Renal Failure

Renal Failure Acute • Reversible • Sudden • Azotemia

Chronic • Irreversible • Progressive • Azotemia

Azotemia = Uremia • Elevated BUN (N = 10-20 mg/dL) • Elevated Uric Acid (2.5 – 8 mg/dL) • Elevated Creatinine (N = .4-1.2 mg/dL) • Most accurate test: Creatinine Clearance

Causes • Prerenal - any decrease in kidney’s blood supply • Intrarenal – damage to the kidneys • Postrenal – obstruction to the out flow

Stages of ARF Onset

GFR (125) TRR (124125.5)

Oliguric / Anuric

Diuretic

Recovery

Stages of CRF First

Diminished Renal Reserve

Second Stage of Renal Insufficiency

Third

ESRF

Asymptomatic Mild = 25% Moderate = 50 % Severe = 75% Azotemia develops Life threatening

Pathophysiology Excretory Problems: • Middle molecule accumulation or urea  trapping of: • Glucose – hyperglycemia • Keratin  sallow, yellow discoloration of the hair; split ends • Lipids  hyperlipidemia  atherosclerosis  ASHD – Inability of lipids / fatty acids to stimulate adrenal cortex to release sex hormones  amenorrhea, infertility, impotence

• Travel of urea around the body: • Surface to the skin  uremic frost  pruritus • Surface to GI tract  PUD  gastric bleeding • Surface to pericardium  percarditis • Build up outside the blood brain barrier  CNS depression, psychological changes

• Inability to remove uric acid  inability of the kidneys to produce HCO3  metabolic acidosis  destruction of WBC  infection tendencies • Inability to remove uric acid  GOUT • Inability to remove potassium  HYPERKALEMIA  cardiac arrest

Endocrine Problems • Inability to produce REF  decreased BM stimulation  decreased precursor cell production  decreased RBC  anemia  anorexia, N/V

• Inability to produce hydroxyl: – Decreased vitamin D  hypocalcemia  bleeding tendencies (calcium is a clotting factor) – Decreased vitamin D  hypocalcemia  parathyroid gland compensation  hyperparathyroidism  ejection of calcium to the blood  renal osteodystrophy  osteoporosis  risk for fracture

• Decreased urine output  false activation of RAAS  hypertension, CHF, pulmonary edema

Management • Maintain Fluids and Electrolytes Balance – Monitor VS – Monitor ECG – Monitor for edema

• Control nutritional intake – Control fluid intake – High CHO – Prescribed K, Na, P (administer phosphate binding agents) – Limited protein (to decrease urea)

• Prevent infection, fatigue and injury – Avoidance of extreme activities – Asepsis – Isolation if necessary

• Promote comfort –Relieve pruritus –Prevent oral cracking

Medical Management • Control Hyperkalemia – Diet: low K diet – Kayexalate (sodium polysterene sulfonate)  ion reversal – Insulin w/ D50W – Dialysis

Hemodialysis • Replaces exocrine (removal of wastes) but not the endocrine (production of hormones) function • Practice ARM PRECAUTION

Vascular Access AV Shunt (ideal for ARF) • Advantages: – Used immediately – Use is relatively simple

• Disadvantages: – Clotting – Infection – Dislodgement with hemorrhage – Limited longevity

AV Fistula (ideal for CRF) • Advantages: – Longevity – No danger of dislodgement • Disadvantage: – Requires 4-6 weeks to mature

Management • Prevent hypovolemia and shock • Prevent disequilibrium syndrome • Prevent blood loss • Implement standard precautions • Promote comfort • Provide hygienic measures • Maintain activity and nutrition • Facilitate learning

Peritoneal Dialysis • Can be done ambulatory • Not much change in chemistries • Proteins are wasted

• Drain should be greater than the fill • Most common complication: peritonitis – Observe standard precaution

• Warm the dialysate – To prevent abdominal discomfort – To prevent hypothermia – Better removal of urea