Renal (General, AKI and CKD) Flashcards
Drugs that are usually safe in acute kidney injury (AKI)
Some common drugs that are usually safe in AKI are:
- Paracetamol
- Aspirin (at a cardioprotective dose)
- Clopidogrel
- Warfarin
- Statins
- Beta-blockers
Drugs that should be stopped in AKI
These drugs should be stopped as they may worsen an AKI:
- NSAIDs (except low-dose cardioprotective aspirin)
- ACE inhibitors
- Angiotensin II receptor blockers (ARBs)
- Aminoglycosides (e.g. gentamicin)
- Diuretics
Drugs with an increased risk of toxicity in AKI
Drugs that may be stopped as an AKI can increase toxicity, but they do not usually worsen the AKI itself:
- Metformin – due to increased risk of lactic acidosis
- Lithium – due to increased risk of lithium toxicity
- Digoxin – due to increased risk of digoxin toxicity
Drugs causing pre-renal damage
Any drug that causes volume depletion or reduced renal perfusion may cause pre-renal damage. Some examples are:
- NSAIDs
- ACE inhibitors
- ARBs
Drugs causing intrarenal damage
These drugs may be directly nephrotoxic or lead to hypersensitivity reactions:
Drugs that may cause glomerulonephritis:
- Rifampicin
- Sulfonamides
- Penicillamine
Drugs that may cause acute interstitial nephritis:
- Antibiotics – generally penicillins and cephalosporins
- Sulfonamides
- Thiazide diuretics
Drugs that are directly nephrotoxic and may cause acute tubular necrosis:
- Aminoglycosides (e.g. gentamicin)
- Amphotericin
- Ciclosporin
Drugs causing post-renal damage
These drugs may lead to urinary tract obstruction:
- Anticholinergic drugs (e.g. tricyclic antidepressants) may cause acute urinary retention
- Acetazolamide, methotrexate, and sulfonamides can cause crystalluria which can lead to obstruction
Acute kidney injury (AKI)
describes a spectrum of disorders leading to reduced kidney function over hours to days. An AKI can lead to a failure to maintain fluid, electrolyte, or acid-base homeostasis.
An AKI may occur in patients with previously intact renal function or in patients with pre-existing renal disease (known as acute-on-chronic kidney disease).
causes of AKI can be split into
pre-renal
renal
post-renal
Pre-renal causes
- include causes that decrease blood flow to the kidney such as*
- Hypovolaemia (e.g. dehydration), decreased cardiac output (e.g. heart failure)
- Drugs that cause renal hypoperfusion (e.g. ACE inhibitors, angiotensin II receptor blockers and diuretics)
Renal (intrinsic) causes
Toxins and drugs:
- Antibiotics (e.g. aminoglycosides such as gentamicin)
- Radiocontrast media, particularly iodinated contrast
- Chemotherapy drugs (e.g. tacrolimus)
Vascular disease:
- Vasculitis (usually anti-neutrophil cytoplasmic antibody- (ANCA-) associated)
- Thrombotic microangiopathies (e.g. haemolytic uraemic syndrome or thrombotic thrombocytopenic purpura)
- Renal artery stenosis
- Renal vein thrombosis
- Malignant hypertension
Tubular disease:
- Acute tubular necrosis
- Rhabdomyolysis
- Multiple myeloma
- Interstitial disease:
- Acute interstitial nephritis
- Lymphoma infiltration
Glomerular diseases:
- Glomerulonephritis (e.g. anti-glomerular basement membrane disease, IgA nephropathy, post-infectious glomerulonephritis etc.)
