Renal + Bariatric surgeries Flashcards
1
Q
Name 5 indications for bariatric surgery
A
- BMI ≥ 40
OR - BMI > 35 with significant obesity-related comorbidities (e.g. MetS, OSA, Osteoarthritis, HTN, …)
- Acceptable operative risk (risk of surgery < risk of not undergoing surgery)
- Failure of non-surgical weight loss attempts
- Well-informed, compliant, and motivated patient (need to understand lifestyle habits still have to change despite the surgery being done)
2
Q
Name 6 contraindications to bariatric surgery
A
Active substance abuse (drugs, alcohol) Uncontrolled psychiatric illness Cirrhosis Pulmonary hypertension Severe cardiac and respiratory disease Active pregnancy
3
Q
Name 4 disadvantages of gastric bands
A
- Requires frequent adjustments (cannot tighten too much at once; requires adjustments –> better for people who live close to the center)
- Unknown durability of the band (research does not support this procedure, poor long-term outcomes – no longer covered by insurance)
- Can lead to band erosion and damage the tissue of the stomach.
- Band can also leak which requires more surgeries to fix.
4
Q
Where does the common limb start in a RYGB? In a BPD-DS?
A
RYGB: Common limb starts at proximal jejunum
Switch: ≈ 100 cm of the ileum
5
Q
How do we calculate excess weight loss (EWL)?
A
% Excess weight loss (EWL) = (Pre-op BW – CBW)/(Pre-op BW – IBW) x 100
IBW is at BMI 25
6
Q
Why is there a resolution of T2DM in bariatric surgeries?
A
Not d/t weight loss but rather to gut hormone changes
7
Q
What is the pattern of weight loss after bariatric surgery?
A
o Rapid weight loss occurs over first 12 months post-op
o Most significant loss seen in the first 6 months post-op (fastest loss occurs over 6 months; and for the next 6 months about ½ of the weight lost in the first 6 months is lost) –> patients get discouraged
o Stabilizes after 12 months (goal is maintenance)
8
Q
What are the 3 mechanisms of weight loss in bariatric surgeries?
A
- Gastric restriction (all surgeries) –> reduced PO intake
- Alimentary/Roux limb length (RYGB, BPD-DS)
- Longer roux limb means shorter common limb = more malabsorption and vice versa
- Shorter common channel length –> more malabsorption - Gut hormones (RYGB, sleeve, BPD-DS)
- Decreased Ghrelin (orexigenic hormone) secretion - Produced by the parietal cells (in the gastric fundus), which is removed
- Increased leptin (produced by adipocytes)
- PYY hormone involved in DM resolvement – not a lot of evidence
9
Q
Name late complications of bariatric surgeries
A
Ulcer, stricture, obstruction, hernia, nutrition deficiencies, dumping syndrome, weight regain or weight loss failure, psychological complications, malnutrition, gastric reflux
10
Q
Name early complications of bariatric surgeries
A
Bleeding, anastomotic leak, infection, strictures, obstructions
11
Q
What are the nutrition guidelines post op for bariatric surgeries?
A
Texture progression (to prevent vomiting and promote healing)
Clear fluids (1-3 days)
Full fluids/puree (5 weeks) (applesauce, oatmeal, pureed meat…)
Solids (for life)
Portion progression
After surgery, the stomach and SI are swollen and inflamed – can only eat a small amount
o ½ cup to start, increase to 1 cup portions per meal/snack
12
Q
What is the effect of the removal of the stomach fundus on nutrient absorption?
A
Removal of fundus (fewer parietal cells)
Reduced gastric acidity (hydrochloric acid helps in the digestion of protein, calcium and iron)
Reduced intrinsic factor (IF)
13
Q
What are the nutrients to watch for in RYGB? Switch?
A
Gastric bypass nutrients to watch for: • Calcium • Iron • Vitamin D • Folate • Vitamin B12 (intrinsic factor in the stomach)
Duodenal switch nutrients to watch for: • Calcium • Iron • ADEK (fat-soluble vitamins) – they are usually absorbed in the jejunum and beginning of ileum which are bypassed • Folate • Vitamin B12
14
Q
Why is calcium citrate preferred over calcium carbonate after surgery?
A
It is preferred to use calcium citrate instead of calcium carbonate after a surgery because calcium carbonate requires an acidic component to be absorbed while calcium citrate contains an acidic component
15
Q
Which deficiencies may appear later?
A
Zinc and copper deficiencies usually appear later (2-3 years) because they have adequate stores before
16
Q
Differentiate primary protein malnutrition to secondary PM
A
Primary protein malnutrition (PM) or protein-energy malnutrition (PEM)
o Rare but at risk in all bariatric surgeries
o D/t decreased oral intake/volume restriction
Secondary PM or PEM
o RYGB (rare) and BPD-DS (uncommon, but possible)
o D/t malabsorption
17
Q
When is there most LBM loss after surgery? What are the implications?
A
Most LBM loss occurs within 3 months post-op (PO intake is still poor; trying to advance on texture and volumes)
LBM loss may lead to reduced RMR and reduced muscle strength and physical function (and puts them at risk of regaining weight over time)
Importance:
o Inevitable LBM loss, but try to minimize as much as possible
18
Q
What are the protein recommendations in bariatric surgeries?
A
Band, sleeve, RYGB
o 1.0-1.5 g/kg IBW (≈ 60-120g/d); may use Adjusted BW d/t very high BMI
BPD/DS
o 1.5-2.0 g/kg IBW (≈ 90-120g/d) d/t significant malabsorption may use Adjusted BW d/t very high BMI
Based on expert opinion
Focus in high biological value/high quality protein
o High PDCAAS: egg white, whey, casein, soy
o Low PDCAAS: collagen, gelatin
19
Q
Name common tolerance issues after surgery.
