Renal Flashcards
AAV
ANCA Associated Vasculitis
ACR
Albumin:Creatinine Ratio
ADPKD
Autosomal Dominant Polycystic Kidney Injury
APD
Automated Peritoneal Dialysis
ANA
Anti-Nucleic Antibody
ANCA
Anti-Neutrophilic Cytoplasm Antibody
ATN
Acute Tubular Necrosis
AVF
AterioVenous Fistula
CAPD
Continuous Ambulatory Peritoneal Dialysis
CKD
Chronic Kidney Disease
CMV
Cytomegalovirus
CNI
Calcineurin Inhibitors
CHr
Hypochormnic Red Cells
eGFR
Estimated Globerular Filtration Rate
ESA
Erythropoeitin Stimulating Agent
ESRF
End Stage Renal Failure
GN
GlomeruloNephritis
GPA
Glomerulomatous PolyAngitis
HUS
Haemolytic Uraemic Syndrome
MMF
Mycophenolate Mofetil
MPA
Microscopic PolyAngitis
NODAT
New-Onset Diabetes After Transplantation
PCR
Protein: Creatinine Ratio
PD
Peritoneal Dialysis
PND
Paroxysmal Nocturnal Dyspnoea
RRT
Renal Replacement Therapy
RPGN
Rapidly Progressive GlomeruloNephritis
RTA
Renal Tubular Acidosis
SIADH
Syndrome of Inappropriate Anti-Diuretic Hormone
SLE
Systemic Lupus Erythematosus
SVCO
Superior Vena Cava Obstruction
TIN
TubuloInterstital Nephritis
TTP
Thrombotic Thrombocytopenic Purpura
Features to ask out dyspnoea
Exercise tolerance Triggers Relieving factors Diurnal variation Orthopnoea PND Associated symptoms
Features to ask about leg swelling
Site
Severity
Time of onset
Amount of fluid intake
Features to ask about N+V
Triggers Relieving factors Able to keep down food Frequency Associated symptoms Bowel frequency
Features to ask about ENT symptoms
Nasal secretions Sinusitis Epistaxis Haemoptysis Sore throat Visual disturbances Hearing loss
Features to ask about constitutional symptoms
Fever Joint pains Muscle aches Weight changes Lethargy Night sweats Pruritus
Features to ask about lower urinary tract symptoms
Dysuria Frequency Quantity of urine Colour of urine Frothiness Haematuria
Features to ask about flank pain
Duration Radiation Associated symptoms Intensity Aggravating/relieving factors
Presenting complaints of renal history
Dyspnoea Leg swelling N+V Upper airway symptoms Constitutional symptoms Lower urinary tract symptoms Flank pain
Features of PMH of renal histroy
Previous AKI - hospitalisation, requiring dialysis CKD stage Cause of CKD/ESRD CVS risk factors - DM, HTN, Hypercholesterolaemia Recurrent UTIs Childhood infections Surgery Cancer
Types of haemodialysis lines
Perm-cath - tunelled under skin - long term Vas-cath - non-tunelled - short term
Signs of advanced renal disease
Brown nails
Discolouration of skin from uraemia
Under-nutrition leading to muscle wasting
Uraemic frost - urea from sweat crystallises on the skin
Hyper-reflexia, pericardial rub, GI ulceration and bleedin
How to calculate anion gap
[Na+] - ([Cl-] + [HCO3])
Normal anion gap
8-12
What does high anion gap mean
Acidosis caused by increased acid
Causes of high anion gap
Lactic acidosis - anaerobic exercise - sepsis - organ ischaemia Ketoacidosis - diabetic - alcohol abuse - starvation Toxins - ethylene glycol - methanol - isoniazid - aspirin - salicylate Renal failure
What causes a normal anion gap in acidosis
Reduced alkali
Causes of normal anion gap in acidosis
GI losses of HCO3 - vomiting - diarrhoea Renal losses of HCO3 - renal tubular acidosis - mineralocorticoid deficiency (Addison's) Toxins - ammonium chloride - acetazolamide
Causes of hypernatraemia
Usually water deficit
- cellular dehydration - osmotic drag
- vascular shear stress - bleeding and thrombosis
Symptoms of hypernatraemia
Thirst Apathy Irritability Weakness Confusion Reduced consciousness Seizures Hyperfreflexia Spasticity Coma
Causes of hypovolaemic high Na+
Renal free water losses - osmotic diuresis (NG feed) - loop diuretics - intrinsic renal disease Non-renal free water losses - excess sweating - burns - diarrhoea - fistulas
