Nutrition in Kidney Disease: Impact on Renal Failure and Stones
Nutritional Requirements in Kidney Disease
Proteins
This is a subject of controversy. A higher protein intake may not promote a positive nitrogen balance and may result in higher levels of urea.
- 0.5 to 0.8 g/kg for patients not on dialysis
- 1.0 to 2.0 g/kg for those on dialysis
Keeping urea levels <100 mg/dL
Vitamins
- Avoid vitamin A supplements.
- Vitamin C: 30-50 mg/day
- Requirements of K, E, D, B6, and folate are increased in acute renal failure (ARF) and require supplements.
Acute Renal Failure
First Stage
The patient is critically ill and unable to eat.
Nutritional Intervention
Total parenteral nutrition (due to vomiting, diarrhea) and early dialysis. Parenteral administration of glucose, lipids, and a mixture of essential and nonessential amino acids.
Objective: To reduce protein catabolism and urea production until the patient can tolerate oral feeding.
Chronic Renal Failure
Factors contributing to slowing the progression of the disease:
- Protein: a diet low (0.6 g/kg/day) or very low in protein (0.3 g/kg/day)
- Restriction on the quality and quantity of potassium
- Fat: w-3 fatty acids are beneficial
Factors that aggravate progression:
- Proteinuria
- Hyperglycemia
- Hypertension
Nutritional Recommendations in Chronic Renal Failure
- Protein: 0.55-0.6 g/kg/day, 75% of high biological value
- Energy: 35 kcal/kg/day
- Fat: 30% of total kcal
- Phosphate: 5-10 g/kg/day
- Calcium: 1400-1600 mg/day
- Supplementation of vitamins
Nephrolithiasis (Kidney Stones)
Affects 10% of men and 3% of women. It is caused by the crystallization of components in urine. Composition can be calcium salts, uric acid, cystine, or struvite (ammonium salt, magnesium, and phosphate). Clinical features are similar, but they differ in their pathogenesis and treatment.
Recommendation
Regardless of the type of stone and cause, increase water consumption to 1.5 to 3 L/day to produce at least 2 liters of urine per day. This is an effective preventive treatment to decrease the recurrence rate.
The goal is to maintain hydration with dilute urine, preventing the crystallization of stone-forming minerals.
Calcium Oxalate and Calcium Phosphate
80% of stones are calcium oxalate (alone or with a core of calcium phosphate in the form of hydroxyapatite). Primary treatment involves the correction of the specific defect and certain nutritional measures.
Primary Hyperoxaluria
This is a rare inherited metabolic disorder that causes recurrent calcium oxalate deposits in the renal parenchyma. It leads to progressive death of the patient before the third decade of life.
Enteric Hyperoxaluria
Cause: Excessive intestinal absorption of oxalate linked to bowel diseases like Crohn’s disease and celiac sprue.
Treatment: 800 to 1200 mg/day of oral calcium (which binds oxalate) and reduced consumption of certain foods rich in oxalate.
Eight foods that actually raise urinary oxalate excretion are rhubarb, spinach, strawberries, chocolate, wheat bran, nuts, beets, and tea.
Hypercalciuria
Formation of calcium stones occurs when there is over 200 mg of calcium in urine for 24 hours.
Cause: Increased intestinal absorption, renal calcium loss, or bone resorption.
Treatment: A diet low in calcium (400-600 mg/day) only if the patient has impaired renal absorption, due to the risk of bone loss.
There are no studies showing that a lower intake of calcium leads to a lower occurrence of stones.
Epidemiological Studies: Calcium intake forms insoluble calcium oxalate salts in the intestine. Restricting intestinal absorption of calcium oxalate is not appropriate.
Hyperuricosuria
Usually results in the formation of calcium oxalate stones rather than uric acid stones. Uric acid crystals create a nucleus of precipitation where calcium oxalate is deposited.
Treatment: Limit protein consumption. The consumption of animal protein increases the excretion of uric acid and calcium, reduces urinary citrate excretion, and is a risk factor for lithogenesis.