A
Dehydration – hard to drink enough after surgery
Constipation – reduced PO intake = reduced fiber intake (+ we focus more on protein)
Diarrhea o Lactose intolerance (less lactase enzyme if SI has been removed) o Dumping syndrome o Sugar alcohols o Other?
Food intolerances o Dysgeusia (things taste metallic) o Regurgitation (max physical capacity of stomach) o Esophageal dysphagia (hurts)
20
Q
Name possible causes of vomiting post-sx
A
- Esophageal dysphagia?
- Poor chewing
- Overeating
- Eating too quickly
- Eating tough, fibrous foods, doughy breads, dry meat
- Stricture (If a patient vomits everything he/she eats (even pureed foods) but can tolerate water = probably a stricture)
21
Q
With which surgery(ies) is dumping syndrome common?
A
Occurs with RYGB due to the removal of the pyloric sphincter. Occurs in 85% of patients with GB, 30% of those with sleeves. No pyloric sphincter: Undigested food touches SI too soon –> osmosis
22
Q
Describe the 2 phases of dumping syndrome
A
“early” phase:
o Occurs 10-30 minutes PC
o D/t rapid transit of hyperosmotic food into the jejunum (usually simple sugars)
o Symptoms: dizziness, nausea, weakness, rapid pulse, diarrhea (similar to hypo)
“Late” phase:
o Occurs 1-3h PC
o Reactive hypoglycemia due to an exaggerated release of insulin d/t surge of glucose in the SI –> pancreas sends a surge of insulin –> end up with a surge in BG d/t simple sugars entering the blood and then a drop
23
Q
What nutrition interventions are recommended for dumping syndrome?
A
o Healthy snacking
o Advise glucometer
o Avoidance of trigger foods (limiting simple sugars)
o Label reading (≤ 25 g absorbable carb)
* ≥ 25 g absorbable carb can lead to dumping syndrome
24
Q
What is nesidioblastosis and what can be done to avoid?
A
Nesidioblastosis (hyperinsulinemic hypoglycemia) may happen when patients eat high carb low protein meal
Nutrition intervention
o Increase in protein:carb ratio at lunch and PM snack
o If no change in symptoms, see an endocrinologist (may be put on acarbose)
25
What are 3 possible causes of hair loss post surgery?
- weight loss (happens in about 50% of bariatric patients); Shock loss – premature loss of hair before growth of next “batch”
Thinning or shedding of hair d/t weight loss and physiological stress of surgery
Occurs between 3-6 months post-op (early hair loss) – can go on to 9 months
Late hair loss (about 2-3 years after surgery) conduct dietary assessment and bloodwork; calculate protein intake
-Protein deficiency (needs are higher)
- zinc deficiency (gummy MVI have less calcium, iron and zinc…)
Prevalence of zinc deficiency among patients with a switch: 70%
Symptoms of Zn deficiency: Hair loss, dysgeusia
Consider zinc deficiency if…
o Hair loss starts > 6-9 months post-op
o Attaining protein needs
o Insufficient zinc supplementation
26
What can be done to reverse Zn deficiency?
Nutrition intervention
o Zinc supplementation: 60 mg elemental BID
o Monitor plasma zinc in bloodwork
o Suggest complete MVI to patient considering…
27
Name 5 causes for weight regain post-op
• Dietary habits
Increased calories: sugar and fat; Grazing: emotional eating
Not delaying fluids (drinking and eating at the same time)
• Poorly controlled thyroid
• New medications (weight promoting, antidepressants)
• Stopped exercising
• Surgical reasons? (only in 10% of cases; unlikely…)
28
Define GFR
Expression of the quantity of glomerular filtrate formed each minute in the nephrons of both kidneys, calculated by measuring the clearance of specific substances (inulin or creatinine)
29
Name 6 factors that can influence urine creatinine
• Diet, muscle breakdown, lab calibration bias, extra-renal elimination (gut bacteria), age, Antibiotics…
30
Classify the 5 stakes of CKS based on their GFR.
```
Stage 1: Kidney damage with normal or increased GFR
Stage 2: GFR 60-89
Stage 3: GFR 30-59
Stage 4: GFR 15-29
Stage 5: GFR < 15 or dialysis
```
31
How do we calculate dry weight?
1. Total body water – Watson Method (Weight in kg, height in cm)
2. Estimated dry weight
o Liters of actual body water = 142 mEq/L X Liters of total body water/serum sodium (mEq/L)
o Liters of actual body water – liters of total body water = excess body fluid (kg)
o Weight – XS body fluid (kg) = Estimated dry weight
32
What are sodium and fluid needs in patients with CKD?
o If output less than 1L/d: Restrict to 1.0-1.5L and 2g sodium
o If output greater than 1L/d: 2L and 2-4 g sodium
PD: 1-3L and 2-3g sodium
Predialysis stage (1-4): No need for fluid restriction/sodium restriction according to BP
33
What are high P foods?
High phosphorus foods: Dairy products, proteins (livers, oysters, sardines, carp…), legumes (beans, lentils, chickpeas…), bran cereals, seeds, whole grain products, nuts…
34
How do we calculate adjusted serum calcium?
