Renal & acid base Flashcards
definitions of AKI
abrupt (48 hrs) reduction of kidney function defined as
-increase in serum creatinine >/= 0.3mg/dL increase
OR
-50% increase from baseline
OR
-decrease in UO < 05mL/kg/hr for > 6 hours
Oliguria criteria
<400 ml/d
Nonoliguric
> 400 ml/d
staging system used more for AKI
modified RIFLE
- ↑ of sCR >/+ 0.3mg/dL or ↑ >150-200%
- ↑ 200-300% from baseline
- ↑ >300% from baseline
modified RIFLE
most common form of AKI
prerenal
prerenal is typically due to
decreaesd renal perfusion
AKI type:
decreased circulation ( cardiac failure, nephrotic syndrome, cirrhosis, pancreatitis, sepsis, low BP, blood loss, trauma)
fluid loss (n/v/d, fever, increased urination, GIB
prerenal
AKI type:
Acute tubular necrosis
glomerular disease
interstitial disease
intrarenal
3 most common reasons for intrarenal AKI
Acute tubular Necrosis
Glomerular Disease
Interstitial Disease
(typically prerenal progresses)
acute tubular necrosis is caused by
radiographic contrast
lab needed for rhabdomyolosis
creatinine kinase
2 main causes of acute tubular necrosis (leading to INTRARENAL AKI)
ischemia and nephrotoxic exposure
Acute tubular necrosis electrolyte monitoring
↑Mg, ↑Phos, ↑Mg, ↓Ca
rhabdomyolysis
rapid hemolysis (masssive transfusion rx, hemolytic anemia)
Intrarenal (acute tubular necrosis)
Strep, rocky mt spotted fever, sarcoidosis and allergic rx to PCN, sulfas, etc. are all types of
intra renal interstitial nephritis (inside kidney)
eosinophilia (↑) in blood/urine
intrarenal interstitial nephritis
immune related and inflammatory glomerular lesions account for 5% of AKI
intrarenal glomerular nephritis
granular casts may be seen in urine in which type of AKI
intrarenal (ATN)
red cell casts and pyuria are typically seen in what AKI
intrarenal: glomerular
obstruction is the usual cause of which AKI
postrenal
stones
BPH
tumors
masses
clots
strictures
postrenal AKI
muddy brown casts are seen in
ATN
WBC casts are typically seen with
tubules infection/ pyelonephritis
RBC casts are seen with
glomerular nephritis
eosinophils are seen with
acute interstitial nephritis
FeNa is only validated in what 2 patients
oliguria or AKI
FeNa can not be used in
patients with diuretics, CKD, obstruction, acute glomerular disease
test of choice for renal artery stenosis
doppler ultrasound for vascular assessment
cysts, stones, masses, and size of kidneys can be seen on
renal US
what CT is preferred for stones
non contrast
MRI is used in place of
CT with contrast
do not over hydrate in what AKI
postrenal
always consult nephrology for
intrarenal AKI
steroids may be useful in what (2)
glomerural nephritis
&
interstitial nephritis
sepsis, ischemia, and endogenous and exogenous nephrotoxins are causes common causes of
AKI
AKI classifcation
RIFLE criteria stands for
RISK
INJURY
FAILURE
LOSS
ESRD
diminished renal perfusion cause dfrom low blood supply to the kidneys WITHOUT nephron damage
prerenal AKA (60% of AKI cases)
ACE, NSAIDS, diuretics may cause which AKI
prerenal
patient is on max pressors and you notice a drop in UO, this could indicate
prerenal AKI due to vasoconstrictive state
intrarenal sites
abrupt decrease in GFR due to tubular cell damage that results from renal ischemia or nephrotoxic injury leads to
INTRARENAL (intrinsic) AKI
long periods of renal azotemia lead to tubular injury resulting in
ATN
*info card
ENDOGENOUSIS: hemoglobinuria (hemolysis), myoglobinuria (rhabdo), hyperuricemia, multiple myeloma
ATN
*info sheet
EXOGENOUS: aminoglycosides, contrast, ethylene glycol,cyclosporin, heavy metals
ATN
Contrast induced nephropathy is define das
rise in sCreat 25-50% within 48 hrs of IV contrast
Sterp, CMV, rocky mt fever are forms of bacterial pyelo that lead to
acute tubulointerstitial nephritis (intrinsic/intrarenal)
systemic lupus, Sjogrens, sacoidosis, cryoglobulinemia, can all cause
glomerulonephritis (intrinsic/intrarenal)
greatest incidence of recovery and not progressing to ESRD
post renal
conditions that cause obstruction of urinary flow and consequently a decrease in GFR
post renal
never insert a foley into
a patietn with a positive urethrogram
if there is trauma damage to a kidney who do you consult
UROLOGY (not nephro)
3 categories of CKD incidence in USA
> 65 y/o
female > male
AA, hispanic, asian, caucasion (in order)
metalic taste in the mouth, pruritus, brittle nails, SOB, ED are all s/s of
CKD
your patient with CKD comes in with an acutely elevated BUN you should be suspicious of
1 GIB
#2 dehydration
elevated sCreat, low GFR but BUN is really low could be related to
liver disease/ hepatorenal syndrome
ACUTE elevation of creatinine could likely be
toxin or drug induced.
