Chapter 46: acute kidney injury and chronic kidney disease Flashcards by Caleigh Justen

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

Three phases of AKI and how to classify progression

phases: oliguric, diuretic, and recovery

RIFLE classification

Risk
Injury
Failure
Loss
End stage renal disease

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

Recovery phase
how long?

up to 12 months

increased GFR, decreased BUN and creatinine

influenced by severity of injury and complications

How well did you know this?

Not at all

Perfectly

Diagnostic studies for AKI

thorough history
serum creatinine, BUN, and electrolytes
UA
renal ultrasound
renal scan
CT scan
renal biopsy

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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