Week 5: Acute and Chronic Kidney Disease Flashcards
what is the function of the glomerulus and tubular system? what is essential for reabsorption to happen?
glomerulus
- selective filtration of water & solutes from blood
- filtration of blood: 125mL/min but only 1mL/min is excreted as urine
tubular system
- reabsorption of essential minerals; excretion of non-essential ones
- dense capillary network needed for reabsorption ability
what is the nephron’s function and parts of the nephron w/functions?
Functional unit of the kidney working for electrolyte balance and blood pressure
Glomerulus
- capillary network allowing for filtration
Bowman’s capsule
- part containing the glomerulus
Proximal tubule
- reabsorption of 80% electrolytes and water
- majority of absorption occurs here
Loop of henle
- concentration and conservation of water
- ascending limb: Na and Cl
- descending limb: water
Distal tubule
- permeable/impermeable to water and solutes so we can have final concentration
- ADH influences permeability of nephrons (high level = more water reabsorption)
- acid-base balance impact
Collecting duct
- reabsorption of water with ADH
- everything is getting ready for excretion
vascular anatomy of the kidneys: cardiac output
- highly vascular
- receive up to 20% of CO
- 1L to 1.2L/min of blood flow
vascular anatomy of kidneys: renal artery
- divides into arterial branches that become progressively smaller vessels ending with the afferent arterioles
arterial branches:
- afferent arterioles: single afferent supplies blood to each glomerulus
- efferent arterioles: blood exits glomerulus
3 processes involved in urine formation
- glomerular filtration
- tubular reabsorption
- tubular secretion
functions of the kidneys (6)
- elimination of metabolic wastes
- blood pressure regulation: RAAS system, increase BP to have better kidney perfusion. Increase aldosterone also increases BP
- erythrocyte production: production of RBC in bone marrow, renal failure can cause anemia
- Vit D activation: needed for calcium uptake in GI. If GFR > 40, we cannot activate Vit D. We give Calcitriol if pt cannot activate.
- Prostaglandin synthesis: simulate renin production, RAAS system, and impact local constriction/dilation of muscle impacting glomerulus pressure
- Acid-base balance: ex. resp distress causing resp acidosis (increase CO2 increase acid levels), so kidneys kick in to fix it OR they become compromised
Chronic kidney disease characteristics
kidney damage or decreased function for a period greater than 3 months
- decreased function: GFR <60mL/min/1.73 m2
- kidney damage: urinary albumin excretion of ≥30mg/day or equivalent
- develops slowly (adaptive hyperfiltration, increased pressure)
- GFR accompanied by urine sediment or abnormal imaging test results
- kidney biopsy with abnormalities
Acute kidney injury characteristics
- sudden decline in renal function (hours/days)
- increased BUN and CR
- oliguria <400ml/24hr
- hyperkalemia and Na retention
What is important in a history assessment regarding kidney damage? (7) - C P H E I S R
- complaints: onset, location, duration
- predisposing factors: medicines (OTC, antihypertensives), recent infections requiring antibiotic therapy, diagnostics using radiopaque contrast
- recent history: SOB, change in cognition, rapid fluid volume gain, weight gain 2lb+/day, nutritional-metabolic pattern
- signs that suggest extracellular fluid depletion: thirst, decreased skin turgor, lethargy
- Signs implying intravascular fluid volume overload: pulmonary congestion, increasing heart failure, rising BP
- past kidney studies: imaging, biopsy
- risk factors: fam history, hypertension, diabetes mellitus, prior acute kidney failure
what are the 4 ongoing assessments
- weight monitoring
- daily, fluctuations over 1-2lb/day indicates fluid gains and losses
- consider dry weight (wt b4 retention) - intake and output monitoring
- identify +/- fluid balances
- assess hourly in some cases - neurological findings
- LOC changes due to inadequate perfusion, increase in toxins - Hemodynamic monitoring
- assesses volume depletion and volume overload
- heart can be tachycardic to accomodate for inadequate perfusion (↑SNS stimulation)
what are the 11 lab assessment serum components
- blood urea nitrogen (BUN)
- Creatinine
- estimated glomerular filtration rate
- hemoglobin and hematocrit
- albumin
- acidosis
- electrolytes
- BUN to creatinine ratio
- creatinine clearance
- osmolality
- blood gases - anion gap
Lab assessment: blood urea nitrogen (BUN)
- normal range
- considerations
- 3.6-7.1
- by product of protein and amino acid metabolism
- elevated with GFR ↓and resulting ↓ in urea excretion
- ↓ with volume overload, liver damage, severe malnutrition, use of phenothiazines, or pregnancy
