Renal Flashcards
Explain blood flow through the nephron
Aorta
Renal artery
Afferent arteriole
Highly vascular
glomeluar/bowmann’s capsule filters blood
efferent arteriole brings filtered blood into renal vein
Unfiltered blood/filtrate continue into tubule where it will be
- reabsorbed ito peritubular capillary
- secreted into tubule
Main Functions of Kidneys (7)
- Urine formation/regulation of fluid components through filtration, reabsorption, secretion, and excretion
- Acid base balance
- fluid and electrolyte balance
- remove metabolic waste from body
- EPO production: control production of RBC by bone marrow
- Blood pressure regulation through renin release
- Produces most active form of vitamin D: regulates bone density
Explain RAAS system
- Kidneys sense drop in BP and fluid volume
- Release renin which acticates angiotensinogen to angiotensin I
- This is converted from angiotensin II by ACE
- This acts on adrenal gland to release aldosterone
- aldosterone acts on kidney’s to resorb sodium and constrict blood vessels
Normal BUN
2.9-8.2
What does BUN reflect
GFR and urine concentrating capacity
What effects BUN
hydration status, level of catabolism, protein intake, and GI bleeding
BUN increases as GFR _______
decreases
Why is BUN not the most reliable measure of GFR?
Because it is resorbed back into the blood from tubule to peritubular capillary
Normal creatinine
50-110
What is creatinine?
End-product of muscle metabolism
Why is creatinine the most reliable indicator of renal health?
Released back into blood at constant rate
Elimiinated at a rate related to renal function
Not resorbed back into blood
What occurs in the body when kidneys fail?
Less waste is removed, inability to regulate fluid, electrolytes, and pH, creatinine and BUN build in blood
Define AKI and what 3 things does it lead to
Abrupt decrease in kidney function leading to:
1. failure to regulate F/E/A/B
2. rapid decrease in urine output
3. Decreased GFR (elevated BUN/creatinine) leading to azotemia
Rapid, progressive, reversible
Define prerenal AKI
decrease in blood flow to kidney (inadequate perfusion)
Define intrarenal AKI
something that happens to the structures in the kidney (i.e. infection such as acute glomerulonephritis, drug toxicity, etc.)
Define postrenal AKI
obstruction to urine outflow (i.e. kidney stone, prostate cancer, etc.)
Causes of prerenal AKI
Decreased kidney perfusion
- Decreased volume
- hemorrhage
- burns
-diaphoresis
- vomiting/diarrhea
- polyuria (DKA/diuretics)
- decreased CO (HF, MI, cirrhosis)
- shock states - arterial occlusion/emboli
- drugs that alter renal perfusion/nephrotoxic
- ACE/ARBS
- NSAIDS
What lab value characterizes prenal AKI
Increased BUN
Causes of intrarenal AKI
Direct damage to renal parenchyma
- acute tubular necrosis (ischemia, necrosis)
- vascular problems (hypertension)
- Glomerulonephritis and other infections
- nephrotoxic drugs
- rhabdomyolysis clogging up glomeruli causing dark urine
Nephrotoxic drugs
ACEs/ARBs
NSAIDs
CT contrast***
Chemo
Antibiotics (aminoglycosides, gentamycin, cephalosporins, PipTaz, Vanco)
Management of rhabdo to prevent AKI
Massive breakdown of skeletal muscle (trauma)- release of myoglobin (plugs glomeruli- damages lining in tubules)
Dark urine
Monitor CK levels, give fluids
What lab values characterize intra renal AKI
Increased BUN and creatinine
Cause of post renal AKI
Caused by an obstruction to the outflow of urine from the kidneys (bladder, ureters, urethra)
- kidney stone
- prostate cancer
- BPH
- catheter obstruction
What lab values characterize post renal AKI
Increased creatinine
What are the risk factors for AKI?
HEMODYNAMIC CHANGES RESULTING IN DECREASED FLOW TO KIDNEYS
- HTN
- Trauma
- diabetes
- nephrotoxic agents
- exposure to heavy metals
- recent hypotensive episode
- tumor/vascular obstruction
- infection/sepsis
- age
What urinary output changes occur in AKI
Changes in amount and concentration depending on injury
Usually oliguria, which causes fluid to buildup in body
What respiratory changes occur in AKI
Pulmonary edema with fluid buildup
Increased RR as body tries to compensate for metabolic acidosis
What A/B changes occur in AKI and why?
Metabolic Acidosis
decreased excretion of nonvolatile acids via urination and decreased renal synthesis of bicarbonates
What electrolyte changes occur in AKI?
- Potassium excess (high)
- Sodium imbalance (normal, high or low)
- Calcium deficit (low)
- Phosphate excess (high)
What hematological disorders occur in AKI?