((4-albumin mg/dL) x 0.8) + Ca mg/dL
35
Explain the link between CKD and renal bone disease
1. Failure of the endocrine function of the kidneys to produce calcitriol (1,25 - dihydroxy cholecalciferol) results in secondary hyperparathyroidism
2. This deficiency leads to disorders of calcium, phosphorus, magnesium, and bone and muscle metabolism
Supplement with active form of Vit D: “1-alpha” to increase absorption and raise serum calcium level and suppress PTH secretion
Renal bone disease develops in early stages of CRF
• Patients with CKD have decreased Ca absorption 2°:
- altered metabolism of Vit D
- inability to excrete excess phosphate or hyperphosphatemia
Results in decreased serum calcium or hypocalcemia, hyperparathyroidism and renal osteodystrophy
36
How can we control hyperphosphatemia in CKD?
To control hyperphosphatemia:
Restrict dietary phosphorus to 12mg/kg/d or 15 mg/gPro/d
** main foods: dairy products, meat, fish, poultry, legumes, nuts, bran, cola, chocolate, beer
Use phosphorus binders (calcium acetate, calcium carbonate or Sevelamer HCl known as RENAGEL {Calcium free})
Avoid aluminum containing binders, because linked with the development of dementia; if necessary, pulse for 2 weeks.
37
Why do we want to decrease PTH levels?
High calcium x phosphorus product results in metastatic calcification in soft tissue areas:
This is why we want to decrease PTH levels
• Conjunctivae of the eye
• Heart, especially aortic valve and blood vessels
• Lungs
• Extremities
38
Which vitamins should be supplemented in people on dialysis? Why
Water-soluble vitamin supplements
o Increased losses during PD and HD; anorexia; poor intake
o Diet restrictions
o Impaired synthesis
39
Why is zinc supplementation useful in patients on HD?
Researchers suggest that zinc supplementation in the amount of 15 mg/d may improve dysgeusia (loss of taste) and may be helpful in the management of impotence in male hemodialysis patients
40
What are the macronutrient recommendations for patients with CKD?
```
SFA: 7% E
PUFAS: ≤ 10% E
MUFAS ≤ 20% E
Total fat: 25-35% E
CHO: 50-60% E
Protein: 15% E
Cholesterol < 200 mg
Fiber: 20-30g/d with 5-10 g soluble fiber
```
41
Name risk factors for CKD
* Diabetes
* Hypertension
* Autoimmune diseases (e.g. systemic lupus erythematosus)
* Systemic infections
* Urinary tract infections
* Urinary stones or lower urinary tract obstruction
* Neoplasia
* Family history of chronic kidney disease
* History of acute kidney injury
* Reduction in kidney mass
* Exposure to certain drugs
* Low birth weight
* Age older than 60 years
* Exposure to certain chemical and environmental conditions
* Low income/education
* Ethnicity (African Americans, Hispanic Americans, Asians, Pacific Islanders, and American Indians.)
42
Name causes of CKD
Diabetes, HTN, other renal disease (chronic glomerulonephritis, polycystic kidney disease, interstitial nephritis, obstructive nephropathy)
43
Name symptoms of CKD
Asymptomatic in earlier phases but as failure progresses: Increasing fatigue, N/V, anorexia, insomnia, uremic syndrome --> body is intoxicated by nutrients
44
Name and explain the 4 phases of CKD
1. Decreased renal reserves
Diminishing renal function but without accumulation of the end-products of protein metabolism. The patient is asymptomatic
```
2. Chronic renal insufficiency
Further reduction in kidney function
GFR decreases of 30 mL/min (about 90)
Waste products begin to accumulate
CRI can be mild, moderate, or severe --> Severe CRI will eventually progress to ESRD
```
3. Frank Renal Failure
Serum creatinine and BUN rise steadily due to drop in GFR
4. End stage renal disease
Remaining kidney function cannot adequately regulate the balance of fluids, salts, and waste products in the body – uremia
< 15% of normal function (DM); < 10% (no DM)
All body systems are impaired
Dialysis and/or transplant is needed to prevent complications and death
45
Name complications of CKD
* Uremic syndrome (high urea and creatinine)
* Anemia (decreased erythropoietin)
* Fluid imbalances (Na imbalance, edema)
* Electrolyte imbalances (high K, acidity, PO4)
46
What is pre-dialysis? What is the nutritional goal?
Stage 3-4 (GFR 13-50)
| Goal: Minimizing renal impairment while preventing malnutrition (prevent uremia symptoms)
47
What is considered as CKD in diabetes?
CKD in diabetes = Albumin to creatinine ratio (ACR) ≥ 2.0 mg/mmol and/or eGFR < 60 mL/min/1.73 m2
48
What are the nutrition recommendations for CKD stage 1-2?
- Protein
- Energy
- Sodium
- K
- P
- Ca
- Fluid
- Protein: 0.8-1.4
- Energy: 25-35 kcal/kg
- Sodium: < 2400
- K: Unrestricted unless blood level high
- P: Maintain serum P WNL
- Ca: DRI, maintain serum levels WNL
- Fluid: Usually unlimited
49
What are the nutrition recommendations for CKD stage 3-4?
- Protein
- Energy
- Sodium
- K
- P
- Ca
- Fluid
- Protein: 0.6-0.8
- Energy: 25-35 kcal/kg
- Sodium: < 2400
- K: Unrestricted unless blood level high
- P: 800-1000 mg/d
- Ca: DRI, maintain serum levels WNL
- Fluid: Usually unlimited
50
When should we screen diabetic people for CKD?
Screen annually when no transient cause of albuminuria or low eGFR are present, and when AKI or non-diabetic kidney disease is not suspected
T1DM: Annually in postpubertal individuals with duration of diabetes ≥ 5 years
T2DM: At diagnosis and annually thereafter
51
Name possible causes of transient albuminuria
Recent major exercise, UTI, febrile illness, decompensated CHF, menstruation, acute severe elevation in BG, acute severe elevation in BP
52
How do we diagnose CKD in diabetic people?
eGFR ≤ 60 or ACR > ≥ 2.0 mg/mmol?
