Renal Failure

Cards (61)

  • Acute Renal Failure (ARF)

    Abrupt loss of kidney function and decrease in glomerular filtration rate (GFR) over hours to days
  • Acute Renal Failure (ARF)
    • Typically reversible clinical condition
    • Mortality rate: 40% - 60%
  • Categories of Acute Renal Failure
    • Pre-renal azotaemia (50-65%)
    • Intrinsic renal azotaemia (20-35%)
    • Post-renal azotaemia (15%)
  • Pre-renal azotaemia
    Inadequate perfusion of kidneys
  • Intrinsic renal azotaemia

    Intrinsic renal disease (damaged renal parenchyma or nephron)
  • Post-renal azotaemia
    Urinary tract obstruction
  • Causes of pre-renal azotaemia
    • Hypovolemia
    • Diminished cardiac output
    • Renal artery disease
    • Hepatorenal syndrome
  • Pathophysiology of pre-renal azotaemia
    1. Auto-regulation: Afferent arteriole dilation and efferent arteriole constriction
    2. Release of renin: Activates Renin Angiotensin Aldosterone System (RAAS)
  • Pre-renal azotaemia
    • Decrease urine output or oliguria (<400ml/ day)
    • Increase urine specific gravity
    • Decrease urine Na
  • Nursing interventions for pre-renal azotaemia
    1. Early identification and treatment
    2. Increase fluids
    3. Strict I/O charting
    4. Lung assessment
    5. Treat cardiac arrhythmia
    6. Monitor any increase in cardiac output
    7. Monitor BUN, creatinine, and GFR
    8. Monitor/ restrict use of ACE-I and NSAIDs
  • Causes of intrinsic renal azotaemia
    • Acute tubular necrosis (ATN) either ischemic or toxic
    • Nephrotoxic agents
    • Environmental agents
    • Heavy metals
    • Plant and animal substances
    • Trauma or radiation to kidney
    • Obstruction
    • Pregnancy-related disorders
    • Inflammatory processes
    • Immune processes
    • Intravascular haemolysis
    • Systemic and vascular disorders
  • Pathophysiology of ischemic ATN
    1. Prolonged hypoperfusion and kidney ischemia
    2. Failure of renal autoregulation, sympathetic nervous system (SNS) responses, RAAS, and endothelin production
    3. Tubular cellular damage results in decrease glomerular blood flow, glomerular hydrostatic pressure, and GFR
  • Pathophysiology of toxic ATN
    1. Toxic event refers to exposure to toxic products, organisms, and/or nephrotoxic agents
    2. ATN begins by causing injury to tubular epithelial cells
  • Phases of acute tubular necrosis (ATN)
    • Onset
    • Oliguric
    • Diuretic
    • Recovery
  • Onset phase of ATN
    • Initial injury to nephrons
    • Renal blood flow 25% of normal
    • May last hours to days
    • Kidney dysfunction can be reversed or prevented by early intervention
  • Oliguric phase of ATN

