Chronic Renal Failure and Transplant: Concept Map & Case Study
An assignment submitted in partial fulfillment of the requirements for the degree of Associate
Degree of Science in Nursing in the Undergraduate School of North Central Texas College.
By submitting this paper for grading I am certifying that it is entirely my own work, with any
words and/or ideas from other sources properly indicated (words with quotation marks), cited
in-text, and referenced. I have not submitted this paper to satisfy the requirements of any other
course.
By
Kailee Burnside
RNSG 2435 - Integrated Care Management
7 April 2021
, CHRONIC RENAL FAILURE AND TRANSPLANT 2
Chronic Renal Failure and Transplant: Concept Map and Case Study
Pathophysiology
Chronic kidney disease (CKD) is initially described as diminished renal reserve or renal
insufficiency, which may progress to renal failure (end-stage renal disease). Initially, as renal
tissue loses function, there are few noticeable abnormalities because the remaining tissue
increases its performance (renal functional adaptation).
Decreased renal function interferes with the kidneys’ ability to maintain
fluid and electrolyte homeostasis. The ability to concentrate urine declines
early and is followed by decreases in ability to excrete excess phosphate,
acid, and potassium. When renal failure is advanced (glomerular filtration
rate [GFR] ≤ 15 mL/min/1.73 m2), the ability to effectively dilute or concentrate urine is
lost; thus, urine osmolality is usually fixed at about 300 to 320 mOsm/kg, close to that of plasma
(275 to 295 mOsm/kg), and urinary volume does not respond readily to variations in water
intake.
Creatinine and urea
Plasma concentrations of creatinine and urea (which are highly dependent on glomerular
filtration) begin a hyperbolic rise as GFR diminishes. These changes are minimal early on. When
the GFR falls below 15 mL/min/1.73 m2 (normal > 90 mL/min/1.73 m2), creatinine and urea
levels are high and are usually associated with systemic manifestations (uremia). Urea and
creatinine are not major contributors to the uremic symptoms; they are markers for many other
substances (some not yet well defined) that cause the symptoms.