Lab assessment: Creatinine
- normal range
- considerations
male: 53-106 mmol/L
female: 44-97 mmol/L
- byproduct of muscle and normal cell metabolism
- completely excreted when kidney function is normal
- even small increases represent significant decrease in GFR
Lab assessment: GFR
- normal range
- considerations
90-120 mL/min/2.73 m2
- based on creatinine level, age, sex
- defined: amount of blood filtered by glomeruli in a given time
- great indicator of renal function
Lab assessment: hemoglobin and hematocrit
- considerations
- indicates increases/decreases in intravascular fluid volume
- increase in hematocrit indicated fluid volume deficit resulting in hemoconcentration
- decrease in hematocrit indicates fluid volume excess because of dilutional effect of extra fluid load
Lab assessment: albumin
- considerations
- responsible for colloid osmotic pressure maintenance
- decreases levels result in fluid shift from plasma to interstitium, creating peripheral edema
Lab assessment: acidosis
- considerations
- pH < 7.35
- severe acute kidney insult
- metabolic acidosis occurs as a result of accumulation of un-excreted waste products
Lab assessment: electrolytes
- considerations
imbalances indicating renal failure
- no excretion or retainment
- risk for hyperkalemia which impacts cardiac function
Lab assessment: BUN to creatinine ratio
- consideration
- BUN and CR levels elevated and maintained at 10:1, disorder is intrarenal or affecting tubules of kidneys
- > 10:1 cause is most likely prerenal
Lab assessment: creatinine clearance
- normal range
- considerations
85-135mL/min
- amount excreted in urine and amount in blood over 24h
- renal failure: ↓ in urine and ↑ in blood
Lab assessment: osmolality
- considerations
- elevated = hemoconcentration or dehydration
- decreased = hemodilution or volume overload
Lab assessment: blood gases - anion gap
- considerations
- increases level reflects overproduction or decreased excretion of acid products and indicated metabolic acidosis
- decreased anion gap indicates metabolic alkalosis
what do we look for in a urinalysis
- urine appearance
- urine pH
- urine specific gravity
- urine osmolality
- urine protein
- urine glucose
- urine ketones
- urine electrolytes
- urine sediment
- hematuria
what is a urine toxicology screen
urine drug screen (UDS)
- used to find cause of altered LOC
- detects alcohol, illegal drugs, prescription and nonprescription meds, other substances
what are the 6 diagnostic procedures of kidney disease and what do they look for?
- ultrasound
- physiologic traits, masses, cysts, renal arterial stenosis, obstruction - CT - kidneys, ureters, bladder
- urolithiasis (kidney stones) - X-ray
- masses, fluid collections, obstructions - bladder scan
- amount of urine in bladder - contrast/radiopaque dye
- potentially nephrotoxic
- require adequate hydration pre and post
- may need to hold certain medications (Ex. metformin) - kidney biopsy
- diagnosis of kidney disease
what are the 3 most impactful comorbidities of chronic kidney disease
hypertension
diabetes
cardiovascular disease
what are the stages of CKD
Stage 1: >90; (normal or GFR) normal renal function, with proteinuria
Stage 2: 60-89; mild loss of kidney function, with proteinuria
Stage 3: 30-59; mild to moderate loss of kidney function, with proteinuria
Stage 4: 15-29; severe loss of kidney function, with proteinuria
Stage 5: <15; end stage renal disease, with proteinuria
what are the clinical manifestations of CKD
- affects every system
- onset of ESRD results in a constellation of signs and symptoms referred to as Uremia (end stage renal disease)
what are the goals of care for CDK
Prevention or slowing of progression
Early identification
- Preserve existing function
- Treat clinical manifestations
- Prevent complications
- Educate patients and family
- Prepare patients for RRT (renal replacement therapy)
detect and treat potential reversible causes when kidney disease is diagnosed
referral to nephrologist when GFR <30
what are the things we want to prevent in CDK
- avoid medications with neurotoxic side effects
- avoid nonsteroidal anti-inflammatory meds (NSAIDs) in patients with elevated creatinine levels
- delay use of intravascular contrast dye until patient is fully rehydrated
how do we slow the rate of progression of CDK
- have appropriate interventions
- manage secondary factors: hypertension, diabetes, smoking, chronic metabolic acidosis, protein restriction
what are some reversible causes of CDK
- decreased renal perfusion
- administration of nephrotoxic meds
- urinary tract obstruction
what are the CDK urinary system clinical manifestations
early stages:
- polyuria: ↓renal concentrating ability, urine production >2.5-3 L over 24h, often at night
late stages:
