WK (2nd half of 3-wk 4) Flashcards
At what stage does calcium wasting usually begin in CKD patients?
Calcium wasting begins in about stage 3 of kidney failure
What are indications that a patient is wasting calcium?
- Typically, circulating calcium stays in the low-normal, progressing toward frank hypocalcemia
- In response to this, you’ll see PTH levels go up
- Which, in turn, leads to increase phosphorus absorption from food, so higher phosphorus levels in the blood
- As renal disease progresses, you’ll also see vitamin D activation problems as kidney tissue becomes progressively less active
- But, you can also see hypercalcemia as a result of treatment, especially if active vitamin D forms are used
- Hypercalcemia – N/V, tetany, palpitations, hypertension, CMS – confusion (may look like stroke)
- Hypercalcemia > hypertension > worsening kidney disease, so you really don’t want to see that
What are approaches to preventing and mitigated calcium wasting?
A. You’ll want to try to triangulate three different measures:
1. Calcium in the normal range (so about 8.5 – 10.2 mg / dl) 2. Phosphorus levels below 5.5 mg/dl (that’s below 1.8 mmol / L in Canadian) 3. PTH below about 110 pg/ml (normal is up to about 55, so we’re setting target at twice the top of normal range)
B. We can do this through use of the following tools
1. Calcium from the diet and supplements
a. Careful of dairy, though, as a high phosphorus food
2. Activated vitamin D (e.g., calcitriol)
a. Note that this medication is VERY potent, and needs to be monitored carefully
3. Phosphorus binders (e.g., calcium carbonate, sevelamer carbonate) taken w/ meals
4. Parathyroid removal surgery
C. Note that these management goals will only become more difficult as disease progresses, one among many reasons to consider a renal nutrition specialist referral
What are various options for lowering phosphorous intake, considering diet, nutrients, and drugs?
- Phosphorus restriction below 1 g/day may be necessary fairly early on
- High phosphorus foods: dairy, (preserved) meats, soda, seeds, legumes
- Use binders appropriately as mentioned above
How is anemia of chronic disease differentiated from iron deficiency?
- DDX of anemia of chronic disease from iron deficiency: Iron panel finds all low in ACD, but finds elevated TIBC in iron deficiency anemia. LOW TIBC in ACD
- Ferritin may not be a good marker here, as inflammatory mediators can drive it up (although ferritin > 70 makes IDA awfully unlikely)
- The presence of ACD doesn’t necessarily rule out folate or B12 or copper or other potential etiologies, and you may need to consider them if treatment does not resolve sx
- Clinical pearl: Rule of 3’s
a. Normal HCT – 36-40 (men usually 3% higher)
b. Hb (divide HCT by 3) – 12
c. RBC count (Hb/3) - 4
How is anemia of CKD treated? What are potential problems with erythropoietin?
The National Kidney Foundation guidelines on CKD management speak very directly on how to manage anemia treatment to minimize clot risk from erythropoietin treatment. Note that iron (especially I.V.) may enhance EPO treatment effect even in the absence of iron deficiency
At what stage is a protein-restricted diet usually recommended for CKD patients?
Low protein diets have been a mainstay of treatment for mid- to late-stage renal failure - frequently prescribed as patient transitions to stage 4 disease
What clinical effects can be expected from a protein-restricted diet in terms of progression of CKD? How does it work? Does it treat the cause(s) of CKD?-> NO!
- In the best clinical research trial, no benefit from protein restriction was seen
- A clinical management note: dietary protein elevates GFR, so you’ll see a quick but small drop in GFR (about 3 or so) related to the shift to a low-protein diet
- Note, there is no association between protein intake and kidney function in healthy people – this conversation is limited to patients with existing renal disease
- The theory here is that the acidity in the nephron as a result of (some types of) protein breakdown leads to increases in endothelin-1, angiotensin II, and aldosterone
a. Ignore talk of protein “straining” kidney function, or about dehydration in the nephron. Neither are correct. - These mediators in turn tend to promote the progression of nephropathy via increased glomerular pressure and hyperfiltration (Brenner Hypothesis)
a. Note that the latter is the big controversy here – it is not fully clear if or why filtering more damages the kidney - Note that animal-source proteins tend to be more acid forming than plant-based foods (due to higher sulphur content)
What is the protein limit for late stage CKD?
- Try to limit protein down to about 0.6 g/kg body weight/day, or down to RDA level
a. Some sources hold this recommendation until GFR < 25, with 0.8 for GFR 25-55
b. This is very hard to do – it’s about 40 g protein for an avg adult
c. About half the protein should be from high biological value protein (egg albumin is reference) - Dairy and eggs tend to hit over 90%
- Meat and fish tend to be 70-80%
- Other than soy and quinoa, most plant food proteins are going to be below 70%
What are adverse effects of a protein-restricted diet?
- Protein calorie malnutrition can result from these recommendations, and this becomes a potential issue later on in dialysis
- It is really hard to do, especially when you have some other big dietary limitations (e.g., low potassium diet, low simple carb diet, low fat diet). What is your patient supposed to eat? (see question 41)
- May be quite at odds with other recommendations (prevent CVD), so you’ll have to choose your battles appropriately
At what stage should salt be restricted in CKD patients? To what level?
Aim for about 2 g of sodium / day, while regularly monitoring electrolyte levels.
1. In renal failure, benefits of sodium restriction are magnified 2. Due to the risk for edema – low sodium diets cut the risk by more than half 3. Reduce the need for blood pressure meds 4. Sodium restriction does appear to manage proteinuria progression, but not to significantly reduce the rate of progression on its own
What are indications for easing salt restriction?
- Remember that sodium restriction is always going to reduce fluid volume
- This will always have the potential to limit kidney perfusion
- As such, if you have a patient following a low sodium diet, and they develop hypotension or their creatinine starts to go up quickly, you’ll want to undo this recommendation
Concomitant use of what drugs can cause a problem when combined with salt restriction?
The potential for hypovolemic symptoms is magnified when diuretics are on board
What is the effect of thiamine on diabetic nephropathy?
High doses of thiamine (or benfotiamine) ==> potential tx for diabetic nephropathy.
Thiamine supplements can prevent the development of early-stage nephropathy (kidney disease) in people with type 2 diabetes. As a treatment for general peripheral neuropathy, thiamine therapy helped reverse diuresis (increased urine flow) and glucosuria (excretion of glucose into the urine), and it also helped normalize cholesterol and triglyceride levels.
What causes metabolic acidosis in late-stage CKD?
- Alkali treatment is recommended for pts with a serum total CO2 < 22 mM
- This is metabolic acidosis, and an accompanying loss of ability to compensate with increase in respiratory rate
- Alkali treatment is either sodium citrate or sodium bicarbonate
- Note that the sodium here is at odds with our prior recommendation for sodium restriction
How is metabolic acidosis in late-stage CKD managed?
A. Note that this is not a primary care management step – this needs to happen via a nephrologist
B. As long as potassium levels are still controlled, you can use food intervention (which means fruits and vegetables) to help balance acid load.
1. This is almost certainly going to be a stage 4 patient, not stage 5
