Renal Flashcards
What is AKI?
An acute drop in kidney function
How do you diagnose AKI?
AKI is diagnosed by measuring the serum creatinine
Criteria for diagnosing AKI…
Rise in serum creatinine 26µmol/L or more in 48 hours or > or equal to 50% rise in creatinine over 7 days or fall in urine output to less than 0.5ml/kg/hour for more than 6 hours in adults (8 hours in children) or more than or equal to 25% fall in eGFR in children/young adults in 7 days
What are the stages of AKI?
Stage 1= increase in creatinine to 1.5-1.9x baseline or increase in creatinine by > or equal to 26.5
Or reduction in urine output to <0?5ml/kg/hour for more than or equal to 6 hours
Stage 2= Increase in creatinine to 2.0 to 2.9 times baseline, or
Reduction in urine output to <0.5 mL/kg/hour for ≥12 hours
Stage 3= Increase in creatinine to ≥ 3.0 times baseline, or
Increase in creatinine to ≥353.6 µmol/L or
Reduction in urine output to <0.3 mL/kg/hour for ≥24 hours, or
The initiation of kidney replacement therapy, or,
In patients <18 years, decrease in eGFR to <35 mL/min/1.73 m2
When would you refer to a nephrologist in terms of AKI?
Renal tranplant ITU patient with unknown cause of AKI Vasculitis/ glomerulonephritis/ tubulointerstitial nephritis/ myeloma AKI with no known cause Inadequate response to treatment Complications of AKI Stage 3 AKI (see guideline for details) CKD stage 4 or 5 Qualify for renal replacement hyperkalaemia / metabolic acidosis/ complications of uraemia/ fluid overload (pulmonary oedema)
What are the risk factors for AKI?
Chronic kidney disease Heart failure Diabetes Liver disease Older age (>65) Cognitive impairement NSAIDS/ACE-I Use of contrast medium
What are the causes of AKI?
They can be split into pre renal, renal and post renal
Pre renal= inadequate blood supply ie: dehydration, hypotension and heart failure
Renal= intrinsic disease in the kidney, leading to a reduced filtraton of blood, may be due to…
- glomerulonephritis
- interstitial nephritis
- acute tubular necrosis
Post renal….
- obstruction to the outflow
- kidney stones
- cancer in abdo or pelvis
- ureter or uretral strictures
- enlarged prostate/prostate cancer
What are the investigations for 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.
What is the management of 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
What are the complications of AKI?
Hyperkalaemia
Fluid overload, heart failure and pulmonary oedema
Metabolic acidosis
Uraemia (high urea) can lead to encephalopathy or pericarditis
What pain relief do you use for renal colic?
IM diclofenac 75mg
What is anaemia in CKD caused by?
What is the management of anaemia in CKD?
A variety of factors
the main one is reduced erythropoietin levels
Usually a normochromic normocytic anaemia
Becomes apparent when the eGFR <35ml/min
Causes of anaemia in renal failure;
- Reduced EPO
- Reduced erythropoeisis due to toxic effects of uraemia on bone marrow
- Reduced absorption of iron
- Anorexia/Nausea due to uraemia
- Reduced red cell survival (Especially in haemodialysis)
- Blood loss due to capillary fragility and poor platelet function
- Stress ulceration leading to chronic blood loss
Need to check iron levels before giving erythropoiesis stimulating agents, may require ferrous sulphate or IV iron if on haemodialysis before giving ESA
What is hyperkalaemia classified as?
Mild: 5.5-5.9
Moderate: 6-6.4
Severe: >6.5
What are the features of hyperkalaemia on ECG?
Peaked or tall tented T waves
Loss of P waves
Broad QRS
Sinusoidal wave patterns
How do you treat hyperkalaemia?
