Renal Flashcards
Acute Kidney Injury
Acute kidney injury (AKI) is defined as an acute drop in kidney function. It is diagnosed by measuring the serum creatinine.
NICE criteria for AKI
Rise in creatinine of ≥ 25 micromol/L in 48 hours
Rise in creatinine of ≥ 50% in 7 days
Urine output of < 0.5ml/kg/hour for > 6 hours
Risk factors for AKI
Consider the possibility of an acute kidney injury in patients that are suffering with an acute illness such as infection or having a surgical operation. Risk factors that would predispose them to developing acute kidney injury include:
Chronic kidney disease
Heart failure
Diabetes
Liver disease
Older age (above 65 years)
Cognitive impairment
Nephrotoxic medications such as NSAIDS and ACE inhibitors
Use of a contrast medium such as during CT scans
Pre-renal causes of AKI
Pre-renal pathology is the most common cause of acute kidney injury. It is due to inadequate blood supply to kidneys reducing the filtration of blood. Inadequate blood supply may be due to:
Dehydration
Hypotension (shock)
Heart failure
Renal causes of AKI
This is where intrinsic disease in the kidney is leading to reduced filtration of blood. It may be due to:
Glomerulonephritis
Interstitial nephritis
Acute tubular necrosis
Post-renal causes of AKI
Post renal acute kidney injury is caused by obstruction to the outflow of urine from the kidney, causing back-pressure into the kidney and reduced kidney function. This is called an obstructive uropathy. Obstruction may be caused by:
Kidney stones
Masses such as cancer in the abdomen or pelvis
Ureter or uretral strictures
Enlarged prostate or prostate cancer
Investigating AKI
Urinalysis for protein, blood, leucocytes, nitrites and glucose.
Leucocytes and nitrites suggest infection
Protein and blood suggest acute nephritis (but can be positive in infection)
Glucose suggests diabetes
Ultrasound of the urinary tract is used to look for obstruction. It is not necessary if an alternative cause is found for the AKI.
Managing AKI
Prevention of acute kidney injury is important. This is achieved by avoiding nephrotoxic medications where possible and ensuring adequate fluid input in unwell patients, including IV fluids if they are not taking enough orally.
The first step to treating an acute kidney injury is to correct the underlying cause:
Fluid rehydration with IV fluids in pre-renal AKI
Stop nephrotoxic medications such as NSAIDS and antihypertensives that reduce the filtration pressure (i.e. ACE inhibitors)
Relieve obstruction in a post-renal AKI, for example insert a catheter for a patient in retention from an enlarged prostate
In a severe acute kidney injury or where there is doubt about the cause or complications, input from a renal specialist is required. They may need dialysis.
Complications of AKI
Hyperkalaemia
Fluid overload, heart failure and pulmonary oedema
Metabolic acidosis
Uraemia (high urea) can lead to encephalopathy or pericarditis
Chronic kidney disease
Chronic kidney disease describes a chronic reduction in kidney function. This reduction in kidney function tends to be permanent 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 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
Investigating 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.
Stages of CKD
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 of CKD
Anaemia
Renal bone disease
Cardiovascular disease
Peripheral neuropathy
Dialysis related problems
When to refer CKD
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
Managing CKD
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 in CDK
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 CKD
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 of renal bone disease
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.
Managing renal bone disease
Management involves a combination of:
Active forms of vitamin D (alfacalcidol and calcitriol)
Low phosphate diet
Bisphosphonates can be used to treat osteoporosis
Renal dialysis
Dialysis is a method for performing the filtration tasks of the kidneys artificially in patients with end stage renal failure or complications of renal failure. It involves removing excess fluid, solutes and waste products.