COPD, emphysema, PNA, and asthma typically cause what acid base imbalance
resp acidosis
hyperventilation, fever, pain, anxiety, high altitude typically cause what acid base imbalance
resp alkalosis
shock, DKA, AKI, diuretics, sepsis typically cause what acid base imbalance
met acidosis
excess base, antacids, gastric suctioning, and vomiting typically cause what acid base imbalance
met alkalosis
only type of hyponatermia that requires treatment
HYPOTONIC HYPONATERMIA
hyperlipidemia is a common cause of what electrolyte imbalance
isotonic hyponatremia
hyperglycemia, mannitol and radiocontrast is a common cause of what electrolyte imbalance
hypertonic hyponatermia
what lab do you use to determine cause of hypotonic hypovolemia hyponatermia
urine sodium
<10: dehydration, D/V
>20: diuretics, ACE, steroid deficiency, etc
correction dose/tx for acute hypernatremia
correct no faster than 1-2mEq/L/hr
(0.5 for chronic)
beer, SIADH, diuertics, CKD are all causes of what electrolyte imbalance
hypotonic euvolemic hyponatermia
what serious electrolyte abnormality must you always correct with Na if needed
K
hyponatermic tx with seizures
- fluid restriction <1000ml/24
- 100 ml 3% over 10m; repeat if needed;
- 3% @ 0.5-2ml/kg/hr
MAX CORRECTION OF LOW NA
12 mEq/L/24
OR
20mEq/L/48
no more than 4-6mEq
fluid options for mild, oder, sev volume depletion with hypernatermia
mild: D5W
mod: 1/2 NS, free water
sev: 9%NS then 1/2 NS
metabolic disease, catecholamine excess, and IV insulin for DKA all cause what electrolyte disturbance
hypoKalemia
Action of Glomerulus & drug at site
Filters plasma
Acetazolamide
Action at proximal convoluted tube
bicarb, sugars, & drugs re-absorbed
Action and drugs at ascending loop of henle
Site for loop diuretics
drugs at descending loop of henle
Osmotic diuretics (mannitol)
Action & drug site at Distal Convoluted tubule
(Tip ** last stop to fix everything before collecting duct)
Reabsorption of water, K+ acid/base balance effected by ADH and aldosterone.
Site of Action for Thiazides – HCTZ
Action & drug site for Collecting Duct
Last step in water and Na+ balance.
Site of action for Potassium Sparing diuretic - Spironolactone
Acute glomerual injury, ATN, acute acute interstitial nephritis & AKI may have what in urine
EOSINOPHILS
Renal epithelial cells in urine indicate what
Tubular injury
If the glomerulus is not working what lab will be abnormal
High creatinine ( because it is the only place in the kidney where it is absorbed)
Stage 1- kidney damage
GFR > 90% (normal)
GFR 60-89
Stage 2 CKI
GFR 45-59
Stage 3 a CKI
GFR 30-44
Stage 3b CKI
GFR 15-29
Stage 4 CKI
GFR < 15
Stage 5/ kidney failure
An acute increase in BUN with CKD may indicate
Acute GIB
Acute decrease in BUN with CKD may indicate
Liver disease
Edema/weeping, high lipids, hypoalbuminemia, proteinuria, increase bleeding/clotting all could be signs of
Nephrotic syndrome
When BUN/Creat rise tighter it’s called 15:1 signifying
INTRA renal failure
Nephrotic Meds “cake man c”
Cyclosporine - ACE - keppra - erythromycin - metformin - amphotericin - NSAIDS - contrast
Urinary casts: red cell
Glomerulonephritis
Vasculitis
Urinary casts: white cell
Acute interstitial nephritis
Urinary casts: fatty
Nephrotic syndrome
Urinary casts: muddy brown
ATN
