QuestionSBA
QuestionChoice
Cinacalcet is a treatment used to treat secondary hyperparathyroidism, although it is reserved for patients on dialysis. It mimics the action of calcium on the tissues (calcimimetic) and increases the sensitivity of calcium receptors on parathyroid cells to reduce PTH
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Cinacalcet
QuestionChoice
Calcitriol is the active form of vitamin D - 1,25-dihydroxycholecalciferol. It increases calcium uptake in the gastrointestinal tract, increases renal absorption of calcium, and stimulates osteoclastic activity. This then sequentially suppresses parathyroid hormone, helping to prevent progression from secondary hyperparathyroidism into tertiary hyperparathyroidism
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Calcitriol
QuestionChoice
Colecalciferol should not be used to reduce PTH in those with normal vitamin D as an attempt to reduce the risk of progression into tertiary hyperparathyroidism. It can worsen hyperphosphataemia and lead to hypercalcaemia which can worsen cardiovascular morbidity. This would be exacerbated by additional calcium carbonate supplementation and would not improve survival benefit
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Colecalciferol with calcium carbonate
QuestionChoice
Calcitonin can occasionally be used in the treatment of hypercalcaemia by inhibiting osteoclast activity in bones and inhibiting renal reabsorption of calcium and phosphate. This patient is hypocalcaemic, and so this would reduce serum calcium levels further
33075
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Calcitonin
QuestionChoice
Colecalciferol (vitamin D3) is the major form of vitamin D that provides nutritional supplementation. It should not be used to reduce PTH in those with normal vitamin D as an attempt to reduce the risk of progression into tertiary hyperparathyroidism. It can worsen hyperphosphataemia and lead to hypercalcaemia which can worsen cardiovascular morbidity
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Colecalciferol
QuestionComment
Explanation for this question doesn't make sense: it says you should not use cholecalciferol as it can increase phosphate levels and worsen hypocalcaemia; but calcitriol will do the exact same thing!
8505
User
subscriber
Juice Complement
QuestionComment
why is his calcium low?

43116
QuestionComment
most likely secondary hyperparathyroidism
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subscriber
Acute Myopathy
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Neoplasia Nightshift
Concept
Chapter
# Summary

Chronic Kidney Disease (CKD) is a condition characterised by abnormal kidney function for over three months, with a decrease in glomerular filtration rate (GFR) and/or markers of kidney damage such as proteinuria. Classification is based on the cause of CKD, GFR and heaviness of proteinuria. Common causes include diabetes, hypertension and age-related decline. Most patients are asymptomatic in the early stages; signs and symptoms that may develop include lethargy, breathlessness, anorexia and oliguria. First-line investigations include blood tests for U&Es to determine serum creatinine and estimated GFR (eGFR), urine albumin:creatinine ratio and investigations to screen for a cause (e.g. renal tract ultrasound to look for structural abnormalities or obstruction). Management involves regular monitoring for complications (such as anaemia or bone disease), optimising risk factors such as blood pressure and diabetic control, and considering options for renal replacement therapy (RRT) in patients who have end-stage renal disease.

# Definition

CKD is defined by KDIGO as abnormal kidney function or structure for over 3 months, with implications for health. 

Glomerular filtration rate (GFR) refers to the volume of fluid filtered by the kidney's nephrons per minute. This can be estimated (eGFR) from serum creatinine although this may be less reliable in patients with extremes of muscle mass.

A GFR below 60 ml/min/1.73m<sup>2</sup> is considered significantly abnormal kidney function.

Examples of abnormal kidney structure include:

- Urinary albumin:creatinine ratio > 3 mg/mmol
- Urinary sediment abnormalities e.g. haematuria, pyuria or casts
- Biochemical abnormalities (e.g. acidosis, electrolyte disturbance) due to tubular disorders
- Histological abnormalities e.g. glomerulosclerosis, tubular atrophy
- Structural abnormalities e.g. polycystic kidneys or reflux nephropathy
- Previous renal transplant

# Epidemiology

- CKD is very common, with an estimated global prevalence of 9%
- Diabetes is the commonest cause, accounting for up to 50% of cases
- As the early stages of CKD are often asymptomatic, many cases are likely undiagnosed
- Prevalence is rising due to the ageing population and increased prevalence of chronic diseases such as diabetes and hypertension
- 50% of people over the age of 75 have CKD
- Risk factors include:
	- Family history of CKD
	- Black or Hispanic ethnicity
	- History of acute kidney injury (AKI)
	- Older age

