Clinical Medicine 9/20/16--Kirila Flashcards
Acute Kidney Injury
- increase in serum creatinine +/- decrease in urine output over hours to days
- electrolyte disturbances, acid-base disturbances (metabolic acidosis), inability to excrete nitrogenous waste, intravascular volume overload
Orthostatic hypotension
- volume contraction or ECV depletion (dehydration)
- due to fluid losses from nausea and vomiting
Fractional excretion of sodium
- calculated using a random urine sample close to time of the blood draw–helps sort between pre-renal and intrinsic renal
- (Una/Pna)/(Ucr/Pcr)x100
FeNa less than 1% means
tubules intact and are sodium avid i.e. retaining sodium as would be expected in dehydration
FeNa greater than 1-2% means
tubular function not intact
Pre-renal origin suggests
-that the tubules and glomeruli were not the initial location of pathology, though they will eventually become affected and possibly permanently
BUN/Creatinine in AKI
- elevation in serum Creatinine by 50% or by 0.5-1.0mg/dL (affected by muscle mass available to generate creatinine)
- BUN also elevated due to retention of nitrogenous wastes
Elevated BUN=
azotemia
Elevated BUN plus confusion=
uremia
eGFR=
175x (serum creatinine)^-1.154x(age)x0.742 [if female] x 1.22 [if black]
Pre renal causes of acute kidney injury
- anything that compromises renal perfusion
- hypovolemia: dehydration, viral syndromes, acute pancreatitis, diuretics
- low cardiac output: CHF
- altered renal/SVR ratio: sepsis, cirrhosis
- renal hypo perfusion with impaired autoregulation: NSAIDS
- hyperviscosity syndrome (rare): myeloma
- not something that started in the kidney! Something before you got to the kidney
Effective Volume depletion
- 3rd space
- results in decreased kidney perfusion as seen in pre-renal disease
Pre renal treatment
- hypovolema: fluid replacement IV; treat underlying cause
- even with effective volume depletion such as pancreatitis, large quantities of IV fluids are indicated, with close monitoring for systemic volume overload
Intrinsic renal failure
- renovascular obstruction: renal artery obstruction e.g. embolism, dissecting aortic aneurysm (can be pre renal or intrinsic renal)
- disease of glomeruli or microvasculature: accelerated HTN
- acute tubular necrosis: iodinated contrast dye–used with CTs, vascular studies, IVP’s, etc
- interstitial nephritis: acute pyelonephritis, NSAIDs, also can be contrast dye induced, other drugs
- intratubular deposition and obstruction: myeloma
- renal allograft rejection
Post renal AKI
-blockage
Ureteric blockage
-calculi (stones), blood clot, sloughed papilla, cancer, external compression (tumor, retroperitoneal fibrosis)
Bladder neck blockage
-neurogenic bladder, prostatic hypertrophy, calculi, cancer, blood clots
Urethra blockage
-stricture, congenital valve, phimosis
If AKI unresponsive to conservative measures,
- consider temporary hemodialysis in the following:
- volume overload refractory to diuretics
- hyperkalemia
- encephalopathy otherwise unexplained
- pericarditis, pleuritis
- severe metabolic acidosis comprising respiratory or circulator function
Chronic Kidney disease
- long-standing, irreversible impairment of renal function
- uremia: clinical syndrome resulting from profound loss of renal function
Glomerular filtration rate
- Creatinine clearance: 24 hour urine sample measured for creatinine in addition to obtaining serum creatinine
- can use inulin as substance to measure, but has to be given IV and assay for inulin not available in most labs
CKD Stage 1
-kidney damage with normal or increased GFR>or = 90
CKD Stage 2
-mild decrease in GFR
60-89
CKD Stage 3
moderate decrease in GFR
-30-59