CKD Flashcards
Definition of CKD
Describes a chronic reduction in kidney function - tends to be permenant and progressive
Causes of CKD
Diabetes
Hypertension
Age-related decline
Glomerulonephritis
Polycystic kidney disease
Medications such as NSAIDS,
proton pump inhibitors and lithium
Risk factors for CKD
older age
Hypertension
Diabetes
Smoking
Use of medications that affect the kidneys
Presentation of CKD
Usually asyptomatic and diagnosed on routine testing - number of signs/ symptoms that suggest chronic kidney disease:
- Pruritus (itching)
- Loss of appetite
- Nausea
- Oedema
- Muscle cramps
- Peripheral neuropathy
- Pallor
- Hypertension
Investigations for CKD:
- eGFR - can be checked using U&Es (2 tests 3 months apart for diagnosis)
- Proteinuria - can be checked using urine albumin:creatinine ratio (ACR) (result of >=3mg/mmol is significant)
- Haematuria - can be checked using urine dipstick. significant result of 1+ for blood.
- Renal ultrasound - used to investigate ptx with accelerated CKD, haematuria, PCKD, or evidence of obstruction
2 methods of staging CKD:
G score (using eGFR)
A score (using ACR)
G- Score:
G1 = eGFR >90
G2 = eGFR 60-89
G3a = eGFR 45-59
G3b = eGFR 30-44
G4 = eGFR 15-29
G5 = eGFR <15 (known as “end-stage renal failure”)
A score:
ACR
A1 = < 3mg/mmol A2 = 3 – 30mg/mmol A3 = > 30mg/mmol
Diagnosis/ excluding CKD using the scores:
The patient does not have CKD if they have a score of A1 combined with G1 or G2. They need at least an eGFR of < 60 or proteinuria for a diagnosis of CKD.
Complications of CKD:
Anaemia
Renal bone disorder
Cardiovascular disease
Peripheral neuropathy
Dialysis related problems
When should you refer to specialist: (NICE)
eGFR <30
ACR >= 70mg/mmol
Accelerated progression - defined as disease in eGFR of 15 OR 25% OR 15ml/min in 1 year
Uncontrolled hypertension despite >=4 antihypertensives
Aims of management in CKD:
- Slowing progression
- Reducing the risk of cardiovascular disease
- Reducing the risk of complications
- Treating the complications
Management to slow the progression of CKD:
- optimise diabetic control
- optimise hypertensive control
- treat glomerulonephritis
Management to reduce risk of complications in CKD:
- exercise, maintain a healthy weight and smoking cessation
- Special dietary advice about:
- Phosphate, sodium, potassium, and water intake
- Offer atorvastatin 20mg for primary prevention of cardiovascular disease
Treating metabolic acidosis in CKD:
oral sodium bicarbonate
Treating anaemia in CKD:
Iron supplementation and erythropoietin
Treating renal bone disease in CKD:
vitamin D supplementation
Management options in end-stage renal failure:
Dialyisis
Transplant
Criteria for offering ACE inhibitors for patients with CKD:
Meet one of these criteria:
- Diabetes plus ACR > 3mg/mmol
- Hypertension plus ACR > 30mg/mmol
- All patients with ACR > 70mg/mmol
Blood pressure targets:
- <140/90
- or < 130/80 if ACR > 70mg/mmol
Monitoring serum potassium in CKD:
Needs to be monitored as both ACE inhibitors and CKD cause hyperkalaemia
Anaemia of CKD:
Healthy kidney cells produce erythropoietin (EPO).
- Which stimulates RBC production
Damage to kidney cells in CKD cause decreased EPO - therefore a drop in RBC production
Treatment of anaemia of CKD
Iron deficiency should be treated first if present (IV iron is usually preferred)
Exogenous erythropoietin
- Blood transfusions should be limited in transplant patients as they can sensitise the immune system - ‘allosensitisation’ so that transplanted organs are more likely to get rejected
3 main features of renal bone disease:
Oseteomalacia - (softening of bones)
Osteoporosis (brittle bones)
Osteosclerosis ( hardening of bones)
Why does osteomalacia take place in renal bone disease?
Occurs due to increased turnover of bones without adequate calcium supply
Why does osteosclerosis take place in renal bone disease:
Occurs when osteoblasts respond by increasing their activity to match the osteoclasts by creating new tissue in the bone
- however, due to low calcium level this new tissue is not properly mineralised
Osteoporosis in CKD
Can exist alongside renal bone disease because of compounding risk factors - such as use of steroids and age
Pathophysiology of renal bone disease:
High serum phosphate occurs due to reduced phosphate excrestion
- low active vitamin D because the kidney is essential in metabolising vitamin D into active form
Active vitamin D is essential in calcium absorption from the intestines and kidneys
- vitain D also regulates bone turnover
- SECONDARY HYPERPARATHYROIDISM:
- occurs because parathyroid glands react to the low serum calcium and high serum phosphate by excreting more PTH.
- This leads to increased osteoclast activity - which leads to the absorption of calcium from bone
XR changes in renal bone disease
Spine xray shows sclerosis of both ends of the vertebra (denser white) and osteomalacia in the centre of the vertebra (less white). This is classically known as “rugger jersey” spine after the stripes found on a rugby shirt.
Management of renal bone disease:
Active forms of vitamin D (alfacalcidol and calcitriol)
Low phosphate diet
Bisphosphonates can be used to treat osteoporosis
