Management of Acute Kidney Injury and Chronic Kidney Disease
Manual of Clinical Nutrition Management III- 112 Copyright © 2013 Compass Group, Inc.
Chronic Kidney Disease
Chronic kidney disease (CKD) is the result of the progressive deterioration of kidney tissue during several
months or years as scar tissue is substituted for viable kidney tissue. Patients who have lost 85% or more of
their kidney function have stage V CKD and require maintenance renal replacement therapy (dialysis) or
renal transplantation (5,6).
Causes of CKD include:
diseases of the glomeruli (glomerulonephritis)
blood vessel damage in the kidney by nephrosclerosis from high blood pressure
inherited diseases, such as polycystic kidney disease
obstructive diseases, such as kidney stones
congenital birth defects of the kidney and urinary tract
systemic or metabolic diseases, such as diabetic nephropathy, systemic lupus erythematosus, and
hyperuricemia, in which the kidneys and urinary tract are irreversibly damaged
abuse of analgesic or illicit drugs
Nutrition Assessment and Nutrition Intervention in CKD
When evaluating the patient for nutrition intervention, the dietitian should use established practice
guidelines (5) and the norms established at the institution-specific guidelines for a particular dialysis unit.
Biochemical levels for dialysis patients will seldom be the same as for healthy individuals, since dialysis
cannot completely replace kidney function. Various nephrologists may define normal levels differently, and
the goal levels may be different based on the stage (1-5) of CKD and the management therapies. The
following text outlines the biochemical parameters that are affected by CKD. These biochemical parameters
should be routinely evaluated following institution-specific guidelines, especially guidelines that are certified
by the Centers for Medicare and Medicaid Services.
Albumin: The presence of acute or chronic inflammation limits the specificity of albumin and other acute-
phase hepatic proteins as nutritional markers in CKD (12). The normalized protein catabolic rate may be a
better marker of nutritional status in the CKD patient who receives renal replacement therapy. Uremia
depresses albumin metabolism, which can affect the albumin concentration. Mean albumin levels are lower
in CKD patients who have a glomerular filtration rate (GFR) that is less than 60 mL/min. Compared with
normal levels, however, this decreased albumin level may be a reflection of decreased protein intake (5).
Albumin losses are greater in patients who receive peritoneal dialysis. The National Kidney Foundation
guidelines have not been updated to reflect the current evidence documenting the limitations for using
albumin as an indicator for diagnosing nutrition related disorders or malnutrition in patients with chronic
disease. The 2000 K/DOQI guidelines recommend for individuals with a GFR < 20 mL/min, protein-energy
nutrition status be evaluated by serial measurements of a panel of markers including albumin and normalized
protein nitrogen appearance (nPNA) (12). (See the discussion of protein requirements in “Medical Nutrition
Therapy for Chronic Kidney Disease” in Section IG.)
Lipids: Increased lipid levels are associated with accelerated cardiovascular disease in patients who have
renal failure. Cardiovascular disease is responsible for approximately 50% of all deaths in dialysis patients
(13). The primary abnormality is a reduction in the catabolism of lipoproteins with unchanged or low hepatic
synthesis. Dialysis patients commonly have increased levels of total cholesterol, very low-density lipid
cholesterol, and triglycerides and decreased levels of high-density lipoprotein cholesterol (5). The National
Kidney Foundation Task Force on Cardiovascular Disease has recommended the National Cholesterol
Education Program Adult Treatment Panel III guidelines for patients who have chronic renal disease.
Individuals who have low, low-normal, or decreasing serum cholesterol levels should be examined for
nutritional deficits (12).
Blood (serum) urea nitrogen: A nitrogenous waste product of protein metabolism, the level of blood urea
nitrogen increases with increased protein intake, catabolism, gastrointestinal bleeding, glucocorticoid use, or
decreased dialysis efficiency. A low level of blood urea nitrogen may indicate decreased protein intake, loss
of protein through emesis or diarrhea, frequent dialysis, protein anabolism, or overhydration. Values greater
than 90 to 100 mg/dL may lead to azotemia.
Potassium: Hyperkalemia, which is a potassium level greater than 5.5 mEq/L, is potentially life-threatening
and may precipitate cardiac arrest if not treated. When hyperkalemia occurs in patients who have chronic