Acute and chronic renal failure Flashcards
What causes renal disease?
Inflammation, inherited (RTA, polycystic kidneys), metabolic disease (DM), obstruction (renal calculi, carcinoma)
What is the difference between CKD and AKI?
CKD develops slowly, whilst AKI have a rapid onset of kidney failure. CKD is irreversible whilst AKI isnt.
CKD is the progressive loss of glomerular and tubular function until end stage renal disease. CKD have significant morbidity and mortality, which is also true for AKI as it can be fatal
Define CKD - lay terms
This is an abnormality of kidney function or structurepresent for >3 months
Define CKD - Technical
GFR <60ml/min/1.73m2 on at least 2 occasion seperated by a period of at least 90 days, with ACR>3mg/mmol
State some risk factors of CKD
Age, ethnicity, family history, DM, smoking, hypertension, obesity, structural renal disease/renal stones and cardiovascular disease
What are some symptoms of early CKD?
Typical symptoms are changes in urinary quantity and frequency, but this tends to go unnoticed as technically you are asymptomatic to all other symptoms.
State the biochemical complications of CKD
Increased serum creatinine and urea Hyponatraemia Hyperkalaemia Metabolic acidosis Hyperphosphataemia Hypocalceamia
How does CKD affect glucose, lipid and red cell production?
Glucose - impaired glucose tolerance and decreased insulin secretion
Lipid - increased triglyceride, decreased HDL with significant effects to cardiovascular system
Red cell - decreased produciton, causing normocytic, normochromic anaemia because secretion of erythropoietin decreases.
How does protein loss affect a CKD patient?
Patient will become catabolic, meaning patient is breaking down or losing overall mass, both fat and muscle
What is the main goal in treating CKD?
Aim to prevent or delay the progression and reduce the risk of complications and CVD. Also covers managing anaemia and hyperphosphatemia associated with CKD.
According to NG23
What population requires regular screening?
Risk population; DM, CVD, hypertension, multisystemic disease, family history, nephrotoxic drugs (some antibiotics and chemo). Incidental findings of proteinuria or haematuria require further testing.
Hows eGFR calculated?
CKD-EPI or CDK-MDRD formulas
EPI is the most accurate
What assay is used to determine serum creatinine?
An enzymatic assay
What patient preparations are necessary ahead of a creatinine/eGFR test?
No meat 12hr before
Is creatinine an accurate measure of kidney function?
No becuase it is affected by muscle mass. A patient with a large body mass will have a really high creatinine which will be odd
If ACR is 3-70mg/mmol we need to …
confirm by a subsequent EMU
If ACR is >70mg/mmol we need to …
Nothing required because its a clear indication
What are some investigation apart from eGFR and ACR to examine CKD presence?
Other investigations possible is urine sediment abnormalities, electrolyte, and other abnormalities due to tubular disorders, histology, imaging to detect structural abnormalities.
What is necessary for patients in G3a/G3b?
We need to rule in or out CKD using a eGFRcystatinC
When should the eGFR cystatin C be considered?
A. Symptomatic with eGFR creatinine of 85ml/min/1.73m2
B. Pregnancies
C. eGFRcreatinine of 45-59ml/min/1.73m2 sustained for at least 90 days and no proteinuria
D.eGFRcreatinine of 45-59ml/min/1.73m2 sustained for at least 90 days and presence proteinuria
C
Is the MDRD formula validated for every patient group?
No it is not validated for use in children, AKI, amputees, pregnancies, malnourished, or muscle wasting disease
- only validated for black ethnicities
In a validated group when is MDRD and EPI most accurate?
MDRD underestimates GFR (>60), compared to EPI which is especially accurate for GFR>60
Why are most CKD patients asymptomatic?
They are asymptomatic due to the large reserve capacity of the kidney. 50-60% loss of functioning kidney occurs before symptom/biochemical abnormalities seen
Describe the progression of CKD
As the kidney begins to lose parts of its reserve the kidney adapts by hyperfiltrating other remaining nephrons. Hyperfiltration causes an inflammatory response involving cellular infiltration, T-cell activation, fibroblast activity increased leading to ECM synthesis (fibrosis), disruption to renal flow causing ischaemic damage
