Renal Flashcards
Acute kidney injury
A significant deterioration in renal function occurring over hours or days. Severity is defined by 3 stages (1 to 3).
prerenal AKI
decreased perfusion to the kidney– hypoperfusion (sudden/severe drop in BP), atherosclerosis/ischaemia
Prerenal causes of AKI
Renal artery stenosis
Heart failure
Haemorrhage
Renal AKI
(intrinsic renal disease) – direct kidney damage, inflammation, infection, drug, autoimmune disease
4 causes of Renal AKI
Acute tubular injury
Glomerulonephritis
Acute interstitial nephritis
Renal vasculitis
postrenal AKI
obstruction to urine flow
postrenal causes of AKI
Benign prostatic hyperplasia
Kidney stones
Tumour
Pathology of Prerenal AKI
Low vascular volume
Decreased cardiac output
Systemic vasodilation
Renal vasoconstriction
pathology of renal AKI
Glomerular
Interstitial
Vessels
pathology of post renal AKI
Extrinsic compression
3 clinical manifestations of AKI
Oliguria (passing small volumes of urine)
Fatigue or tiredness
Shortness of breath
4 complications of severe AKI
pulmonary oedema, encephalopathy and pericarditis
hyperkalaemia
differential diagnoses for AKI
Chronic kidney disease
Hyperkalaemia/ hypernatremia
Acute tubular necrosis
First line investigations for AKI
Rise in creatinine of >26 micromol/L in 48 hours
Rise in creatinine of >50% from baseline in 7 days
Urine output of <0.5ml/kg/hr for >6 hours
Determine cause: urea:creatinine ratio – pre-renal (>100:1), intrarenal (<40:1), post-renal (40-100:1)
Metabolic panel and urine output monitoring: raised serum creatinine, low urine output, raised potassium, metabolic acidosis (raised H+)
Urinalysis: leucocytes and nitrates (infection), proteinuria and haematuria (acute nephritis)
Gold standard investigations for AKI
Metabolic profile: U&E (GFR) and creatinine – raised serum creatinine, reduced urine output
management of AKI
Identification of risk factors
Dialysis may be needed whilst renal function improves
Manage complications
Dependent on the underlying aetiology
Management of Hypovolaemic AKI
fluid resuscitation;
Renal perfusion will improve with volume replacement
Give crystalloid
management of hypervolaemic AKI
Oxygen supplementation if required
Fluid restriction. Consider oral and IV volumes.
Diuretics – only in symptomatic fluid overload
Renal replacement therapy
Chronic kidney disease
abnormalities of kidney structure or function, present for >3 months, with implications for health. Irreversible loss of nephrons.
4 abnormalities of kidney function
Decreased glomerular filtration rate (GFR)
Increased albuminuria
Urinary sediment abnormalities
Electrolyte and other abnormalities due to tubular disorders
4 main causes of CKD
Acute renal failure, hypertension, diabetes, kidney disease e.g. polycystic kidney disease
4 rarer causes of CKD
Dysplastic kidneys
Reflux nephropathy
Obstructive nephropathy
Infections/ drugs/ systemic diseases that affect the kidney
pathology of CKD
Injury may primarily affect glomeruli, vessels, or the tubulo-interstitium, but eventually it leads to reduction in nephron mass with reduction in renal function.
The reduction in nephron mass may then cause haemodynamic stress in remaining nephrons, leading to further nephron loss.
Manifestation of early CKD
asymptomatic and can only be picked up if GFR is measured in at-risk patients e.g. diabetics, hypertensives