Causes of euvolaemic high Na+
Renal losses - diabetes insipidus - hypodipsia Extra-renal losses - insensible - respiratory losses
Causes of hypervolaemic high Na+
Primary hyperaldosteronism Cushing's syndrome Hypertonic dialysis Hypertonic sodium bicarbonate Sodium chloride tablets
Features of diabetes insipidus
Dilute urine - urine osmolatlity < 300
Polydipsia
Polyuria - not always hypernatraemic
Causes of cranial DI
Impaired release of ADH
- trauma/post op
- tumours
- cerebral sacroid/TB
- infections - meningitis/encephalitis
- cerebral vasculitis - SLE/Wegener’s
Causes of nephrogenic DI
Resistance to ADH
- congenital
- drugs - lithium, amphoterecin, demeclocycline
- hypokalaemia
- hypercalcaemia
- tubulointestinal disease
Treatment of hypernatraemia
Free water
Symptoms of hyponatraemia
Decreased perception and gait disturbance Yawning Nausea Reversible ataxia Headache Apathy Confusion Seizures Coma
Features of pseudohyponatraemia
Low plasma sodium (<135 mmol/L) due to increased plasma lipid and/or plasma protein concentration
Causes of hypovolaemic hyponatraemia
Renal loss - [Urine Na+ > 20 mmol/L]
- diuretics - thiazides
- osmotic diuresis - gluocse, urea in recovering ATN
- Addison’s disease - mineralocorticoid deficiency
Non-renal loss - [Urine Na+ < 20 mmol/L]
- diarrhoea
- vomiting
- sweating
- third space losses - burns, bowel obstruction, pancreatitis
Treatment of hypovolaemic hyponatraemia
IV fluids - 0.9% NaCl at 1-3 nl/kg/hour
Give K+ if necessary
Causes of euvolaemic hyponatraemia
Hypothyroidism
Primary polydipsia - urine osmolality < 100
Glucocorticoid deficiency - adrenal insufficiency, SIADH
Features of SIADH
Low serum osmolality
Inappropriately concentrated urine - urine osmolality > 100
Urine Na+ > 20
Clinical euvolaemia
Not on diuretics
Diagnosis of elimination - normal renal, thyroid and adrenal function
Management of SIADH
Fluid restrict < 800 ml/day
PO sodium chloride
May give furosemide
Demeclocycline induces DI - reversing ADH effect
Causes of hypervolaemic hyponatraemia
CCF
Nephrotic syndrome
Liver cirrhosis
Treatment of hypervolaemic hyponatraemia
Fluid restrict
Consider furosemide
Rate of correcting hyponatraemia
<12 mmol/L/day
- too rapid correction leads to central pontine/osmotic myelinosis
Treatment of hyponatraemia
Acute
- 3% hypertonic salive IV bolus +/- furosemide
Chronic
- hypertonic saline bolus if having seizures
- isotonic saline and furosemide
Asymptomatic
- water restriction
- stop offending drug
- restore volume if dehydrated
- Na+, water restriction and diuretics if overloaded
Causes of hyperkalaemia
CKD - rich diet with CKD - dried fruit, potatoes, oranges, tomatoes, avocados, nuts Drugs - ACEi - ARBs - Spironolactone - Amiloride - NSAIDs - Heparin - B-blockers Hypoaldosteronism Addison's disease Acidosis DKA Massive haemolysis Rhabdomyolysis
Features of hyporeninaemic hypoaldosteronism
Decreased angiotensin 2 production as well as intra-adrenal dysfunction
Hypertensive with increased extra-cellular fluid volume
- renin down-regulated by fluid overload
Causes of hyporeninaemic hypoaldosteronism
Diabetic nephropathy NSAIDs Ciclosporin Sickle cell Lupus nephritis
Treatment of hyporeninaemic hypoaldosteronism
Low K+ diet
Loop diuretic if overloaded
ECG changes of hyperkalaemia
Tented T waves Prolonged QRS Slurring of ST segment Loss of P waves Asystole
Treatment of hyperkalaemia
Stabilising myocardium - prevent arrhythmias
- 10mls of 10% calcium gluconate over 5-10 mins
Shifting K+ back to intracellular space
- 10 units fast acting insulin IV (actrapid) and IV glucose/dextrose 50% 50mls
- 500mls 1.4% sodium bicarbonate - if acidotic
- 5-10mg salbutamol via nebuliser