# Aetiology

- Diseases causing intrinsic kidney damage:
	- Diabetes
	- Hypertension
	- Glomerulonephritis, which may be primary or secondary
	- Conditions causing urinary tract obstruction:
	- Recurrent urolithiasis
	- Structural abnormalities (e.g. ureteropelvic junction obstruction)
	- External compression (e.g. from a pelvic mass)
	- Bladder voiding problems (e.g. benign prostatic hyperplasia, neurogenic bladder)
- Iatrogenic causes:
	- Radiotherapy
	- Nephrotoxic drugs, e.g. aminoglycosides, lithium, NSAIDs
- Renal involvement secondary to multisystem diseases:
	- HIV
	- Myeloma
	- Vasculitis
	- Systemic lupus erythematosus (lupus nephritis)
	- Amyloidosis
	- Genetic kidney diseases
	- Autosomal dominant polycystic kidney disease (ADPKD)
	- Alport's syndrome
	- Tuberous sclerosis
	- Cystinosis
	- Recurrent urinary tract infections
	- Often secondary to vesico-ureteric reflux or other anatomical defects
	- Leads to chronic pyelonephritis which may lead to end-stage renal disease

# Classification

The KDIGO classification is used to stratify patients by risk of adverse outcomes from CKD based on their GFR and urinary albumin:creatinine ratio (ACR).

||A1 - normal to mildly increased ACR (< 3 mg/mmol)|A2 - moderately increased ACR (3 to 30 mg/mmol)|A3 - severely increased ACR (over 30 mg/mmol)|
|---------------|-----------|---------------|-----------|
|**G1 - normal or high GFR (> 90 ml/min/1.73m<sup>2</sup>)**|Low risk/not CKD if no other markers of kidney damage|Moderate risk|High risk|
|**G2 - mild reduction in GFR (60 - 89 ml/min/1.73m<sup>2</sup>)**|Low risk/not CKD if no other markers of kidney damage|Moderate risk|High risk|
|**G3a - mild to moderate reduction in GFR (45 - 59 ml/min/1.73m<sup>2</sup>)**|Moderate risk|High risk|Very high risk|
|**G3b - moderate to severe reduction in GFR (30-44 ml/min/1.73m<sup>2</sup>)**|Moderate risk|High risk|Very high risk|
|**G4 - severe reduction in GFR (15 - 29 ml/min/1.73m<sup>2</sup>)**|High risk|Very high risk|Very high risk|
|**G5 - renal failure (< 15 ml/min/1.73m<sup>2</sup>)**|Very high risk|Very high risk|Very high risk|


# Signs and Symptoms

CKD is often asymptomatic, however especially in later stages patients may have non-specific symptoms such as:

- Lethargy
- Anorexia
- Headaches
- Weight loss (or gain due to fluid overload)
- Nausea and vomiting
- Itching (uraemic pruritus)
- Shortness of breath (due to anaemia, pulmonary oedema, pleural effusion or acidosis)
- Muscle cramps, especially at night
- Bone pain (due to renal osteodystrophy)
- Taste changes
- Cognitive impairment
- Urinary symptoms: 
- Polyuria or oliguria may occur
- Nocturia
- Frothy urine (due to proteinuria)

Examination findings may include:

- Hypertension
- Pallor (due to anaemia)
- Abnormal fluid status
- Fluid overload with peripheral and/or pulmonary oedema
- Dehydration
- Cachexia
- Ammonia-like smelling breath due to uraemia
- Tachypnoea (due to anaemia, pulmonary oedema, pleural effusion or acidosis 
- Flank mass(es) may be palpable due to malignancy or renal cysts (e.g. in ADPKD)
- Patients on renal replacement therapy may have additional signs such as:
- Arteriovenous fistula (AVF)
- Peritoneal dialysis catheter
- Renal transplant scar (usually right iliac fossa)
- Parathyroidectomy scar may be present in patients requiring surgical management of secondary or tertiary hyperparathyroidism