Other:
* Eclampsia
Post-renal causes
include causes of obstruction to urine outflow such as:
- Renal stones
- Prostatic hyperplasia/cancer
- Urinary retention, which may be secondary to drugs (e.g. tricyclic antidepressants)
- Blocked catheter
investigations for AKI
- U&Es
- Urea:creatinine ratio
- Urinalysis
- Renal US
Others
- FBC
- Blood cultures if sepsis suspected
- liver function tests (hepatorenal syndrome)
- CK (rhabdomyolysis)
- CRP or ESR
- Virology tests
- Kidney biopsy
UEs in AKI
- Urea, creatinine, and potassium may be elevated
- Creatinine tends to rise around 24 hours following the start of an AKI
Urea:creatine ratio AKI
Urea:creatinine ratio – can help determine if the cause is pre-renal, renal, or post-renal:
Calculated by dividing urea by creatinine, ensuring the units are the same
1) A ratio of >110:1 suggests a pre-renal cause
- A disproportionate increase in urea suggests hypoperfusion
2) A ratio of <40:1 suggests a renal cause
- Suggests decreased urea absorption due to intrinsic renal damage
3) A ratio of 40-110:1 suggests a normal result or post-renal cause
- This suggests urea reabsorption is within normal limits
urinalysis in AKI
dipstick testing for blood, protein, leukocytes, nitrites, and glucose should be performed in all patients with AKI
Renal ultrasound and AKI
- If there is an AKI with no identifiable cause or those at risk of urinary tract obstruction
- Performed within 24 hours of assessment
An AKI can be diagnosed if any of the following apply:
- A rise in creatinine of ≥26 µmol/L in 48 hours or
- A ≥50% rise in creatinine over 7 days or
- A fall in urine output to <0.5 mL/kg/hr for >6 hours in adults or 8 hours in children or
- A ≥25% fall in the estimated glomerular filtration rate (eGFR) in both children and young people over 7 days
AKI staging
Stage 1 AKI:
- An increase in creatinine to 1.5-1.9 times the baseline or
- A reduction in urine output to <0.5 mL/kg/hr for ≥6 hours
Stage 2 AKI:
- An increase in creatinine to 2.0-2.9 times the baseline or
- A reduction in urine output to <0.5 mL/kg/hr for ≥12 hours
Stage 3 AKI:
- An increase in creatinine to ≥3.0 times the baseline or
- A reduction in urine output to <0.5 mL/kg/hr for ≥24 hours
AKI vs. CKD
Features supporting CKD:
- Anaemia – due to anaemia of chronic disease and reduced erythropoietin release from the kidneys
- Hypocalcaemia – due to reduced activation of vitamin D, which takes place in the kidneys
- Increased phosphate also leads to the deposition of calcium in calcium phosphate, which is insoluble, and therefore removed from the circulation
- Hyperphosphataemia – dysfunction of the kidneys leads to decreased phosphate excretion
- Small kidneys on ultrasound – this may not always be seen:
- E.g. in polycystic kidney disease, a cause of CKD, the kidneys may be enlarged
Features supporting AKI:
- Acutely unwell patients or hypovolaemia make CKD less likely and AKI more likely.
Presentation of AKI
The presentation depends on the underlying cause. Many patients may not experience clear symptoms, however, as urea and electrolytes become more deranged in AKI, symptoms may emerge such as:
- Decreasing urine output with or without increasing serum creatinine
- Nausea and vomiting
- Arrhythmia – if hyperkalaemia develops
- Dehydration
- Confusion
- Features of Uraemia
management of AKI
STOP
- Sepsis – screen for sepsis and treat
- Toxins – stop and identify any nephrotoxic drugs/agents
- Optimise blood pressure – correct hypovolaemia, withhold drugs that contribute to AKI, consider critical care escalation for vasopressors if patients are still hypotensive despite fluid resuscitation
- Prevent harm – identify and treat reversible causes, treat complications, and review medications
May need haemodialysis
Indications for haemodialysis
Remembered with AEIOU:
- Acidosis
- Electrolytes (hyperkalaemia)
- Ingestion or overdose of medications/drugs
- Overload of fluid causing heart failure and pulmonary oedema
- Uraemia leading to pericarditis or encephalopathy
complications of AKI
Hyperkalaemia
Acidosis
