Renal Medicine Flashcards
What are some renal presenting complaints
dysonoea, swelling, tiredness, flank pain, Nausea+vomiting
Questions to ask for Dyspnoea
Exercise tolerance? Triggers? Relieving factors? Diurnal variation? Orthopnoea, PND? Associated symptoms?
Questions for leg swelling
Site, Severity, Onset, fluid intake
Qs for Nausea and Vomiting
triggers, relieving factors,
able to keep down food, frequency, associated
symptoms, bowel frequency
ENT Symptom questions
– nasal secretions, sinusitis,
epistaxis, haemoptysis, sore throat, visual
disturbances, hearing loss
Constitutional Symptoms Questions
– fever, joint pains,
muscle aches, weight changes, lethargy, night
sweats, pruritus
Lower Urinary Tract Symptoms
dysuria,
frequency, quantity of urine, colour of urine,
frothiness, haematuria
Questions for Flank Pain
– duration, radiation, associated
symptoms, intensity, aggravating/relieving factors
PMH
Previous AKI - previous hospitalisation / ITU
Requiring dialysis?
CKD stage (if known)
Cause of CKD/ESRF
Cardiovascular Risk factors – DM, HTN,
Hypercholesterolaemia
Recurrent Urinary Tract Infections
Childhood infections
Surgery
Cancer
Dx
What drug
Dose
Frequency
Route
Patient Adherence
Also ask about over the counter drugs / herbal
medicines ESPECIALLY NSAIDs
Fx
Renal disease
Cardiac disease
Diabetes
Hypertension
Genetic conditions
WHO Performance Status
0 Normal - Fully active without restriction
1 Restricted in physically strenuous activity but ambulatory and
able to carry out light work e.g., light house work, office work
2 Ambulatory and capable of all self-care but unable to carry
out any work activities. Up and about more than 50% of waking
hours
3 Capable of only limited self-care, confined to bed or chair
more than 50% of waking hours
4 Completely disabled. Cannot self-care. Totally confined to
bed or chair
5 Dead
What are the different types of tests to check Renal Function
Bloods, Urine, Imaging
Which are bloods relevant to renal function
FBC – Anaemia, infection, allergic reactions,
Haematinics – Iron/Folate/B12 deficiency
U&Es – Potassium, Urea, Creatinine, Bicarbonate
Bone profile – Calcium, Phosphate, PTH, Alkaline Phosphatase
CRP – Infection/Inflammation
HbA1c – Diabetic control
Which urine tests are relevant to renal function
Urine Dipstick – Infection (leukocytes, nitrites); Glomerular pathology (blood, protein)
Urine Protein:Creatinine Ratio – Quantifies the amount of all protein in the urine
Urine Albumin:Creatinine Ratio – Quantifies just albumin (good for diagnosing and monitoring diabetic
nephropathy)
Urine microscopy, culture and sensitivity
What imaging is relevant to renal function
US KUB – look for peri-nephric collection, size of kidneys, corticomedullary differentiation, hydronephrosis
Venous Blood Gases
Metabolic Alkalosis or Acidosis
Metabolic acidosis causes
GI losses
o Diarrhoea
o Vomiting
Renal losses
o Primary hyperaldosteronism
o Tubular transporter defects
o Diuretics
Intracellular shift
o Hypokalaemia
How do you work out anion gap
Can be useful to work out what could be causing the
acidosis
Anion Gap = Sodium - (Chloride + Bicarbonate)
[Na+] – ([Cl-] + [HCO3-])
Normal Anion gap is 8-12
Causes of High and Low Anion Gap?
Case 1 – a 26 year old female admitted with
overdose of multiple drugs and AKI stage 3
On air pH 7.28, pCO2 3.6, PO2 14.5, HCO3
13, Na 145, Chloride 107, Urea 31,
Creatinine 308, Potassium 5.9
Metabolic Acidosis with incomplete
respiratory compensation
Anion Gap = 145 – (107+13) = 25
She admits to taking 36 tablets of Aspirin
THEREFORE Acidosis related to
combination of Toxin and AKI
Case 2 – a 15 year old male, admitted with diabetic
ketoacidosis
On air pH 7.16, pCO2 3.0, PO2 13.3, HCO3
10, Na 131, Chloride 98, Urea 18, Creatinine
214, Potassium 5.3
Metabolic Acidosis with incomplete
respiratory compensation
Anion Gap = 131 – (98+10) = 23
Patient has high BM and ketones
THEREFORE Metabolic acidosis, with high
anion gap, due to diabetic ketoacidosis, with
AKI
Electrolyte and fluid Balance Topics (Not a Qs)
Hyper/HypoNatraemia (Hyper,hypo,euvolaemia) + Diabetes Insipidus + SIADH + Potassium Imbalances
Causes of HYPERnatraemia
Usually due to water deficit.
