What is AKI?
Sudden, acute drop in kidney function and GFR occurring over a period of
hours, days, or weeks
Is AKI reversible?
May be reversible depending on cause or may lead to permanent renal failure
What is AKI characterized by?
fluid, electrolyte and acid-base imbalances and wasting
How can AKI be defined in terms of numbers?
- Increase in SCr by ≥ 0.3 mg/dl (≥ 26 μmol/l) within 48 hours
- Increase in SCr to ≥ 1.5 times baseline, which is known or presumed to have occurred within the prior 7 days;
- Urine volume <0.5 ml/kg/h for 6 hours.
what are the 3 AKI classifications according to etiology?
prerenal
intrarenal
postrenal
Describe prerenal AKI
causes, dietary intervention
• Impaired blood flow to kidneys resulting in decreased urine output and retention of N waste products
Causes:
• Hypovolemia: hemorrhage, burns, diarrhea ,vomiting, inadequate fluid replacement
• Increased vascular capacity and leakiness:sepsis,anaphylaxis
• Heartis compromised: heart failure, cardiogenic shock after an MI
• Renal stenosis: Fibromuscular dysplasia, atherosclerosis causing stenosis
• Minimal dietary intervention required; reversible if underlying problem treated
Describe intrarenal AKI
causes, dietary intervention
Damage within kidney cells due to ischemia, toxins and tubular obstruction
Cause: acute tubular necrosis (ATN) = death of epithelial cells in the renal tubular that cause obstruction of the lumen and fluid back-up.
• Prerenal issue causing lack of blood flow
• Exposure to nephrotoxic exogenous compounds: (antibiotics), heavy metals, ethylene glycol
• Exposure to nephrotoxic endogenous compounds: myoglobin (released from muscle damage cells), uric acid (destruction of DNA/RNA re. chemotherapy), hemoglobin
• Interstitial nephritis and glomerulonephritis
• Nutrition management is critical
Describe postrenal (obstructive) AKI causes, dietary intervention
- Obstruction in urine flow (urinary tract obstruction)
- Causes: bladder cancer, benign prostate hyperplasia, strictures, blood clots, renal stones
- Minimal dietary intervention and reversible if underlying problem corrected
what are the phases of AKI
• Onset: Kidney injury occurs (hours to days)
• Oliguric (or anuric) phase: Urine output decreases from renal tubule damage (8 – 14 days…)
• Diuretic phase: Healing and urine output increases (7 to 14 days)
- Decreasing BUN/Cr, potassium, phosphorus and Magnesium
• Recovery: Tub (Months ++)
what are the stages of AKI? at what stage is dialysis given?
1, 2, 3
dialysis is usually started in stage 2 or 3
is AKI hyper or hypo metabolic
hyper
Clinical manifestations of AKI
- extremely low urine output
- fluid and electrolyte disorders
- azotemia
- wasting, particularly if they are both oliguric and hypercatabolic (common complications of AKI)
AKI has a poor __ and a high __ rate associated with the degree of __ and __.
AKI has a poor prognosis and a high mortality rate associated with the degree of hypercatabolism and infection.
Symptoms and signs of AKI
•Fluid retention/overload
- Swelling in the hands, face, or feet
- SOB (worse during activity or when lying down)
- Tachycardia and enlarged neck veins
• Electrolyte abnormalities (K, Mg, Na often high)
- Muscle cramps
- Irregular heartbeat
- Neurological problems, (tingling, paralysis, confusion)
• Metabolic acidosis
- Nausea, vomiting, and loss of appetite
- Muscle fatigue
- Rapid breathing
- Headache
- Confusion or lethargy
• Anemia
- Paleness
- Shortness of breath
- Fatigue
- Irregular heartbeat
AKI complications
• Hematuria
• Reduced urine output (oliguria)
• Dehydration: may lead to excess thirst, dizziness, weak rapid pulse
• Uremia (high levels of urea in the blood): may affect the digestive system, brain, heart, lungs, and other parts of
the body.
• Side or lower back pain: If obstruction in urinary tract
• HYpercatabolism, high levels of protein breakdown
metabolic complications of AKI
- Hypertension
- hyperglycemia
- insulin resistance
- high cholesterol
- high triglycerides
- decreased protein synthesis
- increased protein breakdown
- azotemia
- changes in electrolytes up or down
- hypocalcaemia
- metabolic acidosis
- anaemia
AKI: Nutritional goals
- Minimize uremia and maintain the chemical composition of the body as close to normal as possible
- Preserve body protein stores until renal function returns
- Maintain fluid, electrolyte, and acid-base homeostasis
- Nutritional support
AKI: General Dietary Guidelines
- Controlled protein, PO4, Na, K, fluid
- Energy to meet requirements and minimize lean body mass breakdown
- Consider: clinical condition, lab values, fluid status, type/frequency of dialysis
- Supplementation of water soluble vitamins due to losses in dialysis
- IBW vs actual weight vs dry weight
does AKI require dialysis?
AKI often requires RRT
• Continuous renal replacement therapy (CRRT)
Energy reccs for AKI
20-30 kcal/kg/d
Based on actual body weight (ideal body weight if obese)
Protein reccs for AKI
- 0.8–1.0 g/kg/d of protein in noncatabolic AKI patients without need for dialysis
- 1.0–1.5 g/kg/d in patients with AKI on RRT
- up to a maximum of 1.7 g/kg/d in patients on continuous renal replacement therapy (CRRT) and in hypercatabolic patients.
Minerals, electrolytes, trace elements reccs for AKI
Maintain serum level
Fluid reccs for AKI
Output + 400-500 ml
what should be monitored in AKI?
Daily intake and output Serum electrolytes levels Blood pressure
Weight
TSF/MAMC (Triceps skinfold /midarm muscle circumference): Useful in stable patients–affected by hydration status
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Diabetes90
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Readings75
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Insulin therapy36
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Diabetes complications71
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Insulin pumps60
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GD77
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Diabetes in Culturally Diverse Populations16
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Physical activity and insulin calculation39
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Bariatric surgery42
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Renal133
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Nutrition and Chronic Kidney Disease111
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AKI34
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Transplant33
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eating disorders49
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Pediatrics intro108
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pediatrics: nutr assessment131
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neonatal nutrition134