Eliminating K+ from body
- 15-45g oral or rectal Calcium Resonium - mixed with sorbitol or laculose
- 20-80mg Furosemide - depending on hydration status
- dialysis if resistant to medical treatment
Symptoms of hypokalaemia
Fatigue Constipation Proximal muscle weakness Paralysis Cardiac arrhythmias Worsened glucose control in diabetics Hypertension
Causes of hypokalaemia
Pseudohyokalaemia - acute leukaemia Extra-renal losses - inadequate PO intake - gut losses Redistribution - delirium tremens - beta agonists - insulin - caffeine - doxazosin Refeeding syndrome Primary hyperaldosteronism Cushing's syndrome Renal losses - diuretics - RTA - glucocorticoids - hypomagnesaemia
ECG changes in hypokalaemia
Small T waves
U wave
Increased PR interval
Treatment of hypokalaemia
Replace magnesium
Oral K replacement
IV K replacement - 0.9% NaCl
Risk factors for AKI
Diabetes CKD IHD / CCF Elderly > 75 Sepsis Medications - ACEi - ARBs - NSAIDs - Antibiotics
Stages of AKI
Stage 1 - 1.5-1.9 x baseline serum creatinine - or 26.5 μmol/L increase - urine output < 0.5ml/kg/hr for 6-12 hours Stage 2 - 2.0-2.9 x baseline serum creatinine - urine output < 0.5ml/kg/hr 12 hours Stage 3 - 3 x baseline serum creatinine - or 353.6 μmol/L increase - or initiation of renal replacement therapy - urine output < 0.3ml/kg/hr for > 24 hours - or anuria for > 12 hours
Prerenal causes of AKI
Hypovolaemia Decreased CO Decreased effective circulating volume - CCF - liver failure Impaired renal autoregulation - NSAIDs - ACEi/ARBs - Cycloporine
Postrenal causes of AKI
Bladder outlet obstruction
Bilateral pelvoureteral obstruction - unilateral obstruction of solitary functioning kidney
Intrinsic causes of AKI
Glomerular - acute glomerulonephritis Tubules and interstitium - ischaemia - sepsis - nephrotoxins Vascular - vasculitis - malignant hypertension - TTP-HUS
Nephrotoxins that can cause AKI
Exogenous - iodinated contrast - aminoglycosides - cisplatin - amphotericin B Endogenous - haemolysis - rhabdomyolysis - myeloma - intratubular crystals
Investigations in AKI
Urine dip - abnormal protein and blood
Daily bloods - FBC, U&Es, LFTs, bone profile, CRP
Urine - PCR, MC+S, USS KUB
Management of AKI
Discontinue nephrotoxic agents if possible
Ensure volume status and perfusion pressure
- if dehydrated give IV fluids
- if overloaded give diuretics
Be aware of 3rd space losses
- patient may look overloaded but JVP and BP low
Monitor urine output
Avoid hyperglycaemia
Treat underlying cause
Indications for renal replacement therapy in AKI
Resitant to medical therapy - hyperkalaemia - metabolic acidosis - fluid overload Uraemic pericarditis Uraemic encephalopahty Intoxications
Symptoms of uraemic encephalopathy
Vomiting
Confusion
Drowsiness
Reduced consciousness
Features of nephrotic syndrome
Oedema
Albumin < 30
Urine PCR > 350
Hypercholesteraemia
Complications of nephrotic syndrome
Higher risk of infection Venous thromboembolism Progression of CKD Hypertension Hyperlipidaemia
Causes of nephrotic syndrome
Minimal change disease - commonest form in children
Focal segmental glomerulosclerosis
Membranous nephropathy
Membranoproliferative glomerulonephritis - commonly presents as nephritic syndrome
Lupus nephritis
Presentation of nephritic syndrome
AKI Mild to moderate oedema Proteinuria < 3.5g/24hrs Hypertension Sometimes visible haematuria
Causes of nephritic syndrome
Post-infectious GN IgA nephropathy Small vessel vasculitis Anti-GBM disease Thin basement membrane disease Alport syndrome Lupus nephritis Membranoproliferative glomerulonephritis
Associations of post-infectious GN
Weeks after group A, B-haemolytic streptococci infections - 1-2 weeks post tonillitis/pharyngitis - 3-4 weeks post impetigo/cellulits Usually children 3-12 yrs Can lead to PRGN in some cases