# Differential Diagnosis

- **Acute kidney injury (AKI)** is the main differential 
	- It may be difficult to differentiate AKI from CKD based on investigations showing renal impairment at a single point in time 
	- To diagnose CKD markers of kidney damage or an eGFR of < 60mL/min/1.73m_ need to be present on two occasions at least 3 months apart
	- Abnormal kidneys on imaging (atrophy e.g. in chronic pyelonephritis, or enlarged kidneys e.g. in ADPKD) are indicative of CKD rather than AKI
	- Complications of CKD such as anaemia or secondary hyperparathyroidism may also be useful in differentiating the two
	- The two may co-exist if there is an acute insult causing AKI in a patient with pre-existing CKD (whether this is diagnosed or not)
- **False-positive low eGFR results** may occur due to high serum creatinine results, for example in patients with high muscle mass, or after consumption of meat
- **Urinary ACR** may also be high due to menstruation, strenuous exercise, orthostatic proteinuria or UTI

# Investigations

**Bedside tests:**

- **Urine dipstick** to screen for haematuria and proteinuria
- Urine positive for haematuria should be sent for **MC&S** to screen for infection
- Malignancy should also be considered in patients with persistent unexplained haematuria
- **Early morning albumin:creatinine ratio** should be done in all patients 
- If this is between 3 and 70 mg/mmol it should be repeated within 3 months for confirmation

**Blood tests:**

- **U&Es** for creatinine, eGFR, urea and electrolytes
- Patients should be advised not to eat meat 12 hours prior to the test
- If eGFR is < 60 mL/min/1.73m_, this should be repeated within 2 weeks
- If it remains low with no evidence of ongoing AKI, U&Es should be repeated in 3 months to diagnose CKD
- **Full blood count** looking for anaemia secondary to CKD, which is usually normochromic and normocytic
- **LFTs** may show a raised ALP due to bone disease; albumin may be low due to malnourishment or nephrotic syndrome
- **Bone profile** may show an abnormal calcium; phosphate is usually high
- **HbA1c** to screen for diabetes as a cause of CKD
- **Bicarbonate** may be low due to metabolic acidosis
- **Lipid profile** as dyslipidemia is common in CKD and is a modifiable risk factor for cardiovascular disease
- **Clotting screen** in case renal biopsy is required
- **Parathyroid hormone** often rises as renal function declines (secondary or tertiary hyperparathyroidism)
- **HIV and hepatitis B and C serology** especially in patients for whom renal replacement therapy is being considered
- **An autoimmune screen** may be sent if an underlying autoimmune condition is suspected
	- Antinuclear antibodies
	- ANCA antibodies
	- dsDNA antibodies
	- Anti-GBM antibodies
	- Serum complement 
- **Myeloma screen** i.e. immunoglobulins, protein electrophoresis and serum free light chains if this is suspected

**Imaging:**

- **Renal tract ultrasound** is not required in all patients, but should be offered to the following patients:
- Accelerated progression of CKD (sustained decrease in GFR of 15 ml/min/1.73m_ per year **or** 25% or more **and** a change in GFR category within 12 months)
- GFR < 30ml/min/1.73m_
- Patients planned for renal biopsy
- Suspected urinary tract obstruction
- Persistent or visible haematuria
- Family history of polycystic kidney disease
- Kidneys are usually atrophic in advanced CKD
- Large kidneys are seen in polycystic kidney disease and in the initial stages of diabetic nephropathy
- **CT KUB** is the most sensitive imaging modality if renal stones are suspected
- **CT or MRI angiography** may be indicated for suspected renal artery stenosis - **radionuclide scanning** is also an option

**Special tests:**

- **Renal biopsy** is not required in every case of CKD but may be indicated after initial investigations have been completed, for example if the cause of renal impairment is unclear, where there is rapid progression of CKD or where glomerulonephritis is suspected
- Important contraindications include active pyelonephritis, uncontrolled hypertension or coagulopathy; biopsying a patient with a single kidney should be avoided where possible due to the (very rare) risk that a nephrectomy may be required to treat complications