Causes cellular dehydration (osmotic drag).
Creates vascular shear stress (bleeding and
thrombosis)
Symptoms of hypernatraemia
thirst, apathy, irritability, weakness,
confusion, reduced consciousness, seizures, hyperreflexia,
spasticity & coma.
Causes of HyperNa in Hypovolaemia, Euvolaemia and Hypervolaemia
Hypovolaemic High Na
Renal free water losses (Osmotic diuresis [NG feed
etc], loop diuretics, intrinsic renal disease)
Non-Renal free water losses (Excess sweating, Burns,
Diarrhoea, Fistulas)
Euvolaemic High Na
Renal Losses (Diabetes Insipidus, Hypodipsia)
Extra-Renal Losses (Insensible, Respiratory losses)
Hypervolaemic High Na (Sodium Gains)
Primary hyperaldosteronism, Cushing’s Syndrome,
Hypertonic dialysis, Hypertonic Sodium Bicarbonate,
Sodium Chloride tablets
What is Diabetes insipidus + Symptoms
(differential = psychogenic polydipsia)
– dilute urine (Urine osmolality <300)
Can be Cranial or Nephrogenic
POLYDIPSIA AND POLYURIA
Causes of Diabetes Insipidus (Cranial DI)
Causes - Trauma/post-op, tumours, cerebral
sarcoid/TB, infection (meningitis/encephalitis), cerebral
vasculitis (SLE/Wegener’s)
Causes of Diabetes Insipidus (Nephrogenic DI)
Causes - Congenital, Drugs (lithium,
amphoterecin, demeclocycline), hypokalaemia,
hypercalcaemia, tubulointerstitial disease
Cranial DI vs Nephrogenic DI
Cranial = Impaired release of ADH.
Nephrogenic = Resistance to ADH
Treatment for HyperNa
Free Water
HypoNa symptoms?
Low Na causes decreased perception and gait disturbance,
yawning, nausea, reversible ataxia, headache, apathy,
confusion, seizures, coma.
What are some causes of HypoNa
Pseudohyponatraemia – occurs with high lipids, myeloma,
hyperglycaemia, uraemia etc.
What are some investigations for fluid imbalances?
– plasma osmolality (if normal or raised
then pseudohyponatraemia),
hypokalaemia/hypomagnesaemia potentiates ADH release,
Urine sodium (if <20 then non-renal salt losses, if >40 then
SIADH) (diuretics may confound), TSH and 9am cortisol,
Calcium, albumin, glucose, LFT, CT head or chest if
suspect SIADH.
Describe causes if Hypo,Hyper ,Euvolaemic HypoNa
Hypovolaemic Hyponatraemia
Renal loss [Urine Na+ >20mmol/L]
Diuretics (thiazides), Osmotic diuresis (glucose, urea in
recovering ATN), Addison’s disease (mineralocorticoid
deficiency)
Non-renal loss [Urine Na+ <20mmol/L]
Diarrhoea, Vomiting, Sweating, Third space losses
(burns, bowel obstruction, pancreatitis)
Treatment – give IV fluids (0.9% NaCl at 1-3ml/kg/hour)
Give K if necessary
Euvolaemic Hyponatraemia
Hypothyroidism, Primary polydipsia – (if urine
osmolality <100), Glucocorticoid deficiency – adrenal
insufficiency, SIADH
Hypervolaemia Hyponatraemia
CCF, Nephrotic syndrome, Liver cirrhosis
Treatment – fluid restrict and consider furosemide
Risk of correcting hyponatraemia quickly
Too rapid correction of chronic hyponatraemia leads to
central pontine/osmotic myelinosis. Aim to correct <12
mmol/L/day
What is SIADH and how do we diagnose?