If so, do random urine ACR --> is it ≥ 20 mg/mmol?
NO --> order SCr and 2 repeat random urine ACRs over next 3 months
Is GFR ≤ 60 OR ACR 2/3 ≥ 2 mg/mmol?
DIAGNOSIS
53
Name 4 ways to reduce the progression of diabetic nephropathy
* Optimal glycemic control
* Optimal BP control
* ACEi or ARB
* SGLT2i (less certain, but evidence going there)
54
What do we need to do before starting new drug therapy in CKD?
Before starting new drug therapy: Check serum K and Creat
At baseline
Within 1-2 weeks of initiation or titration
During acute illness
If K+ becomes elevated or Creat > 30% increase review therapy; recheck serum K and Creat
55
What to do in case of moderate/mild hypokalemia? Severe hypokalemia?
Mild to moderate stable hyperkalemia
o Counsel on a low potassium diet
o If persistent, consider adding non-potassium sparing diuretics and/or oral sodium bicarbonate (in those with metabolic acidosis)
o Consider temporarily holding or discontinuing ACEi, ARB or Direct Renin Inhibitor (DRI)
Severe hyperkalemia
o Hold or discontinue ACEi, ARB or DRI
o Emergency management strategies
56
Name symptoms of CKD/uremia
Weight loss, weakness, vomiting, loss of appetite, fatigue, nausea, SOB, leg cramps, itching, chest pain, easy bruising, swelling of ankles and legs, bad taste in the mouth, restless legs, forgetfulness, difficulty sleeping, cold intolerance, skin color changes, decreased sexual desire
57
What can be secondary causes of anemia in CKD?
* Residual blood loss in dialyzer contributes
* Inflammation due to infection and co-morbid conditions
* Hyperparathyroidism can be an adjunctive cause
58
Why is constipation common in CKD? What can be done to help?
* Low fluid intake
* Inactivity
* Use of calcium containing phosphorus binders
* Fruit and vegetable avoidance related to K content
* Low fiber food choices
Treatment:
• Add foods high in fiber content
• Increase fluid intake if possible, dispel fears (patients may be used to restricting fluid)
• Add fiber in forms of psyllium hydrophilic mucilloid, known as Metamucil
• Use stool softeners routinely such as Docusate sodium (Colace)
59
What are the 2 main characteristics of AKI?
• Characterized by: Fluid and electrolyte imbalances and muscle wasting
60
Define AKI
* Sudden, acute drop in function occurring over a period of hours, days, or weeks
* May be reversible depending on cause or may lead to permanent renal failure
Acute kidney injury can be defined as:
Increase in SCr by ≥ 0.3 mg/dL (≥ 26.5 umol/L) within 48 hours (rapid)
Or
Increase in SCr to >= 1.5 times baseline, which is known or presumed to have occurred within the prior 7 days;
OR
Urine volume <0.5 ml/kg/h for 6 hours.
61
What can cause AKI?
```
Caused by a combination of events including sepsis, hypotension, exposure to nephrotoxic drugs…
• Sepsis
• Critical illness
• Circulatory shock
• Burns
• Trauma
• Cardiac surgery
• Major noncardiac surgery
• Nephrotic drugs
• Radiocontrast agents
• Poisonous plants and animals
```
62
Describe the stages of AKI
Stage 1:
SCr 1.5-1.9x baseline or ≥ 0.3 mg/dL increase
Urine < 0.5 ml/kg/h for 6-12h
Stage 2:
SCr 2.0-2.9x baseline
Urine < 0.5 ml/kg/h for > 12h
Stage 3:
SCr 3.0 times baseline
OR
Increase in serum creatinine to >=4.0 mg/dl (>=353.6 mmol/l)
OR
Initiation of renal replacement therapy OR,
In patients <18 years, decrease in eGFR to <35 ml/min
Urine output < 0.3 ml/kg/h for >= 24 hours
OR
anuria for >= 12 hours
63
Who is more susceptible to AKI?
* Dehydration or volume depletion
* Advanced age
* Female gender
* Black race
* CKD
* Chronic diseases (heart, lung, liver)
* Diabetes mellitus
* Cancer
* Anemia
64
Name symptoms of AKI
```
• Too little urine leaving the body
• Swelling in legs, ankles, and around the eyes
• Fatigue or tiredness
• Shortness of breath
• Confusion
• Nausea
• Seizures or coma in severe cases
• Chest pain or pressure
In some cases, AKI causes no symptoms and is only found through other tests done by your healthcare provider.
```
65
Name and explain the 3 categories of AKI
1. Prerenal
Impaired blood flow to kidneys --> decreased urine and retention of N waste products
Hypoperfusion of an otherwise functioning kidney leads to enhanced reabsorption of sodium and water, resulting in oliguria (urine output < 500 mL/day) with high urine osmolality and low urine sodium.
Minimal dietary intervention possible
2. Intrarenal
Damage to kidney parenchyma or acute tubular necrosis (ATN)
Glomerular disease reduces glomerular filtration rate (GFR) and increases glomerular capillary permeability to proteins and red blood cells; it may be inflammatory (glomerulonephritis) or the result of vascular damage due to ischemia or vasculitis.
Tubules may become obstructed by cellular debris, protein or crystal deposition, and cellular or interstitial edema.
Interstitial inflammation (nephritis) usually involves an immunologic or allergic phenomenon. These mechanisms of tubular damage are complex and interdependent, rendering the previously popular term acute tubular necrosis an inadequate description.
3. Postrenal
Obstruction in urine flow (urinary tract obstruction)
66
What are possible causes of prerenal AKI?
