Kidney disease 2 Flashcards
What is AKI?
“It is a clinical syndrome characterised by a rapid reduction in renal excretory function due to several different causes…”
AKI risk factors
AGE >65 Clinical Acutely unwell/ sepsis Hypovolemia (diarrhoea, vomiting, increased fluid loss or reduced intake Hypotensive Systolic Bp <100mmHg or more than 40mmHg less than baseline Co-morbidities Chronic kidney disease (CKD 3-5) Heart failure Diabetes mellitus Liver disease Atherosclerotic vascular disease Nephrotoxic drugs ACE/ ARB, NSAIDs, Diuretics, Contrast
AKI common drug causes
Inherent nephrotoxic potential Dose Duration of therapy Frequency Route of administration Previous exposure Drug interactions – additive effect if 2 nephrotoxic drugs are given together
How is AKI detected
Detection by any of the following:
A rise in serum creatinine of 26micromols/l or more within 48 hours
A 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days
A fall inurine output to less than 0.5ml/kg/hour for more than 6 hours in adults and more than 8 hours in children and young people
25% of greater fall in eGFR in children and young people within the past 7 days
AKI life threatening?
Clinical symptoms/signs
Can be life threatening – mortality in hospital ~50% if require dialysis
Frequently reversible and rapid recognition and treatment may preserve function
More common in older patients (esp 80-89 yr old) and those with CKD
Abrupt fall in glomerular filtration rate
Sustained rise in urea and creatinine
Potentially life threatening due to volume overload, hyperkalaemia and metabolic acidosis
Causes of AKI types and percentages
Pre-renal = reduced renal perfusion =85% Renal = 10% Post-renal = obstruction = 5%
functions of kidney
specific
filtration
regulation
Filtration - removal of nitrogen-containing waste products
Regulation - acid/base, blood volume, haemoglobin, electrolytes
Pre-renal causes of AKI
dehydration sepsis hypotension shock hepatorenal syndrome severe heart failure intra-abdominal hypertension/compartment syndrome
Renal causes of AKI
NSAIDS ACEi ARBs Gentamicin GN/vasculitis (GN=glomerulonephritis) contrast interstitial nephritis myeloma rhabdomyolosis
post-renal causes of AKI
prostrate enlargement
renal stones
pelvic cancer
Potential causes by drugs
SAD MAN
Sulphonylureas e.g. gliclazide ACE and ARB e.g. ramipril/losartan Diuretics e.g. furosemide Metformin Aldosterone antagonists e.g. spironolactone NSAID e.g. ibuprofen, naproxen
When to consider haemodialysis
Fluid overload-resistant High K (hyperkalaemia) > 6.5 with ECG changes or >7 mmol/l even with normal ECG-resistant Pericardial rub Uraemia/Encephalopathy Metabolic acidosis-resistant
Common nephrotoxic drugs
drugs of abuse - cocaine, herione etc statins - gemfibrozil antibiotics -aminoglycosides, ciprofloxacin, tetracycline, quinolones Heavy metals Chemotherapy Immunosuppresants
Renal replacement therapy
Dialysis
Haemodialysis
Peritoneal dialysis
Transplantation
Live donor
Cadaveric
Non-heartbeating
Dialysis
Diffusion of molecules in solution across a semi permeable membrane along an electrochemical concentration gradient.
