Renal Disease 1 Flashcards
Prevalence of CKD in Canada?
12.5% of the population
Prevalence of Stage 3-5 in Canada? What % has diabetes and/or hypertension?
3.1%
75%
Prevalence of CKD in adults over 65 years?
30.8%
Provide 5 risk factors for CKD
- Diabetes
- Hypertension
- Autoimmune diseases
- Systemic infections
- Urinary tract infections
Provide 4 sociodemographic risk factors for CKD
- Age > 60 years
- Exposure to certain chemicals and environmental conditions
- Low incomes/education
- Ethnicity
Which ethnicities are at a higher risk of CKD?
- African American
- Hispanic Americans
- Asians
- Pacific Islanders
- American Indians
What is CKD?
The irreversible damage of nephrons, where urea can no longer be properly filtered, leading to the build-up of uremic toxins within the blood
What are the symptoms of CKD?
-Asymptomatic in earlier phases, but as failure progresses leads to increased fatigue, nausea, vomiting, anorexia, insomnia, uremic syndrome and itching
What is a uremic toxin?
An identified substance, which is higher in uremia with associated symptoms which are studies at in vivo levels
What are the confirmed toxins?
- Water
- Sodium
- Potassium
- Hydrogen
- Inorganic Phosphate
- Urea
- Cyanate
- Oxalic Acid
- B2-Microglobulin
What are the suspected toxins?
- Leptin
- AGE’s
- Uric Acid
- Creatinine
- Mg
- Homocysteine
What are the 3 stages of CKD?
1) Decreased renal reserve
2) Chronic renal insufficiency
3) Frank renal failure
4) End stage renal disease
Discuss decreased renal reserve
Diminishing renal function but without the accumulation of the end-products of protein metabolism, the patient is asymptomatic
Discuss chronic renal insufficiency
- Further reduction in kidney function, where GFR decreases to 30 ml/min and waste products can begin to accumulate (“tipping point”)
- Can be mild, moderate or severe
- Severe will eventually progress o ESRD
Discuss Frank renal failure
-Serum creatinine and BUN will rise steadily due to the drop in GFR
Discuss End Stage Renal Disease (ESRD)
- The remaining kidney function cannot adequately regulate the balance of fluids, salts and waste products within the body, and uremia accumulates
- All body systems will become impaired
What is the % function cut-off for ESRD for those with and without diabetes?
With: <15%
Without: <10%
What is needed in ESRD?
Dialysis and or transplant to prevent complications and death
What is the main consideration when initiating dialysis?
-Symptoms, such as fatigue, poor appetite, fluid overload and electrolyte abnormalities
Discuss creatinine in the Mild, asymptomatic CKD patient
- Creatinine clearance will rapidly drop off as GFR decreases
- Serum creatinine slowly rises
Discuss creatinine in the Moderate, compensated CKD patient
- Creatinine clearance will continue to steadily decrease from a lower baseline
- Serum creatinine levels rapidly rise
Discuss creatinine in the severe, decompensated CKD patient
- Creatinine clearance reaches nearly 0
- Serum creatinine continue to rapidly rise, then slightly decrease
CKD complications?
Uremic sundrome
Anemia
Fluid imbalances
Electrolyte imbalances
Uremic syndrome?
High urea and creatinine
Anemia?
Decreased kidney function and less erythropoietin to stimulate RBC production in bone marrow
Fluid imbalances?
Na imbalance and edema
Electrolyte imbalances
High K+, acidity (H+ retained), PO
CKD tests?
- Creatinine and creatinine clearance rates
- BUN, electrolytes
- Iron status measurement
- 24h protein/sodium
- PTH
- Renal biopsy
When may we use 24 hr urine collection?
To estimate Na intake in steady state patient s(as urine sodium is usually the most accurate than intake)
How many mg of Na in 1 mmol?
23 mg
How to determine how many mg of Na a patient is consuming based on 24 h urine collection?
(24 h Na in mmol/day) x (23 mg Na/mmol) = Na mg/day
When should we be cautious in interpreting 24 hour sodium?
-If the patient is on diuretics, such as Lasix which are sodium losing
How may CKD be treated?
- Transplant
- Dialysis
- Medication
- Conservative care
What should be reviewed prior to drawing conclusions about symptoms?
- Changes to medications and dosages, such as hyperkalemia within the context of longstanding ACEi use
- ACEi causes the retention of potassium due to increasing aldosterone
- The longer they have been on the medications and showing tolerance, less likely the med is the cause of the new symptom
What is a goal of medication?