- Anemia (EPO production)
- Urea decreases clot formation
What neurological changes occur in AKI?
Related to increased ICP (excess fluids), or increases uremia (build up of nitrogenous waste)
Symptoms: Headache, confusion, irritability, seizure, asterixis (hand tremor)
What CV changes occur as result of AKI?
Fluid overload/HTN
MI - clotting with hypocalcemia
What integument changes occur as a result of AKI?
Uremic frost; dry itchy pale skin – buildup of urea
What GI symptoms can occur as a result of AKI?
N/V secondary to acidosis
malnutrition
ulcers (urea is irritating)
How does hypoproteinemia occur is AKI? What is the result?
The glomerular damages leads to incresed permeability across membrane, leading to proteinuria
The decrease proteins in the blood decreases oncotic pressuure so fluids leak into interstitial spaces causing edema
Normal urine output and at what value is there concern?
1500/2000ml/day ; 1-2ml/kg/hr
0.5ml/kg/hr
Normal BUN:Creatinine and value indicative of AKI
Normally BUN and Creatinine ratio ~ 10:1 or 15:1
* A 20:1 ratio of BUN / Creatinine may indicate AKI
- BUN/Cr ratio can be used to diagnose
When is creatinine elevated?
Creatinine is not elevated until ~25% of the nephrons are not functioning
A decrease in CCR indicates a:
A decrease in creatinine clearance rate indicates a decrease in glomerular function
Doubling of serum creatinine means:
a decrease in GFR of about 50%
Normal GFR
Kidneys control own filtration rate dependent upon fluid volumes and BP
Normal = 125 ml/min
What will be seen in the urinalysis and 24 hour Urine of AKI/how in urine osmolality altered?
When renal function is altered:
Urine osmolality increases and urine specific gravity increases
* How much stuff and how heavy the urine is (how concentrated the urine is)
How is serum osmolality altered in AKI?
Serum (blood) osmolality may stay the same
* Electrolytes (serum & urine)
Give insight into what is being filtered or not
Priorities of Treatment for AKI (9)
- restore perfusion
- fluid overload
- electrolyte imbalance
- infection prevention
- acid-base imbalance
- Impaired gas exchange
- acute confusion
- coagulopathies
- diet challenges
How is fluid overload managed in AKI?
- Diuretics
- Fluid restriction as prescribed
- HR, BP, lungs, heart, ECG
- STRICT Intake and output
- Daily weights
- Watch for electrolyte imbalances
- Monitor for evidence of heart failure with fluid overload that has been happening; has heart been able to compensate?
What electrolytes are you most concerned about in AKI
Potassium: acidosis and decreased excretion causing hyper
- arrhythmias (wide QRS)
Sodium: dependent on fluid status
hypo: early due to lack of reabsorption because of lack of healthy nephrons to resorb
hyper: later on which causes cellular dehydration
Why is there increase risk for infection with AKI?
toxin buildup alters inflammatory response
* Changes in leukocyte function
* Altered immune response and function
* Diminished inflammatory response
* Protective mechanisms lost
Why does acid-base imbalance occur in AKI? What is the typical ABG?
Kidneys unable to excrete acid load; defective regeneration and absorption of HCO3
* Metabolic Acidosis
Why is gas exchange impaired in AKI?
Pulmonary edema
Why does acute confusion/decreased cognition occur in AKI?
- Increased ICP in fluid overload (hyponatremia)
- Toxic effects of azotemia
Why doe coagulopathies occur in AKI?
- Bleeding (EPO deficiency)
- Toxic buildup reduces platelet adhesion
What diet challenges occur in AKI?
- High state of catabolism (breaking proteins down into amino acids)
- Therefore: high calorie, low protein, AVOID K, Na
- Lack appetite
What 5 reasons would dialysis by used in AKI?
- Refractory acidosis (not responsive to correction)
- Electrolytes (refractory; severe increased K+)
- Acute intoxication on salicylic acid, lithium, magnesium laxatives, ethylene glycol
- Overload with fluid (pulls fluid off without having to administer diuretics that may be damaging to kidneys)
- Uremic complications (pericarditis, platelet dysfunction leading to bleeding)
Define CKD
Slow, progressive, irreversible loss of renal function, affecting nearly all organ systems
What does CKD result from?
- Primary renal condition (polycystic kidney disease, glomerulonephritis)
- Other diseases that produce a long-term renal insult (diabetes, hypertension)
Risk factors for CKD
- diabetes
- HTN
- proteinuria
- family history
- increasing age/wear out over time
Why is diabetes a risk factor for CKD?
- Excess glucose stiffens efferent arteriole causing it to stiffen and narrow so blood cannot leave glomerulus
- Leads to hyperfiltration and increased glomerular pressure, expanding size and stiffness of glomerular
Why is HTN a risk factor for CKD?
