MANAGEMENT OF ADULT RENAL FAILURE:  ACUTE RENAL FAILURE AND CHRONIC KIDNEY DISEASE

Description
Acute renal failure (ARF) generally presents with a sudden onset of symptoms.  The medical history will include a recent isolated insult to the kidneys.  The most common causes include (1-2):

• Shock, a sudden loss of blood supply to the kidneys from trauma, surgical complications, or both.
• Exposure to a nephrotoxic chemical or drug (eg, radiologic dyes, cleaning solvents, pesticides, and gentamicin).
• Recent streptococcal infection.  If the insult occurred to a previously healthy kidney, the kidney will eventually rejuvenate if diet and/or dialysis can support the patient.  Dialysis is usually a temporary therapy for these patients.

Approaches in ARF
Acute renal failure occurs in approximately 5% of all hospitalized patients and is associated with a 50% to 90% mortality rate (1).  Patients with ARF are both hypermetabolic and hypercatabolic as a result of neurohumoral response associated with acute injury and include the loss of glucose homeostasis, muscle wasting, protein catabolism, electrolyte imbalance, and acidosis (1).  Nutrition support plays an important role in the setting of ARF and may help determine the patient’s course and ultimate outcome (2).  The primary goal of medical nutrition therapy is to decrease the degree of protein catabolism and decrease the severity of negative nitrogen balance while complimenting medical and therapeutic interventions.  Guidelines for Nutrition Care of Renal Patients have recently been updated, and specific guidelines for Nutrition Care of Adult Acute Renal Failure Patients are found in reference 2.  A summary of the guidelines for medical nutrition therapy follows (2):

• Calories: Individualize or determine based on indirect calorimetry (if available) or use 30 to 40 kcal/kg of  actual or ideal body weight (IBW).
• Protein: Without dialysis, 0.5 to 0.8 g/kg of actual or IBW with dialysis, 1.0 to 2.0 g/kg of actual or IBW (consider underlying disease state and type of renal replacement therapy).
• Sodium: During anuric/oliguric phase (<500-mL urine output in 24 hours), less than 2,000 mg/day.  During diuretic phase, replace losses depending on urinary output, edema, dialysis, and serum sodium levels
• Potassium: During anuric/oliguric phase, individualize per laboratory values.  Diuretic phase may need to replace losses depending on urinary volume, serum and urinary potassium levels, frequency of dialysis, and drug therapy.
• Phosphorus, calcium, and magnesium: Individualize based on laboratory values.
• Fluids: During anuric/oliguric phase: 500 mL plus total urine output (including urine, vomitus, and diarrhea) per day.
• Vitamin and mineral supplementation: Individualize based on assessment of laboratory values and documented deficiencies or if routine renal therapy is being used. 

Also refer to the Acute Renal Failure Medical Nutrition Therapy Protocol found in Nutrition Care Protocols for the Acute Care Setting, Atlanta, Ga: Morrison Management Specialists Inc, 2006, for detailed monitoring guidelines. 

    Chronic kidney disease (CKD) is the result of progressive deterioration of kidney tissue over several months or years as scar tissue is substituted for viable kidney tissue.  When about 90% or more of kidney function is lost, the person has reached end-stage renal disease (ESRD) and usually will require renal replacement therapy (dialysis) or renal transplantation (1).

    Some causes of CKD are:

• diseases of the glomerulus (glomerulonephritis)
• damage to the blood vessels 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 and/or metabolic diseases, such as diabetic nephropathy in which the kidney and urinary tract are irreversibly damaged, systemic lupus erythematosus, and hyperuricemia
• abuse of analgesic or “street” drugs

Approaches in CKD
When evaluating the patient for nutrition intervention, the dietitian should be guided by established practice guidelines (2) and norms established at the particular dialysis unit.  Normal levels will seldom be the same as for healthy individuals, since dialysis cannot completely replace real kidney function.  Note that various nephrologist may define normal levels differently.  The following outlines the significance of biochemical parameters that CKD affects.

    Albumin: Serum albumin is a valid and clinically useful measure of protein-energy nutritional status in maintenance dialysis patients.   The presence of acute or chronic inflammation limits the specificity of albumin as a nutritional marker (3).  Uremia appears to depress albumin metabolism, and this can affect its concentration.  Mean albumin levels are lower in patients with CKD with a glomerular filtration rate (GFR) less than 60 mL/min.  Compared with normal levels, however, this may be a reflection of decreased protein intake (2).  Albumin losses are greater with peritoneal dialysis.  (See the discussion of protein requirements in Medical Nutrition Therapy for Chronic Kidney Disease.)

    Lipids: Elevated lipid levels have been associated with accelerated cardiovascular disease in renal failure. Cardiovascular disease is responsible for approximately 50% of all deaths in dialysis patients (4). The main abnormality seems to be a reduction in the catabolism of lipoproteins with unchanged or low hepatic synthesis.  Most commonly, dialysis patients show elevated cholesterol, very-low-density-lipid (VLDL) cholesterol, and triglyceride levels and decreased high-density-lipoprotein (HDL) cholesterol levels (2).  The National Kidney Foundation Task Force on Cardiovascular Disease has recommended the use of the (National Cholesterol Education Program (NCEP) Adult Treatment Panel III) guidelines for patients with chronic renal disease (1).  Individuals with low, low-normal, or declining serum cholesterol levels should be investigated for possible nutritional deficits (3).