# Management

**Conservative management:**

- Patients with CKD are often managed in primary care, however the following should prompt referral to secondary care renal services:
	- End-stage renal disease
	- Rare or genetic cause for CKD known or suspected (e.g. ADPKD)
	- Suspected renal artery stenosis
	- Diagnostic uncertainty
	- Complications of CKD e.g. malnutrition, hyperkalaemia, anaemia, mineral and bone disorder, acidosis
	- Uncontrolled hypertension despite four antihypertensives
	- 5-year risk of needing RRT > 5% (see references for calculator)
	- Accelerated progression of CKD
	- Urinary ACR > 70 mg/mmol (or > 30 mg/mmol with persistent haematuria)
	- Patient with obstructive causes of CKD should be referred to urology
	- Individualised education on CKD including safety netting regarding complications and risk of AKI
- Some patients may require additional counselling e.g. genetic counselling and advice regarding screening family members in ADPKD
- Lifestyle advice should be provided, including:
	- Smoking cessation
	- Moderating alcohol intake
	- Maintaining a healthy weight with regular exercise
	- Maintaining a healthy diet
	- Avoid over-the-counter nephrotoxics e.g. NSAIDs, dietary supplements and herbal remedies
- Dietician input may be required for end-stage renal disease (e.g. reducing phosphate, salt and potassium intake)
- Regular monitoring of eGFR, urinary ACR and for any complications should be undertaken, more frequently in patients with more advanced CKD
- Patients may benefit from education and/or support groups 
- In the later stages, psychological support and/or access to specialist nurse input may be helpful
- Many patients with end-stage renal disease may not want or not be suitable for RRT - in these cases - conservative management is an important alternative (also referred to as "supportive care")

**Medical management:**

- Treat the underlying cause of CKD e.g. optimise diabetic control; specialist input for immunosuppressive treatments in autoimmune conditions
- Review medications and consider reducing or stopping nephrotoxic drugs (e.g. NSAIDs, diuretics)
- Treat hypertension with up to four antihypertensives 
- Aim for a target blood pressure of <140/90 if ACR is < 70 mg/mmol
- Aim for < 130/80 if ACR is > 70 mg/mmol
- Patients over 80 with type 1 diabetes should aim for < 150/90
- An ACE-inhibitor or angiotensin-receptor blocker (ARB) should be first line if ACR is > 30 mg/mmol (if less then manage as per usual hypertension guidelines)
- ACE-inhibitors or ARBs may be initiated in patients with diabetes and ACR > 3 mg/mmol in the absence of hypertension
- However these should be avoided in patients with a potassium of > 5 mmol/L 
- They should be stopped if potassium rises to > 6 mmol/L on treatment
- Consider starting a statin (usually atorvastatin 20mg) in all patients with CKD - the dose should be uptitrated to achieve effect lipid-lowering
- Consider an antiplatelet (e.g. aspirin) for secondary prevention of cardiovascular disease (balanced against bleeding risk)
- Sodium-glucose cotransporter-2 (SGLT-2) inhibitors may be considered in some patients on maximal ACE-inhibitor or ARB treatment who meet certain criteria (based on presence of type 2 diabetes, ACR and eGFR)
- Ensure patients are up to date with vaccinations:
- Annual influenza vaccine
- 5-yearly pneumococcal vaccine (PPV23)
- Covid vaccination as per national guidance
- Medical management is often required for complications of CKD - see "Complications" section for more details

**Surgical/interventional management:**

- Renal replacement therapy is covered in detail in another chapter
- Options include haemodialysis, peritoneal dialysis (which may be automated and mainly done overnight, or continuous and ambulatory) and renal transplant
- Patients should be referred for consideration of RRT ideally at least a year before this is anticipated to be required
- Indications include:
- eGFR approximately 5-7 ml/min/1.73m_
- Symptomatic uraemia affecting quality of life
- Refractory fluid overload
- Refractory biochemical abnormalities
- Various options exist for dialysis access which may require surgical formation (e.g. an arteriovenous fistula)
- Other surgical interventions may be required to treat complications of CKD, for example parathyroidectomy may be indicated in some patients with refractory hyperparathyroidism