Low serum osmolality
Inappropriately concentrated urine – Urine osmolality >100
Urine Na >20
Clinical euvolaemia
Not on diuretics
Diagnosis of elimination – normal renal, thyroid, adrenal
function
How is SIADH managed?
Management of SIADH – Fluid restrict <800ml/day. PO
sodium chloride, may give furosemide, Demeclocycline
induces diabetes insipidus (reversing ADH effect),
alternatively Tolvaptan
What is the treatment of ACUTE HypoNaWhat
Acute (tends to be iatrogenic, polydipsia, colonoscopy prep,
ecstasy)
If acute hyponatraemia (within 48 hours) and symptomatic
– Give 3% hypertonic saline IV boluses +/- Furosemide
What is the management of CHRONIC HypoNa
Chronic
If chronic (>48 hours) and symptomatic – hypertonic saline
boluses if having seizures. Otherwise isotonic saline and
furosemide – aim to correct 8mmol/L in 24 hours
If chronic and asymptomatic – water restriction, stop
offending drug, if dehydrated – restore volume, if
overloaded – Na and water restriction and diuretics
What are some causes of HyperK+?
CKD, K rich diet with CKD (dried fruit, potatoes,
oranges, tomatoes, avocados, nuts)
Drugs (ACEi/ARBs/Spironolactone/Amiloride/NSAIDs/
Heparin/ LMWH/Cyclosporin or calcineurin
inhibitors/High dose Trimethoprim/ Digoxin toxicity/Bblockers)
Hypoaldosteronism (T4RTA), Addison’s disease,
Acidosis, DKA (insulin deficiency), Rhabdomyolysis,
tumour lysis, Massive haemolysis, Succinylcholine use
Rarer – Hyperkalaemic periodic paralysis, Gordon’s
syndrome
Artifact Hyperkalaemia – haemolysis, leucocytosis,
thrombocytosis
What are some causes in HypoK+
Pseudohypokalaemia – acute leukaemia
Extra-renal losses - Inadequate PO intake, Gut
losses (vomiting, NG losses, secretory Diarrhoea,
laxatives, VIPoma, Zollinger-Ellison, Ileostomy,
enteric fistula)
Redistribution – Delirium tremens, beta agonists,
insulin, caffeine, theophylline, alpha-blockers
(Doxazosin), hypokalaemic periodic paralysis
(inherited or acquired from thyrotoxicosis – Asian
males)
Refeeding syndrome, alkalosis, vigorous exercise,
glue-sniffing (Toluene can cause Fanconi/RTA II
with renal potassium wasting)
Primary hyperaldosteronism (conn’s syndrome)
Cushing’s syndrome, Secondary
hyperaldosteronism (liver failure, heart failure,
nephritic syndrome),
Renal losses (diuretics, RTA, Tubulopathies -
Bartters/Liddles/Gittelmans), liquorice,
glucocorticoids, hypomagnesaemia.
How do hyperkalaemics present?
Often hypertensive with increased extra-cellular fluid
volume (renin often down-regulated by fluid overload)
What are treatments for for Hyper and Hypo K+
Treatment of hyperkalaemia involves:
1. Stabilizing the myocardium to prevent arrhythmias
10mls of 10% Calcium Gluconate over 5-10
minutes
2. Shifting potassium back into the intracellular space
IV fast acting insulin (actrapid)
10 units and IV glucose/dextrose 50% 50mls
Sodium Bicarbonate
500mls of 1.4% Sodium Bicarbonate
Only effective at driving Potassium intracellullarly
if the patient is acidotic
Salbutamol
5-10mg via nebulizer
3. Eliminating Potassium From the Body:
Calcium Resonium
15-45g orally or rectally, mixed with sorbitol or
lactulose
Frusemide
20-80mg depending on hydration status
Dialysis
If resistant to medical treatment
Hypo:
Replace magnesium
Oral K replacement
IV K replacement (Usually in 0.9% NaCl - avoid in
dextrose as induces further hypokalaemia)
What ECG changes do we see in K+ Imbalances?
Hyper:
Tented T waves
Prolonged QRS
Slurring of ST segment
Loss of P waves
Asystole
Hypo: Small T waves
U wave (after T)
Increased PR interval
What are risk factors for AKI?