    Blood (serum) urea nitrogen (BUN): A nitrogenous waste product of protein metabolism, BUN most commonly becomes elevated with increased protein intake, catabolism, gastrointestinal bleeding, glucocorticoid use, or decreased dialysis efficiency.  A low BUN value may be an indication of 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 (potassium level greater than 6.0 mEq/L) is potentially life-threatening and may precipitate cardiac arrest if not treated.  When hyperkalemia occurs in chronic renal failure, it is usually due to oliguria (urine output <500 mL per 24-hour period), excessive potassium intake, acidosis, the catabolic stress of infection, surgery, trauma, or glucocorticoid administration or hypoaldosteronism.  In clinical practice, excessive potassium intake is frequently related to the use of potassium-containing salt substitutes and dietary noncompliance. Hypokalemia (potassium level less than 3.5 mEq/L) may be caused by decreased dietary intake, vomiting, diarrhea, use of a potassium-depleting diuretic, excessive use of the potassium binder sodium polystyrene sulfonate (Kayexalate), or dialysis against a low-potassium bath.

    Sodium: Serum sodium levels must always be interpreted with current fluid status in mind.  Hypernatremia can be caused by excessive water loss through diarrhea and vomiting (dehydration) and aggressive diuretic therapy without sodium restriction.  Signs of hypernatremia include flushed skin, dry tongue and mucous membranes, and thirst.  Hyponatremia can be caused by fluid overload and sodium depletion from sodium restriction along with sodium-losing nephropathy.  Symptoms of hyponatremia include abdominal cramps and hypotension.

    Calcium: The Renal Diet tends to be low in calcium, and there is decreased calcium absorption secondary to the abnormal metabolism of vitamin D.  Hyperphosphatemia also leads to decreased serum calcium levels, which contribute to secondary hyperparathyroidism and renal osteodystrophy (1).  The goal of therapy is to achieve a normal range of serum calcium, with the optimum level being 8.5 to 10.5 mg/dL (2).  The presence of calcium in the dialysate helps to normalize serum calcium levels in patients receiving hemodialysis, along with the use of an activated source of vitamin D (Calcitriol), an oral calcium supplement, vitamin D analog (doxercalciferol or paricalcitol) (5-7) and a phosphorus binder.  A “corrected calcium” should be considered when the albumin level—not the serum calcium—is low.

    Phosphorus: Low levels of serum phosphate may lead to phosphorus depletion and osteomalacia.  The goal of therapy is to maintain the phosphorus level between 2.5 to 5.0 mg/dL for patients with Pre-ESRD, and 4.0 to 6.0 mg/dL in patients receiving renal replacement therapy (2).

    Calcium-phosphorus product: It is best to maintain the calcium-phosphorus product (the result of multiplying the serum values of both) below 55 mg2/dl2, to prevent soft-tissue calcification (4-6).

    Creatinine: Creatinine, another form of nitrogenous waste, is a product of muscle metabolism. Creatinine is used as a tool to assess renal function.  A twice-normal serum creatinine level (normal, 0.5 to 1.5 mg/dL) suggests a greater than 50% nephron loss, whereas a serum creatinine level of 10 mg/dL suggests a 90% nephron loss or ESRD.  Serum creatinine assessment can be used in determining the consistency of dialytic therapy, when serial measurements are used.  Eventually a normal creatinine level can be established for each dialysis patient for his or her muscle mass and dialysis prescription.  The predialysis or stabilized serum creatinine and the creatinine index reflect the sum of dietary intake of foods rich in creatine and endogenous creatinine production minus the urinary excretion, dialytic removal, and endogenous degradation of creatinine.  Individuals with low predialysis or stabilized serum creatinine (less than approximately 10 mg/dL) should be evaluated for protein-energy malnutrition and wasting of skeletal muscle (3). Sudden increases in serum creatinine levels usually can be traced to changes in the dialysis regimen, such as skipped treatments, decreased dialysis time, or poor blood flow through an access.  Elevated BUN and serum potassium levels accompanied by a suddenly elevated serum creatinine level and a decrease in carbon dioxide, usually indicate decreased waste product removal.

    Glucose:Ideally, normal glucose levels should be maintained in all dialysis patients to prevent the complications of hypoglycemia and hyperglycemia.  Abnormal carbohydrate metabolism resulting in hyperglycemia has been noted in individuals approaching ESRD.  The cause is not specifically known, but it does seem to resolve after several weeks of dialysis therapy or transplantation.  High blood glucose levels can increase thirst, decrease serum sodium, and increase serum potassium.  Acidosis (indicated by decreased carbon dioxide and increased anion gap) increases protein catabolism and often accompanies the elevated blood glucose levels in chronic renal failure (8,9).

