Chapter 46: acute kidney injury and chronic kidney disease Flashcards
AKI
what?
accompanied by?
Rapid loss of kidney function with
-rise in creatine and/or fall in urine output
-High BUN and K+
-Azotemia = accumulation of nitrogenous wastes
High mortality rate! –> usually affects people with other issues
Prerenal causes of AKI
factors that reduce systemic circulation, causing less renal bloodflow, leading to oliguria –> dehydration, heart failure, low CO
Autoreg mechs try to preserve the flow
-retains water and sodium and decreases urine output
Intrarenal causes of AKI
conditions that cause direct damage to kidney tissue
-prolonged ischemia
-nephrotoxins
-hemoglobin released from hemolyzed RBCs
-myoglobin released from necrotic muscle cells
-kidney diseases – acute glomerulonephritis and SLE
Intrarenal causes of AKI: acute tubular necrosis: ATN
-Hypoperfusion
-Results from ischemia, nephrotoxins, or sepsis
-ischemia disrupts basement membrane and creates patches in tubular epithelium
-nephrotoxic agents kill tubular epithelial cells and clog the tubules
-possible reversible
Postrenal causes of AKI
mechanical obstruction of outflow –> leads to reflux in renal pelvis, fucking up renal function —> BPH, prostate cancer, calculi, trauma, and extrarenal tumors
Bilateral ureteral obstruction is even worse! –> hydronephrosis –> Might be able to recover if you clear the obstruction within 48 hours
Three phases of AKI and how to classify progression
phases: oliguric, diuretic, and recovery
RIFLE classification
Risk
Injury
Failure
Loss
End stage renal disease
Oliguric Phase: urinary changes
Oliguria
-less than 400 ml/day
-happens within 1-7 days after injury
-lasts 10-14 days (your probs gonna die if it lasts longer)
-urinalysis = casts, RBCs, WBCs, protein
-specific gravity is 1.010
-osmolality is 300 mOsm/kg
Half of people with AKI don’t even have oliguria though
Oliguric phase: fluid volume
Hypovolemia might worsen AKI
Less urine output leads to retension
-neck and veins distended
-bounding pulse
-edema
-hypertension
Fluid overload can lead to heart failure, pulmonary edema, and pericardial and pleural effusions
Oliguric phase: metabolic acidosis
messed up kidneys can’t get rid of H+ or acids
serum bicarbonate production goes down -> defective reabsorption and regeneration
severe acidosis –> Kussmaul respirations increase exhaled CO2
Oliguric phase: sodium and potassium
loss of sodium due to messed up tubules –> low Na can cause cerebral edema
Too much K bc kidneys can’t get rid of it
-increased risk with massive tissue trauma
-usually asymptomatic
-ECG stuff
Oilguric phase:
hematologic disorders
waste accumulation
neurologic disorders
Hematologic
-leukocytosis - infection may be fatal - side effects in urinary and respiratory system
waste
-more BUN and creatinine
Neurologic
-fatigue and difficulty concentrating
-seizures, stupor, coma
Diuretic phase
how long?
urine output?
1-3 weeks
1-3 L, but up to 5
Osmotic diuresis from high urea and inability of tubules to concentrate urine
Monitor for hypo- volemia, tesion natremia, kalema and dehydration
Recovery phase
how long?
up to 12 months
increased GFR, decreased BUN and creatinine
influenced by severity of injury and complications
Diagnostic studies for AKI
thorough history
serum creatinine, BUN, and electrolytes
UA
renal ultrasound
renal scan
CT scan
renal biopsy
AKI diagnostic study contraindictions for contrast
MRI or MRA with gadolinium contrast could KILL the person –> CIN
Diabetics need to stop taking melformin 48 hrs before and after contrast to avoid lactic acidosis
If absolutely necessary to use contrast in risky situation, use low dose and optimal hydration
Interprofessional care: fluid
make sure intravascular volume and CO are good
-use loop or osmotic diuretics
monitor intake during oliguric phase
-fluid restriction calculation : O for past 24 hrs + 600 mL
Interprofessional care: hyperkalemia therapies
move K into cells with insulin and sodium bicarbonate –> for acute issues
use calcium gluconate to stabilizy myocardium
use kayexalate or Veltessa or dialysis to excrete K –> slower, not for acute cases
dietary restriction
Indications for renal replacement therapy RRT
volume overload
high K
metabolic acidosis
BUN > 120 mg/dL (43 mmol/L)
significan mental status changes
pericarditis, pericardial effusion, or cardiac tamponade
clinical status of patient
Types of RRT
Peritoneal dialysis (PD)
- not common –> most closely resembles actual kidney func
Intermittnet hemodialysis (HD)
-emergent therapy
Continuous renal replacement therapy (CRRT)
-cannulation of artery and vein
-continuously 24 hrs
Nutrition therapy
get enough calories –> mostly carbs and lots of fat (to prevent ketosis)–> also enough protein to prevent breakdown
limit Na, K and phosphate
Ca supplements of Phosphate-bidig agents
enteral or parenteral nutrition
Why are old ppl more susceptible to AKI?
slower GFR already due to aging
Dehydration from polypharmacy, illness, and immobility
HT, diuretic therapy, aminoglycoside therapy, obstructive disorders, surgery, infection, and contrast medium
less able to recover –> can still do RRT though
Chronic kidney disease
more or less common than AKI? Why?
more common
aging population, obesity, diabetes, HTN
How does KDIGO define CKD?
