6- CKD and AKI Flashcards
What is an AKI
Renal function deterioration over hours/days
What rises in AKI (Blood)
Urea and creatinine
Is AKi reversible
Can be
Consequences of AKI
Volume overload, metabolic acidosis, hyperkalemia
What causes the most AKIs
Pre renal cause
Pre-renal causes
Hypovolemic
Shock
Renal artery stenosis
NSAIDs and ACEI
How do NSAIDs and ACEI cause AKI
Impair mechanism of renal autoregulation
Intrinsic causes of AKI
Acute tubular necrosis- ischemia, rhabdomyolysis, drug toxicity, toxins
Acute interstitial nephritis- drugs, hypercalcemia, myeloma
Glomerular disease- acute glomerulonephritis, rapidly progressive glomerulonephritis.
Vascular disease- vasculitis, malignant hypertension, thrombotic microangiopathies
What is a sign of Rhabdomyolysis
Dark urine. Muscle breakdown–> myoglobin –> filtered but toxic.
Post renal causes of AKI
Bladder outflow obstruction
Tumour
Stone- bilateral to cause AKI
Retroperitoneal fibrosis causing ureteral obstruction
Basic investigations
Urine test- microscopy, dipstick, cytology
Bloods
Imaging
What biochemical changes occur
Increased plasma urea, creatinine, urate, phosphate, potassium
Decreased plasma sodium, calcium
Metabolic acidosis
Increased anion gap
How to manage AKI
Fluid replacement to optimise flow and correct hypovolemia
Correct electrolyte imbalances
Catheter if obstruction
What are the life threatening complications of AKI
Hyperkalemia
Pulmonary oedema
Bleeding
What is CKD
Progressive loss of function over months and years
Is CKD reversible
No, renal tissue replaced by extracellular matrix in response to damage.
Whats a good GFR
> 90
Stage 2
60-89
Stage 3
30-59
Stage 4
15-29 RRT
Stage 5
<15 -dialysis or transplant
Increased incidences in what people
Ethnic, elderly, multi-morbid, social deprivation, diabetes, hypertension
Pathology of CKD- what happens to kidney
Medulla maintains but cortex (where nephrons are) thin.
Who gets CKD screening
Diabetes
Hypertension
CVD
Those on nephrotoxic drugs
What blood tests to use
U&Es eGFR Bone biochemistry FBC CRP Iron PTH
Other investigations for CKD
USS- kidney size
Biopsy
CT
MRI
Management
Lifestyle modification Uncontrolled diabetes control Hypertension control Proteinuria - ACEI Lipid control
What are the functions of the kidneys
BP, volume, pH, electrolytes, osmolality, excretion of waste, metabolism of drugs
What is the endocrine function of the kidneys
Inactive Vit D, renin, EPO
Water handling in kidney during CKD
Reduced GFR means lost ability to maximally dilute and concentrate urine.
Nocturia in CKD
Small filtrate but same solute loads causes osmotic diuresis- reduces maximum concentrating ability and response to ADH
Effect on low GFR on K+ (and ACEI)
Hyperkalaemia
Need to stop ACEI as aldosterone helps to excrete K+ by increasing ROMK expression
CKD and bone mineral disease
Decreased activation of Vit D = less Ca = PTH stimulated = bone breakdown. As kidneys aren’t functioning well then PO4 isn’t excreted = precipitates = vessels, joints, skin. Manage: give Vit D supplements
Drug sensitivity in CKD
Increased as elimination is impaired.
Accumulation of waste products- symptoms
Uraemic symptoms- reduced appetite, nausea and vomiting, pruritus
End stage renal failure
GFR < 15mls/min
Requires RRT
Symptoms of dialysis
Tiredness, sleep issues, concentration issues, volume overload, nausea, restless legs, sexual dysfunction, increased infection
Hemodialysis times and pills
4 hrs x 3 times a week + 19 tablets, EPO and iron
Peritoneal dialysis
4-5 bags and day or overnight
Transplant
Reduced morbidity and mortality
QOL
Infection risk
Immunosuppressants- diabetes, hypertension risk
