Chronic Kidney Disease Flashcards
Causes of CKD
Diabetes
Hypertension
Age-related decline
Glomerulonephritis
Polycystic kidney disease
Medications such as NSAIDS, proton pump inhibitors and lithium
Risk factors of CKD
Older age
Hypertension
Diabetes
Smoking
Use of medications that affect the kidneys
Presentation of CKD
Usually chronic kidney disease is asymptomatic and diagnosed on routine testing. A number of signs and symptoms might suggest chronic kidney disease:
Pruritus (itching)
Loss of appetite
Nausea
Oedema
Muscle cramps
Peripheral neuropathy
Pallor
Hypertension
Investigations of CKD
Estimated glomerular filtration rate (eGFR) can be checked using a U&E blood test. Two tests are required 3 months apart to confirm a diagnosis of chronic kidney disease.
Proteinuria can be checked using a urine albumin:creatinine ratio (ACR). A result of ≥ 3mg/mmol is significant.
Haematuria can be checked using a urine dipstick. A significant result is 1+ of blood. Haematuria should prompt investigation for malignancy (i.e. bladder cancer).
Renal ultrasound can be used to investigate patients with accelerated CKD, haematuria, family history of polycystic kidney disease or evidence of obstruction.
Staging of CKD
The G score is based on the eGFR:
G1 = eGFR at or above >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”)
The A score is based on the albumin:creatinine ratio:
A1 = < 3mg/mmol
A2 = 3 – 30mg/mmol
A3 = > 30mg/mmol
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 (decrease erythropoietin, decreased production of RBCs)
Renal bone disease (can lead to hypoparathyroidism - may lead to rugger jersey spine)
Cardiovascular disease
Peripheral neuropathy
Dialysis related problems
NICE suggest referral to a specialist when there is:
eGFR < 30
ACR ≥ 70 mg/mmol
Accelerated progression defined as a decrease in eGFR of 15 or 25% or 15 ml/min in 1 year
Uncontrolled hypertension despite ≥ 4 antihypertensives
Aims of management
Slow the progression of the disease
Reduce the risk of cardiovascular disease
Reduce the risk of complications
Treating complications
Slowing the progression of the disease may include?
Optimise diabetic control
Optimise hypertensive control
Treat glomerulonephritis
Reducing the risk of complications may include?
Exercise, maintain a healthy weight and stop smoking
Special dietary advice about phosphate, sodium, potassium and water intake
Offer atorvastatin 20mg for primary prevention of cardiovascular disease
Treating complications of CKD
Oral sodium bicarbonate to treat metabolic acidosis
Iron supplementation and erythropoietin to treat anaemia
Vitamin D to treat renal bone disease
Dialysis in end stage renal failure
Renal transplant in end stage renal failure
Treating Hypertension in CKD
ACE inhibitors are the first line in patients with chronic kidney disease. These are offered to all patients with:
Diabetes plus ACR > 3mg/mmol
Hypertension plus ACR > 30mg/mmol
All patients with ACR > 70mg/mmol
Aim to keep blood pressure <140/90 (or < 130/80 if ACR > 70mg/mmol).
Serum potassium needs to be monitored as chronic kidney disease and ACE inhibitors both cause hyperkalaemia.
Anaemia of Chronic Kidney Disease Pathophysiology
Healthy kidney cells produced erythropoietin. Erythropoietin is the hormone that stimulates production of red blood cells. Damaged kidney cells in CKD cause a drop in erythropoietin. Therefore there is a drop in red blood cells and a subsequent anaemia.
Anaemia can be treated with erythropoiesis stimulating agents such as exogenous erythropoeitin. Blood transfusions should be limited as they can sensitise the immune system (“allosensitisation”) so that transplanted organs are more likely to be rejected.
Iron deficiency should be treated before offering erythropoetin. Intravenous iron is usually given, particularly in dialysis patients. Oral iron is an alternative.
Renal Bone Disease in CKD is known as?
chronic kidney disease-mineral and bone disorder (CKD-MBD).
Features of CKD-MBD?
Osteomalacia (softening of bones)
Osteoporosis (brittle bones)
Osteosclerosis (hardening of bones)
Xray Changes of CKD-MBD?
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.
Pathophysiology of CKD-MBD
High serum phosphate occurs due to reduced phosphate excretion. Low active vitamin D because the kidney is essential in metabolising vitamin D to its active form. Active vitamin D is essential in calcium absorption from the intestines and kidneys. Vitamin D also regulates bone turnover.
Secondary hyperparathyroidism occurs because the parathyroid glands react to the low serum calcium and high serum phosphate by excreting more parathyroid hormone. This leads to increased osteoclast activity. Osteoclast activity lead to the absorption of calcium from bone.
Osteomalacia occurs due to increased turnover of bones without adequate calcium supply.
Osteosclerosis occurs when the osteoblasts respond by increasing their activity to match the osteoclasts by creating new tissue in the bone, however due to the low calcium level this new tissue is not properly mineralised.
Osteoporosis can exist alongside the renal bone disease due to other risk factors such as age and use of steroids.
Management of CKD-MBD involves a combination of:
Active forms of vitamin D (alfacalcidol and calcitriol)
Low phosphate diet
Bisphosphonates can be used to treat osteoporosis
Definition of CKD?
Reduction in kidney function for 3 or more months
eGFR <60
or
ACR >3 (urine albumin to creatinine ratio) also known as microalbumin
Peritoneal dialysis
Peritoneal membrane is filtering membrane
Dialysis solution added to peritoneal cavity (contains dextrose)
Continuous ambulatory peritoneal dialysis
- No machine, dialysis solution in peritoneum all times
Automated Dialysis
- Machine carries out dialysis over night (8-10hrs)
Haemodialysis
Various regimes
Can be hospital or at home
Blood filtered by a haemodialysis machine
Requires an A-V fistula
Surgical operation with 1 to 4 month maturation period
Infections
Increased risks of blood cltos
STEAL syndrome
High output heart failure
