CKD Flashcards
Patients at risk for CKD
> 60yo (likely in stage 2 from 1ml/year decrease)
HTN or diabetes
family history
nephrotoxic drugs
AKI history
Lupus
GFR >90
stage 1
GFR 60-89
Stage 2
GFR 45-59
Stage 3a
GFR 30-44
Stage 3b
GFR 15-29
Stage 4
GFR <15 or dialysis
stage 5
ACR <3 mg/mmol
A1 Normal ACR levels
ACR 3.0-30 mg/mmol
A2 moderate increase
ACR >30 mg/mmol
A3 severely increased
Diabetes mellitus pathology
Na hyperfiltration from glucose load and increased glycosylation of mesangial cells causes causing hypertrophy of mesangial cells and then filtering basement membrane causing glomerular scarring and death. Loss of albumin then leads to edema.
HTN pathology
RAAS system activation causes AG2 secretion which constricts efferent arteriole increasing BP, this increases permeability and albuminuria. Aldosterone also causes constriction and causes retention of H2O and Na+. Maladaptive hypertrophy and tubular damage/oxidative stress causes renal failure
CKD progression factors
Hyperglycemia
HTN
smoking
obesity
proteinuria (causes inflamm and fibrogenic pathways leading to damage)
CKD symtoms
Pericarditis, edema (Aldosterone H2O retention and albumin loss), pruritus from waste, restless leg syndrome from increased electrolytes, cramps, anemia
Diagnosis
eGFR <60 and ACR>3 (retest both and order urinalysis)
If GFR is 30-60 and/or ACR 3-60 then no referral
but if GFR <30 ACR >60 or any hematuria then refer
Lifestyle changes
Low phosphate and sodium diet
Limit protein to 0.8g/kg G3-G5
limit alcohol to <2 drinks/day
physical activity
smoking cessation
weight management when required
ACE renoprotective
Shown to reduce progression of albuminuria in normotensive patients with type 1 and 2 diabetes
ARB renoprotective
Shown to prevent decline in renal function
ACEi and ARB monitoring
-Titrate dose every 3-4 days, watching for BP and proteinuria target.
-A/E, dry cough (ACE), angioedema, hyperkalemia (aldosterone block)
-Hold during sick days
-Expect 25-30% increase of SrCr and GFR decrease in first 1-2 weeks
-Get baseline SrCr and K+ and test Q1-2W for titration then Q3-6M
Proteinuria
ACE and ARBs are first line as they reduce hyper filtration
-non-dihydropyridine Ca+ channel blockers are second line
-Spironolactone may be of help in patinents already on ACE/ARB and SGLT2i with normal K+ and GFR >25
-Finerenone, has some efficacy in diabetic CKD and GFR>25
Non-dihydropyridine Ca+ channel blockers CKD
Used as second line treatment of proteinuria (diltiazem, verapamil)
spironolactone CKD considerations
Can be used for persistent proteinuria in patients on ACE/ARB and SGLT2i with normal K+ and GFR >25
- Monitor for hyperkalemia
Finerenone
has some effect on proteinuria in diabetic CKD with GFR >25
SGLT2i
First line for glycemic control, Works to slow progression of DM and non DM patients (dapagliflozin)
SGLT2i mechanism
prevents SGLT2 from glucose and Na up take, this lowers BP and sympathetic activity. Na+ retention causes macua dense to decrease blood flow and slow hypertrophy
SGLT2 initiation
Do not start if GFR <30, unless DM on ACE/ARB then >20 is ok
-Once on therapy continuation below 20 is fine
-Do not initiate if starting dialysis
SGLT2 monitoring
-Monitor for GFR decrease which should stabilize after 4weeks, if >20-25% decline F/U and if >30% D/C
-A/E UTIs, increased urination, diabetic ketoacidosis
Check A1c Q6M, want <6.5 or <8 for DM, Anemia can artificially lower A1C
Diabetic ketoacidosis Sx
difficulty breathing, thirst, confusion, abdominal pain, nausea/vomiting
GLP-1
second line for glycemic control, can reduce CV outcomes. For use in DM when SGLT and metformin don’t control A1c
Statin medications
Given to all patients >50yo or 18-49yo with moderate to high risk of CV
SADMANS
Sick day protection of kidneys
-Sulfonylureas
-ACEi
-Diuretics
-Metformin
-ARBs
-NSAIDs
-SGLT2i
Urgent dialysis signs
Acidosis
electrolyte imbalance (K+ especially)
Fluid overload causing pulmonary edema
Uremia, causes itch over body from waste
CKD anemia
Kidneys not longer produce EPO leading to hypo proliferative normocytic and normochromic anemia. Can also be due to lack of iron from inflammatory conditions
- Stage 4 >50% of people have it
Anemia testing intervals
Stage 3 - Hgb annually
Stage 4-5 every 6 months
Stage 5 on dialysis every 3 months
Increasing frequency when under therapy
anemia symptoms
fatigue, lethargy, cold intolerance, angina, dizziness, pallor
Anemia cardiac impact
ventricular volume overload can lead to dilation and hypertrophy increasing mortality of floppy heart.
Types of iron
Serum iron (bound to transferrin)
Transferrin (iron transport)
Ferritin (main storage in GI)
Iron labs
Total iron binding capacity (TIBC)
Transferrin saturation (TSAT)
Hgb
Ferritin
TIBC
total iron binding capacity, indirect measure of transferrin capacity
TSAT
transferrin saturation, Serum iron/TIBC*100, lets us know how much iron is ready for use by bone marrow
Hepcidin
Liver produce hormone, degraded and excreted by kidneys. Stimulated by iron uptake, inflammation or infection. Causes reduced absorption and prevents iron release from macrophages, duodenum and hepatocytes
Functional anemia
You have adequate stores but low mobilization from increased hepcidin or ESA treatment
Normal or elevated Ferritin with TSAT <20%
Absolute anemia
You have low iron stores and little delivery to bone marrow, low ferritin with TSAT <20%
When to start iron therapy
When Hgb is low (<120) females (<130) males and TSAT <30% and ferritin <500 ug/LI
Iron therapy goals
TSAT 20-40% no more than 40%
Ferritin, >100ug/L or >200 for dialysis, and <500
Oral iron
150-300 elemental iron in divided doses titrated up
Take with food and Vit C
——–
-nausea and vomiting
-Dyspepsia
-constipation
-Can go away with continued therapy
————-
Monitor ferritin, TSAT, Hgb every 3 months Stage 3-5
Or every month for dialysis
Fumarate, sulfate and gluconate iron
Cheap but need stomach acid for absorption and therefore prefer empty stomach which increases side effects
Polysaccaride iron
no stomach acid needed so can be taken with or without food (most preferred form)
Heme iron
More bioavailable and does not need to be taken with or without food
Separate iron dose from
-Antacids
-Synthroid
-Bidphosphonates
-levodopa/methyldopa
-quinolone or tetracycline antibiotics
ESA treatment initiation
For dialysis patients with Hgb 90-100, for non-dialysis patients it is individualized choice
-Target is 100-110 and not to be used past 115
-Iron supplementation is required during use
-Epoetin alfa or darbepoetin
-A/E HTN, clotting (stroke), pure red cell aplasia, ESA resistance
ESA monitoring
Inadequate dose indicated by <10g/L increase in 4 weeks (increase dose by 25%
Overdose is >10 in 2 weeks or >20 in 4 weeks. Decrease dose by 25 or 50%
can also change frequency instead of dose
