Renal Lab Eval Flashcards
Kidney’s fxn?
- excretion of waste products of metabolism
- regulate excretion of water and solutes (Na, K, and H), through changes in tubular reabsorption or secretion
- secretes hormones: renin, prostaglandins, and bradykinin
erythropoietin, Ca2+, phosphorus, (and calcitriol)
Sxs of kidnney disease?
- gross hematuria, flank pain
- edema, HTN, signs of uremia
- many pts are asx, only sign is elevated serum creatinine or abnorm uirnalysis
Azotemia?
- elevated BUN and/or creatinine, buildup of abnormally large amounts of nitrogenous waste products in the blood
Oliguria?
- urine output of less than 400 ml a day, or less tahn 20 cc/hr
Anuria?
- hardly any output at all
- less than 100 mL/day
Causes of pre-renal failure?
- volume contraction (dehydration)
Causes of intrinsic renal failure?
- arteriolar damage (acute HTN)
- glomerulonephritis
- ATN (acute tubular necrosis)
Causes of post-renal obstruction?
- ureteral obstruction
- bladder outlet obstruction
What does the GFR tell us? normals? influenced by?
- sum filtration rate of all fxning nephrons
- men norm: 130 mL/min
- women: 120 mL/min
- influenced by: age, sex, body size, RBF and HP in glomerulus
How can the GFR be measured?
- CrCl
- urea clearance
- inulin clearance - 100% filtered, gold std for GFR
What is CrCl? Normals?
- endogenous substance used to assess GFR
- men (Up to 40): 107-139 ml/min
- women: 87-107
- overestimates true GFR by up to 40% because of active tubular secretion of creatinine
How does GFR correlate with kidney disease?
- level of GFR has prognostic indications but isn’t the exact correlate to loss of nephron mass
- stable GFR: doesn’t imply stable disease
- some pts with renal disease may go unrecognized b/c of normal GFR
What is BUN (blood urea nitrogen)
- urea nitrogen is what is formed when protein breaks down
- normal range: 6-20 mg/dL
- many drugs can effect the BUN
- usually measured with creatinine to monitor kidney fxn
What causes an increase in BUN?
increases when protein is broken down and more ammonia forms:
- renal disease
- excessive protein breakdown (catabolism - tissue necrosis)
- very high protein diet
- GI bleeding***
- burns
- tetracycline
- fever
- decreased GFR: less BUN presented at glomerulus to be removed from the blood
slower transport time through PCT allows more reabsorption
What causes a decrease in BUN?
- liver disease (liver unavailable to convert ammonia to urea then the BUN will decrease and the ammonia increases)
- starvation
Where does BUN come from?
- protein is cleaved from the AA and a nitrogen is left behind so it takes up 3 H+ to form ammonia
- NH3+ is then processed through the liver to become urea
- when urea enters to blood stream it is called BUN
- then it is excreted by the kidney
How does decreased GFR lead to increased BUN?
- 2 ways
1. decreased flow through glomerulus
2. slower transport time allows more BUN to be resorbed at level of PCT
What is creatinine?
- formed from normal breakdown of muscle
- more muscle mass the higher creatinine
- lower the muscle mass the lower the creatinine (normal reduction in creatinine as a person ages and loses muscle mass)
Normal range of creatinine?
- waste product of protein breakdown excreted by the kidneys
- normal range: men - 0.8-1.4
women: 0.6-1.2 - 50% loss of renal fxn is needed to increase serum creatinine from 1-2 mg/dL
- used in ratio with BUN to determine types of azotemia
In what situations is creatinine increased?
- renal failure
- diet: increased digestion of meats
- meds: ACEIs, diuretics, NSAIDs
- muscle disease/breakdown: muscular dystrophy, rhabdomyolysis
- blockage at sites in DCT that allow for active secretion
- decreased GFR as there is less creatinine presented at glomerulus to be filtered out
when would creatinine be decreased?
- pregnancy: normal occurence
- range in pregnancy: 0.4-0.6 mg/dL (increased volume)
What happens to creatinine with a decreased GFR?