To correct electrolyte imbalance
K supplements?
- Indicated in peritoneal dialysis
- Poor intake, meds, vomiting, diarrhea can cause depletion
PO4 binders?
- may used adjunct to dietary restriction
- Examples are Sevelamer, Lanthanum, Calcium carbonate or citrate
Ca supplements?
- Typically more used as a binder to phosphate than to supplement calcium
- Due to altered Vitamin D metabolism, decreased Ca absorption, high P04
- Monitor for hypercalcemia
Antihypertensives?
- ACE inhibitors
- Diuretics
- Ca Channel blockers
- B-blockers
K Depleting meds?
- Thiazides and Loop (Will deplete Na and K+, but retain H20)
- Excessive fluid can develop, and caution with hyponatremia and edema
Erythropoietin?
- Given often in late stage or on dialysis
- Decreased kidney function means the hormone cannot signal to the bone marrow to make RBCs, may lead to anemia
Iron supplementation?
- At risk of anema
- Start with oral, and progress to IV
- Most patients on dialysis are on EPO and Iron supplementation
Discuss dysregulation of Vitamin D and calcium
- Decreased kidney function means decreased calcitriol, and will fail to increase absorption of calcium from GI , and retain calcium from kidneys.
- Blood calcium will be low, stimulating PTH to demineralize bone –> leading to potential osteodystrophy
- Recall that vitamin D is activated in the liver, then in the kidneys
Should we supplement with inactive vitamin D?
No, as the kidney already has reduced function, less likely to activate as calcitriol
Active vitamin D supplements?
- Calcitriol
- Alfacalcidiol
Primary indications of active vitamin D deficiency?
-Secondary hyperparathyroidism (stimulation of PTH to promote bone breakdown and osteoblasts)
Which electrolytes may be altered after we supplement with active vitamin D?
-Can increase the absorption of phosphate alongside calcium, caution with hyperphosphatemia
How are antihyperglycemic agents indicated to be administered?
Varies, but based on when GFR reached a certain lower threshold, usually <30
Which meds are contraindicated when GFR is less than 30?
- Alpha-glucosidase inhibitors
- GLP-1 receptor agonists
- Insulin secretagogues
- SGLT-2 inhibitors
Which meds can be used at a lower kidney function, <15?
- DPP-4 inhibitors, as long as there is less urine output
- If they are diabetic, there will be a high urine output and the meds will be less effective
What is the mechanism of DPP-4 inhibitors?
-Increase incretin levels: GLP-1 and GIP which will inhibit glucagon release, increase insulin secretion, decrease gastric emptying and decrease blood glucose levels
What happens in late stage CKD?
- There is alterations in insulin resistance and retention
- Blood sugars are hard to control
- Caution with insulin meds
When is CKD indicated?
When there is kidney damage OR GFR <60 ml/min per 1/73m^2 for 3 or more months
What is key when interpreting changes in GFR and lab values?
- Their change over time
- Cannot look at a singular number
Normal?
GFR >/= 60 with not kidney damage
Stage 1?
-Normal or increased GFR (>/= 90 with kidney damage
Stage 2?
-Mildly decreased GFR (60-89) with kidney damage
Stage 3a?
-Mild to moderately decreased GFR (45-59)
Stage 3b?
-Moderately to severely decreased GFR (30-44 )
Stage 4?
Severely decreased GFR (15-29)
Stage 5?
Kidney failure, GFR <15
How is kidney damage assessed?
-Albuminuria or proteinuria
Normal to mildly increased albuminuria? (A1)
<30 mg/g
<3 mg/mmol
Moderately incresed albuminuria ? (A2)
30-300 mg/g
3-30 mg/mmol
Severely increased albuminuria? (A3)
> 300 mg/g
>30 mg/mmol
Very high risk for progression?
- All G4 and G5
- G3b with A2 and A3
- G3a with A3
No CKD?
- G1 and A1
- G2 and A1
When may we have normal GFR but high proteinuria?
Sometimes observed in severe diabetic nephropathy
If the _____ is not corrected, then the patient is much more likely to progress to later stage CKD
proteinuria
Why is creatine indicative of kidney function?
-Creatinine is produced from the muscles, where our ability to excrete it will be an indication of kidney function
When is pre-dialysis indicated?
- eGFR between 13-50 ml/min/1.73m2
- Depends on the individual patient
Why may dialysis not be started despite GFR being in range?
- Acceptable laboratory values
- Lack of physical symptoms
- Conservative care
How can we provide dietary intervention in conservative care?