- Narrowed lumen and thickened walls mean less blood and oxygen delivered to the kidney causing ischemic injury
Symptoms of CKD
Sodium/Water Imbalance
- HTN
- increased vascular volume/edema
- HF
Impaired Potassium Balance
-Hyperkalemia
Impaired nitrogenous waste elimination/uremia
- coagulopathies (urea increases bleed rx)
- pericarditis
- impaired immune function
- skin disorders
- GI manifestations
- neuro manifestations
- sexual dysfunction
Decreased EPO production
- anemia
A/B imbalance
- acidosis
Lack of Vit D activation/phosphorous elimination
- hypocalcemia
- hyperPTH
- osteodystrophies
Explain the roles of phosphorous and calcium in the development of osteodystrophies in AKI
- Phospohate
- is retained
- binds to calcium, decreasing serum levels - Calcium
- decreased production of active vit D
- decreased absorption, decreasing serum levels
Both of these things cause PTH release
PTH release releases calcium stored in bones (bone demineralization and density loss)
Serum caclium increases
Phosphate binds again (hyperphosphatemia in AKI) which furthers metastatic calcifications that can lodge in organs in vessels
What are the various sources of anemia in CKD?
hemolysis, bone marrow suppression, decreased erythropoietin and iron
Decreased platelets - bleedings
Nursing care of CKD
- Dialysis
- HTN management
- Nutrition
- hypoxia
- infection risk
- metabolic acidosis
- drugs to treat
* Hyperkalemia
* HTN
* CKD-mineral and bone disorder
* Anemia
* Dyslipidemia
Diet for CKD
- Low protein diet, sodium, potassium, phosphate restrictions
Why does hypoxia occur in CKD
associated with anemia with decreased RBC carrying capacity
Why is infection risk high in CKD
Buildup of nitro waste, azotemia effecting response
When is RRT required
when kidneys are functioning at < 10-15% of their normal rateT
True or false dialysis is a cure
- Doesn’t cure kidney disease or make kidneys well
- Doesn’t fully replace kidney function
- (CKD) must continue to have dialysis for rest of life (unless transplant)
2 Types of RRT
- Hemodialysis (AKI, CKD) 2 types:
- Intermittent (generally 3 x 4hr “runs” per week)
- Continuous renal replacement therapy (CRRT) – AKI patients
- Peritoneal dialysis (CKD)
How does dialysis work
- Dissolved particles are transfused across a semipermeable membrane from one fluid compartment to another
- Corrects fluid, electrolyte and acid-base imbalances, and removes waste products
What is a dialysate?
- Used in both types of dialysis
- Uses osmosis & oncotic pressure to transfer fluids/particles back and forth across the semi-permeable membrane
- Specific solution prescribed based on patient’s current bloodwork to facilitate diffusionA
Advantages of peritoneal dialysis
Can be done on a regular basis so that fluid and electrolyte shift is less dramatic
Can be done at home (don’t need to be in hospital)
Relieves uremic symptoms
Greater flexibility with treatment (can do other activities/work while dialysis happens; can travel)
Disadvantages of peritoneal dialysis
Considerable infection risk (peritonitis)
Permanent catheter in abdomen
Can’t get wet (no swimming)
Dialysis a daily part of life
Slow (slower than hemo)
Abdominal discomfort
Describe the hemodialysis system
- Blood Compartment
- Contains electrolytes, wastes, toxins, excess water
- Exerts oncotic and hydrostatic pressure
- Dialysate Compartment
- Contains electrolytes similar to plasma
- Circulates on the outside of the tubing system
- Has a semi-permeable membrane; forces movement of waste from blood into dialysate
- Adjustable
How to assess arm of fistula for hemodialysis
- High risk!! Clots, bleeds, infection
- DO NOT take BP or blood work on the arm of a fistula!
- Inspect the AV fistula for redness, bruising, pustules, swelling, bulging
- Palpate for a thrill (should have)
Advantages of hemodialysis
Relieves uremic symptoms
Quick and efficient
Requires min. 3 treatments/week (4-8hrs)
Most individuals have suitable vessels to establish an access site
Diadvantages of hemodialysis
New medications, restricted intake of fluids
Requires vascular access each time and anticoagulation
Must plan around hemodialysis schedule
Travel to dialysis unit
Restricts activity level
Who is CRRT used for?
- For patients who are hemodynamically unstable
- Has less hemodynamic side effects than intermittent hemodialysis
- Useful in AKI
- Allows for more gradual removal of excess electrolytes/fluid
- Critical care setting ONLY
- Uses different methods to clear excess fluids, fluids and solutes, electrolytes, creatinine, and urea.