Investigation findings of post-infectious GN
Postive anti-streptococcal antibodies
Low serum C3
Biopsy - immune complex deposition
- IgG, IgA, C3
Treatment for post-infectious GN
Usually self limiting
Supportive therapy
- ACEi/ARB for proteinuria and hypertension
- low sodium diet
Associations for IgA nephropathy
Episodic gross haematuria during or directly after URT and GI infections or strenuous exercise
Male > Female
2nd-3rd decade of life
Investigation findings for IgA nephropathy
Asymptomatic michrochaematuria with intermittent visible haematuria
Increase serum IgA
Normal C3 and C4
Biopsy
- mesangial immune complex depositis in glomeruli
Treatment for IgA nephropathy
Supportive therapy
- ACEi/ARB for proteinuria and hypertension
Types of small vessel vasculitis (ANCA associated)
Granulomatosis with polyangitis (GPA)
Microscopic polyangitis (MPA)
Eosinophilic granulmatosis with polyangitis (Churg-Stauss syndrome)
Associations with GPA
Pulmonary and nasopharyngeal involvement
- haemoptysis
- nasal ulcers / polyps
Investigation findings for GPA
c-ANCA (PR3)
Biopsy
- segmental necrotising GN
Associations for MPA
Usually only mild respiratory symptoms
Investigation findings for MPA
p-ANCA (MPO)
Biopsy
- segmental necrotising GN
Associations for eosinophilic granulomatosis with polyangitis
Patients have
- asthma
- allergic rhinitis
- purpura
- peripheral neuropathy
Investigation findings for eosinophilic granulomatosis with polyangitis
p-ANCA Bloods - eosinophilia Biopsy - segmental necrotising GN
Treatment for ANCA associated vasculitis
Immunosuppression
Associations for anti-GBM disease (Goodpasture syndrome)
Two peaks - 3rd and 7th decade
Antibodies against type IV collagen
- react with pulmonary basement membrane causing pulmonay haemorrhage
Can lead to PRGN
Investigation findings for anti-GBM disease
Anti-GBM antibodies
Pulmonary infiltrates on CXR
Biopsy
- linear deposition of IgG along basement membrane
Treatment for anti-GBM disease
Plasma exchange
Immunosuppression
Associations for thin basement membrane disease
Heriditary
Abnormalities of type IV collagen
Good prognosis
Investigations for thin basement membrane disease
Persistent microscopic haematuria
- possible intermittent visible haematuria
Biopsy
- diffuse thining of GBM
Treatment for thin basement membrane disease
Monitor renal function
Supportive treatment
Associations for Alport syndrome
X-linked - usually affects males
Mutation in gene coding for type V collagen
Associated with hearing loss and abnormalities of the eyes
Often leads to ESRF
Investigation findings for alport syndrome
Persistent microscopic haematuria with intermittent visible haematuria
Sensorineural hearing loss
Biospy
- splitting of GBM
- alternating thickening and thinning of GBM
Genetic studies - family history
Treatment for alport syndrome
Supportive treatment
Renal replacement therapy
Renal transplant
- can lead to development of anti-GBM sdisease
Associations for lupus nephritis
Complication of SLE
Can be nephrotic or nephritic
Investigation findings for lupus nephritis
ANA and anti-dsDNA postitive
Biopsy
- 6 different classes have different presentation
Treatment for lupus nephritis
Supportive therapy
Immunosuppressive therapy based on classification/presentation
Management of glomerulonephritis
Supportive - ACEi/ARB for proteinuria - control BP - salt and water restriction if fluid overloaded - diuretics for fluid overload - statins for hypercholesterolaemia Immunosuppressive - specific to cause - oral corticosteriods, IV pulsed methylprednisolone, tacrolimus, ciclosporin, reiuximab, MMF, azathioprine Invasive - RRT / haemodialysis - severe AKI or ESRF - plasma exchange for AAV and anti-GBM