    • Urine output decreases from renal tubule damage (below 400mL/day)
    • Increases blood urea nitrogen (BUN) and creatinine levels
    • Electrolytes disturbances, acidosis and fluid overload
    • May last for 8 to 10 days or even longer
  • Diuretic phase of ATN
    • Urine output gradually increases
    • GFR increases
    • Serum creatinine, BUN, and electrolytes stop rising and begins to decrease
    • Possible electrolytes depletion
    • Usually last for 1 to 2 weeks
  • Recovery phase of ATN
    • Decreased oedema
    • Fluid and electrolytes balance gradually start to normalize
    • If significant damage, residual renal impairment may occur
    • 45% of cases will make complete recovery
    • Takes several months to 1 year
  • Treatment goals for intrinsic renal azotaemia
  • Nursing interventions for intrinsic renal azotaemia
    1. Identify high risk groups
    2. Avoid nephrotoxic agents whenever possible
    3. Monitor urine output, creatinine, and BUN levels
    4. Administer IV fluids as tolerated
    5. Monitor vital signs for signs and symptoms of fluid overload
  • Post-renal azotaemia
    Obstruction that develops anywhere from collecting ducts of kidney to urethra
  • Pathophysiology of post-renal azotaemia
    1. Bilateral renal obstruction ➔anuria related to impedance of urine flow past obstruction
    2. Urine congestion ➔retrograde pressure through collecting system and nephrons ➔tubular fluid flow rate and GFR
    3. Prolonged post renal obstruction ➔collecting system dilates ➔compress parenchymal tissue ➔nephron injury ➔dysfunction of concentrating/ diluting system ➔urine osmolality and Na plasma ➔loss of renal function
  • Nursing interventions for post-renal azotaemia
    1. Assess and remove cause of obstruction
    2. Monitor vital signs, mental status, and level of consciousness
    3. Monitor and treat cardiac dysrhythmias
    4. Monitor or avoid use of ACE-I and NSAIDS if necessary
    5. Monitor renal function by urinary output and serum electrolytes
    6. Administer IV fluids, IV diuretics, and IV NaHCO3
  • Chronic Renal Failure (CRF)
    • Progressive and irreversible loss of renal function for months to years
    • Inability to maintain metabolic, fluid and electrolyte balance ➔azotaemia and uraemia
  • Causes of Chronic Renal Failure (CRF)
    • DM
    • Hypertension
    • Interstitial nephritis
    • Chronic pyelonephritis
    • Congenital disorders
    • Glomerulonephritis
    • Vasculitis
    • Obstructive disorders
    • Hereditary disease
    • Cystic disease
  • Glomerular Filtration Rate (GFR)

    • Most accurate indicator for renal function
    • Formula: urine volume (per min) X urine creatinine / serum creatinine
  • Diuresis
    Fluid volume deficit
  • Treatment for diuresis
    1. Administer IV fluids
    2. Administer IV diuretics
    3. Administer IV NaHCO3
  • Renal dose
    Adjustment of medication dosage for patients with kidney disease
  • Quick reaction to renal dose adjustment
    Can let ARF become reversible
  • Chronic Renal Failure (CRF)
    • Progressive and irreversible loss of renal function for months to years
    • Inability to maintain metabolic, fluid and electrolyte balance leading to azotaemia and uraemia
  • Incidence of CRF is increasing, particularly among older adults
  • In Hong Kong, the percentage of CRF ranges between 15-20% of the population, meaning 1 in 5 may be affected
  • Chronic Renal Failure (CRF) Etiology
    • DM
    • Hypertension
    • Interstitial nephritis
    • Chronic pyelonephritis
    • Congenital disorders
    • Glomerulonephritis
    • Vasculitis
    • Obstructive disorders
    • Hereditary disease
    • Cystic disease
  • Glomerular Filtration Rate (GFR)

    Most accurate indicator for renal function
  • Calculating GFR
    1. 24-hour urine for creatinine clearance
    2. Formula: (urine volume per min X urine creatinine) / serum creatinine
  • Normal GFR for an adult is more than 90 mL/min/1.73 m2
  • GFR declines with age, even in people without kidney disease
  • Stages of Chronic Kidney Disease
    • Stage I: GFR 90+, Kidney damage with normal kidney function
    • Stage II: GFR 60-89, Kidney damage with mild loss of kidney function
    • Stage IIIa: GFR 45-59, Mild to moderate loss of kidney function
    • Stage IIIb: GFR 30-44, Moderate to severe loss of kidney function
    • Stage IV: GFR 15-29, Severely loss of kidney function
    • Stage V: GFR <15, Kidney failure (End-stage)
  • Symptoms of Uraemia
    • Loss of appetite
    • Nausea and vomiting
    • Headache
    • Shortness of breath
    • Itching
    • Bone disease (osteoporosis)
    • Anaemia
    • Proteinuria
    • Weakness
    • Insomnia
    • Hypertension
    • Oedema