Pulmonary oedema
Uraemic encephalopathy or pericarditis
management of mild hyperkalaemia (5.5-5.9 mmol/L)
- Identify and treat underlying cause
- Consider cation exchange resin to remove K+ from body (e.g. calcium resonium)
management of moderate hyperkalaemia (K+ of 6.0-6.4 mmol/L)
- Perform ECG. If changes are present, treat as severe hyperkalaemia
- If no ECG changes present: IV insulin and glucose infusion – moves potassium intracellularly
- Consider adjunct nebulised salbutamol – avoid if tachyarrhythmia present
management of severe hyperkalaemia (K+ ≥6.5 mmol/L):
- Seek advice from nephrology/intensive care and monitor in a high-dependency area
- Immediate IV calcium gluconate or IV calcium chloride – for cardioprotection and prevents arrhythmia
- Seek senior advice if the ECG does not normalise after one dose
Pulmonary oedema
This may occur due to the underlying cause of AKI (e.g. heart failure, renal artery stenosis) or due to excessive IV fluid resuscitation
- Sit the patient upright – allows for better gas exchange as fluids settle in the lung bases
- Give high-flow oxygen at 15 L/min via a reservoir mask
- Consider IV glyceryl trinitrate if systolic blood pressure is >90 mmHg and there is no valvular heart disease
- Loop diuretics may be considered by specialists if the patient is haemodynamically stable and not dehydrated
Seek senior support
Refer for renal replacement therapy
acidosis
- IV sodium bicarbonate may be needed due to the risk of volueme overload or hypernatraemia (pH <7.20)
- refer for renal replacement therapy
Uraemic encephalopathy or pericarditis
Refer for renal replacement therapy
Chronic kidney disease (CKD)
is defined as a reduction in kidney function, structural damage, or both for more than 3 months with associated health implications.
CKD can lead to fluid and electrolyte imbalance, and protein and/or blood leakage into the urine, causing proteinuria and haematuria.
2 main causes of CKD
- Diabetic nephropathy ( most common )
- Hypetensive nephorpathy (second)
causes of CKD
- Diabetic nephropathy – the most common cause
- Hypertensive nephropathy – the second most common cause
- Hypertension can cause CKD and CKD can cause hypertension
- Glomerulonephritis
- Current or previous acute kidney injury (AKI)
- Nephrotoxic drugs
- Causes of obstructive uropathy (e.g. recurrent renal stones)
- Systemic disorders that may involve the kidneys (e.g. systemic lupus erythematosus, vasculitis, multiple myeloma)
- Polycystic kidney disease
- Alport’s syndrome
- Cardiovascular disease
- Obesity with metabolic syndrome (obesity alone is not a risk factor)
- Gout
- Solitary functioning kidney
presentation of CKD
CKD is often asymptomatic, and it is often detected on routine blood tests. As kidney function decreases, symptoms may emerge including:
- Uraemia – accumulation of urea due to failure of renal clearance:
- Reduced appetite
- Nausea with or without vomiting
- Pruritus
- Restless legs
- If severe, patients may have seizures or coma
- Reduced urine output– may lead to fluid overload which may present with:
- Peripheral oedema
- Weight gain
- Orthopnoea
- Pulmonary oedema
-
Anaemia – due to reduced anaemia of chronic disease (AOCD) secondary to erythropoietin (EPO) deficiency:
* Fatigue
* Shortness of breath
* Headache - Foamy urine – due to proteinuria
- Dark urine – due to haematuria
investigations for CKD
- UEs and calcium
- Creatinine
- eGFR
- Urinary albumin: creatinine ration (ACR)
- Urine dipstick
CKD classification
how haemodialysis work
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.
Peritoneal dialysis
How it works
- Home based therapy
- Reliant on the patients’ own peritoneal membrane acting as the dialysis membrane.
- Solutes (electrolytes, urea, creatinine) move from the patient’s blood, across the peritoneal membrane, down the concentration gradient into the dialysate fluid.
- Osmotic gradient is created by high concentration of glucose (occasionally amino acid or glucose polymer solutions are used) in the dialysate fluid, which removes water from the patient.