Definition of CKD
Presence of kidney damage
- manifested by abnormal albumin excretion or decreased kidney function
- quantified by eGFR
- persists for more than 3 months
CKD classification
ACR categories - A1 = < 3 - A2 = 3-30 - A3 = > 30 GFR categories G1 = > 90 G2 = 60-89 G3a = 45-59 G3b = 30-44 G4 = 15-29 G5 = < 15 (kidney failure)
Causes of CKD
Diabetes Hypertension Glomerulonephritis Renovascular disease Polycystic kidney disease Obstructive nephropathy - urological problems Chronic/recurrent pyelonephritis
Complications of CKD
Anaemia of chronic kidney disease
Chronic kidney disease - mineral and bone disease
Secondary and tertiary hyperparathyroidism
Hypertension
CVS disease
Malnutrition/sarcopenia
Dyslipidaemia
Complications of advanced CKD
Electrolyte disturbances Fluid overload Metabolic acidosis Uraemic pericarditis Uraemic encephalopathy
Management of CKD
Treat underlying disease Reduced CVS risk - statin, control BP and diabetes, weight loss and exercise, stop smoking Reduce progression of CKD - reduce proteinuria - ACEi/ARB - monitor blood and BP Prevent complications - low phosphate/potassium diet - phosphate binders - IV iron/folate/vit B12 - EPO
Features of diabetic nephropathy
Type 1 or long duration type 2
Associated with other diabetic microvascular complications
- retinopathy
- peripheral neuropathy
Diagnosis of diabetic nephropathy
Most diabetic patients will undergo screening for diabetic nephropathy
- raised urine albumin:creatinine ratio
- evidence of long standing/poorly controlled DM
- evidence of other microvascular disease
Treatment of diabetic nephropathy
ACEi/ARB - reduce proteinuria
Anti-hypertensives - BP control
CVS risk modification
Screen for other microvascular complications
Features of hypertensive nephropathy
Chronic raised BP causing nephrosclerosis
- hard to tell if HTN caused renal impairment or renal impairment caused HTN
Investigations for hypertensive nephroapthy
24 hour urinary metanephrines - phaeochromocytoma
Aldosterone:renin ratio - primary aldosteronism
Cortisol and dexamethasone suppression test - Cushing’s syndrome
TSH - hyperthyroidism
MRA - renal artery stenosis
Features of polycystic kidney disease
2 types - autosomal dominant
- type 1 - PKD1 mutation on chromosone 16
- type 2 - PKD2 mutation on chromosone 4
Symptoms related to
- size of kidney
- infection of cysts - flank pain, haematuria, fever
- asymptomatic
Diagnosis of polycystic kidney disease
Family history
USS
Treatment of polycystic kidney disease
Control BP
Tolvaptan - vasopression recptor-2 antagonist
Genetic counselling and testing
Features contributing to anaemia of chronic kidney disease
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
Management of anaemia of CKD
Measure haematinics - vitamin B12, folate, ferritin, iron, transferrin saturation, CHr
Replacement of any deficiencies
Aim for Hb 100-120
Diagnosis of CKD mineral bone disease
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
- low turnover states
- adynamic bone disease
- osteomalacia
- high turnover states
- osteitis fibrosa
Featues of CKD MBD
Increased fibroblast growth factor 23 Increased alkaline phosphatase and PTH Increased phosphate Decreased serum calcium Decreased 1,25-vitamin D
Causes of tertiary hyperparathyriodism
PTH release continues despite raised serum calcium levels
- parathyroid gland nodular hyperplasia
- advanced CKD
Management of CKD MBD
Reduce occurrence/severity of renal bone disease
CVS morbidity and mortality caused by elevated serum levels of PTH and high phosphate levels and calcium overload
Features of peritoneal dialysis
Reliant on patients own peritoneal membrane