STABILISATION OF THE CARDIAC MEMBRANES (DOES NOT ACTUALLY DECREASE SERUM K+ LEVELS)= IV CALCIUM GLUCONATE
short term shift in K+ from ECF to ICF- combined insulin/ dextrose infusion, nebulised salbutamol
Removal of K+ from the body- Calcium resonium (Orally or enema), this actually removes K+ from the body
Loop diuretics
Dialysis
How can you differentiate between Acute tubular necrosis and acute interstitial nephritis?
Acute interstitial nephritis is an inflammatory process so there would be white cells in the urine, whereas acute tubular necrosis is not inflammatory so has no cellular compartment
How do you work out alcohol units?
ml x %
What are the causes for normal anion gap metabolic acidosis?
ABCD
A- addisons
B- bicarbonate loss
C- Chloride
D- drugs
What type of alkalosis is seen in vomiting?
Hypochloraemic, hypokalaemic metabolic alkalosis
What is the mainstay of treatment rhabdomyolysis?
Rapid IV fluid rehydration
What are the features of rhabdomyolysis?
AKI with disproportionally raised creatinine elevated CK Myoglobinuria Hypocalcaemia Elevated phosphate Hyperkalaemia Metabolic acidosis
Seizure/collapse/ectasy/crush injury/statins
What is the anticoagulation of choice in AKI/CKD?
warfarin
What are the causes of CKD?
Diabetes Hypertension Age related decline Glomerulonephritis Polycystic kidney disease NSAIDS, PPIs, lithium
What are the risk factors for CKD?
Older age Hypertension Diabetes Smoking NSAIDS PPIS lithium
What are the features of CKD?
Usually CKD is asymptomatic and diagnosed on routine testing, a number of signs and symptoms might suggest CKD…
Pruritus (itching) Loss of appetite Nausea Oedema Muscle cramps Peripheral neuropathy PallorHypertension
Whatbinvestigations do you do for CKD?
Estimated eGFR can be checked using a U and E blood test
Two eGFR tests 3 months apart can confirm the diagnosis of CKD
Proteinuria can be checked using a urine albumin: creatinine ratio
A result of > or equal to 3mg/mmol is significant
Haematuria can be checked using a urine dipstick
Renal ultrasound can be used to investigate patients with accelerated CKD, haematuria, FHx of PCKD or evidence of obstruction
What is needed for a diagnosis of CKD?
EGFR of <60 or proteinuria
What are the complications of CKD?
Anaemia Renal bone disease CVD Peripheral neuropathy Dialysis related problems
How do you treat the complications of CKD?
Iron supplements for the anaemia
Vit D for renal bone disease
Dialysis in end stage renal failure
Oral sodium bicarbonate to treat metabolic acidosis
How do you treat hypertension due to CKD?
ACE-I
Offered to all pts with;
Diabetes plus ACR >3mg/mmol
Hypertension plus ACR >30mg/mmol
All patients with ACR >70mg/mmol
Serum potassium also needs to be monitored as both CKD and ACE- I both cause hyperkalaemia
What are the features of renal bone disease?
Osteomalacia (softening of bones)
Osteoporosis (brittle bones)
Osteosclerosis (hardening of bones)
What is the pathophysiology behind renal bone disease?
High serum phosphate occurs due to reduced phosphate excretion
Low active vit D because the kidney is essential in metabolising vit D to its active form
Active vit D is essential in calcium absorption from the intestine and kidneys, vit D also regulates bone turnober
Secondary hyperparathyroidism occurs because the parathyroid glands react to low serum calcium and high serum phosphate by excreting more parathyroid hormone, this leads to an increased osteoclast activity
Osteoclast activity leads to absorption of calcium from bone.
What is the management of bone disease caused by CKD?
Active forms of vitamin D (alfacalcidol and calcitriol)
Low phosphate diet
Bisphosphonates can be used to treat osteoporosis
What are the indications for Acute dialysis?