Kidney damage and low GFR
Kidney damage
-pathologic abnormalities
-markers of damage = blood, urine, and imaging tests
Low GFR
-less than 60 mL/min/1.73m^2 for over 3 months
Leading causes of CKD
Diabetes - 50%
HTN - 25%
Other - glomerulonephritis, cystic diseases, urologic diseases
ppl with CKD are often asymptomatic and go untreated
Stages of GFR during CDK
1) >90
2) 60-89
3a) 45-59
3b) 30-44
4) 15-29
5) <15 or dialysis –> ESRD
clinical action plan for stages of CDK
1) diagnose and treat –> reduce CVD risk
2) estimation of progression
3a) evaluate and treat complications
3b) get more aggressive with treatment
4) prepare for RRT (dialysis or transplant)
5) RRT if uremia present and patient wants treatment (alternative is death)
Ethnicity CKD
blacks 4x more likely than whites (HTN)
native americans 2x more likely (diabetes)
Hispanics 1.5x more likely
how much does medicare cover?
80%
Early stages of CDK manifestations
no change in urine output
polyuria might be present due to diabetes
as CDK progresses, increase fluid retention –> need diuretic
After a while on dialysis, patients become anuric
Clinical manifestations of CDK: hyperkalemia
most serious electrolyte disorder of kidney disease
Fatal dysrhythmias –> when K reaches 7-8
Decreased excretion, breakdown of cellular protein, bleeding, and metabolic acidosis lead to increased K
—-also foot, dietary supplements, drugs and IVs
Clinical manifestations of CDK: sodium
could be high, low, or normal
Impaired excretion –> Na and water retention
Dilutional hyponatremia could happen –> edema, HTN, heart failure
CDK clinical manifestation: metabolic acidosis
From kidney’s inability to excrete acid
Also defective reabsorption and regeneration of bicarbonate
Plasma bicarbonate level usually falls to 16-20 mEq/L
clinical manifestations of CDK: Anemia
Bc less EPO produced –> usually stimulates bone marrow to make RBCs
Also, nutritional deficiencies, RBCs die quicker, more hemolysis, blood sampling, GI bleeding, HD, and increased PTH
Decreased iron stores
Folic acid lost in dialysis
Which condition is closely linked with CKD? Why?
Cardiovascular disease
-myocardial infarction , ischemic heart disease, peripheral arterial disease, HF, cardiomyopathy, and stroke
Traditional CV risk factors that are common in CDK patients = HTN and high lipids
Nontraditional CV risk factors = vascular calcification and arterial stiffness
HTN in CKD patients
Both a cause and a consequence
- aggravated by Na and H2O retention
-increased renein production might contribute
HTN, ECF volume overload, and anemia might dvlp into left ventricular hypertrophy which could lead to cardiomyopathy and HF
-HTN can cause retinopathy, encephalopathy, nephropathy
What’s one of the most important goals in CKD treatment?
What causes dysrhythmias?
Uremic pericarditis progression and presentation
BP cotrol
Hyperkalemia and decreased coronary artery perfusion
progresses to effusion and tamponade –> friction rub, chest pain, and fever
Clinical manifestation of CDK: Integumentary issues
Pruritus
- calcium-phosphate deposits and sensory neuropathy
-itching might be intense –>leads to bleeding or infection
Uremic frost
-urea crystalizes on skin
-happens when BUN > 200 mg/dL
Clinical manifestations of CKD: Reproductive issues
Infertility and decreased libido
-dudes have low sperm count –> girls have amenorrhea
Sexual dysfunction
-physical, psychological, and medication side effects
Pregnancy during dialysis is super risky for mom and baby
How to treat CKD: Hypertension
weight loss (if indicated)
Therapeutic lifestyle changes
Diet recommendations (DASH Diet)
Antihypertensive drugs –> usually need 2+
***if diabetic, give ACE inhibitors and ARBs
How to treat CKD: anemia –> EPO
Get them EPO
-Epoetin alfa (epogen and procrit)
-Darbepoeitin alfa (Aranesp)
-Give IV or subcutaneously
-HGB and Hct might take 2-3 weeks to increase
-Side effects = thromboembolism and HTN
How to treat CKD: anemia –> supplements
Iron supplements
-Give if plasma ferritin level is <100 ng/mL
-Side effects: gastric irritation and constipation
-Might make stool dark in color
Folic acid supplements
-needed for RBC formation
-removed by dialysis
What to avoid when treating CKD –> esp when it comes to anemia
blood transfusions
-increase the development of antibodies –> makes finding kidney donor hard
-might lead to iron overload
Can do it if significant blood loss or symptomatic anemia
