Renal Flashcards
Define AKI
Acute reduction in renal function following an insult to the kidneys.
What are the pre-renal causes of an AKI?
Hypotension from sepsis or hypovolaemia from blood loss
Renal artery stenosis
What are the renal causes of an AKI?
(1) Vasculitis – affects the vessels
* Small vessel (microangiopathic) = HUS, TTP, DIC, GPA, eGPA
o HUS (E. coli toxin 0157; triad S/S: MAHA, thrombocytopenia, AKI)
o TTP (pentad S/S: MAHA, thrombocytopenia, AKI, neurological impairment, fever)
* Large vessel (obstructive) = renal artery/vein thrombosis/embolus
(2) Glomerulonephritis – affects the glomerulus (i.e. membranous, membranoproliferative, etc.)
* Most common in children -> minimal change disease -> 2/3 relapse; 1/3 complete recovery
* Most common in adults -> membranous glomerulonephritis
(3) ATN – affects the tubules (i.e. post-hypovolaemia, rhabdomyolysis)
(4) AIN / interstitial nephritis – affects the surrounding tissue; 4-7 days after exposure
* S/S: rash, fever, eosinophilia (± sterile pyuria, white cell casts), nephrotic syndrome
* Drugs = 75% (NSAIDs, penicillin, sulfa-drugs, PPIs, ciprofloxacin, allopurinol, furosemide)
* I.E. CAP treated with amoxicillin returns with fever, rash and arthralgia with rising creatinine
What are the post-renal causes of an AKI?
This is where there is an obstruction to the urine coming from the kidneys resulting in things ‘backing-up’ and affecting the normal renal function.
Classify as luminal, mural, extra-mural
Who is at an increased risk of AKI?
Risk factors for AKI include:
* chronic kidney disease
* other organ failure/chronic disease e.g. heart failure, liver disease, diabetes mellitus
* history of acute kidney injury
* use of drugs with nephrotoxic potential (e.g. NSAIDs, aminoglycosides, ACE inhibitors, angiotensin II receptor antagonists [ARBs] and diuretics) within the past week
* use of iodinated contrast agents within the past week
* age 65 years or over
* oliguria (urine output less than 0.5 ml/kg/hour)
* neurological or cognitive impairment or disability, which may mean limited access to fluids because of reliance on a carer
What are the symptoms and signs of a AKI?
- reduced urine output
- pulmonary and peripheral oedema
- arrhythmias (secondary to changes in potassium and acid-base balance)
- features of uraemia (for example, pericarditis or encephalopathy)
What ix results would be expected in an AKI?
Detect acute kidney injury, in line with the (p)RIFLE, AKIN or KDIGO definitions, by using any of the following criteria:
* a rise in serum creatinine of 26 micromol/litre or greater within 48 hours
* a 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days
* a fall in urine output to less than 0.5 ml/kg/hour for more than 6 hours in adults and more than
if patients have no identifiable cause for the deterioration or are at risk of urinary tract obstruction they should have a renal ultrasound within 24 hours of assessment.
How do we stage an AKI?
How should we manage an AKI?
Supportive
* Review medications
* Hyperkalaemia also needs prompt treatment to avoid arrhythmias which may potentially be life-threatening.
-Stabilisation of the cardiac membrane: 10ml 10% Intravenous calcium gluconate
-Short-term shift in potassium from extracellular to intracellular fluid compartment: Combined insulin/dextrose infusion or Nebulised salbutamol
-Removal of potassium from the body: Calcium resonium (orally or enema) or Loop diuretics or Dialysis
- Specialist input from a nephrologist is required for cases where the cause is not known or where the AKI is severe.
- All patients with suspected AKI secondary to urinary obstruction require prompt review by a urologist
What are the indications of dialysis?
- Refractory hyperkalaemia [K+ >6.5]
- Refractory fluid overload
- Metabolic acidosis [pH <7.1]
- Uraemic symptoms (encephalopathy, nausea, pruritis, malaise, pericarditis)
- CKD stage 5 (GFR <15mL/min) / often planning starts <20 and dialysis starts <12
What RRT is used on ITU?
haemofiltration (uses ultrafiltration and subsequent convection to remove solutes)
What is this?