AEIOU
A= acidosis
E= electrolyte abnormalities
I= intoxication
O= oedema (severe and unresponsive pulmonary oedema)
U= uraemia symptoms- seizures or reduced consciousness
What are the indications for long term dialysis?
End stage renal failure (CKD stage 5)
Any of the acute indications continuing long term
What are the complications relating to kidney transplant?
Complications relating to the transplant:
Transplant rejection (hyperacute, acute and chronic)
Transplant failure
Electrolyte imbalances
Complications related to immunosuppressants:
Ischaemic heart disease
Type 2 diabetes (steroids)
Infections are more likely and more severe
Unusual infections can occur (PCP, CMV, PJP and TB)
Non-Hodgkin lymphoma
Skin cancer (particularly squamous cell carcinoma)
What is 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.
What are the 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
What are the indications for long term dialysis?
End stage renal failure (CKD stage 5)
Any of the acute indications continuing long term
What are the options for dialysis?
Continuous Ambulatory Peritoneal Dialysis
Automated Peritoneal Dialysis
Haemodialysis
What is 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.
What is continous ambulatory peritonal 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.
What is 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.
What are the comolications 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.
What are the complications of A-V fistula?
Aneurysm Infection Thrombosis Stenosis STEAL syndrome High output heart failure
What are the main complications of tunnel cuffed catheter?
Infection an blood clots
What is 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.
How can a fistula cause 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.
What are the features of nephritic syndrome?
Haematuria means blood in the urine. This can be microscopic (not visible) or macroscopic (visible).
Oliguria means there is a significantly reduced urine output.
Proteinuria is protein in the urine. In nephritic syndrome, there is less than 3g / 24 hours. Any more and it starts being classified as nephrotic syndrome.
Fluid retention
What are the features of nephrotic syndrome?
Peripheral oedema
Proteinuria more than 3g / 24 hours
Serum albumin less than 25g / L
Hypercholesterolaemia
What is glomeruloscerosis?
Glomerulosclerosis is a term to describe the pathological process of scarring of the tissue in the glomerulus. It is not a diagnosis in itself and is more a term used to describe the damage and scarring done by other diagnoses. Glomerulosclerosis can be caused by any type of glomerulonephritis or obstructive uropathy (blockage of urine outflow), and by a specific disease called focal segmental glomerulosclerosis.
What are the specific types of glomerulonephritis?
Each disease listed has its own epidemiology, causes and treatments. It is easy to get overwhelmed and confused since they are very similar names. I would suggest not trying to learn every detail until you really understand the basics. If you understand the basics you will be ahead of most of your colleagues.
Minimal change disease Focal segmental glomerulosclerosis Membranous glomerulonephritis IgA nephropathy (AKA mesangioproliferative glomerulonephritis or Berger’s disease) Post streptococcal glomerulonephritis (AKA diffuse proliferative glomerulonephritis) Mesangiocapillary glomerulonephritis Rapidly progressive glomerulonephritis Goodpasture Syndrome
What are most types of glomerulonephritis treated with?
Immunosuppression (e.g. steroids)
Blood pressure control by blocking the renin-angiotensin system (i.e. ACE inhibitors or angiotensin-II receptor blockers)
Give examples of glomerulonephritis
IgA nephropathy
Membranous glomerulonephritis
Post streptococcal glomerulonephritis
Goodpasture
What are most type of g,omerulonephritis treated with?
Immunosuppression (e.g. steroids)
Blood pressure control by blocking the renin-angiotensin system (i.e. ACE inhibitors or angiotensin-II receptor blockers)
What is the most common cause of glomerular pathology and chronic kidney disease in the UK?
Diabetes nephropathy
The chronic high level of glucose passing through the glomerulus causes scarring, this is called glomerulosclerosis
Why is proteinuria a key feature of diabetic nephropathy?
Damage to the glomerulus allows protein to be filtered from blood to urine
How do you regularly screen for diabetic nephropathy?