- Help prevent malnutrition, maintain quality of life, and avoid hypophosphatemia (causes chronic itching), manage potassium to prevent cardiac issues
- Conservative care is not palliative care
What are the 3 key nutritional goals of CKD?
1) Delay the progression of CRF
2) Preventing or alleviating the symptoms of uremia and restoring biochemical balance
3) Maintaining/improving QOL and Health where possible
How can we delay the progression of CRF?
-Provide adequate calories to maintain or achieve ideal body weight
What is the paradox with the renal and diabetic diets?
- They contradict each other
- Low potassium in renal, whereas important sources of fibres for diabetics will contain the potassium
What are the nutrition goals for pre-dialysis?
- Low or normal protein
- Restricted phosphorus diet
- Restricted potassium
- Restricted sodium
- Adequate kcals
- Healthy foods and eating habits
What is the overarching theme of nutritional intervention in renal disease?
Minimizing renal impairment while preventing malnutrition
Protein CKD stages 1-2?
0.8-1.4
Protein CKD stages 3-4?
0.6-0.6
Energy CKD?
25-35 kcal/kg and adjust for weight loss and weight gain
Na CKD?
<2400 mg
K+ CKD?
Usually unrestricted unless serum level is high
Phosphorus CKD stages 1-2?
-Maintain serum P and PTH WNL
Phosphorus CKD stages 3-4?
-800-100 mg/day
-
Calcium CKD?
- DRI
- Maintain serum levels WNL
Fluid in CKD?
Usually unrestricted
What is the #1 cause of new cases of ESRD
- Diabetes
- Diabetics are most common on dialysis
When is CKD indicated in diabetes?
-When ACR >/= 2 mg/mmol
AND/OR
-eGFR <60
What is ACR?
Albuminuria:Creatinine ratio, which is more accurate is assessing kidney damage and proteinuria than the individual values
What does a progressive increase in proteinurea cause in diabetes?
-Will cause declining renal function, and then followed by ESRD
When should we continue to screen annually?
- No transient increase in albuminuria
- no low GFR
- No acute injury or non-diabetic kidney disease is suspected
When should we screen for CKD in type I diabetics?
-Screen annually in post-pubertal individuals with duration of diabetes >/= 5 years
When should we screen for CKD in Type 2 diabetes?
-At diagnosis and annually after
If CKD is suspected, which lab values should be ordered?
- Random urine ACR
- Serum creatinine for eGFR
What are potential causes for transient albuminuria?
- Recent major exercise
- Urinary tract infection
- Febrile illness
- Decompensated congestive heart failure
- Menstruation
- Acute severe elevation in blood glucose or blood pressure
What are the common causes of Diabetic nephropathy, which leads to CKD?
- Hypertension
- Renovascular complications
What is one of the hallmark signs of CKD and diabetes?
The slow progression and loss of kidney function, those with other renal diagnoses will often have rapid changes, extreme proteinuria and rapidly falling GFR
Discuss factors which favour a diagnosis of diabetic nephropathy
- Persistant albuminuria
- Bland urine sediment
- Slow progression of disease
- Reduced eGFR associated with overt proteinuria
- Known diabetes >5 years, with complication**
Discuss factors which favour an alternate renal diagnosis
- Extreme proteinuria (>6 g/day)
- Persistent hematuria or active urinary sediment
- Rapidly falling GFR
- Reduced eGFR with little or no proteinuria
- Known duration of diabetes <5 years, with no complications
- family history of non-diabetic kidney disease
What has been shown to reduce the development and progression of nephropathy?
- Optimal glycemic control in type I and type II diabetes (Up to 50% risk reduction with intensive therapy)
- Reduction in proteinuria through ARB/ACEi
- Optimal BP control
How is albuminuria often controlled?
- With ACE or ARB
- These favour the retention of potassium, which is contraindicated in renal disease
- However, we know that decreased proteinuria may improve outcomes in the CKD progression of diabetics
Why are diabetics with CKD prone to hyperkalemia?
- Likely due to ACE and ARB medications
- We need to closely monitor potassium and intervene with a low-potassium diet
- This is especially indicated when creatinine is >30%
When should serum K+ and Creatinine need to be checked?
- At baseline
- Within 1-2 week of initiation or titration
- During acute illness
What should we do when K+ becomes elevated or CR>30% increase?
- Review therapy, especially ACE/ARB
- Then, re-check serum K+ and Cr
Intervention in mild to moderate stable hyperkalemia?