# Complications

- **Anaemia** is often multifactorial, due to reduced erythropoietin production, iron deficiency and reduced red blood cell survival
	- Other contributing factors include B12 and folate deficiency, haemolysis due to dialysis and the underlying cause of CKD (e.g. myeloma, sickle cell disease)
	- Typically anaemia is normocytic and normochromic
	- Patients should be investigated if haemoglobin (Hb) is < 110 g/L or if symptomatic
	- If eGFR is > 60 ml/min/1.73m_, anaemia is unlikely to be due to CKD
	- Other investigations may be required to rule out other causes of anaemia (e.g. gastrointestinal bleeding, B12/folate deficiency)
	- All patients should be investigated for iron deficiency with percentage of hypochromic red blood cells being first-line (> 6% indicates functional iron deficiency)
	- Ferritin < 100 mcg/L is also indicative of iron deficiency
	- Iron supplementation may be either oral or IV (with IV usually preferred for patients on haemodialysis)
	- Ferritin should be monitored and iron supplements stopped before ferritin increases over 800 mcg/L
	- Once iron stores are replete, erythropoiesis-stimulating agent (ESA) treatment should be considered
	- These are usually given subcutaneously, with examples of ESAs including epoetin or darbepoetin
	- Roxadustat is a new oral alternative to ESAs which also acts to stimulate erythropoiesis (it is a hypoxia-inducible factor prolyl hydroxylase inhibitor)
	- Blood transfusion should be avoided, especially in patients who may require a renal transplant (due to the risk of allosensitization)
	- Target Hb is 100-120 g/L
- **Mineral and bone disorder (MBD)** occurs due to abnormal metabolism of phosphate, vitamin D, calcium and parathyroid hormone
	- There is a spectrum of disease that involves abnormal bone turnover and mineralisation as well as vascular and soft tissue calcification
	- Risk of CKD-MBD increases once eGFR is < 60 mL/min/1.73m_
	- Phosphate retention occurs due to renal dysfunction -> calcitriol (active form of vitamin D) is downregulated, and is also decreased due to reduced renal activation of vitamin D -> calcium falls -> PTH rises (secondary hyperparathyroidism) -> calcium is released from bone
	- Tertiary hyperparathyroidism may also occur if there is longstanding secondary hyperparathyroidism (both may be treated with parathyroidectomy)
	- "Renal osteodystrophy" refers to a range of bone abnormalities seen in CKD including bone resorption, osteosclerosis and osteopenia
	- There is an increased risk of fracture - bone density assessment (e.g. DEXA scanning) and bone protection should be considered
	- Patients with at least stage 3a CKD should be regularly monitored with serum calcium, phosphate and PTH levels 
	- Management involves normalising serum phosphate via dietary restriction of phosphate and phosphate binders (e.g. calcium carbonate, sevelamer)
	- Severe hyperparathyroidism may be treated with calcitriol and cinacalcet (a calcimimetic)
	- Vitamin D supplementation with ergocalciferol or cholecalciferol may be considered
	- Dialysis settings can be adjusted to remove excess phosphate and calcium
- **Cardiovascular risk** is significantly increased, including myocardial infarction, stroke, peripheral arterial disease and heart failure
	- There is a high prevalence of comorbid conditions increasing cardiovascular risk (e.g. hypertension, hypercholesterolaemia, diabetes)
	- Patients also have additional CKD-related risk factors, including vascular calcification due to CKD-MBD, uraemia, oxidative stress and anaemia
	- Dialysis further increases the risk of cardiovascular disease, including ischaemic heart disease, valvular disease and hypertensive cardiomyopathy
- **Uraemia** typically becomes symptomatic in patients with end-stage renal disease
	- Symptoms include nausea, vomiting, anorexia, taste disturbance, confusion, muscle cramps, pruritus and restless legs
	- Complications include pericarditis, neuropathy and encephalopathy
	- Symptomatic uraemia is an indication for renal replacement therapy
- **Hyperkalaemia** is a common issue in CKD due to impaired potassium excretion
	- Medications such as ACE-inhibitors and ARBs also contribute to hyperkalemia
	- Dietary intake of potassium should be limited
	- Medical treatment with potassium binders may be required (e.g. sodium zirconium cyclosilicate (Lokelma), calcium resonium or patiromer)
	- Treatments such as sodium bicarbonate (for metabolic acidosis) and diuretics (for fluid overload) may also help to reduce serum potassium
- **Metabolic acidosis** is common due to reduced renal acid excretion once eGFR < 50 ml/min/1.73m_
	- Chronic metabolic acidosis further increases kidney injury and fibrosis, bone demineralisation and muscle wasting and risk of cardiovascular events
	- Oral sodium bicarbonate should be considered for patients with an eGFR < 30 ml/min/1.73m_, or if serum bicarbonate is < 20 mmol/litre
- **Fluid overload** with both pulmonary and peripheral oedema may occur in the later stages of CKD
	- Fluid restriction may be advised
	- Diuretics may also be used, with loop diuretics (e.g. furosemide) being first-line in most cases
- **Malnutrition** is common, especially as CKD progresses
	- Uraemia may cause anorexia and taste disturbance
	- Low mood may also contribute to poor oral intake
	- Protein catabolism is promoted by acidosis and chronic inflammation
	- Patients should be regularly screened for malnutrition
	- Specialist renal dietician input should be offered for patients at risk of malnutrition
	- Oral nutritional supplements may be indicated in some cases (or less commonly enteral tube feeding or parenteral nutritional support) 
- **Acute kidney injury** - patients with CKD are at increased risk of AKI
	- Risk increases in patients with an eGFR of < 60 mL/min/1.73m_
	- There is also a risk of increased CKD progression with episodes of AKI
	- Triggers include intercurrent illness, especially with diarrhoea and vomiting, medications e.g. NSAIDs, antibiotics and urinary tract obstruction
- **Increased risk of malignancy** especially of renal and thyroid cancers
	- Immunosuppressive medications further increase malignancy risk (e.g. after renal transplant)
	- Chronic uraemia is also a contributing factor
- **Hypertension** both contributes to the development of CKD and is caused by CKD
	- Mechanisms include sodium dysregulation, upregulation of the renin angiotensin aldosterone system, and sympathetic nervous system hyperactivity
	- Regular monitoring of blood pressure and effective treatment is therefore key to minimising progression of CKD as well as other adverse cardiovascular events
- **Reduced quality of life**, especially in patients with more severe CKD
	- As with any chronic disease, depression and anxiety are common