Albumin: creatinine ratio
UEs
What is the management of diabetic nephropathy?
Optimising blood sugar levels and blood pressure
ACE-I are the trearment of choice in diabetes for blood pressure control, ace inhibitors should be started in patients with diabetic nephropathy even if they have normal blood pressure.
What is interstitial nephritis?
Interstitial nephritis is term to describe a situation where there is inflammation of the space between cells and tubules (the interstitium) within the kidney. This is different to glomerulonephritis, where there is inflammation around the glomerulus. There are two types of interstitial nephritis: acute interstitial nephritis and chronic tubulointerstitial nephritis.
How does acute interstital nephritis present?
What causes it?
What is the management?
Presents with AKI and hypertension
There is acute inflammation of the tubules and interstitium
It is usually caused by a hypersensitivity reaction to…
- drugs (NSAIDS or abx
- infection
Other features of a generalised hypersensitivity reaction can accompany the acute kidney injury…
Fever
Rash
Eosinophilia
Management involves treating the underlying cause, steroids have a role in reducing inflammaton and improving recovery
What is chronic tubulointerstitial nephritis?
Chronic tubulointerstitial nephritis involves chronic inflammation of the tubules and interstitium. It presents with chronic kidney disease.
It has a large number of underlying autoimmune, infectious, iatrogenic and granulomatous disease causes.
Management involves treating the underlying cause. Steroids have a role when guided by a specialist.
What is acute tubular necrosis?
Acute tubular necrosis is damage and death (necrosis) of the epithelial cells of the renal tubules. It is the most common cause of acute kidney injury. Damage to the kidney cells occurs due to ischaemia or toxins. The epithelial cells have the ability to regenerate making acute tubular necrosis reversible. It usually takes 7-21 days to recover.
What are the causes of acute tubular necrosis?
Ischaemia can occur secondary to hypoperfusion in:
Shock
Sepsis
Dehydration
Direct damage from toxins can occur due to:
Radiology contrast dye
Gentamycin
NSAIDs
What is found on urinalysis of acute tubular necrosis?
Muddy brown casts” found on urinalysis is a pathognomonic finding specific to acute tubular necrosis. There can also be renal tubular epithelial cells in the urine.
What is the management of acute tubular necrosis?
Treatment is the same as with other causes of an acute kidney injury:
Supportive management
IV fluids
Stop nephrotoxic medications
Treat complications
What is renal tubular acidosis?
Where there is a metabolic acidosis due to pathology in the tubules of the kidney
What is haemolytic uraemic syndrome (HUS)?
When there is thrombosis in small blood vessels throughout the body
HUS is triggered by a bacterial toxin called the shiga toxin
What is the classic triad of HUS?
Haemolytic anaemia
AKI
Low platelet count (thrombocytopenia)
What is the most common cause of HUS?
The most common cause is a toxin produced by the bacteria e. coli 0157 called the shiga toxin. Shigella also produces this toxin and can cause HUS. The use of antibiotics and anti-motility medications such as loperamide to treat the gastroenteritis increase the risk of developing HUS.
What is the pathophysiology of HUS?
The formation of blood clots consumes platelets, leading to thrombocytopenia. The blood clots within the small vessels chop up the red blood cells as they pass by (haemolysis), causing anaemia. The blood flow through the kidney is affected by the clots and damaged red blood cells, leading to acute kidney injury.
What is the presentation of HUS?
E. coli 0157 causes a brief gastroenteritis often with bloody diarrhoea.
Around 5 days after the diarrhoea the person will start displaying symptoms of HUS:
Reduced urine output Haematuria or dark brown urine Abdominal pain Lethargy and irritability Confusion Hypertension Bruising
What is the management of HUS?
HUS is a medical emergency and has up to 10% mortality. The condition is self limiting and supportive management is the mainstay of treatment:
Antihypertensives
Blood transfusions
Dialysis
70-80% of patients make a full recovery.
