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
Why do progressed CKD patients have bone pain
Bone decalcification due to metabolic acidosis
What is metabolic derangement
Increased sodium and water retention due to decreased GFR – vomiting and diarrhoea
differential diagnoses for CKD
Acute kidney injury
Diabetic nephropathy
Chronic glomerulonephritis
First line investigations for CKD
FBC (anaemia of CKD), U&E (raised creatinine, phosphate, potassium. Decreased eGFR), urinalysis (haematuria, proteinuria), raised urine albumin (albumin:creatinine >3mg/mmol), renal USS (bilateral renal atrophy)
Gold standard investigations for CKD
U&E for estimated GFR
(eGFR < 60mL/min/1.73m2 or, eGFR <90mL/min/1.73m2 + signs of renal damage)
5 steps to management of CKD
Appropriate referral to nephrology
Treatment to slow renal disease progression
Treatment of renal complications of CKD
Treatment of other complications of CKD
Preparation for renal replacement therapy (dialysis/ transplant)
treatment to slow renal disease progression
Target to lower blood pressure
Offer treatment with renin-angiotensin system antagonist – ace inhibitors
Treatment of renal complications of CKD
Anaemia: treat underlying cause
Acidosis: consider sodium bicarbonate supplements
Oedema: restrict fluid and sodium intake
CKD bone mineral disorders: give vitamin D supplements
why does CKD increase risk of CVD
due to high blood pressure, vascular stiffness, inflammation, oxidative stress, and abnormal endothelial function.
treatment of CVD caused by CKD
Antiplatelets for CKD at risk of atherosclerotic events
Atorvastatin for primary and secondary prevention of CVD
Preparation for renal replacement therapy
Should begin in progressive CKD when the risk of renal failure is 10-20% within a year.
All suitable patients should be listed for a deceased donor transplant 6 months before the anticipated start of RRT.
main complication of CKD
High incidence of cardiovascular disease due to a combination of hypertension, vascular calcification, and hyperlipidaemia
Patients are much more likely to die of CVD than to need renal replacement therapy.
complications of calcium and phosphate metabolism derangement by CKD
leads to renal bone disease, which is a complex mixture of hyper-parathyroid bone disease, Osteomalacia and osteoporosis.
7 Symptoms of renal failure that lead to RRT being needed
Inability to control volume status, including pulmonary oedema
Inability to control blood pressure
Serositis
Acid-base or electrolyte abnormalities
Pruritus
Nausea/ vomiting/ deterioration in nutritional status
Cognitive impairment
Features of Haemodialysis
Blood is passed over a semi-permeable membrane against dialysis fluid flowing in the opposite direction.
A hydrostatic gradient is used to clear excess fluid as required (ultrafiltration).
Access is preferentially via an arteriovenous fistula which provides increased blood flow and longevity.
Haemodialysis is needed 3 times/week or more.
features of Peritoneal dialysis
Uses the peritoneum as a semi-permeable membrane.
Catheter is inserted into the peritoneal cavity and fluid infused. Solutes diffuse slowly across.
Ultrafiltration is achieved by adding osmotic agents to the fluid.
It is a continuous process with intermittent drainage and refilling of the peritoneal cavity, performed at home.
features of Haemofiltration
Water cleared by positive pressure, dragging solutes into the waste by convention.
The ultrafiltrate (waste) is replaced with an appropriate volume of clean fluid.
Low haemodynamic instability so used in critical care when HD not possible due to low BP.
3 complications of RRT
Cardiovascular disease: increased BP, calcium/phosphate dysregulation, inflammation
Renal bone disease: high bone turnover, renal osteodystrophy
Infection: uraemia causes granulocyte and T-cell dysfunction with increased sepsis-related mortality.
2 types of renal transplants
Living donor: best graft function and survival, especially if HLA matched.
Deceased donor