Renal Function Flashcards
Kidney Anatomy
2 bean shaped organs
cortex & medulla housed in fibrous capsule of connective tissue
nephrons
kidney function
eliminate NPN compounds
water & electrolyte balance maintained
acid-base balance
endocrine functions
Nephron
glomerulus - end of renal tubule, capillary tuft, sits in Bowman capsule proximal convoluted tubule loop of henle distal convoluted tubule collecting duct
Glomerular filtration
depends on blood pressure through glomerular capillaries & integrity of semi-permeable glomerular membrane
membrane is negatively charged so proteins & others are repelled
GFR
volume of blood filtered per minute
glomerular filtration rate
Proximal convoluted tubule
returns 75% of water, Na, Cl
100% of glucose, amino acids, vitamins, proteins, & varying amounts of urea, uric acid & ions like Mg, Ca, K, HCO3
water & cl are passive transport; everything else is active
Loop of Henle
opposing flows result in osmolality changes & hypo-osmole urine
COUNTER CURRENT MULTIPLIER
ascending limb of henle
Na & Cl are reabsorbed into medulla interstitial fluid along limb impermeable to water -> hyperosmotic medulla diluting limb (!)
descending limb of henle
highly permeable to water but does not reabsorb Na & Cl
water leaves for the medulla
fluid in loop is hypo-osmotic urine
Distal convoluted tubule
adjusts the electrolyte & acid-base homeostasis via ADH & aldosterone actions
aldosterone
acts on distal tubule stimulates Na reabsorption & excretion of K & H+
Urea
ammonia from amino acid degradation made into urea in liver
40-60% reabsorbed into medulla to maintain high osmolality
creatinine
waste from muscle
not reabsorbed by tubules
Uric acid
waste from purine metabolism
only 6-12% of original uric acid is excreted; can contribute to crystal in urine, gout & calculi
water balance
controlled by ADH, proximal, distal & collecting ducts
sodium balance
aldosterone system (RAS) governs Na reabsorption
Potassium balance
excretion controlled by kidneys
actively reabsorbed through nephron; negatively effected by aldosterone
Chloride balance
maintenance of extracellular balance; passive reabsorption in proximal tubule
Phosphate, Mg, Ca balance
PTH controls proximal tubule reabsorption of phosphates
Mg filtered by tubule & reabsorbed via PTH action
calcium under PTH & calcitonin control so tubule reabsorption is not significant
Endocrine function
makes EPO, 1,25-dihydroxy vitamin D3, & prostaglandins
Kidney renin
made by juxtaglomerular cells of renal medulla; released when blood pressure decreases
activates renin-angiotensin system
EPO production
made by cells close to proximal tubule, production regulated by 02 levels in blood within 2 hour window
1,25-dihydroxy vitamin D3 production
made when kidney enzyme converts 25-hydroxy vit D to this form
adds a methyl group & becomes an active vitamin
Prostaglandins
made from arachidonic acid
increase blood flow, Na & water excretion & renin release
oppose renal vasoconstriction due to angiotensin II & norepinephrine
Creatinine clearance
creatinine clearance to assess glomerular filtration rate
males: 97-137 ml/min
females: 88-128 ml/min
Urea clearance
urea 40% reabsorbed by tubules- not used now
Cystatin C
low molecular weight protein from nucleated cells; freely filtered by glomerulus;
reabsorbed & catabolized by proximal tubule
constant rate unaffected by age, gender, race, muscle mass;
may be better early indicator of decreased GFR
Cystatin C vs Creatinine
creatinine - more stable w/in a person so fluctuations seen indicate renal function over time
cystatin C- doesn’t change much between people but within a person there is bioflux; marker better at detecting minor renal impairment
Urine electrophoresis
normally excrete 50-150 mg/24 hrs
increases in protein indicate disease states
do electrophoresis to ID proteins & define disease type
Beta2-Microglobulin
small, non-glycosylated peptide found on surface of nucleated cells
shed at constant rate normally
elevated levels indicate myeloproliferative & lymphoproliferative disorders, inflammation or renal failure
filtered by kidney & then 99.9% reabsorbed
elevated b2 microglobulin in transplant patients
can indicate rejection
Myoglobin
associated w/ muscle injury (rhabdomyolysis) overloads kidney proximal tubule & see acute renal failure
increased in serum can be early indicator of renal disease
Microalbumin
increased in diabetics w/ nephrophathy
nephrophaty
renal hypertrophy
increased glomerular thickness
tubular basement membrane dysfunction
increased microalbumin, blood pressure & leads to increased renal damage
Kidney Diseases
glomerular diseases tubular diseases infections & obstructions renal failure renal hypertension
Glomerular diseases
damage renal glomerulus directly & lead to tubular disease over time:
actue glomerularnephritis
chronic glomerularnephritis
nephrotic syndrome
acute glomerularnephritis general
inflamed glomeruli w/ decreased capillary lumen
can recover from acute
acute glomerularnephritis labs
hematuria, proteinuria, increased BUN, creatinine
Na & water retention
acute glomerularnephritis causes
group A Beta hemolytic strep drug related infections systemic lupus bacterial endocarditis
Chronic Glomerularnephritis general
lengthy glomerular inflammation
leads to scarring & loss of function of nephrons
chronic glomerularnephritis
increased BUN & other nitrogen compounds
hematuria
proteinuria
labs for nephrotic syndrome
proteinuria (>3.5g/day!!), decreased oncotic pressure leading to increased edema, w/ hyperlipidemia
Tubular diseases
occur as decreased GFR due to progressive tubular defects
damage to excretion/reabsorption functions of tubules
renal tubular acidosis
acute inflammation of tubules & surrounding interstitium
Renal tubular acidosis (RTA)
primary tubular disease
distal RTA- tubule cannot keep up w/ pH gradient between blood & tubular fluid
proximal RTA- decreased HCO3 reabsorption, resulting in hyperchloremic acidosis
acute inflammation of tubules & surrounding interstitium
may occur due to analgesics/drugs or radiation toxicity, methicillin hypersensitivity reaction, renal transplant rejection, infections
decreased GFR, decreased metabolic acid excretion
see WBC casts
issues w/ Na control
urinary infections
pyelonephritis, cystitis micro >105 colonies/ml hematuria pyuria WBC casts
urinary obstructions
gradual rise in intra-tubular pressure until nephrons necrose & get chronic renal failure maybe from repeated infections decreased urine concentrating capacity decreased metabolic acid excretion decreased GFR decreased blood flow to kidney
urinary obstructions
gradual rise in intra-tubular pressure until nephrons necrose & get chronic renal failure maybe from repeated infections decreased urine concentrating capacity decreased metabolic acid excretion decreased GFR decreased blood flow to kidney
renal failure
acute renal failure & chronic renal failure
acute renal failure diseases
pre-renal failure: blood supply defect prior to kidney
renal failure: defect in kidney; often dacute tubular necrosis
post renal failure: defect after urine exits; obstruction or bladder rupture
Chronic Renal Failure
when progressive loss of GFR occurs & patient has additional factors of risk-> end stage renal failure
chronic renal failure increases with:
diabetes mellitus age obesity metabolic syndrome hypertension decreased HDL increased triglycerides increased glucose
Renal hypertension
decreased perfusion to all of kidney (ischemia) decreased perfusion to part of kidney increased Na decreased serum K increased urine K
Dialysis
use semi-permeable membrane in dialysate bath
hemodialysis
dialysate & blood running in opposite directions to filter out waste
peritoneal dialysis
less clearance but continuous
transplantation
survivals vary; living donor lasts longer
3 year survival 65-85%