- oliguria: <400mL/24h - occurs as CDK worsens
- anuria: urine output <40mL per 24h
what are the CDK respiratory system clinical manifestations
- Kussmaul respiration: deep and laboured
- dyspnea
- pulmonary edema
- uremic pleuritis
- pleura effusion
- predisposition to resp infection
how do we care for fluid overload in CDK
- dietary sodium restriction <2g/day
diuretic therapy: loop diuretics
- Furosemide (lasix)
- moderate CDK - 80mg furosemide
- severe CDK - 200mg furosemide
- oliguric AKI - up to 500mg of intravenous furosemide
how do we care for hypertension in CDK
lifestyle changes
- weight loss, exercise, avoid alcohol, stress management, smoking cessation
Diet recommendations
- sodium and fluid restriction
antihypertensive drugs
- ACE inhibitors (ramapril, enalapril)
- ARB agents (losartan)
fluid overload: loop diuretics, SGLT2 inhibitors, thiazide diuretics
nondiabetic: goal is <130-140/90 mmHg
diabetic: goal < 125-130/80 mmhg
what are some clinical manifestations of metabolic disturbances
Waste product accumulation:
- As GFR ↓, BUN ↑ and serum creatinine levels ↑
- N/V, lethargy, fatigue, impaired thought processes, headache
Altered carbohydrate metabolism
- Caused by impaired glucose use (cellular insensitivity to insulin)
Elevated triglycerides
- Hyperinsulinemia stimulates hepatic production of triglycerides
- Altered lipid metabolism :↓ levels of enzyme lipoprotein lipase (important in lipoprotein breakdown)
Metabolic Acidosis
- Due to increasing tendency to retain hydrogen ions
- Defective reabsorption/regeneration of bicarbonate
what is the care for metabolic acidosis
bicarbonate supplements (sodium bicarbonate)
- Requires careful monitoring of volume status
Decreased protein intake
- Diminishes acid and sulfate generation
Increased fruit intake
- Provides citrate that is converted to bicarbonate
- Fruits can be high in K
what are the clinical manifestations of electrolyte imbalances
- Hyperkalemia: Fatal dysrhythmias
- Sodium: Low or normal, Hyponatremia (water shifts into cells-swelling)
- Calcium and phosphate
- Magnesium
- Metabolic acidosis: results from inability of kidneys to excrete acid load (primarily ammonia), Defective reabsorption/regeneration of bicarbonate
what is the care for hyperkalemia
nonpharm: <5.5mmol/L
pharmaco: >5.5mmol/L
- stop supplements
- low K diet (<2g/day)
- insulin with glucose
- calcium gluconate
- removal of K from body: diuretics, gastrointestinal cation exchangers (decreases dysrhythmia risks - ex. Kayexalate), dialysis
what is important for nutritional therapy
- consult with dietician
- protein moderately restricted
- water restriction
- Na and K restriction
- Phosphate restriction
- Glycemic control
what are the clinical manifestations for the hematological system
Anemia
- due to ↓ erythropoietin production due to decreased erythropoiesis in bone marrow and ↓functioning in renal tubular cells
- deficient iron stores
- folic acid (removed with dialysis)
bleeding tendencies (uremic bleeding)
- defect in platelet function
infection
- changes in leukocyte function
- altered immune response and function
- diminished inflammatory response
what is the care for anemia in CKD
Erythropoietin (Epogen, Darbepoetin)
- Erythropoiesis-stimulating agents (ESAs) - Administered IV or subcutaneously
- Increased hemoglobin and hematocrit in 2 to 3 weeks
- Side effect: hypertension
Iron supplements
- Side effects: gastric irritation, constipation, dark stools
Folic acid supplements
- Needed for RBC maturation
- Removed by dialysis
clinical manifestations of MSK system in CDK
Mineral and bone disorder
- Abnormalities of calcium, phosphorus, PTH or Vitamin D metabolism
- Abnormalities in bone turnover, mineralization, volume, linear growth or strength (renal osteodystrophy)
- Vascular or other soft tissue calcification
- Results in skeletal and extra skeletal complications
what is the care for mineral and bone disorders in CDK
Phosphate intake restricted to <1 g/day
Phosphate binders (with meals)
-Calcium carbonate (Caltrate, Tums)
- Calcium acetate (PhosLo): Binds phosphate in bowel and excretes
Supplementing vitamin D
- Calcitriol (Rocaltrol)
- Serum phosphate level must be lowered before calcium or vitamin D is administered
what is the care for dyslipidemia in CDK
- statins for patients with stage 1-3
what are the complications of drug therapy in CDK
- absorption, distribution, metabolism elimination
- dialysis: impact on drug doses and frequency
what is the uremic state in CDK
- manifestations
- treatment
manifestations
- anorexia, N/V, pericarditis, peripheral neuropathy, central nervous system abnormalities
treatment = kidney replacement therapy
- hemodialysis
- peritoneal dialysis
- kidney transplantation
clinical manifestations of GI in CDK
Every part of GI is affected.
