Summary
Summary Kidney Failure
- Course
- N164 (N164)
- Institution
- Samuel Merritt University
Renal Failure & Kidney Issues: Complete guide to understanding acute and chronic renal failure, dialysis, and related therapies.
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N164: Managing Care of Adults IIIAcute and Chronic Renal Failure Ch. 51 W3
Kidney (Renal) Failure " Partial or complete impairment of kidney function that results in inability to excrete metabolic waste
products and water.
• Affects all body systems
• Treatments and dietary changes are challenging
o Impacts lifestyle, occupation, family relationships, and self-image
• Classified as Acute or Chronic
o Acute kidney injury (AKI) has a rapid onset
o Chronic kidney disease (CKD) is gradual with a progressive decline in kidney function
Kidney Anatomy
Comparison of AKI and CKD Criteria AKI CKD
Onset Sudden Gradual, often over many years
Most common cause Acute tubular necrosis Diabetic nephropathy
Diagnostic criteria Acute reduction in urine output GFR < 60 mL/min/1.73m2 for > 3 months
AND/OR AND/OR
↑ Serum creatinine Kidney damage > 3 months
Reversibility Potentially Progressive and irreversible
Cause of death Infection Cardiovascular disease
Acute Kidney Injury " Ranges from slight deterioration to severe impairment
" Rapid loss of kidney function with:
o Rise in serum creatinine and/or reduction in urine output
o Elevated BUN and K+
o Azotemia—accumulation of nitrogenous waste products
• Develops over hours or days
• High mortality rate; usually affects people with other life-
threatening conditions
• Often follows severe, prolonged hypotension, hypovolemia, or
exposure to a nephrotoxic agent
• Prerenal AKI
o Causes: Factors that reduce systemic circulation causing
reduction in renal blood flow which leads to oliguria.
• Severe dehydration, heart failure, decreased Cardiac Output.
o Autoregulatory mechanisms attempt to preserve blood flow
o Prerenal azotemia results in Na+ excretion, increased Na+ and H2O retention and ↓ urine output
• Intrarenal AKI
o Causes: 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
o *Acute tubular necrosis (ATN)
• Results from ischemia, nephrotoxins, or sepsis
• Severe ischemia causes disruption in basement membrane and patchy destruction of tubular
epithelium
• Nephrotoxic agents cause necrosis of tubular epithelial cells—clog tubules
• Potentially reversible
, • Postrenal AKI
o Causes: Mechanical obstruction of outflow which results reflux into renal pelvis, impairing kidney
function.
• Benign prostatic hyperplasia, prostate cancer, calculi, trauma, and extrarenal tumors
o Bilateral ureteral obstruction—hydronephrosis; relieve obstruction in 48 hours increased chance
of recovery.
• Clinical Manifestations
o Three phases: oliguric, diuretic, and recovery
o RIFLE Classification
o (R) Risk
o (I) Injury
o (F) Failure
o (L) Loss
o (E) End-stage renal disease
o Oliguric Phase
• Urinary changes—*oliguria
º Urinary output less than 400 mL/day
º Occurs within 1 to 7 days after injury
º Lasts 10 to 14 days (longer à poor prognosis)
º Urinalysis—casts, RBCs, WBCs, protein
º Specific gravity 1.010
º Osmolality 300 mOsm/kg
• 50% patients non-oliguric; greater than 400 mL urine/day
• Fluid volume
º Hypovolemia may exacerbate AKI
º Decreased urine output leads to fluid retention
· Neck veins distended
· Bounding pulse
· Edema
· Hypertension
º Fluid overload can lead to heart failure, pulmonary edema, and pericardial and pleural
effusions
• Metabolic Acidosis
º Impaired kidney cannot excrete hydrogen ions or acid products of metabolism
º Serum bicarbonate production is decreased
· Reabsorption and regeneration defective
º Severe acidosis develops
· Kussmaul respirations—increasing exhaled CO2
• Sodium Balance
º Increased excretion of sodium—damaged tubules
º Hyponatremia can lead to cerebral edema
• Potassium Excess
º Impaired ability of kidneys to excrete K+
º Increased risk with massive tissue trauma
º Usually asymptomatic
º ECG changes—peaked T waves, widened QRS, ST depression
• Hematologic Disorders
º Leukocytosis—infection may be fatal
· Urinary and respiratory infections
• Waste Product Accumulation
º Increased BUN and *serum creatinine levels
• Neurologic Disorders
º Fatigue and difficulty concentrating
º Seizures, stupor, coma
o Diuretic Phase (1 to 3 weeks)
• Daily urine output is 1 to 3 L; up to 5 L
º Osmotic diuresis from high urea and inability of tubules to concentrate urine
º Monitor for hypovolemia, hypotension, hyponatremia, hypokalemia, and dehydration
o Recovery Phase (up to 12 months)
• Increased GFR, decreased BUN and creatinine
º Influenced by severity of injury and complications
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