Haemodialysis
Synthetic membrane
Peritoneal dialysis
Endogenous (peritoneum)
Management of ESRF with haemodialysis
advantage of HD
disadvantages
advantages
-good removal of electrolytes
Disadvantages anaemia hypotension anaphylactic reaction to filter air embolism access surgically introduced cost clotting and blocked lines infections cramps pain - chest and back pruiritis dysrhythmia
How to deal with hypotension associated with dialysis and what is the cause
Cause: Too much fluid is being removed too quickly
Bolus of NaCl 0.9%
Omit blood pressure medicines
reduce rate of fluid removal
how to deal with cramps associated with dialysis and what is the cause
Caused by hypotension and fluid removal
Give:
IV fluid
Quinine tablets
Re-assess weight
Cause of chest and back pain associated with dialysis and how to treat
Complement activation
Inducement of angina
Treatment:
More biocompatible dialysiser
Paracetamol
Advantages of PD (Peritoneal dialysis)
- Fluid balance less tight
- renal function declines less rapidly
Disadvantages of PD
Complications (long-term)
Constipation Infections Pleural effusions Scelorising peritonitis diabetes electrolyte removal not as good as with HD
Long term complications: CVD, sepsis
types of kidney transplant donor
cadaver
Living
Related
Matched unrelated
Non heart beating
Immunosuppressive agents used in kidney transplant
Induction Therapy given in transplant centres at time of transplant
Maintenance therapy taken daily may include a combination of
Ciclosporin or tacrolimus +/- prednisolone
Ciclosporin or tacrolimus +/- prednisolone +/- mycophenolate or azathioprine
prednisolone +/- mycophenolate or azathioprine
Sirolimus
Aggressive treatment for rejection given in hospital methylprednisolone, ATG
Plasma exchange
Rituximab
Ciclosporin
Tacrolimus
Sirolimus
Monitoring
Therapeutic changes
Cautions
Immunosuppressants
Require therapeutic drug monitoring as narrow therapeutic range
The therapeutic range changes over time since transplant
Caution with drug interactions
Caution with different brands (should be brand prescribing even for “generics”)
Drugs that increase ciclosporin/tacrolimus levels
- Amiodarone
- Erythromycin
- Clarithromycin
- Ketoconazole
- Fluconazole
- Diltiazem
- Nifedipine
- Progestogens
Drugs that decrease ciclosporin/tacrolimus levels
Rifampicin Carbamazipine Phenytoin Phenobarbitone St John's Wort
Management of common CKD complications
reduce gastric acidity with ranitidine or PPIs eg omeprazole
vitamin supplementation (Vit C, Vit Bs) caution with vitamin A accumulation
Quinine/ clonazepam for restless legs syndrome
Constipation due to fluid restriction
hyperlipidaemia: treating is controversial as currently less evidence than in general population
Antiplatelet therapy vs risk of bleeding
Effect on bioavailability
GI absorption is decreased in patients with ureamia
GI symptoms are common eg nausea
small bowel absorptive function is decreased
first pass metabolism is altered
systemic concentration may be increased or decreased.
Effects of kidneys on distribution
Apparent volume of distribution (Vd) of drugs is affected by renal insufficiency
oedema and ascities increase the Vd of highly water soluble drugs or protein bound drugs resulting in lower plasma concentrations
dehydration or muscle wasting may have the reverse effect
Altered protein binding can be seen
Effect of kidneys on metabolism
Renal failure affects drug biotransformation: reduction & hydrolysis
normal rates of glucuronidation, sulphated conjegation and microsomal oxidation occur
many active or toxic drug metabolites depend on renal function for elimination, consequently pts with RF experience a high incidence of adverse drug reactions
Renal excretion depends on?
What are some important factors to consider?
Depends on
glomerular filtration
renal tubular secretion
re-absorption.
Important factors to consider are water solubility, protein binding, molecular size, distribution.
Patient adhere in CKD
Patients with CKD take on average 10 medicines per day – not automatically exempt from prescription charges
Long term condition = long term drug therapy
Experience increased incidence of side effects
May be managed by multiple health care providers eg – Specialists in hospital, GP, Practice Nurse
Analgesics in kidney disease
Dos and don’ts
First choice - paracetamol,
consider reduced dose.
NSAIDs – ibuprofen, diclofenac both available OTC.
Avoid where possible, recommend short course only. Increased risk of adverse effects
Opiods
with caution – accumulation of metabolites
Use of topical preparations may carry less risk
capsaicin rub
Opiods
Morphine
metabolised to morphine 6- glucuronide & morphine 3- glucuronide
M6G active metabolite excreted by kidneys therefore will accumulate in renal failure
half life increased to ~ 50 hours
Alternative choices – oxycodone, fentanyl, hydromorphone
Remember codeine is metabolised to morphine
coughs and colds in patient’s with kidney disease
Patients with kidney disease are immunocompromised
Increased risk of infections
Symptomatic relief but early referral
Consider blood pressure effects of sympathomimetics – eg pseudoephedrine
Recommend simple measures eg, simple linctus, steam inhalations.
alternative/complementary medicines
alternative therapy
Herbal medicines have been estimated to account for ~35% of acute renal failure in some African countries
Base compounds may be safe however some products contain traces of other chemicals which may cause harm
