Renal Medicine Flashcards
advantages of haemodialysis?
can be done at home
4 days free of treatment
long term survivers, proven to be effective
better provision, resources having been increased for it
disadvantages of haemodialysis?
nausea, cramps and low BP during and after due to rapid fluid shifts
significant dietary restrictions
transport to dialysis unit
difficulty with vascular access
advantages of peritoneal dialysis?
low tech, at home, taught quickly
less fluid shifts as continuous therapy
mobility
disadvantages of peritoneal dialysis?
infection, sclerosing peritonitis- bowel becomes fibrosed and obstructed=LT risk
limited survival
life-threatening consequences of AKI?
volume overload-pulmonary oedema
hyperkalaemia
metabolic acidosis
uraemia?
prevention strategies in AKI?
maintaining adequate BP
ensuring adequate volume status
avoid potentially nephrotoxic drugs e.g. gentamicin
commonest cause of intrinsic renal disease?
acute tubular necrosis (ATN)
name of criteria used to classify AKI based on degree and outcome?
RIFLE criteria
This defines 3 degrees of increasing severity of AKI, and 2 possible outcomes.
what is the RIFLE criteria?
the risk, injury and failure, and loss and end-stage renal disease=classification system of AKI.
Risk of renal dysfunction: 50% increase creatinine, or >25% decrease GFR AND/OR urine output less than 0.5ml/kg/hr for at least 6 hrs.
Injury to kidney: 2 fold increase creatinine or >50% decrease GFR AND/OR urine 75% decrease GFR, or creatinine more than 350 AND/OR urine 4wks but
what is the KDIGO staging of severity of AKI?
kidney disease improving global outcomes staging, based on creatinine or urine output.
3 stages of increasing severity
how is renal blood flow and GFR normally kept constant through autoregulation?
myogenic resonse
tubuloglomerular feedback- based on NaCl delivery to DCT and detection by macula densa cells, which subsequently control release of adenosine and ATP, and PGs and NO, which cause vasoconstriction or vasodilation of afferent arteriole respectively.
efferent arteriole vasoconstriction-AngII
in what circumstances is GFR maintenance part. AngII-dependent?
in cases of renal artery stenosis or volume depletion
site of ACE production?
lungs-surfaces of pulmonary and coronary endothelial cells
if ibuprofen is being used by a pt in the setting of volume depletion e.g. severe diarrhoea, why might AKI occur with acute GFR decline?
ibuprofen= NSAID-COX inhibitor, so inhibiting PG synthesis which acts to vasodilate, and NA and AngII high in vol depletion, so unopposed action of local vasoconstrictors on both afferent and efferent arterioles, so inadequate renal perfusion.
Give 4 overall causes of pre-renal AKI, and causes for each of these.
hypovolaemia-haemorrhage, GI losses-diarrhoea and vomiting, urinary losses-glycosuria, post-obst diuresis, diuretics and fluid redistribution e.g GI obstruction, pancreatitis.
hypotension- cardiogenic shock e.g. post MI, distributive shock e.g. sepsis, anaphylaxis, with vasodilation.
renal hypoperfusion- reduced perfu plus impaired autoregulation, AAA, renal artery stenosis/occlusion, hepatorenal syndrome.
oedema states- CHF, hepatic cirrhosis, nephrotic syndrome partic. minimal change nephropathy. Fluid o.load can damage kidneys, and fluid in interstitium reduces perfusion to kidneys?
commonest cause of intrinsic renal AKI in intensive care?
sepsis
3rd commonest cause of hospital-acquired AKI?
radiocontrast nephropathy
important clinical consequence of relieving AKI caused by obstruction?
substantial diuresis, requires careful monitoring and appropriate fluid replacement to avoid vol depletion.
how is obstructive nephropathy rapidly diagnosed?