Solutes move from patients blood across peritoneal membrane, down concentration gradient
Osmotic gradient created by high concentration of glucose in dialysate fluid - removes water from patient
Advantages of peritoneal dialysis
Quality of life
Good when patients have some residual native renal function
Regimes designed on a more individual basis
Disadvantages of peritoneal dialysis
Patients need to be able to manage technical aspects of dialysis
Unsuitable in patients with stoma/previous surgery
Risk of infection
Complications of peritoneal dialysis
Drianage problems Malposition Leaks Herniae Hydrothorax Long term use -> encapsulating peritoneal sclerosis
Features of automated PD
Automated cycler machine performed at night
- 10-12L exchanged over 8-10 hours
Features of continuous ambulatory PD
4-5 dialysis exchanges per day - 2L each
Regular intervals throughout day with long overnight dwell
Advantages of haemodialysis
Efficient
Unit-based - plenty of support from staff
Disadvantages of haemodialysis
Less freedom - fixed days at haemodialysis unit
Food and fluid restrictions
Use of needles
Complications of haemodialysis
Infection/bacteraemia Haemodynamic instability Reaction to dialysers Haematomas Risk of bleeding Muscle cramps Anaemia - clotted lines AVF steal syndrome SCVO - central lines
Advantages of renal transplantation
Near normal lifestyle
Better mortality/morbidity
Disadvantages of renal transplantation
Criteria to meet suitability to safely undergo operatio Compliance with lifelong medication Risk of rejection Risk of malignancies over time Risk of infection - immunosuppression Long waiting times for cadaveric organ
Active conservative management
When RRT offers no survival benefit
- insuitable for or choose not to have invasive therapy
Considerations for active conservative management
Age > 08
WHO performance score of 3 or more
Features of active conservative management
Symptom control to enhance quality of life Respect patients preferred place of care Advanced care plan MDT approach Support for patient and family
Contraindications for kidney transplanation
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
Types of kidney transplant
Living related donor
Living unrelated donor
Cadaveric donor
Features of living related donor transplant
Best possible option
- elective procedure
- may have good compatibility
Time to transplantation - months
Features of living unrelated donor transplant
Comparable outcomes to live-related donors
Time to transplantation - months
Types of living unrelated donor transplant
Live-donor paired exchange
Live-donor/deceased-donor exchange
Live-donor change
Altruistic donation
Features of deceased donor transplant
60%
Little time for preparation
Time to transplantation - years
Survival of kidney allograft and patients are significantly low compared to live donor transplantation
Induction treatment for renal transplant
At the moment of transplantation - potent immunosuppression to create tolerance of the graft
- methylprenisolone
- basiliximab
- thymoglobulin
- alentuzumab
- rituximab
Maintenance treatment for renal transplant
Steroids - prednisolone Calcineurin inhibitors - tacrolimus - cyclosporine - voclosporin Antimetabolite medications - mycophenolate - azathioprine Rapamycin inhibitors - sirolimus - everolimus T-cell regulation - belatacept - belimumab
Long term care for renal transplant patient
Monitor GFR, CNI levels, proteinuria, Ca, phosphate, PTH, lipids and glucose
Screen for infections
Vaccination - except live or live attenuated viral vaccines
Monitor CVS disease, bone and mineral metabolism disease
Screen for malignancies
- 3x more likley to have cancer
- anunual skin checks
