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Acute Kidney Injury/Acute Renal Failure (Risk Factors (Chronic Kidney…
Acute Kidney Injury/Acute Renal Failure
Key Facts
AKI has now replaced the term ARF
AKI is often recognised by a falling urine output and rising serum urea and creatinine, or both
In contrast, CKD implies long-standing and usually progressive impairment in renal function
Two classifications are RIFLE and KDIGO
An abrupt (over hours to days) sustained rise in serum urea and creatinine due to a rapid decline in GFR leading to a failure to maintain fluid, electrolyte and acid-base homeostasis - it is usually but not always reversible or self-limiting
Epidemiology
Severe AKI affects about 130-140 per million population per year
Common in the elderly
About 25% of patients with sepsis and 50% of patients with septic shock will have AKI
Associated with:
Diarrhoea
Haematuria
Haemoptysis
Hypotension
Urine retention
AKI is common, occurring in 18% of hospital patients
Aetiology
Pre-renal (40-70%)
Hypotension without hypovolaemia - cirrhosis or septic shock
Low cardiac output
Hypovolaemia of any cause
Renal hypoperfusion e.g. NSAIDs
Renal hypoperfusion e.g. hypotension
Intrinsic renal (10-50%) - renal biopsy required for diagnosis
Acute tubular necrosis - common cause, caused by pre-renal damage
Vascular
Renal parenchyma damage
Glomerular
Interstitial
Commonest are ischaemia, sepsis and nephrotoxins
Post-renal (10-25%)
Luminal: stones, clots or sloughed papillae
Mural (wall) - malignancy, BPH, strictures
Urinary tract obstruction at ureter, bladder or prostate
Extrinsic compression from malignancy
Risk Factors
Chronic Kidney Disease
Past history of AKI
History of urinary symptoms
Hypovolaemia
Poor fluid intake/increased losses
Haemotological malignancy
Sepsis
Diabetes
Chronic liver disease
Prostate cancer
Peripheral vascular disease
Nephrotoxic drugs
Heart failure
Repeated use of radiological contrast
Age >75
Clinical Presentation
Breathlessness occurs from a combination of anaemia and pulmonary oedema secondary to volume overload
Pericarditis occurs with severe untreated uraemia and may be complicated by a pericardial effusion, tamponade or pericardial rub
Symptoms of high urea - fatigue, weakness, anorexia, confusion, seizures etc.
Impaired platelet function causing bruising and exacerbates GI bleeding
Irregular heartbeats (arrhythmias) due to hyperkalaemia
Infection due to immune suppression
Oliguria (very small amount of urine) occurs in early stages
Postural hypotension
On examination there may be palpable bladder, palpable kidneys, abdominal/pelvic masses, rashes
Oedema
Depends on underlying cause or severity
Thirst - indicated fluid depletion and dehydration
Differential Diagnosis
Abdominal aortic aneurysm, alcohol toxicity, alcoholic & diabetic ketoacidosis, chronic renal failure, dehydration, GI bleed, heart failure, metabolic acidosis
Diagnosis
Urine and blood cultures to exclude infection
Mid-stream specimen of urine sent for microbiology culture and sensitivity
Blood count - anaemia and very high ESR suggests myeloma or vasculitis as underlying cause
Ultrasound - give assessment of renal size & can be used to distinguish obstruction and hydronephrosis
Urine dipstick - suggest infection and glomerular disease
CT-KUB
Serum Ca, phosphate and uric acid
ECG - to look for hyperkalaemic changes e.g. arrhythmia
Suspect chronic if - small kidneys on ultrasound, anaemia, low Ca, high phosphate or high creatinine
CXR - to look for pulmonary oedema
Aim is to establish whether AKI is pre-renal, renal or post-renal
Renal biopsy - intrarenal causes of AKI, perform on every patient with unexplained AKI and normal kidneys
Treatment
Treat acidosis with sodium bicarbonate
Optimise fluid balance
Treat pulmonary oedema using diuretics
Stop nephrotoxic drugs e.g. NSAIDs, ACE-inhibitor, Gentamicin, Amphotericin
Diet - Na & K restriction, supply vitamin D
Treat underlying cause
Intrinsic renal - refer early to nephrology if concern over tublointerstitial or glomerular pathology
Post-renal
Pre-renal - correct volume depletion with fluids, treat sepsis with antibiotics
Renal Replacement Therapy
Treat hyperkalaemia - insulin & glucose to drive K into cells