Diabetes
CKD
IHD/CCF/CVD
Any major medical co-morbidity
Elderly >75
Sepsis
Medications – ACEi, ARBs, NSAIDs, Antibiotics
Causes of AKI
What are the investigations we can do for AKI?
gations in AKI
- URINE DIPSTICK is vital (look for abnormal protein and blood)
- Daily FBC, U&Es, LFTs, Bone profile, CRP – incl. serum bicarbonate (CK if rhabdomyolysis suspected)
- Urine PCR, Urine MC+S, USS KUB (to rule out obstruction)
- If blood and protein on urine dipstick – perform c-ANCA (PR3) + p-ANCA (MPO) too look for vasculitis, anti-GBM, ANA,
C3, C4 to look for lupus nephritis, serum immunoglobulins and electrophoresis to look for myeloma
- If suspected post-streptococcal GN – do Anti-Streptolysin O Titres
- In case of associated thrombocytopenia consider HUS/TTP/Disseminated Intravascular Coagulopathy, request
haemolysis screen - blood film, LDH, bilirubin, reticulocytes, haptoglobin, and call Renal SpR urgently.
- Check cryoglobulins if unexplained rash, peripheral neuropathy, hypocomplementaemia, known hepatitis C, history of
lymphoproliferative disorder, or +ve RhF.
How do we manage AKI?
Discontinue nephrotoxic agents if possible
Ensure volume status and perfusion pressure – If dehydrated give IV fluids, If overloaded give diuretics, aim for euvolaemia
Be aware of third space losses (patient may look overloaded but JVP & BP may be low indicating intravascular depletion)
Consider function haemodynamic monitoring with Central Venous Pressure (CVP) line/Arterial line
Monitor urine output and daily bloods (catheterise if necessary)
Avoid hyperglycaemia
Check for changes in drug dosing (antibiotic doses etc adjusted to renal function)
Treat underlying cause
Refer to specialist for consideration of renal replacement therapy
Consider ICU admission
Indications for Renal Replacement Therapy for AKI
Hyperkalaemia refractory to medical therapy
Metabolic acidosis refractory to medical therapy
Fluid overload refractory to diuretics (anuric)
Uraemic pericarditis
Uraemic encephalopathy – vomiting, confusion, drowsiness, reduced consciousness
Intoxications – ethylene glycol, methanol, salicylates, lithium
Nephrotic Syndrome Indicators
Oedema
Albumin <30
Urine PCR >350 (more than 3.5 grams of protein in 24 hours)
o Hypercholesteraemia
Complications of Nephrotic Syndrome
Higher risk of Infection
Venous thromboembolism
Progression of CKD
Hypertension
Hyperlipidaemia
What are causes of Nephrotic Syndrome
Minimal Change Disease – most common form of GN in children
Focal Segmental Glomerulosclerosis – Idiopathic or secondary to infection, malignancy, drugs etc.
Membranous Nephropathy – Idiopathic or secondary to infection, malignancy, drugs etc.
Membranoproliferative Glomerulonephritis (more commonly presents as nephritic syndrome)
Amyloidosis/Myeloma/Diabetes may have nephrotic range proteinuria but not necessarily other nephrotic features
Nephritic Syndrome Indicators
Presentation can vary in a combination of some or many of the following:
AKI (sometimes GFR can drop drastically)
On urine dipstick: blood +/- and/or protein+/- Mild to moderate oedema
Proteinura <3.5g/24 hours
Hypertension
Sometimes visible haematuria
Table Summary
How do you manage Glumeronephritis?
Supportive therapy
If suspect GN – discuss with Renal team
MDT approach depending on underlying diagnosis
ACEi/ARB for proteinuria
Control BP
Salt and water restriction if volume overloaded
Diuretics for fluid overload
If hypoalbuminaemic <20g/dl then higher risk for VTE – consider therapeutic LMWH
Statins for hypercholesterolaemia
Immunosuppressive therapy:
Specific to cause of GN – decided by Renal team (+/- Respiratory / Rheumatology teams if lung or systemic
involvement )
Oral Corticosteroids, IV pulsed methylprednisolone, Cyclophosphamide, Tacrolimus, Ciclosporin, Rituximab, MMF,
Azathioprine
Invasive therapy
Renal replacement therapy/haemodialysis for those in severe AKI or ESRF
Plasma exchange for AAV (with lung involvement), anti-GBM
What is CKD
CKD is defined as the presence of kidney damage,
manifested by abnormal albumin excretion or decreased
kidney function, quantified by measured or estimated GFR
that persists for more than three months.