Contraception obligatory in 1st year
- counsel about pregnancy after
Causes of mortality for transplant patient
CVS disease
Infections
Malignancy
Acute complications of transplant
Surgical complications
Infection
- < 4 weeks - nosocomial infections or related to donor
- 1-12 months - activation of latent infections, relapsed, residual or opportunistic infections
- > 12 months - community aquired
Common pathogens in post transplant infection
CMV Hepatitis B HSV Varicella zoster EBV BK Aspergillus Listeria TB
Chronic complications post renal transplantation
New-Onset Diabetes After Transplant (NODAT)
Malignancy
Simultaneous kidney transplantation options
Liver-kidney - liver failure or cirrhosis and ESFR Pancreas-kidney - selected patients with type 1 DM - simultaneous or sequential Re-transplant - transplant patients who progress into ESRF
Examples of loop diuretics
Furosemide
Bumetanide
Torsemide
Main indications of loop diuretics
Fluid overload
Action of loop diuretics
Inhibits Na+K+Cl- transporter in Loop of Henle
Pharmacokinetics of loop diuretics
Metabolised - kidney and liver
Excreted - urine
Common side effects of loop diuretics
Hyponatraemia Hypokalaemia Diuresis Dehydration Alkalosis
Features of loop diuretics
Furosemide 40mg = Bumetanide 1mg
IV better absorbed if gut oedema present
Protein-bound = low volume of distribution
Examples of thiazide and thiazide-like diuretics
Bendroflumethiazide
Indapamide
Main indications of thiazide and thiazide-like diuretics
Hypertension
Fluid overload
Method of action of thiazide and thiazide-like diuretics
Inhibits NaCl channel in distal convoluted tubule
Pharmacokinetics of thiazide and thiazide-like diuretics
Metabolised - kidney
Excreted - urine
Common side effects of thiazide and thiazide-like diuretics
Hyponatraemia Hypokalaemia Dehydration Hypercalcaemia Hyperuricaemia Hypomagnesaemia Alkalosis
Examples of K-sparing diuretics
Aldosterone antagnosists
- spironolactone
Epithelial Na channel blockers
- amiloride
Main indications of K-sparing diuretics
K-losing tubulopathies
Hypertension
Heart failure
Method of action of K-sparing diuretics
Block epithelial Na channel
Antagonises the action of aldosterone at mineralocorticoid recptors
Common side effects of K-sparing diuretics
Hyperkalaemia
- caution when combined with ACEi/ARBs
Gynaecomastia
Examples of carbonic anhydrase inhibitors
Acetazolamide
Brinzolamide
Main indications of carbonic anhydrase inhibitors
Glaucoma
Benign intracranial hypertension
Method of action of carbonic anhydrase inhibitors
Inhibits carbonic anhydrase
- causes increased renal excretion of Na, K, HCO3 and H2O
Decreases production of aqueous humour
Common side effects of carbonic anhydrase inhibitors
Flushing
Metabolic acidosis
Agranulocytosis
Liver failure
Examples of corticosteriods
Prednisolone - PO
Hydrocortisone - IV, IM
Dexamethasone - PO, IV
Triamcinolone - IM
Main indications of corticosteriods
Supress inflammation, allergy and immune responses
Method of action of corticosteriods
Alters gene transcription
- anti-inflammatory
- immunosuppressive
- increased gluconeogenesis
- decreased glucose utilisation
- increased liver protein catabolism
Pharmacokinetics of corticosteriods
Metabolised - liver
Excreted - urine
Common side effects of corticosteriods
Adrenal suppression - courses > 3 weeks Hyperglycaemia Psychosis Insomnia Indigestion Mood swings
Long term side effects of corticosteriods
Diabetes Cataracts Glaucoma Peptic ulceration Susceptibility to infections Osteoporosis Muscle wasting Skin thinning Cushingoid appearance
Cautions of long term corticosteriods
Long-term course should not be withdrawn abruptly
Additional medication
- PPI - GORD
- Bisphosphonates - bone protection
