Renal Flashcards
How many mL’s per kg should a patient have to measure urine output per hour?
0.5 mL per kg is how many mL’s of urine a patient should have
Metabolic acidosis
Metabolic acidosis (Hydrogen ions being reabsorbed) is the most common form in kidney issues
ADH
Used to reabsorb water in distal tubule
Diabetes Insipidus is a dysfunction of this. Nephrogenic DI is when kidney isn’t responding to ADH.
Renin
Released when theres low BP/Renal perfusion
RAAS constricts to perfuse kidneys, causes BP increases.
Aldosterone is excreted so water and sodium are reabsorbed. If kidney damage is present, third spacing occurs
AKI
***Characterized by rapid loss of renal function with progressive azotemia
Prerenal failure
Before the actual kidney structure
BUN/Cr ratio of >10:1
Intrarenal failure /Intrinsic failure
Within the kidney and organ structures
***Most common is Acute Tubular Necrosis (ATN). Contact dyes/Nephrotoxic drugs cause this
Prolonged ischemia, nephrotoxins, hemolysis, myoglobin, acute glomerulonephritis, lupus
Postrenal failure
Injury occurring after the kidney structure
*Mechanical obstruction, BPH, prostate CA, calculi, trauma and extra renal tumors
Alters bone metabolism because of Vitamin D
Pathophysiology of Prerenal AKI
Decreased blood supply to the kidney
Stimulation of renin-angiotensin-aldosterone system
Retention of sodium and water
Signs/Symptoms
***Decreased urinary output (<400 mL/day)
Elevated BP
Lab values
- **Increased urine specific gravity (Concentrated because not enough water to dilute the solutes)
- **Decreased urine sodium
Treatment and Nursing Care for AKI: Early Identification
Increase IV fluids
Usually fluid challenge of 250 cc NSS
***Look for increased urinary output and no crackles in the lungs (back up into lungs)
- **Increased cardiac output
- **Watch for changes in BNP (HEART FAILURE INDICATOR)
Treat any cardiac rhythm disturbances
Monitor use of ACE inhibitors (less perfusion to kidneys) and NSAIDs (can make worse, nephrotoxic)
*****Monitor (Increased) BUN, (normal) creatinine, GFR
AKI Labs
Increased urine osmolality & specific gravity (>1.025)
Decreased urine Na+
Increased BUN & creatinine (increased BUN to serum creatinine ratio 10:1)
Serum creatinine may be normal to high normal
AKI Nursing Interventions
Goal to increase renal perfusion
Most commonly fluid challenges/bolus
If no increase in urine output - bolus should be repeated
Monitor closely for S/S of fluid overload
Respiratory distress, elevated blood pressure
Monitor urine output
***Monitor blood pressure & SaO2 (May drop)
Monitor body weight daily
Monitor for acid-base changes
Pathophysiology of Intrarenal AKI
Direct damage to kidney tissue (nephrons, cortex) from acute tubular necrosis (ATN) or ischemia (decreased blood supply)
Results in tubular swelling and eventually necrosis
Kidney cells block kidney blood and filtrate flow
Ischemia causes the renal tubular cells to swell & become necrotic
Treatment for Intrarenal AKI
High index of suspicion
**High, uncontrolled glucose levels
Decreased urinary output
**High BUN and creatinine
Forcing IV fluids as tolerated
***Administration of acetylcysteine (Mucomyst)
Acute Kidney Injury Intrarenal Findings
Client findings Oliguria ***Increased blood urea nitrogen (BUN) ***Elevated serum creatinine levels Urine: high sodium; ***presence of casts; fixed SG (1.010) Difficult to differentiate from prerenal
Acute Kidney Injury Intrarenal Interventions
Administer fluid challenges
***Administer loop diuretics
Administer Ca+ channel blocker &/or Dopamine to restore vascular tone & promote renal perfusion
Low dose Dopamine is “renal-protective” & dilates the renal artery, high dose Dopamine constricts the peripheral arteries
Teaching to Prevent the Acceleration of AKI
Maintain a normal BP and glucose control
Drink fluids and avoid becoming dehydrated
Monitor weight frequently
Avoid medications that can accelerate renal failure (dyes, aminoglycoside antibiotics)
Exercise
Take ACE inhibitors or ARBs as directed
Moderate protein ingestion with low-cholesterol diet
Acute Kidney Injury (AKI) Postrenal
Often called “Obstructive or Disrupted” Acute Renal Failure
Results from disruption or obstruction of the flow of urine from the kidneys
Problem/obstruction may occur anywhere after the filtered urine is collected in the renal calyces.
When urine flow is obstructed, pressure increases in the nephron and the glomerular filtration rate (GFR) begins to slow. As back pressure increases or is prolonged, nephron damage can occur
Serum creatinine and BUN begin to rise
Treatment and Nursing Care for Postrenal AKI
High index of suspicion
Relieve the obstruction by mechanical or surgical methods
***Watch for post-obstructive diuresis and resultant fluid volume deficit
CKD Stage 1
Normal glomerular function >90 to 125mL/min/1.73m2
Stage One
Normal GFR or >90mL/min/1.73m2
At risk, or has had kidney disease or comorbid conditions that indicated kidney damage of three consecutive months
Should be diagnosed quickly as “high-risk” & disease preventative strategies should be implemented.
Controlling HTN
Controlling blood sugar
Monitoring for protein (microprotein) in urine
Controlling hypotensive or decreased cardiac output states
Stage 2 CKD
Stage Two
GFR 60 to 89mL/min/1.73m2
Clients should be followed closely
Clients need education about renal protection
Clinicians should attempt to slow, or hopefully prevent further renal & cardiovascular damage
Stage 3 CKD
Stage Three
GFR 30 to 59mL/min/1.73m2
Complications of reduced function begin at this stage
Treatment of anemia, bone disease and other metabolic disorders may be warranted at this point.
Stage 4 CKD
GFR 15 to 29mL/min/1.73m2
Clients should be prepared for RRT
Clients begin to C/O of generalized fatigue and social isolation
Loneliness & depression frequently ensue
Stage 5 CKD
GFR <15 mL/min/1.73m2
RRT (HD, PD, or scheduled transplantation should be initiated upon evidence of uremia)
Treatment will endure for a life-time
Management of metabolic complications will provide better client outcomes when the client starts on RRT
Ideally the client should start the RRT in a non-acute, community care setting
Clients are classified as ESRD, once they begin RRT
End Stage Renal Disease
Irreversible GFR of <15ml/min
CKD stage 5 is considered ESRD
Leading cause of death for clients with ESRD is cardiovascular disease
Cardiovascular disease is the second-leading cause of long-term hospitalization
Because of multi-system organ involvement most clients will require ICU admission for stabilization & treatment of systemic infections & multiple organ dysfunction (MOD)
Diuretic Phase of ATN
Usually 1-2 weeks
Urinary output gradually increases
Hypovolemia can result
Nonoliguric ATN does not do this
Complications
Hypovolemia
Hypokalemia
ESRD postop
Treatment of choice: Renal transplantation
Management of hemodynamic status, acid-base balance, fluid and electrolytes, blood glucose, respiratory management, immunosuppression monitoring and patient education
Ambulation
Frequents assessment for complications
***Hypotension, hypokalemia, hyperglycemia (steroids)
Graft rupture - hemorrhage
Acute rejection
Acute tubular necrosis
Urologic infections or complications- monitor Foley patency
Renal tubular acidosis – frequent administration of NaHCO3 until kidney begins to function well
Assessment of circulatory function
Bowel elimination
Daily weights & assessment of fluid volume balance
Hourly I&O
Replace mL for mL if diuresing