Vascath (central venous catheter) for haemofiltration
What is the first line for RRT? What are the complications?
peritoneal dialysis (APD- automated peritoneal dialysis [done overnight by machine] or CAPD- Continuous ambulatory peritoneal dialysis [pt. operated in day])
Cx: infection (CoNS (S. epidermidis) > other gram +ve (S. aureus) > gram -ve)
Tenckhoff catheter
What is the second line for RRT? What are the complications
haemodialysis [1st line if IBD]; AV fistula made 4-6 weeks before HD commences
Before a fistula can be formed, you can use a Tesio line (a type of central line)
* Cx (AV fistula): thrombosis, stenosis, infection, bleeding, aneurysm, steal syndrome
* Cx (Tesio): sepsis, peritonitis, DIC, fluid overload, DDS
o DDS = Dialysis Disequilibrium Syndrome = cerebral oedema
AV fistula
What is this? Describe the entry points?
Tessio Line
Tesio line = central line to Internal Jugular and RA, tunnelled under skin and has 2 lumens entering skin
* Central line entry points:
o Internal jugular vein 2 lumens = Tesio line
o Subclavian vein 3 lumens = Swan-Gantz line
o Femoral vein
How is haemodialysis carried out?
3x/week, for 4 hours per session
Uses diffusion and oncotic pressures to remove excess solutes
What is the 3rd line of RRT?
Transplant
What is scar C?
Rutherford Morisson scar from renal transplant
What medication needs to be given with a transplant?
Immunosuppression mx = calcineurin inhibitors, anti-proliferative (MMF/azathioprine), steroids
What are the types of transplant rejection? What are the RFs? How should they be managed?
Rejection = immune-mediated organ dysfunction; mx: depends on type of rejection:
* Hyperacute (<24hrs) = ABs in recipient serum attack donor ABO/HLA; mx: explantation
o RFs: previous blood transfusion, previous transplant, multiple pregnancies
* Acute (<6m):
o Antibody-mediated (weeks-months) mx: IVIG, plasmapheresis, anti-CD20, anti-C5
o T-cell-mediated (weeks-months; most common) mx: steroids, OKT3, ATG
* Chronic (>6m) = unknown aetiology – mx: needs to go back on dialysis
What should be done in transplant failure?
organ fails to function (not immune-mediated); mx: dialyse patient and wait
What HLAs need to matched before transplanting?
DR > B > A
How do we estimate kidney function?
Serum creatinine may not provide an accurate estimate of renal function due to differences in muscle.
For this reason, formulas were developed to help estimate the glomerular filtration rate (estimated GFR or eGFR). The most commonly used formula is the Modification of Diet in Renal Disease (MDRD) equation, which uses the following variables:
* serum creatinine
* age
* gender
* ethnicity
Factors which may affect the result
pregnancy
muscle mass (e.g. amputees, body-builders)
eating red meat 12 hours prior to the sample being taken
How do we classify CKD?
When do we refer CKD to a nephrologist?
o In CKD, a referral (routine) to a nephrologist can take place if…
- eGFR <30mL/min/1.73m2
- eGFR decrease >25% or >15mL/min/1.73m2 in 12 months
What are the causes of CKD?
diabetic nephropathy
chronic glomerulonephritis
chronic pyelonephritis
hypertension
adult polycystic kidney disease
What is the presentation of CKD?
Chronic kidney disease is usually asymptomatic and is generally diagnosed following abnormal urea and electrolyte results. However, some patients with undetected late-stage disease may become symptomatic.
Possible features include:
oedema: e.g. ankle swelling, weight gain
polyuria
lethargy
pruritus (secondary to uraemia)
anorexia, which may result in weight loss
insomnia
nausea and vomiting
hypertension
What are the consequences of CKD?
What is the management of CKD?