Glomerular Filtration Rate (Creatinine Clearance) (1,2)
Creatinine clearance is the most commonly used measure of GFR.  Normal GFR is 125 mL/min.  Direct urinary clearance measurements are useful in determining the degree of renal dysfunction at lower levels of clearance (1,2).  The estimated GFR will provide a useful “ballpark” value for the GFR (ie, <25 mL/min) (3) .

    In principle, a reciprocal relationship between serum creatinine and creatinine clearance exists.  To estimate creatinine clearance, factors such as body weight, age, and sex must be considered since creatinine increases with body weight and musculature and decreases with age.  The relationship between serum creatinine and creatinine clearance is not valid for patients receiving dialysis, patients with ARF, or patients in a catabolic state in whom muscle mass is being destroyed.

    The most widely used method for estimating GFR is the Cockcroft-Gault equation (10).

References

1. Wolk R.  Nutrition in renal failure.  In: Gottschlich M, ed.  The Science and Practice of Nutrition Support: A Core-Based Curriculum.  Dubuque, Ia: Kendall/Hunt Publishing Co; 2001.
2. Wiggins KL, ed.  Guidelines for Nutrition Care of Renal Patients.  Chicago, Ill: American Dietetic Association; 2002.
3. NKF-DOQI Clinical practice guidelines for nutrition in chronic renal failure. Am J Kidney Dis. 2000:35(suppl 2):S17-S104. 
4. Block GA, Friedrich KP. Re-evaluation of risks associated with hyperphosphatemia and hyperparathyroidism in dialysis patient: recommendations for a change in management. Am J Kidney Dis. 2000;1226-1237.
5. Moe SA. Calcium and Phosphorus Balance in ESRD: Implications and Management. Cambridge, Mass: Genzyme Corp; 2001.
6. Slatopolsky E, Martin KJ, Sherrard DJ. Should vitamin D analogs be the therapy of preference for ESRD patients with secondary hyperparathyroidism? Dial Transplantation;2001;30:190-195.
7. Malluxhe HH, Monier-Faugere MC. Hyperphosphatemia: pharmacologic intervention yesterday, today, and tomorrow. Clin Nephrol. 2000;54:309-317.
8. Weldy NJ. Body Fluids and Electrolytes. 7th ed. St. Louis, Mo: Mosby; 1996:104-106,108-112.
9. Mitch WE, Klahr S. Handbook of Nutrition and the Kidney.3rd ed. Philadelphia, Pa: Lippincott-Raven; 1998:79-80,170-177.
10. Cockcroft DW, Gault MH.  Prediction of creatinine clearance from serum creatinine.  Nephron.  1976; 16:31-41.

American Dietetic Association. Guidelines for nutrition care of the adult dialysis patient. Renal Nutr Forum. 1998;17(2)(insert).
Inman Felton A, Smith K.  Adult acute renal failure medical nutrition therapy protocol.  In: Inman Felton A, Smith K, eds.   Nutrition Care
Protocols for the Acute Care Setting. Smyrna, Ga: Morrison Management Specialists Inc; 2000.
Mitch WE, Klahr S. Nutrition and the Kidney. 2nd ed.  Boston, Mass: Little, Brown & Co; 1993.
Wilkens KG.  Medical nutrition therapy for renal disorders.  In: Mahan LK, Escott-Stump S, eds. Krause's Food, Nutrition and Diet Therapy. 10th ed.  Philadelphia, Pa: WB Saunders Co; 2000:833-866.

*Kt/V indicates clearance of the dialyzer ´ time/volume; URR, urea reduction rate; CAPD, continuous ambulatory peritoneal dialysis; and nPNA, protein equivalent of nitrogen appearance.

References

1. Wiggins KL, ed.  Guidelines for Nutrition Care of Renal Patients.  Chicago, Ill: American Dietetic Association; 2002.
2. NKF-DOQI Clinical Practice Guidelines for Treatment of Anemia of Chronic Renal Failure, Quick Reference Clinical Handbook. New York, NY: National Renal Foundation; 1998.
3. Wilkens KG.  Medical nutrition therapy in renal disorders.  In: Mahan K, Escott-Stump S, eds.  Krause’s Food, Nutrition and Diet Therapy.  10th ed. Philadelphia Pa: WB Saunders Co; 2000:851-853.
4. Stover J, ed. A Clinical Guide to Nutrition Care in End Stage Renal Disease. 2nd ed. Chicago, Ill: American Dietetic Association; 1994:160.
5. Moe SA. Calcium and Phosphorus Balance in ESRD: Implications and Management. Cambridge, Mass: Genzyme Corp; 2001.
6. Sherman RA. Interdialytic weight gain and nutrition parameters in chronic hemodialysis patients. Am J Kidney Dis. 1995;25:279.
7. Wolk R.  Nutrition in renal failure.  In: Gottschlich M, ed.  The Science and Practice of Nutrition Support: A Core-Based Curriculum.  Dubuque, Ia: Kendall/Hunt Publishing Co; 2001.

Manual of Clinical Nutrition Management                                                     
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