Inflammation of mucosa due to excessive urea:
- Mucosal ulcerations
- Stomatitis (inflammation of the tongue and lips)
- Uremic fetor (urinous odour of breath)
- GI bleeding
- Anorexia, nausea, vomiting, constipation
clinical manifestations of the neurological system in CDK
Restless legs syndrome
Muscle twitching
Irritability
Decreased ability to concentrate
Peripheral neuropathy
Seizures (uncommon)
Coma (uncommon)
clinical manifestations of the integ system
pruritus
uremic frost (rare)
clinical manifestations of psychological changes in CDK
personality and behavioural changes
emotional lability
withdrawal
depression
CDK nursing care (11)
- systems assessment
- maintaining skin integrity
- monitoring excess fluid overload
- daily weights
- risk for infection
- monitoring nutrition
- risk for constipation
- risk for injury
- balancing activity and rest
- patient teaching
- anticipatory grieving
what is prerenal acute kidney injury
- %, what it is and cause
55-60%
- any condition that decreases blood flow, blood pressure, or kidney perfusion before arterial blood reaches the renal artery
- when arterial hypoperfusion due to low CO, hemorrhage, vasodilation, thrombosis, or other cause reduces the blood flow to the kidney, glomerular filtration decrease, urine output decreases
what is intrarenal acute kidney injury
35-40%
- any condition that produces an ischemic or toxic insult directly at parenchymal nephron tissues
- Acute tubular necrosis is most common from ischemia, nephrotoxic exposure, or sepsis
what is postrenal acute kidney injury
5%
- any obstruction that hinders the flow of urine from beyond the kidney through the remainder of the urinary tract
what is the clinical course of AKI (3 phases)
- what occurs, how long it lasts
- initiation phase: increased creatinine and BUNN, decreased urine output, lasts hours to days
- maintenance phase: days to weeks
- recovery phase: return of BUN, creatinine and GFR towards normal
when does the recovery phase of AKI begin, end, last, and result in
begins when urine output gradually increases
ends with acid-base, electrolyte, BUN, and Cr normalizing
Lasts several months to a year
results in some scar tissue
what are the age-related considerations for AKI
most common in older population
- decreased # of functioning nephrons
- impaired other organ function
- kidney less able to compensate for changes in fluid volume, solute overload, cardiac output
- dehydration, hypotension, diuretic therapy, aminoglycoside therapy, obstructive disorders, surgery, injection, radiocontrast agents
what are the gollas of care for AKI
treatment of underlying disease!
manage signs and symptoms
prevent complications while kidneys recover
how do we care for fluid overload in AKI
diuretics
- loop: 80-200mg IV furosemide (dose is adequate when urine output >200mL within 2h)
- thiazide diuretics (hydrochlorothiazide)
- osmotic diuretic (mannitol)
fluid restriction
- 600mL + previous 24h output
- includes diarrhea, emesis, urine, drainage
RRT: renal replacement therapy
how do we care for fluid depletion in AKI
- goal of volume replacement is to replace fluid and electrolyte losses and to prevent ongoing loss
Crystalloids = first choice, and colloids
- crystalloids: 0.9 NaCl, 0.45 NaCl
- colloids: albumin, pentaspan, hetastarch
- initially 1-3L, assessment of patient’s response is v important
when do we provide pharmacological interventions and nonpharmacological interventions with hyperkalemia
nonpharm: <5.5 mmol/L
pharm: >5.5 mmol/L
when do we do renal replacement therapy for metabolic acidosis? what med is considered?