What are some causes of CKD
Diabetes
* Hypertension
* Glomerulonephritis
* Renovascular Disease
* Polycystic Kidney disease
* Obstructive nephropathy – urological problems
* Chronic/recurrent Pyelonephritis
* Others
What are some complications of CKD
Anaemia of Chronic Kidney Disease
* Chronic Kidney Disease – Mineral & Bone Disease
* Secondary & Tertiary Hyperparathyroidism
* Hypertension
* Cardiovascular Disease – No 1 cause of Mortality
* Malnutrition/sarcopenia
* Dyslipidaemia
* As CKD progresses
* Electrolyte disturbances
* Fluid overload
* Metabolic acidosis
* Uraemic pericarditis
* Uraemic encephalopathy
What is the management for CKD?
Treat underlying disease
Treat and monitor diabetic control
Treat hypertension
Treat infections promptly
Tolvaptan if meets criteria for ADPKD
How do we reduce the CV risk?
Start on statin
Control BP
Improve control of diabetes
Advise weight loss
Advise exercise
STOP SMOKING
How do we reduce progress of CKD
Reduce progression of CKD
Reduce proteinuria – ACEi/ARB
Monitor blood tests
Control BP
How do we prevent and treat complications of CKD
Prevent or treat complications of CKD
Dietary advice regarding low phosphate/low
potassium diet
Phosphate binders
IV Iron/Folate/Vit B12 replacement
EPO (Erythropoesis stimulating agent)
Replace Vitamin D deficiency
Consider Calcimimetics for tertiary
hyperparathyroidism
Dietician input
How do we plan for the future for CKD Patients?
Plan for the future
Start discussions of what options they have if they
reach ESRF
Home care team input
Discuss disadvantages & advantages of types of
RRT
o Home therapies – APD, CAPD, Home HD
o Unit-based therapies – Nocturnal HD,
conventional HD
o Active conservative management
o Transplant
Refer for fistula
o Venous mapping
Refer for PD tube insertion
Work-up for transplant
o Further tests
o Refer to Transplant work-up clinic
How do we diagnose Diabetic Nephropathy?
Diagnosis – most diabetic patients will undergo screening for
diabetic nephropathy
Raised Urine Albumin: Creatinine Ratio/PCR
Evidence of long-standing/poorly controlled DM
Evidence of other microvascular disease
How do we treat Diabetic Nephropathy?
Treatment
ACEi/ARB to reduce proteinuria
Anti-hypertensives for BP control
Cardiovascular risk modification
Continue other screens for microvascular
complications – eye checks and foot checks
What is hypertensive nephropathy?
Chronic raised BP causing nephrosclerosis.
Often difficult to tell if advanced renal disease at presentation
whether HTN caused the renal impairment or renal
impairment caused secondary HTN
Investigations to identify if primary or secondary HTN (based
on clinical findings and index of suspicion):
24 hour Urinary metanephrines
(Phaeochromocytoma)
Aldosterone: Renin ratio (Primary aldosteronism)
Cortisol & Dexamethasone suppression test
(Cushing’s syndrome)
TSH (hyperthyroidism)
MRA (Renal artery stenosis)
Treated with Hypertensives
What is polycystic Kidney Disease?
2 Types (both are autosomal dominant)
Type 1 (85%; PKD1 mutation on Chromosome 16)
Type 2 (15%; PKD2 mutation on Chromosome 4)
Symptoms can be related to the size of the kidney, infection
of the cysts (flank pain, haematuria, and fever) or can be
asymptomatic
Diagnosis
Family history is KEY
USS
Treatment
Control BP
As per CKD management
Tolvaptan (Vasopression receptor-2 antagonist) is
available for some patients to slow progression of
CKD.