Diet:
* Reduce dietary PO42-, Na+, K+, fluid restrict
* Avoid ETOH, too much tea/coffee, processed food, chocolate, bananas
PO4^-2 binders
* Aluminium-based binders (less commonly used)
* Calcium-based binders (SE: hypercalcaemia, vascular calcification)
* Sevelamar (non-calcium-based binder)
o More commonly used
o Binds to dietary phosphate and prevents absorption
o Reduces uric acid levels and improves lipid levels in those with CKD
Vitamin D: alfacalcidol, calcitriol
Parathyroidectomy (rarely)
What antihypertensives are used in CKD?
ACEi + Furosemide
With ACEi, NICE suggest that a decrease in eGFR of up to 25% or a rise in creatinine of up to 30% is acceptable, although any rise should prompt careful monitoring and exclusion of other causes (e.g. NSAIDs). A rise greater than this may indicate underlying renovascular disease.
How do we manage anaemia in CKD?
Management
the 2011 NICE guidelines suggest a target haemoglobin of 10 - 12 g/dl
determination and optimisation of iron status should be carried out prior to the administration of erythropoiesis-stimulating agents (ESA). Many patients, especially those on haemodialysis, will require IV iron
ESAs such as erythropoietin and darbepoetin should be used in those ‘who are likely to benefit in terms of quality of life and physical function’
Define anti-glomerular basement membrane disease
Anti-glomerular basement membrane (GBM) disease (previously known as Goodpasture’s syndrome) is a rare type of small-vessel vasculitis associated with both pulmonary haemorrhage and rapidly progressive glomerulonephritis
What serology would be expected in Anti-GBM disease?
It is caused by anti-glomerular basement membrane (anti-GBM) antibodies against type IV collagen
What serology would be expected in Anti-GBM disease?
It is caused by anti-glomerular basement membrane (anti-GBM) antibodies against type IV collagen
Who is Anti-GBM disease seen in?
Goodpasture’s syndrome is more common in men (sex ratio 2:1) and has a bimodal age distribution (peaks in 20-30 and 60-70 age bracket). It is associated with HLA DR2.
What is the presentation of anti-GBM disease?
Goodpasture’s syndrome is more common in men (sex ratio 2:1) and has a bimodal age distribution (peaks in 20-30 and 60-70 age bracket). It is associated with HLA DR2.
What is the presentation of anti-GBM disease?
- pulmonary haemorrhage
- rapidly progressive glomerulonephritis
- this typically results in a rapid onset acute kidney injury
- nephritis → proteinuria + haematuriaGoodpasture’s syndrome is more common in men (sex ratio 2:1) and has a bimodal age distribution (peaks in 20-30 and 60-70 age bracket). It is associated with HLA DR2.
What are the ix for Anti-GBM disease?
renal biopsy: linear IgG deposits along the basement membrane
raised transfer factor secondary to pulmonary haemorrhages
What is the management of anti-GBM disease?
plasma exchange (plasmapheresis)
steroids
cyclophosphamide
What increases the likelihood of pulmonary haemorrhage from anti-GBM disease?
One of the main complications is pulmonary haemorrhage. Factors that increase the likelihood of this include:
* smoking
* lower respiratory tract infection
* pulmonary oedema
* inhalation of hydrocarbons
* young males
Define Alport’s syndrome.
It is due to a defect in the gene which codes for type IV collagen resulting in an abnormal glomerular-basement membrane (GBM).
How is Alport’s syndrome inherited? Who is it worse in?
Alport’s syndrome is usually inherited in an X-linked dominant pattern*.
The disease is more severe in males with females rarely developing renal failure.
Why would an Alport’s patient have a failing renal transplant?
This may be caused by the presence of anti-GBM antibodies leading to a Goodpasture’s syndrome like picture.
How does alport’s syndrome present?
Alport’s syndrome usually presents in childhood. The following features may be seen:
* microscopic haematuria
* progressive renal failure
* bilateral sensorineural deafness
* lenticonus: protrusion of the lens surface into the anterior chamber
* retinitis pigmentosa
* renal biopsy: splitting of lamina densa seen on electron microscopy
