CKD Flashcards

1
Q

What is CKD?

A

Chronic kidney disease describes a chronic reduction in kidney function. This reduction in kidney function tends to be permanent and progressive.

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2
Q

Causes?

A

Diabetes
Hypertension
Age-related decline
Glomerulonephritis
Polycystic kidney disease
Medications such as NSAIDS, proton pump inhibitors and lithium

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3
Q

Risk factors?

A

Older age
Hypertension
Diabetes
Smoking
Use of medications that affect the kidneys

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4
Q

Presentation

A

Pruritus (itching)
Loss of appetite
Nausea
Oedema
Muscle cramps
Peripheral neuropathy
Pallor
Hypertension

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5
Q

Investigations?

A

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.

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6
Q

Stages

A

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.

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7
Q

Complications

A

Anaemia
Renal bone disease
Cardiovascular disease
Peripheral neuropathy
Dialysis related problems

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8
Q

Referral to a Specialist?

A

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

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9
Q

Management

A

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

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10
Q

Treating complications

A

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

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11
Q

Treating Hypertension

A

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.

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12
Q

Anaemia of Chronic Kidney Disease

A

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.

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13
Q

Renal Bone Disease features and x-ray?

A

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.

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14
Q

Pathophysiology and management of renal bone disease?

A

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

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