- increases
- instead of creatinine being reabsorbed in the tubules like BUN with a decreased GFR the creatinine is just dumped out
- in the DCT creatinine is actively secreted from the body to be eliminated by the kidneys
- this active secretion at the DCT can be blocked by drugs such as cimetidine and trimethoprim therefore increasing serum creatinine
Normal range of BUN/creatinine ratio?
- normal: 10-20.1
- elevated: greater than 20.1
- increased ratio in a low flow (low BP) state
- BUN/serum creatinine
When is BUN/creatinine ratio increased with normal creatinine?
- prerenal disease (decreased renal perfusion)
- catabolic state with increased tissue breakdown
- GI hemmorrhage
- high protein intake
- certain drugs: tetracycline, steroids
When is BUN/creatinine ratio increased with elevated creatinine?
- postrenal disease (obstructive uropathy)
- prerenal disease superimposed on renal disease
When is decreased BUN/creatinine (less than 10:1) with decreased BUN occur?
- acute tubular necrosis (intrarenal disease)
- low protein diet, starvation, severe liver disease
- repeated dialysis
- SIADH
- pregnancy
When is BUN/Creatinine decreased with increased creatinine?
- rhabdomyolysis
- muscular pts who develop renal failure
Normal values for Na and K?
- Na+: 135-145 mmol/L
- K+: 3.8-5.5 mmol/L
Normal values for anions?
- chloride: 98-106 mmol/L
- bicarb: 21-28 mmol/L
- total CO2: 23-30 mmol/L
substances that are normally reabsorbed in the kidneys?
- Na+
- K+
- urate
- chloride
- Ca2+
- phosphate ions
- glucose
- AAs
What substances are normally secreted in the kidneys?
- H+
- K+
- urate
Sodium reabsorbtion in the kidneys? Impt of Na+?
- freely filtered at glomerulus
- 60% reabsorbed isotonically in PCT
- reabsorbed in loop of Henle
- reabsorbed in DCT, secondary to aldosterone effect
- normall daily Na excretion balances daily intake (body needs for Na can be met by as little as 500 mg/day)
- Na+ is extracellular ion, doesn’t move freely across the membrane, impt in cardiac and neuro fxn (too low - seizures)
What is hyponatremia primarily due to? Correction?
- most common electrolyte disorder
- primarily due to intake of water that can’t be excreted
- excess Na+ loss relative to water loss occurs via renal or extrarenal routes
- therapy: correct underlying problem, Na+ and fluid replacement
When does hypernatremia occur?
- occurs when there is an excessive loss of water, relative to Na+
- causes include renal and extrarenal routes
- therapy: approp fluid replacement combined with use of diuretics to rid body of excess Na+
Gains and losses of K+?
- major cation in intracellular compartment
- gains: normally derived from dietary sources
balance usually maintained in healthy persons by daily intake of 50-100 mEq - losses: kidneys are the main source of K loss (80-90% lost in urine, remainder lost in stool or sweat)
Why is it so impt to be efficient at regulating K+?
- small change (1-2% of EC volume) can lead to dangerously high serum levels
- norm: 3.5-5 mEq/L
What is K+ homeostasis dependent on?
- pH (acid-base disturbance causes K+ shifts b/t fluid compartments, in acidosis K+ levels go up as bringing K+ out of cells into blood - diabetic ketoacidosis)
- renal fxn including effects of diuretics aldosterone and renal parenchyma
- GI fluid losses (excessive K+ loss with V/D)
What does hypokalemia result from?
- K+ shifting to ICF w/o change in total amt of K+ in the body
- depletion of body stores (diuretic therapy w/o K+ replacement)
When does hyperkalemia occur?
- acidosis
- from cellular damage (fever, hemolysis, rhabdomyoylsis - K+ leaking out of destroyed cells)
- renal and adrenal diseases
- meds (ACEIs)
- artifical hyperkalemia: hemolyzed blood specimens, thrombocytosis or leukocytosis
When does hypochloremia occur?
- excessive loss of Cl-: GI losses DKA mineralocorticoid excess salt-losing renal diseases high bicarb levels