Indications for acute dialysis
The mnemonic is AEIOU can be used to remember the indications for acute dialysis in patients with a severe AKI:
A – Acidosis (severe and not responding to treatment)
E – Electrolyte abnormalities (severe and unresponsive hyperkalaemia)
I – Intoxication (overdose of certain medications)
O – Oedema (severe and unresponsive pulmonary oedema)
U – Uraemia symptoms such as seizures or reduced consciousness
Indications for long term dialysis
End stage renal failure (CKD stage 5)
Any of the acute indications continuing long term
Options for maintenance dialysis
There are three main options for dialysis in patients requiring it long term:
Continuous Ambulatory Peritoneal Dialysis
Automated Peritoneal Dialysis
Haemodialysis
The decision about which form to use is based on:
Patient preference
Lifestyle factors
Co-morbidities
Individual differences regarding risks
Peritoneal dialysis
Peritoneal dialysis uses the peritoneal membrane as the filtration membrane. A special dialysis solution containing dextrose is added to peritoneal cavity. Ultrafiltration occurs from the blood, across the peritoneal membrane, in to the dialysis solution. The dialysis solution is then replaced, taking away the waste products that have filtered out of the blood into the solution.
Peritoneal dialysis involves a Tenckhoff catheter. This is a plastic tube that is inserted into the peritoneal cavity with one end on the outside. It allows access to peritoneal cavity. This is used for inserting and removing the dialysis solution.
Continuous Ambulatory Peritoneal Dialysis
This is where the dialysis solution is in the peritoneum at all times. There are various regimes for changing the solution. One example is where 2 litres of fluid is inserted into the peritoneum and changed four times a day.
Automated Dialysis
This involves peritoneal dialysis occurring overnight. A machine continuously replaces dialysis fluid in the abdomen overnight to optimise ultrafiltration. It takes 8-10 hours.
Complications of peritoneal dialysis
Bacterial peritonitis. Infusions of glucose solution make the peritoneum a great place for bacterial growth. Bacterial infection is a common and potentially serious complication of peritoneal dialysis.
Peritoneal sclerosis involves thickening and scarring of the peritoneal membrane.
Ultrafiltration failure can develop. This occurs when the patient starts to absorb the dextrose in the filtration solution. This reduces the filtration gradient making ultrafiltration less effective. This becomes more prominent over time.
Weight gain can occur as they absorb the carbohydrates in the dextrose solution.
Psychosocial effects. There are huge social and psychological effects of having to change dialysis solution and sleep with a machine every night.
Haemodialysis
With haemodialysis, patients have their blood filtered by a haemodialysis machine. Regimes can vary but a typical regime might be 4 hours a day for 3 days a week.
They need good access to an abundant blood supply. The options for this are:
Tunnelled cuffed catheter
Arterio-venous fistula
Tunnelled Cuffed Catheter
A tunnelled cuffed catheter is a tube inserted into the subclavian or jugular vein with a tip that sits in the superior vena cava or right atrium. It has two lumens, one where blood exits the body (red) and one where blood enters the body (blue).
There is a ring called a “Dacron cuff” that surrounds of the catheter. It promotes healing and adhesion of tissue to the cuff, making the catheter more permanent and providing a barrier to bacterial infection. These can stay in long term and be used for regular haemodialysis.
The main complications are infection and blood clots within the catheter.
A-V Fistula
An A-V fistula is an artificial connection between an artery to a vein. It bypasses the capillary system and allows blood to flow under high pressure from the artery directly into the vein. This provides a permanent, large, easy access blood vessel with high pressure arterial blood flow. Creating an A-V fistula requires a surgical operation and a 4 week to 4 month maturation period without use.
They are typically formed between an artery and vein in the patient’s forearm:
Radio-cephalic
Brachio-cephalic
Brachio-basilic (less common and more complex operation)
Examining an A-V fistula
Skin integrity
Aneurysms
Palpable thrill (a fine vibration felt over the anastomosis)
Stereotypical “machinery murmur” on auscultation
A-V fistula complications
Aneurysm
Infection
Thrombosis
Stenosis
STEAL syndrome
High output heart failure
STEAL Syndrome
STEAL syndrome is where there is inadequate blood flow to the limb distal to the AV fistula. The AV fistula “steals” blood from the distal limb. The blood is diverted away from where is was supposed to supply and flows straight into the venous system. This causes distal ischaemia.
High output heart failure
Where there is an A-V fistula blood is flowing very quickly from the arterial to the venous system through the fistula. This means there is rapid return of blood to the heart. This increases the pre-load in the heart (how full the heart is before it pumps). This leads to hypertrophy of the heart muscle and heart failure.
TOM TIP: NEVER take blood from a fistula! This is a lifeline for the patient to allow them access to dialysis. If it gets damaged it will set them back and you will be in big trouble.
