Polycystic Kidney Disease

Answer 123

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)

Question 124

Diagnosis of PKD

Answer 124

Ultrasound and genetic testing are used for diagnosis.

Question 126

how is tolvaptan used in PKD

Answer 126

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.

Question 127

Management for PKD may involve:

Answer 127

* 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