Chapter 26: Acute Renal Failure & Chronic Kidney Disease

Question 0

Describe the course of acute tubular necrosis in terms of the initiation, maintenance and recovery phases.

Answer 0

Destruction of tubular epithelial cells
Caused:
-Sepsis, nephrotoxins, medication, obstruction, infection
-Coagulation process & rbc lysis = crystals, toxins
-Results in hypoxia & ischemia
-Often reversible

INITIATION PHASE
Onset Phase (hours to days)
Development up to time of ischemia

Maintenance Phase
-Marked decreased GFR & urinary output
Edema, pulmonary congestion, HTN
-Retention of urea/K+/sulfate, creatinine
CNS symptoms due to toxin build-up

Recovery Phase
-Gradual increased output

Question 1

Differentiate the prerenal, intrinsic, and postrenal forms of acute renal failure in terms of the mechanisms of development and manifestations

Answer 1

PRERENAL - Due to decreased blood flow to kidney
Causes:
hypovolemia
Heart failure, cardiogenic shock
Sepsis
Medications, toxins

Manifestations:
Marked decrease in urinary output
Elevation of Bun in proportion to creatinine to 20:1 (normal is 10:1)
Azotemia
Most common indicator of acute renal failure

INTRINSIC- Disorder within kidney structure
Prolonged ischemia
Injury to tubular structures
Intratubular obstruction
Infection
Nephrotoxic agents

POSTRENAL:
Obstruction of urine output
Ureter (calculi, strictures)
Bladder (tumors, neurogenic bladder)
Urethra (BPH common)

Question 2

State the definition, classifications and diagnostic criteria for chronic kidney disease.

Answer 2

Chronic kidney disease, or stages 3 and 4 kidney disease, are defined as either kidney damage or a GFR of 30 to 59 mL/minute/1.73 m2 for 3 months or longer.

Question 4

List the common problems associated with chronic kidney disease, including alterations in fluid and electrolyte balance and disorders of skeletal, hematologic, cardiovascular, immune, neurologic, skin, and sexual function, and explain their physiologic significance.

Answer 4

Altered Fluid & Electrolytes
can produce Dehydration or fluid overload
Sodium/salt wasting (late stage)
Hyperkalemia (release d/t trauma, acidosis)

Altered Acid-Base Balance
H+ ion buildup

Bone Disease
Decreased calcium absorption (d/t vit d deficiency) increases PTH, breaking down bone
Vitamin D deficiency

Anemia (common and early sign)
d/t chronic blood loss, hemolysis, impaired erythropoietin, iron deficiency

CV Complications:
HTN (increased PVR – peripheral Vascular resistance, increased RAAS), decrease levels of renal vasodilators
-The spectrum of cardiovascular disease due to CKD includes left ventricular hypertrophy, ischemic heart disease, and congestive heart failure.

Accumulation of nitrogenous wastes
Azotemia: elevated BUN (early sign)
Uremia (urine in the blood)
The uremic state is characterized by signs and symptoms of altered neuromuscular function (e.g., fatigue, peripheral neuropathy, restless leg syndrome, sleep disturbances, uremic encephalopathy); gastrointestinal disturbances such as anorexia and nausea; white blood cell and immune dysfunction; amenorrhea and sexual dysfunction; and dermatologic manifestations such as pruritus.

-All aspects of inflammation and
immune function may be affected adversely by the high levels of urea and metabolic wastes, including a decreased granulocyte count, impaired humoral and cell-mediated immunity, and defective phagocyte function. The acute inflammatory response and delayed-type hypersensitivity response are impaired.

• The cause probably is multifactorial and may result from high levels of uremic toxins, neuropathy, altered endocrine function, psychological factors, and medications (e.g., antihypertensive drugs).
• The skin and mucous membranes often are dry, and subcutaneous bruising is common. Skin dryness is caused by a reduction in perspiration owing to the decreased size of sweat glands and the diminished activity of oil glands. Pruritus is common; it results from the high serum phosphate levels and the development of phosphate crystals that occur with hyperparathyroidism.

Impaired drug elimination
Integument (d/t platelet dysfunction)
Platelet dysfunction = bruising, pruritus

Question 5

State the basis for adverse drug reactions in patients with chronic kidney disease.

Answer 5

?

Question 6

Describe the scientific principles underlying dialysis treatment, and compare hemodialysis with peritoneal dialysis.

Answer 6

The walls of the capillary tubes in the dialysis chamber are made up of a semipermeable membrane material which allows all molecules (except for blood cells and plasma proteins) to move from blood to dialysate and back
2-4 x/week for 3-4 hours

Side-effects

• Hypotension, chest pain
• -Weight-gain common between treatment
• Nausea, vomiting
• Cramps, ‘restless leg’
• Dialysis disequilibrium syndrome (DDS)

Question 7

State the goals for dietary management of persons with chronic kidney disease

Answer 7

The goal of dietary treatment is to provide optimum nutrition while maintaining tolerable levels of metabolic wastes

Restriction of dietary proteins may decrease the progress of renal impairment in persons with advanced renal disease. Proteins are broken down to form nitrogenous wastes, and reducing the amount of protein in the diet lowers the BUN and reduces symptoms

Sodium and fluid restrictions depend on the kidneys’ ability to excrete sodium and water and must be individually determined

When the GFR falls to extremely low levels in kidney failure or during hemodialysis therapy, dietary restriction of potassium becomes mandatory