Hypovolemia due to hemorrhage, burns, diarrhea, vomiting, inadequate fluid replacement, decreased cardiac output, liver cirrhosis, renal vasoconstriction (medications, hepatorenal), renal artery occlusion…, NSAIDS, allergic reactions, major surgery
67
What are possible causes of intrarenal AKI?
glomerulonephritis, malignant HTN, prolonged prerenal ischemia, MOSF, systemic lupus, nephrotoxic drugs, hemolytic blood transfusions, myoglobinuria, interstitial inflammation or infection (sepsis), multiple myeloma, scleroderma
68
What are possible causes of postrenal AKI?
bladder cancer, benign prostate hyperplasia, prostate or cervical cancer, strictures, blood clots in the urinary tract, renal stones
69
Name Signs and symptoms of AKI
```
Fluid retention/overload (urination is reduced)
- Swelling in the hands, face, or feet --> calculate dry BW
- SOB (worse during activity or when lying down)
- Tachycardia and enlarged neck veins
Metabolic acidosis
- Nausea, vomiting, and loss of appetite
- Muscle fatigue
- Rapid breathing
- Headache
- Confusion or lethargy
Electrolyte abnormalities (K, Mg, Na)
- Muscle cramps
- Irregular heartbeat
- Neurological problems, (tingling, paralysis, confusion)
Anemia
- Paleness
- Shortness of breath
- Fatigue
- Irregular heartbeat
Symptoms of uremia may develop later as nitrogenous products accumulate
```
70
List and explain the 4 phases of AKI
Anuric phase
o Urine output < 100 mL/d
o Requires aggressive tx with dialysis (temporary)
o Time span: 10-14 days
Oliguric phase
o Urine output < 500 mL/d
o Increased levels: BUN, creatinine, K, P, Mg
o Decreased levels: Na, CO2, Ca, Hct, Hgb
o Dialysis typically necessary
o Time span: 8-14 days (may not progress to next phase)
Diuretic phase
o Increased urine output: 150% - 200% of normal
o Increased risk of dehydration
o Electrolyte imbalances: Low K, high or low Na and BUN – related to hydration and urine concentration ability
o Time span: 10 days
```
Convalescent phase
o Occurs in reversible ARF
o Renal function normalizes
o Lab values stabilize
o Time span: 4-6 months
```
71
Name complications of AKI
* Hematuria
* Reduced urine output
* Dehydration --> may lead to excess thirst, dizziness, weak rapid pulse
* Uremia --> may affect the digestive system, brain, heart, lungs, and other parts of the body.
* Side or lower back pain --> If obstruction in urinary tract
* Hyperkalemia
* Hyperphosphatemia
* Glucose intolerance
* Fluid overload, acidosis, azotemia
72
Why is there hyperglycemia in AKI?
Carbohydrate metabolism in AKI is characterized by hyperglycemia due to peripheral insulin resistance and accelerated hepatic gluconeogenesis, mainly from conversion of amino acids released during protein catabolism that cannot be suppressed by exogenous glucose infusions
73
What are the dietary guidelines for people with AKI?
- Energy
- Protein
- Phosphorus
- Sodium
- Potassium
- Calcium
- Fluid
- Energy: 20-30 kcal/kg
- Protein:
0. 8-1.0 g/kg/d non catabolic, non-dialyzed
1. 0-1.5 g/kg/d on RRT
1. 7g/kg high stress, hypercatabolic, dialysis
- Phosphorus: Maintain serum levels
- Sodium: 2-3g/d as tolerated
- Potassium: Maintain serum < 5 mEq/L, replace losses in diuretic phase
- Calcium: Maintain serum levels
- Fluid: Output + 500 mL
74
What to monitor in AKI?
Weight
Gain >0.5-1 kg/day suggests fluid retention
Loss (compared to dry weight) suggests LBM loss
TSF/MAMC (Triceps skinfold /midarm muscle circumference)
Useful in stable patients – affected by hydration status
Albumin
Useful tool for assessing morbidity/mortality risk
Affected by hydration status, acute episodes, liver status, albumin infusions
Iron status
Must be considered if using transferrin to assess protein status
May be high during DF and low during iron overload
Urea nitrogen appearance (UNA)
Glucose tolerance
Insulin resistance and decreased insulin breakdown even without DM
75
What are the 3 leading causes of CKD?
* Diabetes (38%)
| * Renal vascular disease (including HBP) (16%)
76
What is a dialysate?
Fluid containing physiological concentration of various solutes (calcium, sodium, potassium, glucose…)
Bathes the blood in dialysis
77
What are the 3 processes dialysis does?
Diffusion (movement of solutes from high to low conc.)
Osmosis (mvmt of water from low to high conc)
Ultrafiltration (removal oc XS fluid
78
What are the 2 types of vascular access in HD and what are the pros and cons for each?
Central venous catheters
o Subclavian (tunnelled, more permanent) – on chest
o Jugular (more uncomfortable; usually temporary)
*More risks of infection; try to convince patients to get a fistula
*CANNOT take a shower NOR swim in a lake or public pool. (Take baths)
Patients develop rashes, infections, bacteremia.
Arterio-Venous (AV) Fistula
o Upper arm fistula
o Lower arm fistula
*Vein and artery have been anastomosed; pressure from the artery will dilate the vein which will be needled every time they come for dialysis. Higher pressure in the vein creates dilation and visible bumps in the vein.
*Preferred access, Safer for the patient – lower rate of mortality vs catheter. Less visible than catheter especially if upper arm (can wear a shirt)
* CAN take showers and swim in lakes/pools
79
What is exchange in PD? Dwell time?