USS-detects dilatation of renal pelvis and calyces
principal causes of post renal AKI?
intrinsic: intraluminal=stones, blood clots, papillary necrosis
intramural=urethral stricture, bladder tumour, prostatic hypertrophy or malignancy, radiation fibrosis
extrinsic: pelvic malignancy, retroperitoneal fibrosis
causes of intrinsic renal AKI?
glomerular disease-inflammatory e.g. SLE, thrombotic e.g. DIC, thrombotic microangiopathy
tubular injury-ischameia, toxins-drugs, radiocontrast, pigments, heavy metals, metabolic-hypercalcaemia, crystals e.g. urate, oxalate
interstitial nephritis-drug induced e.g. NSAIDs, Abx, infiltrative e.g. lymhoma, granulomatous e.g. TB, sarcoidosis, infection e.g. post-infective, pyelonephritis.
vascular-vasculitis- usually ANCA assoc., cryoglobulinaemia-blood has large numbers of cryoglobulin proteins insoluble at reduced temps., assoc. with conditions such as multiple myeloma and Hep C infection. Cholesterol emboli, renal artery or vein thrombosis.
HRS
HUS
a disproportional increase in urea:creatinine ratio is indicative of which type of AKI?
pre-renal
characteristics of pulmonary oedema on CXR?
widespread opacification, poorly defined edges, CP angle blunting kerley B lines fluid in fissures upper lobe diversion bats wing hilar shadowing?
in pre-renal AKI, there is typically avid retention of Na+ and H20, why is this and what does this mean for the fractional excretion of Na+?
pre-renal- decreased blood flow to the kidney, often due to hypovolaemia so high levels of ADH, Ang-II and aldosterone (RAAS activation?).
FE less than 1%
key investigations in AKI?
haematology: FBC, blood film, clotting profile-eosinophilia, thrombocytopenia, DIC, anaemia in CKD
immunology
BC: Us and Es, creatinine, blood gas analysis, serum HCO3-, CK, myoglobinuria, CRP, serum Igs, protein electrophoresis, Bence Jones proteins proteinuria
virology-Hep B and C and HIV, as import. for infection control in dialysis area
radiology: renal USS- size, symmetry and evidence of obstruction
Management principles in AKI?**
identify and correct pre and post renal factors
optimise CO and renal b.flow
review meds: cease nephrotoxic agents, adjust doses where approp, monitor levels
accurately mon fluid intake and output and daily body weight
identify and treat acute complications e.g. hyperkalaemia, acidosis, hyperphosphataemia, pulmonary oedema
optimise nutri suppport, but minimise nitrogenous waste prod., and K+ restriction
identify and aggressively treat infection, minimise indwelling lines, remove bladder catheter if anuric
identify and treat bleeding tendency, prophylacis with PPI or H2 antagonist, transfuse if req, avoid aspirin
initiate dialysis before uraemic comp.s emerge
define significant progression of CKD
> 5ml/min decline in eGFR within 1 yr, or >10ml within 5 yrs
why is it important to identify those with early CKD?
CKD has strong assoc. with risk of death, CVD and hospitilisation
and to prevent/delay progression to end stage renal disease (ESRD), assoc. with considerable morbidity, mortality, and high healthcare costs.
stage 5 CKD (end stage renal failure) is defined as what eGFR and what is the typical testing frequency of this?
less than 15ml/min
pts eGFR on average when placed onto RRT is 6ml/min
6 weekly testing
how is CKD routinely assessed for in hypertensive and diabetic pts?
hypertensive pts should have urinary ACR checks and urinalysis for haematuria
all diabetics should have 1st pass urine tests for ACR
according to NICE, people with what RFs should be offered testing for CKD?
diabetes
hypertension
CVD-IHD, chronic HF, PVD or CVD
structural renal tract disease, renal calculi or prostatic hypertrophy
multisystem diseases with potential kidney involvement e.g. SLE
FH of stage 5 CKD or hereditary kidney disease e.g. polycystic kidneys
opportunistic detection of proteinuria or haematuria
factors to bear in mind when checking eGFR?
age ethnicity weight diet exercise gender muscle mass
when might eGFR be less reliable?
AKI pregnancy muscle wasting disorders oedematous states amputees malnutrition
how should eGFR be corrected with afro-caribbean or african pts?
multiply by 1.21
if 1st test eGFR is less than 60ml/min, what should be done?
retest within 2 wks to exclude causes of acute deterioration of GFR