Genetic counselling and testing
What is Anaemic of Chronic Kidney Disease? Refer to MEH
Many factors contribute to Anaemia in CKD
Decreased production of erythropoietin from the
kidney
Absolute iron deficiency (poor absorption and
malnutrition)
Functional iron deficiency (inflammation, infection)
Blood loss
Shortened Red Blood Cell survival
Bone marrow suppression from uraemia
Medication induced
Deficiency of Vit B12 and folate
How do we manage AOCKD
Management of Anaemia of CKD
* Measure haematinics – Vitamin B12, Folate,
Ferritin, Iron, Transferrin Saturation, CHr
* If deficient in any of above – replace this first
* IV Iron may be better tolerated than PO
* Discuss with renal team regarding starting ESA
* Aim for Hb 100-120
What is CKD Mineral Bone Disease?
CKD- MBD can be diagnosed if a patient with CKD has
evidence of one or more of:
* Abnormalities of calcium, phosphate, alkaline
phosphatase, PTH or vitamin D metabolism
* Vascular and/or soft tissue calcification
* Abnormalities in bone turnover, metabolism, volume,
linear growth or strength
o Low turnover states
Adynamic bone disease
Osteomalacia
o High turnover states
Osteitis Fibrosa
CKD leads to …
CKD leads to
Increased Fibroblast Growth Factor-23
Increased Alkaline Phosphatase and PTH
Increase Phosphate
Decreased Serum Calcium
Decreased 1,25 – Vitamin D
As CKD develops, disturbances in the homeostatic pathways
lead to hypocalcaemia, hyperphosphataemia and Vitamin D
deficiency and the development of secondary
hyperparathyroidism
Advantages and Disadvantages of Peri Dialysis
Advantages
* Quality of life
* It is often an excellent first choice for patients
starting dialysis, particularly when they still have
some residual native renal function
* PD regimes are designed on a much more
individualised basis than patients on HD.
Disadvantages
* Patients need to be able to manage technical
aspects of dialysis
* Unsuitable in patients with stoma/previous surgery
* Risk of infection (PD peritonitis)
* Complications – drainage problems, malposition,
leaks, herniae, hydrothorax, long term use
associated with encapsulating peritoneal sclerosis
Distinguish between Automated PD, Continuous Ambulatory PD and Assisted PD
Automated PD
* Carried out with an automated cycler machine
performed at night.
* 10-12L usually exchanged, over 8-10 hours.
* Lifestyle advantages – Leaves the daytime free.
Continuous Ambulatory PD
* Usually consisting of 4-5 dialysis exchanges per
day (usually 2 litres each)
* Exchanges are performed at regular intervals
throughout the day, with a long overnight dwell.
Assisted Automated PD
Trained healthcare assistants visit the patient’s home to
help with setting up APD
HaemoDialysis Advantages vs Disadvantages
The dialysis machine pumps blood from the patient,
through disposable tubing, through a dialyser, or artificial
kidney, and back into the patient. Waste solute, salt and
excess fluid is removed from the blood as it passes through
the dialyser.
Advantages
* Efficient form of dialysis
* Unit-based – plenty of support from staff
Disadvantages/Complications
* Dialysis access needs to be secured
* Infection/Bacteraemia
* Haemodynamic instability
* Reactions to dialysers
* Haematomas/risk of bleeding
* Muscle cramps
* Anaemia due to clotted lines/Haemolysis
* AVF steal syndrome
* SVCO from central lines
What are the different ways of giving HD?