What is rhabdomyolysis?
Rhabdomyolysis is a condition where skeletal muscle tissue breaks down and releases breakdown products into the blood. This is usually triggered by an event that causes the muscle to break down, such as extreme underuse or overuse or a traumatic injury.
The muscle cells (myocytes) undergo cell death (apoptosis). The cell death results in muscle cells releasing:
Myoglobin (causing myoglobinurea)
Potassium
Phosphate
Creatine kinase
What is the most immediately dangerous breakdown product in AKI and why?
Potassium is the most immediately dangerous breakdown product, as hyperkalaemia can cause cardiac arrythmias that can potentially result in a cardiac arrest
How does rhabdomyolysis cause acute kidney injury?
These breakdown products are filtered by the kidney and cause injury to the kidney. Myoglobin in particular is toxic to the kidney in high concentrations. This results in acute kidney injury. The acute kidney injury causes the breakdown products to further accumulate in the blood.
What are the causes of rhabdomyolysis?
Anything that causes significant damage to muscle cells can cause rhabdomyolysis:
Prolonged immobility, particularly frail patients that fall and spend time on the floor before being found
Extremely rigorous exercise beyond the person’s fitness level (e.g. ultramaraton, triathalon, crossfit competition)
Crush injuries
Seizures
What are the signs and symptoms of rhabdomyolysis?
Muscle aches and pain Oedema Fatigue Confusion (particularly in elderly frail patients) Red-brown urine
What Ix would you do for rhabdomyolysis?
Creatine Kinase (CK) blood test is a key investigation in establishing the diagnosis. It will be in the thousands to hundreds of thousands of Units/L. CK typically rises until 12 hours, then remains elevated for 1-3 days, then falls gradually. A higher CK increases the risk of kidney injury.
Myoglobinurea is myoglobin in the urine. It gives urine a red-brown colour. This will cause a urine dipstick to be positive for blood.
Urea and electrolytes (U&E) blood tests for acute kidney injury and hyperkalaemia.
ECG is important in assessing the heart’s response to hyperkalaemia.
ECG is important in assessing the heart’s response to hyperkalaemia.
What is the management of rhabdomyolysis?
Suspect rhabdomyolysis in patients with trauma, crush injury, prolonged immobilisation or excessive exercise.
IV fluids are the mainstay of treatment. The aim is to rehydrate the patient and encourage filtration of the breakdown products.
Consider IV sodium bicarbonate. This aims to make the urine more alkaline (pH ≥ 6.5), reducing the toxicity of the myoglobin on the kidneys. The evidence on this is not clear and there is some debate about whether to use it.
Consider IV mannitol. This aims to increase the glomerular filtration rate to help flush the breakdown products and to reduce oedema surrounding muscles and nerves. Hypovolaemia should be corrected before giving mannitol. The evidence on this is not clear and there is some debate about whether to use it.
Treat complications, particularly hyperkalaemia. Hyperkalaemia can be immediately life threatening as it can cause arrhythmias (particularly ventricular fibrillation).
How do ACE- I damage the kidneys?
They inhibit efferent vasoconstricton leading to dilation of the arteriole
When renal perfusion is low (hypovolaemia) angiotension is needed to constrict the arteriole to maintain a good GFR therefore the ACE- I should be stopped
What are the causes of a raised anion gap?
KUSMAL
Ketoasis Uraemia Salicylate poisioning Methanol ingestion Aldehydes Lactic acidosis
What are the two causes of lactic acidosis?
Reduced perfusion of organs
Short bowel syndrome
What are the causes of a normal anion gap?
Diarrhoea
High output ileostomy
Adrenal insufficiency (addisons)
Renal tubular acidosis type 1 and 4
What are the causes of metabolic alkalosis?
Stems from either the retention of base or loss of acid
Loss of chloride; diarrhoea, vomiting, NG suction, diuretics, cystic fibrosis