- Counsel on low potassium diet
- Consider adding non-potassium paring diuretics and/or sodium bicarb (if acidosis is indicated)
- Consider temporarily holding or discontinuing ACEi, ARB, or Direct Renal Inhibitor (DRI)
Intervention in severe hyperkalemia?
- Hold or discontinue ACEi, ARB or DRI
- Emergency management strategies
Hyperkalemia is often ___
factorial
What may be sources of potassium which should be assessed during hyperkalemia?
- Medication
- Diet
- Medical conditions: decr. renal function, metabolic acidosis, hyperglycemia
- Fever, trauma, infection and stress
- Hemolysis
When is hyperkalemia more common in diabetic patients?
Those with renal tubular acidosis type 4
-Require ACEi or ARB
What is the main source of dietary potassium?
- Preservatives in processed foods
- Potassium lactate, chloride and potassium bitartrate
How can we manage processed foods with the patient?
- Find “better” processed foods with less additives
- Consider organic processed foods
- Cut out cold-cuts, processed meats and teach label reading
Other sources of dietary potassium?
- Fruits and vegetables
- Milk products
- Nuts, seeds, legumes and lentils
- Whole grain and high fibre grains
- Meat and alternatives
Which foods are likely already restricted in renal?
- Milk and meats
- Do NOT further restrict to meet potassium requirement, as the protein requirement is more important
Bioavailability of phosphorus in food additives?
-90-100%
Bioavailability for phosphorous in animal protein sources?
-40-70%
Bioavailability for phosphorus in vegetable protein sources?
-40-50%
What else impacts the bioavailability of phosphorus?
- Many factors, and a complex process
- The less P you eat, often the more you absorb
How should phosphate binders be taken?
WITH food, think of as the “salad dressing”
-Will not function once the nutrients are absorbed into the bloodstream, must act in the GI tract
What should be verified in milk alterntives?
- That the fortified source of calcium is not bound to phosphate
- Calcium carbonate vs. calcium phosphate
Phosphorous recommendation?
800-1200 mg/day, however is quite unrealistic
____ is not as dangerous as high potassium
Phosphorous
There are usually two ____ additives per ______
- Phosphate
- Potassium additive
KDIGO recommendations concerning protein?
0.8 g/kg of IBW when GFR <30 and no more than 1.3 g/kg for individuals at risk for progression
What is the usual range for the relatively “healthy” CKD patient?
1.1-1.2 g/kg/day
Protein requirement for dialysis patients?
- 2 g/kg/day
- Someone not on dialysis should probably be below this 1.2 recommendation
HBA1C target?
7.0%
When should treating to an HBA1C target of 7% be contraindicate?
- Patient at risk of hypoglycemia
- Co-morbidities, reduced life expectancy
How to we teach protein restriction?
- Through renal exchanges
- 1 renal exchange = 6-8 g of -protein
- We consider 50% of protein from HBV sources
KDIGO guidelines concerning sodium?
- 1500-2300 mg/day usually more realistic
- KDIGO specifics <2000 mg/day
- -> Goals need to be individualized and realistic
What may a too-restricted diet cause in renal patients?
Malnutrition
What factors will complicate the treatment of malnutrition?
- Hyperkalemia
- Fluid overload
- HyperP
- HyperG
- Dyslipidemia
- Pat dietary retriction
What is novel approach in nephrology?
Gluten restriction in IgA nephropathy, where we lose protein from the kidney
Discuss tolvapten for polycystic kidney disease -
- PKD patients hava a urine-concentrating defect, and high levels of AVP which play a key role in developing the cysts
- Tolvapten is an AVP-receptor blocker, where if a diet high in solutes and sodium will result in extreme thirst, and copious amount of urine production
- It will dilute the urine no matter what
How can we intervent nutritionally for those on tolvapten?
- Low sodium and protein diet to alleviate extreme thirst and frequent urination
- Reduce Na to <2300 mg and protein to 0.8 g/kg, and fluid according to thirst
How may we achieve the urine dilution effects of tolvapten through solely dietary intervention?
- By prescribing a low osmolar diet and adjusted water intake
- Will result in vasopressin reduction
- The less protein and sodium, the less water needed to achieve the reduced urine osmolality
What is the goal urine osmolality for those with PCKD? Why?
- <280 mOsm/kg
- To suppress vasopressin
Fluid, sodium and protein intake in PCKD?
- High fluid of 2.6-4.8 L per day
- Low sodium of 1500-2300 mg
- Low protein of 0.8 g/kg