Exchange is the process of draining and filling
o 30-40 minutes
Dwell time is the time the dialysate solution is left in the peritoneal cavity
o 4-6 hours
80
Differentiate CAPD from CCPD
CAPD – Continuous Ambulatory Peritoneal Dialysis
o During the day
o 4 exchanges/d
o Usually 2-3 L
CCPD – Continuous Cycle-Assisted Peritoneal Dialysis
o Requires a machine (cycler)
o While the patient sleeps
o 3-5 exchanges per night
81
What are things to think about in terms of the PD dialysate solutions?
• Dextrose based (provides the osmotic “pull”)
o 0.5%, 1.5%, 2.5%, 4.25% (mix of 1.5 and 2.5)
o Consider kcal from dextrose absorption
o Watch for diabetics – adjust insulin, and consider the calories that are absorbed for everyone (can be significant)
o Sclerosing of the peritoneal membrane (can become less permeable if peritonitis)
Special solutions
o Nutrineal (AA 1.1%) – glucose polymer
o Extraneal (Icodextran 7.5%)
o Physioneal – most biocompatible solution
82
What test can be used to assess the permeability of the peritoneal membrane?
PET (Peritoneal Equilibration Test): used to assess permeability of the peritoneal membrane (give us % dextrose absorption)
83
What is the dextrose absorption in CAPD? CCPD?
CAPD ~60-70% dextrose absorbed
| CCPD ~40-50% dextrose absorbed
84
What is the energy absorbed from PD solutions with short dwell time (<6h)? Long dwell time (8h)?
Short: 60%
Long: 86% for dextrose and 25% for extraneal 7.5%
85
What are the energy recommendations for HD? For PD?
For both:
30 kcal/kg for adults > 65
35 kcal/kg for adults ≤ 65
*PD: Consider kcal from dialysate
86
What are the protein recommendations for HD? For PD?
HD:
1.2 g/kg/d ≥ 50% HBV
PD: 1.3-1.5 g/kg IBW ≥ 50% HBV
1.5g/kg/d if peritonitis
87
What are the phosphorus recommendations for HD? For PD?
For both: 800-1200 mg/d
88
What are the sodium recommendations for HD? For PD?
HD: 2000 mg/d
PD: 2000-3000 mg/d
89
What are the potassium recommendations for HD? For PD?
HD:
2340 mg/d
PD:
3000-4000 mg/d
Usually unrestricted unless serum K > 5.5 mmol/L
90
What are the calcium recommendations for HD? For PD?
For both: < 2000 mg/d
| Max 1500 mg from phosphate binders
91
What are the fluid recommendations for HD? For PD?
HD: 1000 ml/d
or 1000 ml + U/O
PD: Ultrafiltration + u/o
92
Why are protein needs higher in PD vs HD?
HD 10-12 g of AA lost across the dialysis membrane each treatment
PD 6-9 g of AA/day (12-20g during peritonitis)
93
Why is star fruit toxic for people with CKD? What are the symptoms of toxicity?
A neurotoxin found in start fruit (Averrhoa carambola) can cause toxicity in patients at later stages of CKD or dialysis
```
Symptoms include:
o Persistent hiccups
o Vomiting
o Muscle weakness
o Slight or partial paralysis
o Muscle weakness
o Slight or partial paralysis
o Muscle twitching
o Insomnia
o Mental confusion
o Convulsion
o Coma and death
```
94
What is the definition of PEM?
Definition: The state of decreased body pools of protein with or without fat depletion or a state of diminished functional capacity caused at least partly by inadequate nutrient intake relative to nutrient demand and/or which is improved by nutritional repletion
95
Why is PEM prevalent in dialysis patients?
- Reduced intake on the days of dialysis
- Dialysis puts the patient in an inflammatory state
- PD: extra weight to carry
Uremia:
Inflammation, inadequate dialysis, anorexia, inadequate nutrient intake, hypercatabolism, chronic acidosis, comorbid conditions (DM, CVD, infection), endocrine disorders
PD:
Loss of nutrients into dialysate, loss of residual renal function, appetite loss due to glucose absorption from dialysate, abdominal discomfort induced by dialysate, peritonitis
96
When should OSN be used in cases of PEM?
* ONS should be given separately from regular meals (not a meal replacement)
* ONS should be given during dialysis session
* Late evening meal or ONS may be useful to reduce the length of nocturnal starvation and the associated increased use of endogenous protein and fat stores
97
Name the pros and cons of meals during HD
PROS
o Counteracts HD related catabolism
o Improved nutritional status (Increased protein synthesis, Increased albumin)
```
CONS
o Patient related risk (Risk of aspiration, Hypotension)
o Patient and unit hygiene
o Infection control
o Inconvenience to staff
```
98
Name the 4 criteria for initiating intradialytic PN
o Unintentional weight loss of > 10% of normal weight or > 5% decrease in dry weight in 3 months
o Failure of EN repletion regimens
o Diagnosis of
- Uremic malabsorption
- Chronic malabsorption syndrome
- Gastroparesis due to uremia and diabetes
- GI disorders *obstruction, diarrhea, N/V
o Failure to thrive, cachexia, serum albumin < 34 g/L
99
Can IDPN by itself represent full nutritional support?
* The patient must be able to meet 50-60% of daily requirements orally
* IDPN by itself does not represent full nutritional support and cannot meet total nutritional requirements!