# Prognosis

- Prognosis is dependent on the underlying cause of CKD, for example ADPKD tends to progress more rapidly than other diseases
- CKD is typically a progressive disease, although most patients die before reaching end-stage renal disease
- Approximately 2% of patients with CKD develop end-stage renal disease
- Progression can be slowed through modification of risk factors such as hypertension and proteinuria
- The leading cause of death in CKD is cardiovascular disease

# NICE Guidelines

[NICE CKS - Chronic Kidney Disease](https://cks.nice.org.uk/topics/chronic-kidney-disease/)

[NICE - Chronic kidney disease: assessment and management](https://www.nice.org.uk/guidance/ng203)

[NICE - Renal replacement therapy and conservative management](https://www.nice.org.uk/guidance/ng107)

[NICE technology appraisal - Roxadustat for treating symptomatic anaemia in chronic kidney disease](https://www.nice.org.uk/guidance/ta807/)

# References

[Patient UK - Chronic kidney disease](https://patient.info/doctor/chronic-kidney-disease-pro)

[Patient UK - Anaemia in chronic kidney disease](https://patient.info/doctor/anaemia-in-chronic-kidney-disease)

[UK Kidney Association eCKD guide](https://ukkidney.org/health-professionals/information-resources/uk-eckd-guide) 

[Kidney Failure Risk Equation]( https://www.kidneyfailurerisk.co.uk/)

[KDIGO CKD Evaluation and Management](https://kdigo.org/guidelines/ckd-evaluation-and-management/)

[KDIGO CKD Mineral and Bone Disorder guideline](https://kdigo.org/guidelines/ckd-mbd/)

[Radiopaedia - Renal osteodystrophy](https://radiopaedia.org/articles/renal-osteodystrophy?lang=gb)

[The Renal Association - Undernutrition in Chronic Kidney Disease Guideline](https://ukkidney.org/sites/renal.org/files/FINAL-Nutrition-guideline-June-2019-RNG-endorsed.pdf)

[NHS Kidney Care - Chronic Kidney
Disease in England: The Human and Financial Cost](https://www.england.nhs.uk/improvement-hub/wp-content/uploads/sites/44/2017/11/Chronic-Kidney-Disease-in-England-The-Human-and-Financial-Cost.pdf)
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Urinary tract infection
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Calcitriol is essential in managing hypocalcaemia, particularly in chronic kidney disease, by enhancing calcium absorption and reducing parathyroid hormone levels.
A 73-year-old man has presented to the GP with occasional palpitations. He has ischaemic heart disease, type 2 diabetes, and chronic kidney disease. Bloods reveal he is hypocalcaemic, with raised parathyroid hormone and phosphate and normal levels of vitamin D. ECG is unremarkable.

Which of the following is the most appropriate pharmacotherapy?
a