wk 11, lec 1 Flashcards
azotemia
reduced GFR –> accumulate nitrogenous waste products (mostly ammonia)
hypo/hypervolemia impact
baroreceptor in afferent arteriole which modulates ATII and renin secretion which vasoconstrictors and effects the GFR
acute kidney injury 3 stages
increasing creatinine in serum and reducing urine output
acute kidney injury
abrupt decline in renal function leading to increased
nitrogenous waste products
3 causes/types of acute kidney injury
- pre renal (inadequate plasma flow or hemodyanmics; fall hydrostatic pressure)
- renal (intrinsic) (in kidney parenchyma)
- post renal (obstruction distal to papillary duct (from renal pelvis to distal urethra)
most common acute kidney injury
pre renal
examples of acute kidney injury
pre renal: liver failure, NSAIDs, congestive heart failure, ACE inhibitors
–> hypovolemia, decreased cardiac output etc
intrinsic/ renal: acute glomerulonephritis, sepsis, ischmia, nephrotoxins, vascultiits
post renal: bladder outlet obstruction
impaired auto regulation and hypovolumia causing pre-renal acute kidney injury
hypovolemia: absolute or effective
impaired auto regulation: medication induced (ACE, NSAIDs impact tubuloglmerular feedback)
auto regulation at glomerulus and what impacts it
Glomerular Autoregulation
A. Normal: Regular perfusion pressure, normal GFR.
B. Reduced perfusion: Still within autoregulation range, GFR maintained.
C. NSAID effect:
Blocks vasodilatory prostaglandins → increased afferent resistance
Lower glomerular pressure → GFR decreases
D. ACE-I/ARB effect:
Inhibits angiotensin II → reduced efferent resistance
Less glomerular pressure → GFR decreases
tubuloglomerular feedback
prostaglandin release –> increase renin and prevent excessive vasoconstriction in afferent arteriole
if increase Na+ then ATP from macula densa will decrease GFR and renin
if decrease Na+ then PDG will increase renin
if increase tubular flow then NO will blunt reduce GFR
absolute vs effective hypovolemia causing pre-renal acute kidney injury
absolute: loss of blood volume (hemorrhage or lose ECF) i.e. vomit, diarrhea, hemorrhage, infection, sweat
effective: no volume loss, but low blood pressure/volume from:
- low cardiac output (heart failure), dysregulated hemodynamics (shock, sepsis)
-third spacing: excess ECF in pathological compartments (cirrhosis)
renal/intrinsic acute kidney injury
damage glomerular filtration barrier
vascular injury (sepsis, vascultiits, renal artery obstruction from plaques)
renal ischemia
nephrotoxins
interstitial
post renal acute kidney injury is uncommon- why>
becasue can function with just 1 kidney/ureter
blood labs for acute kidney injury
eGFR via serum creatinine (for filtration)
BUN (nitrogenous waste and see if pre renal AKI) (i.e if fluid depleted, ADH elevates, preserve urea)
sodium, potassium, calcium, phosphate (electrolytes)
urine dipstick for acute kidney injury
▪ Hematuria
▪ Leukocytes (pyuria)
▪ Nitrites (urease-
producing organisms)
* Enterococci,
staphylococci do
not produce nitrites
▪ (Large amounts of)
protein
▪ Specific gravity
* Urine concentration
key urine labs for acute kidney injury
creatinine clearance
fractional excretion of sodium (should be reabsorbed) (if pre renal AKI then we save sodium and exert less, intrinsic/renal may lose sodium if tubules are broken)
protein in urine (albumin)
fraction excretion of sodium in urine
changes in prernal and renal acute kidney injury
Pre-renal AKI: Kidneys retain sodium to conserve fluid (FENa < 1%).
Intrinsic (renal) AKI: Damaged tubules lose sodium (FENa > 3%).
types of casts in urine and causes
RBC casts (kidney damage): vasculitis, malignant hypertesnion
WBC casts (from infection or inflammation): pyelonephritis, interstitial nephritis
granular casts (tubular damage): vascultitis
eosinophiluria: allergic or inflammatory
crystalluria: toxic or metabolic
ETC SLIDE 24
chronic kidney disease staging via
compare eGFR to amount of albumin lost in urine/day
2 mechanisms of damage in chronic kidney disease
- initiating event: damage nephrons i.e. hypertension, diabetes, inflammation, allergy
as more nephrons are damaged then the healthy ones need to work harder and filter more
hyperfiltration –> higher pressure in viable glomeruli –> distort glomerular capillary and podocyte end feet –> damage filtration barrier –> glomerulosclerosis
compensation in chronic kidney disease
and what it leads to
Hyperfiltration refers to an increased filtration rate in the remaining functional nephrons when some nephrons are lost due to kidney damage.
leads to increase glomerular pressure, proteinuria, glomeruloscleoris
glomerular changes in chronic kidney disease
hyperfiltration and hypertrophy or remaining nephrons
- reduction in nephron
number - enlargement of capillary
lumens - focal adhesions
impacts of proteinuria in chronic kidney disease
albumin leak into tubules and so does pro inflammatory and pro fibrotic cytokines –> inflame and fibrosis of intersititum
oxidized lipoproteins leaks and make ROS
chronic kidney disease for how long
3 months
most common causes of chronic kidney disease
diabetes mellitus and hypertension
findings in chronic kidney disease
albuminuria
proteinuria
hematuria
GFR <60ml/min
uremia
renal excretory failure and metabolic waste products accumulate
azotmeia plus accumulation of metabolic waste
ammonia and other nitrogenous breakdown products more dangerous than urea
uremai can cause
metabolic, endocrine problems: anemia, vitamin D deficiency, secondary hyperparathyroidism
GI
peripheral neuropathy
heart and lung (pleural effusion, CVD)
dehydration, edema, osterodystrophy, myopathy, dermatitis etc
