Chronic kidney disease describes a chronic reduction in kidney function. This reduction in kidney function tends to be permanent and progressive.
Causes
- Diabetes
- Hypertension
- Age-related decline
- Glomerulonephritis
- Polycystic kidney disease
- Medications such as NSAIDS, proton pump inhibitors and lithium
Risk factors
- Older age
- Hypertension
- Diabetes
- Smoking
- Use of medications that affect the kidneys
Presentation
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
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.
Stages
The G score is based on the eGFR:
- 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”)
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
- Anaemia
- Renal bone disease
- Cardiovascular disease
- Peripheral neuropathy
- Dialysis related problems
Referral to a Specialist
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
Management
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
- Optimise diabetic control
- Optimise hypertensive control
- Treat glomerulonephritis
Reducing the risk of complications
- 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
- 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
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
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
Renal bone disease is also known as chronic kidney disease-mineral and bone disorder (CKD-MBD).
Features
- Osteomalacia (softening of bones)
- Osteoporosis (brittle bones)
- Osteosclerosis (hardening of bones)
Xray Changes
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
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 involves a combination of:
- Active forms of vitamin D (alfacalcidol and calcitriol)
- Low phosphate diet
- Bisphosphonates can be used to treat osteoporosis
Last updated April 2019