* Total in the end: 1280 kcal, 21.2 g protein and 800 ml fluid
100
Name 4 possible complications if IDPN
```
o Hyperglycemia
o Allergic reaction to IV fat emulsions
o Post IDPN infusion hypoglycemia
o Fluid overload
--> always encourage ONS daily vs IDPN (3x/d)
```
101
Name 5 reasons for serum sodium to be low
```
Over hydration
Starvation
Nephritis
Hyperglycemia
Diabetic acidosis
```
102
Name 6 reasons for serum K to be high
```
High intake (diet, salt substitutes)
K bath (dialysate)
Meds (ACEi)
GI bleed
Hyperglycemia
Acidosis
```
103
Name 2 reasons for serum calcium to be low
Low albumin
| Meds
104
Name 3 reasons why PTH may be high
High turnover bone disease
High serum PO4 levels
Not enough calcitriol
105
Name 3 reasons why PTH may be low
Adynamic bone disease
Too much calcitriol
Diabetes
High serum calcium levels
106
What is the goal for BUN for patients on dialysis? Is it lower, normal or higher than normal?
15-30 mmol/L
| Higher than normal of 2.7-7.5
107
What is the goal for Hgb for patients on dialysis? Is it lower, normal or higher than normal?
Can be slightly < 120
| Lower than normal
108
What is the goal for phosphate for patients on dialysis? Is it lower, normal or higher than normal?
A bit higher 0.58-1.7 mmol/L vs 0.58-1.32
109
What is the goal for PTH for patients on dialysis? Is it lower, normal or higher than normal?
15-65 pmol/L
| Higher than normal (1.13-7.6)
110
Define CKD-MBD
Chronic kidney disease – Mineral bone disease (CKD-MBD)
Defined by the presence of one of the following symptoms
o Abnormal levels of calcium, phosphate, PTH and active VD
o Abnormal bone morphology “renal osteodystrophy”
o Calcification of blood vessels and other soft tissues (metastatic calcification)
111
Define renal osteodystrophy (RO)
o Form of bone disease related to CKD
o Affects more than 50% of patients with CKD by the time GFR < 50 ml/min
o Most patients develop some form of renal osteodystrophy by the time they require dialysis
o Hyperphosphatemia leading to RO is an independent risk factor for morbidity and mortality
112
What is metastatic calcification?
In the presence of high phosphate levels, calcium is more likely to precipitate into crystals of calcium phosphate which can lead to metastatic calcification
Ca-PO4 crystals deposit in:
o Vascular system can develop ulcers (even+ when patient is diabetic and cannot repair the problems. Many patients need amputation)
o Joints
o Heart, lungs, skeletal muscles, stomach and kidneys (deposition can affect the function of these organs)
o Mucous membranes inside the eyelids
o Epidermis (pruritis – very itchy skin)
113
What are the 3 types of phosphorus and what are their absorption %?
Organic plants --> 20-40%
Organic animals --> 40-60%
Inorganic (additives) --> 100%
114
name sources of phosphorus
```
Beans
Cola
Chocolate
Egg
Cheese
Milk
PB
Chicken
Meat
Yogurt...
```
115
Name 2 calcium-containing P binders
```
Calcium carbonate (500 mg elemental Ca)
Tums
```
116
Name 2 non-calcium containing P binders
Renagel (Lower LDL)
Renvela (lower LDL)
Fosrenol (lanthanum carbonate, potential lanthanum accumulation)
117
In ESRD, what makes constipation so common?
```
Inadequate intake of fluids
Limited fiber intake
- Fruits, vegetables and whole grains = phosphate, potassium…
- Aim for 20-30g/d
Decreased PA (usually older)
Use of phosphate binders
Various medications
```
PD: Translocation of bacteria (peritonitis)
+ the catheter in the peritoneal cavity can get compressed, move (d/t constipation) and that will affect dialysis
PD patients are always on stool softeners or laxatives
118
Name 4 contraindicated laxatives for ESRD
o Milk of magnesia
o Magnolax
o Citro-Mag
o Fleet Phospho-Soda
119
Name other methods to decrease constipation in ESRD
Stool softeners (mild constipation)
o Docusate sodium (Colace)
o Docusate calcium (Surfat)
```
Stimulants
o Senna (Senokot)
o Bisacodyl (Dulcolax)
```
```
Osmotic Laxatives (severe constipation)
o Lactulose
```
Bulking agents
o Unifiber
o Benefiber
o Metamucil and Prodiem (not suitable b/c a lot of water needed)
Suppositories: Glycerine suppositories
Enemas (rare)
120
Why do people on dialysis have high TG? What is a typical dyslipidemia pattern in PD patients?
Typical pattern in PD patients
• Normal cholesterol level
• High TG level
• Low HDL level
Due to both
• Dextrose absorption from dialysate and
• Protein losses into peritoneal dialysate contributes to impaired TG clearance
121
Name 2 advantages and 2 limitations of renal transplantation
Advantages
o Increased survival rate
o Preferred method of treatment – someone may prefer being free of dialysis
Limitations
o Lengthy waiting list
o Long-term immunosuppressive therapy (but they also have meds in ESDR so it balances out)
122
Why do obese patient have more post-surgical problems?
o Higher mortality rate
o Lower graft function
o Increased incidence of wound complications
o More frequent ICU admission
o More frequent re-intubations
o Increased incidence of post-transplant diabetes (immunosuppressors)
123
What is cyclosporin? What are its side effects?
Cyclosporin (immunosuppressant they have to take) has several unwanted side effects:
o Gingival hyperplasia
o GI disturbances
o Hyperglycemia
o Gynecomastia
o Hepatotoxicity, decreased glycogen synthesis
o Nephrotoxicity (bad for new kidney…)
124
Why are corticosteroids used post-transplants and what are their side effects?
* Impaired wound healing
* Avascular necrosis of long bones
* Upper GI ulceration
* Protein catabolism
* HTN
* Steroid-induced diabetes
* Cataract formation
* Stimulation of appetite, weight gain
125
What is the protein recommendation for the acute phase post-transplant? Chronic phase?