RRT when pH <7.1
bicarbonate administration considered
what other collaborative care do we provide for AKI (13)
- hypertension vs hypotension
- assessing intake/output, daily weights
- assessing for uremia (anorexia, N/V, metallic taste, altered mental state)
- home medications (NSAIDs, ACE, ARBs, nephrotoxins, renally cleared, dosing)
- hypocalcemia (treat hyperphosphatemia 1st)
- hyperphosphatemia (phosphate-binding agents (calcium carbonate), restrict dietary phosphorus, rrt)
- hypomagnesemia (IV and po supplements)
- hypermagnesemia (limit intake, diuretics, RRT)
- drug dosing
- anemia
- nutritional therapy
- K+, Na+, PO4 restrictions (glucose, electrolyte levels)
- renal replacement therapy
what are the 4 follow up cares for AKI
- daily weights
- fluid intake and output
- daily electrolytes, creatinine
- follow up assessment to guard against recurrent AKI, development of CKD, end stage renal disease and cardiac events
what is dialysis
- definition
- how is it achieved (3 ways)
movement of fluid and molecules across a semi-permeable membrane from one compartment to another
- correction of gluid and electrolyte imbalances and to remove waste products
achieved by:
1. diffusion: solute movement from [high] to [low]
2. osmosis: fluid movement from [low solute] to [high solute]
3. ultrafiltrate: water and fluid removal when there is an osmotic gradient or pressure gradient across membrane
what are the indications for renal replacement therapy
- volume overload resulting in compromised cardiac/pulmonary status
- elevated K levels
- metabolic acidosis (bicarb <15 mmol/L)
- BUN >43mmol/L, GFR <15, creatinine >
- significant change in mental status
- acute poisoning
- signs of uremia
what is peritoneal dialysis and the 2 types
- intro of sterile dialyzing fluid through implanted catheter into abdominal cavity
- automated peritoneal dialysis (APD)
- continuous cycling, done while pt sleeps, usually leaves fluid in abdomen during the day - continuous ambulatory peritoneal dialysis (CAPD)
- during the day, dialysis fluid always in peritoneal cavity
what are the 5 contraindications of peritoneal dialysis
- history of multiple abdominal surgical procedures or several abdominal pathological conditions
- recurrent abdominal wall or inguinal hernias
- excessive obesity with large abdominal wall and fat deposits
- pre-existing vertebral disease
- severe obstructive pulmonary disease
what are the peritoneal dialysis complications? (11)
- Exit site infections – redness, tenderness, drainage
- Peritonitis
- Abdominal pain
- Outflow problems
- Hernias
- Lower back problems
- Bleeding
- Pulmonary complications
- Protein loss
- Carbohydrate and lipid abnormalities
- Effectiveness
what are the nursing assessments fr hemodialysis
- VS assessment q30-60min
- fluid status assessment
- peripheral edema
- lung and heart sounds
- pre and post weight
- treatment usually 3-5h, at least 3x per week
what are the 3 types of hemodialysis
- AVF: arteriovenous fistula
- surgically connecting a vein and an artery, usually forearm - AVG: arteriovenous graft
- synthetic graft attached to an artery and a vein (2 weeks)
- not suitable for AVF - tunnelled hemodialysis catheter
- temporary or permanent access
- internal jugular or femoral vein
what are the nursing cares for hemodialysis
- SIGN: on kardex & above bed. No BP, venipuncture, IV in arm
- do not access catheter (reinforce dressing)
- EPO and folic acid given in renal unit post HD
- no IMs or invasive procedure 4-6h post
- check for thrill & bruit
- most meds are given post dialysis
how do we assess a fistula
inspection: site and peripheral extremity
palpation: thrill - palpable vibration (normal), pulse (abnormal)
auscultation: bruit - low pitched, soft, rumbling sound (normal)
what are the complications of hemodialysis
hypotension
muscle cramps
loss of blood
hepatitis
infections / sepsis
disequilibrium syndrome
PD vs HD: advantages of PD
- ease of travelling
- do well clinically
- fewer dietary restrictions
- good if poor vascular access
- diabetics do well
- less technically challenging
what is a treatment choice of end stage renal disease
kidney transplant
- improves quality of life
- reduces mortality risk for most patients
palliative care for end stage renal disease
- increase in older patients deciding not to start dialysis
- symptom management: pain, constipation, hypervolemia, N/V, delirium