Home HD – offer training at home for more frequent HD
Nocturnal HD – Overnight slow, long HD
CRRT – continuous renal replacement therapy mainly used
in acute setting (ITU/HDU)
Transplant Advantages VS Disadvantages
Advantages
* Near normal lifestyle
* Better mortality/morbidity
Disadvantages
* Criteria to meet suitability to safely undergo
operation
* Compliance with medication lifelong
* Risk of rejection
* Risk of malignancies over time
* Risk of infection (on immunosuppression)
* Long waiting times for cadaveric organ
Active Conservative Management of ESRF
Decision made after discussion with patient and family
members – often after multiple clinic visits and after patient
is fully informed of risks & benefits of each mode of therapy
Evidence suggests that if
* Age >80 OR
* WHO performance score of 3 or more
…then RRT offers no survival benefit
Often these patients may be unsuitable for or choose to not
have invasive therapy such as PD/HD/Transplantation
Active Conservative Management of ESRF
* Symptom control to enhance quality of life
* Respect patients preferred place of care
* Advanced care plan
* MDT approach
* Support system for patient and family
Contraindications for kidney transplantation
Contraindications for kidney transplantation
* Active infection or malignancy
* Severe heart disease not suitable for correction
* Severe lung disease
* Reversible renal disease
* Uncontrolled substance abuse, psychiatric illness
* On-going treatment non-adherence
* Short life expectancy
Related VS Unrelated Donor
Living Related Donor Transplantation
* This is the best possible transplant as patients
have an elective procedure with a selected donor,
that might have a good compatibility
* Time to transplantation can happen in months
Living Unrelated Donor Transplantation
* 4 forms: a)live-donor paired exchange, b) livedonor/deceased-donor exchange, c)live-donor
chain, d)altruistic donation
* Usually have comparable outcomes to live-related
donors
* Time to transplantation can happen in months
Deceased Donor
Deceased Donor Transplantation
* Approximately 60% of the transplants in the UK
fall into this category
* Patients receive a kidney (or two from the same
donor) with little time for preparation, so transplant
protocols are important to keep updated regularly
* Time to transplantation happen in years
* Survival of kidney allograft and patients are
significantly low compared to live donor
transplantation.
What are the induction treatments to Renal Transplant
Induction treatment
* At the moment of transplantation potent
immunosuppressive drugs are used to create
tolerance of the graft
* With these therapies, hyperacute rejection is now
rarely seen
* These include methylprednisolone in combination
with any of the following: basiliximab and
thymoglobulin; less commonly used are
alentuzumab and rituximab.
What is the maintenance treatment for Renal Transplantation?
Maintenance treatment
* Treatment that will be used immediately after
transplantation and for long term to prevent acute
or chronic rejection
* Drugs commonly used are grouped as:
* Steroids: prednisolone (or prednisone)
Calcineurin inhibitors (CNI): tacrolimus,
cyclosporine, voclosporin
* Antimetabolite medications: mycophenolate,
azathioprine
* Rapamycin inhibitors: sirolimus and everolimus
* T-cell regulation: Belatacept and belimumab
Describe the long term care for transplant patients?
Long term care of the transplant patient
* For the firsts months, follow up happens several
times a month, after 6 months it happens less
often
* Monitor GFR, CNI levels, proteinuria, Ca,
phosphate and PTH, lipids and glucose
* Screen for infections (common and opportunistic)
* Vaccination (except live or live attenuated viral
vaccines)
* Monitor and control cardiovascular disease, bone
and mineral metabolism disease
* Screen for malignancies as patients are three
times more likely to have any cancer
* Annual skin checks for skin cancers
* Contraception is obligatory in the first year,
counsel about pregnancy one year after
* Mortality is related to: cardiovascular disease,
infections and malignancies
What are some complications of transplantation
Acute complications, within the first month are
usually related to surgery or infections
* When considering infections, the timeframe is
important
* <4 weeks: nosocomial infections or
related to donor
* 1 to 12 months: activation of latent
infections, relapsed, residual or
opportunistic infections, community
* >12 months: community acquired
* Important germs to consider: CMV, hepatitis B,
Herpes simplex virus, Varicella zoster, EBV, BK;
Aspergilllus, Pneumocystis jirovecii, Listeria,
Mycobacterium tuberculosis, Toxoplasma gondii
* Within the first year, some patients can develop
new-onset diabetes after transplant (NODAT);
important to remember personal risk factors and
new factors, such as medications and a new
gluconeogenic kidney.
* Because of the increased risk of malignancies
among transplant patients, it’s important to screen
for them, such as: skin, cervix, breast, prostate,
renal and urothelial, liver, colorectal, and
lymphoproliferative disease. This last one in
particular is common in patients with EBV.
Simultaneous Kidney Transplantation
Simultaneous kidney transplantation
* Liver-kidney: patients with liver failure or cirrhosis
and ESRF can be candidates for simultaneous
transplant
* Pancreas-kidney: selected patients with Type 1
diabetes mellitus. Can be done simultaneous or
sequential
* Patients with kidney transplant who progress into
ESRF can be re-transp