Acute phase: 1.3-2.0 g/kg
(2.0-2.5 g/kg with high steroid dose during period of rejection)
Chronic phase: 0.8-1.0 g/kg
126
What is the calorie recommendation for the acute phase post-transplant? Chronic phase?
Acute phase: 30-35 kcal/kg
Chronic phase: Maintain UBW
127
What is the CHO recommendation for the acute phase post-transplant? Chronic phase?
Acute phase: Limit simple CHO with hyperglycemia
Chronic: Emphasize complex CHO and distribute CHO throughout the day
Emphasize dietary fiber
128
What is the fat recommendation for the acute phase post-transplant? Chronic phase?
Acute phase: Meed E needs
Chronic phase: 25-35% of total kcal with saturated fat < 7% of total kcal, up to 10% of kcal from PUFA, and up to 20% of kcal from MUFAs
129
What is the potassium recommendation for the acute phase post-transplant? Chronic phase?
o May slightly restrict in the acute phase (2000-4000 mg/d)
| o Can come back to normal diet (no restriction) in chronic phase (except if hyperkalemia)
130
What is the sodium recommendation for the acute phase post-transplant? Chronic phase?
HTN common, restrict Na if HTN
| 2000-4000 mg/d for acute and chronic phase if HTN (maybe more towards 2000 mg....)
131
What is the calcium recommendation for the acute phase post-transplant? Chronic phase?
1200-1500mg/g for both phases
| Higher needs d/t immunosuppressants (glucocorticoids)
132
What is the phosphorus recommendation for the acute phase post-transplant? Chronic phase?
DRI for both
133
What is the fluid recommendation for the acute phase post-transplant? Chronic phase?
No restriction unless graft not functioning
134
Name a drug nutrient interaction for immunosuppressants
Avoid grapefruit and grapefruit juice. Most lead to N/V, diarrhea, abdominal pain etc which may lead to poor nutritional status
135
What are common risks in post-transplant patients?
CVD
o Increased risk of CVD, dyslipidemias common
o Lipid-lowering medications may be used
Hypomagnesemia
o IV replacement may be required
Weight gain is common, may complicate hyperlipidemia and glucose intolerance
136
What are the nutritional implication of a graft rejection?
* Corticosteroids increase
| * Need for increased protein and kcal requirements (is seen as an acute phase)
137
What is the nephrotic syndrome?
An abnormal condition that is marked by
• Deficiency of albumin in the blood (kidney is excreting TOO MUCH protein)
• Protein excretion in the urine due to altered permeability of the glomerular basement membranes
When protein is lost in the urine, this leads to puffiness or swelling (edema), often of the eyelids, feet and ankles, and eventually the abdomen
If left untreated, this can lead to problems with breathing, eating and infections
- Urinary protein levels > 3.5g/1.73m2/d (measured through albumin)
- Average loss of 6-8 g/d
138
Name symptoms/complications of the nephrotic syndrome
* Proteinuria
* Hypoalbuminemia (< 20 g/L, despite increased synthesis)
* Edema (particularly around eyes, ankles, feet) and weight gain (d/t water retention)
* Sodium retention
* Hyperlipidemia
* Blood clots in veins and lungs
* Peritonitis
* Urinary tract infection
* Low levels of iron
* Hypocalcemia (due to hypoproteinemia and other causes)
* SOB
* Others: Fatigue, loss of appetite
139
What are the 3 main treatments for the nephrotic syndrome?
* Diuretics (reduces BP; excretes extra water)
* ACE inhibitors
* Steroids
* Vaccines (flu shot, pneumococcal)
* Statins/sequestrants (CH reducing meds – not sure at what extent it will prevent mortality)
* Coumadin/heparin
* Early antibiotic intervention
* Diet
140
Why is nephrotic syndrome linked to hyperlipidemia?
- Elevated lipid levels can impair renal function
- Elevations in TC, TG and LDL-C
- HDL-C is reduced or unaffected
- Due to increased lipid synthesis and decreased catabolism
- Correlates with the extent of proteinuria
As you lose protein, there is an accumulation of FFAs --> inhibits LPL, increase VLDL --> hyperlipidemia
141
Name 6 complications of the nephrotic syndrome
* High TC and TG
* Malnutrition (loss of protein, anemia, low levels of VD and calcium)
* High BP
* AKI
* CKD
* Infections
142
Name the 5 goals of nutritional intervention in nephrotic syndrome and what to do to meet those goals.
Reduce proteinuria
o Limit protein intake – 0.7-1.0 g/kg/d
Prevent negative N balance
Control hyperlipidemia
o Decrease fat to < 30% of total kcals
o P:S at least 1:1
Minimize edema
o Decreased sodium < 2000 mg/d
o Fluid restrictions
Delay further progression of renal disease and atherosclerosis
Energy: 35 kcal/kg/d unless weight loss is desired
143
Define nephrolithiasis.
Kidney stones form when calcium, oxalate, struvite, cystine, hydroxyapatite or uric acid are in urine in higher than normal amounts
144
What is the nutrition intervention for nephrolithiasis?
- Increase fluid intake by 3L/d in divided doses (most should be water) – 3L + usual intake?
- No need to avoid dairy (calcium) --> Myth. Should rather limit sodium. (maybe fat also)
o Main recommendation for calcium stones is to avoid sodium
- Avoid > 200 mg/d of vitamin C
- Use of probiotics
- Diets with high intake of animal proteins and low intakes of F&V correlate with more acidic urine and increase risk of stone formation (low pH increases risk)
- DASH diet is recommended (whole grains, dairy, fruits and vegetables)
