CKD Staging
Stage |
GFR (mL/min/1.73m^2) |
1 |
> 90 |
2 |
60-89 |
3a |
45-59 |
3b |
30-44 |
4 |
15-29 |
5 |
< 15 |
Stage |
AER (mg/24h) |
ACR (mg/mmol, approx) |
ACR (mg/g, approx) |
1 |
< 30 |
< 3 |
< 30 |
2 |
30-300 |
3-30 |
30-300 |
3 |
> 300 |
> 30 |
> 300 |
Diuretic Infusions
Diuretic |
Load (mg) |
Rate (CrCl < 25) |
Rate (CrCl 25-75) |
Rate (CrCl > 75) |
Furosemide |
40 |
20-40 mg/hr |
10-20 mg/hr |
10 mg/hr |
Bumetanide |
1 |
1-2 mg/hr |
0.5-1 mg/hr |
0.5 mg/hr |
Torsemide |
20 |
10-20 mg/hr |
5-10 mg/hr |
5 mg/hr |
Chlorthalidone |
100-500 QD |
|
|
|
Complications of Untreated ESRD
- Uremia
- SSx: Encephalopathy, edema, LVH, anorexia, N/V/C, anemia, uremic pruritis
- Treat w/ dialysis
- Hyperkalemia and other electrolyte abnormalities
- Hypernatremia: No need to routinely fluid restrict pts beyong 2g Na or 5g NaCl QD
- Add diuretics if necessary
- Hyperkalemia: NTE 3g QD in ESRD
Mineral and Bone Disorder
High Phos is the cause of all problems. High phos leads to hypocalcemia both directly and indirectly. Indirectly, Phos leads to a decrease in calcitriol in an effort to decrease Phos absorption from the gut, which also decrease Ca absorption and impairs Ca deposition in bone. This hypocalcemia increases the levels of PTH (in combination with the activity of the Phos directly on the PT gland), leading to secondary hyperparathyroidism. PTH leads to increased bone demineralization. The metabolic acidosis and Al overload also commonly seen in these pts contributes to bone demineralization and osteoporosis.
Treatment
- Phosphate Binders (All are given w/ meals and are skipped if not eating)
- CaCO3 (Tums): 500mg (40% elem Ca) PO TID w/ meals (NTE 1500mg elem Ca QD)
- Ca Acetate (PhosLo): 2-3 tab (25% elem Ca) TID w/ meals (NTE 1500mg elem Ca QD)
- SEs: Constipation
- Same elemental dose of Ca Acetate gives 2x Phos reduction compared to Tums and may produce fewer hypercalcemic events
- Sevelamer Carbonate (Renvela): Phos 5.5-7.5 800mg PO TID, ≥ 7.5 1600mg PO TID
- SEs: Mild N/V/D
- Decreases serum uric acid
- Lowers LDL 15-30%
- Lanthanum Carbonate (Fosrenol): 250-750mg TID
- Max Dose: 1500-3000mg QD
- SEs: N/V/D
- Sucroferric Oxyhydroxide (Velphoro): 500mg chewable TID
- Titrate by 1 tab weekly
- Iron may lead to dark stool
- Does not impact TSAT or Ferritin
- Ferric Citrate (Auryxia): 1g tab x2 TID
- May cause dark stool
- Increases TSAT and Ferritin
- Al(OH)3 (Amphojel): 300-600mg PO TID
- AVOID: Aluminum toxicity is common in CKD pts and other agents are available
- Dietary Phos Restriction of 800-1000 mg QD
- Phos > 4.6 in CKD 3-4 or > 5.5 in ESRD or PTH > target range for CKD3-5
- Vit D Repletion
- Vit D2/3 (Ergocalciferol/Cholecalciferol)
- Must be activated by the liver and kidney (therefore not usable in CKD5)
- 50000 IU D2 montly or 1000 IU D3 QD
- Calcitriol (Rocaltrol / Calcijex)
- Rocaltrol: 0.25 mcg PO QD or QOD (increase Q4-8wks up to 0.5-1 mcg QD)
- Calcijex: 0.5 mcg IV three times weekly
- Cheapest, approved for peds, but high risk of hypercalcemia
- SEs: Hypercalcemia
- Paricalcitol (Zemplar)
- 0.04-0.1 mcg/kg IV 2-3 times weekly
- PTH < 500 pg/mL: 1 mcg PO QD or 2mcg PO QOD
- PTH ≥ 500 pg/mL: 2 mcg PO QD or 4 mcg PO QOD
- Approved for peds, less risk of hypercalcemia than calcitriol
- SEs: Hypercalcemia
- Doxercalciferol (Hectorol)
- 2.5-10 mcg PO or IV 2-3x weekly
- Prohormone activated by the liver
- Higher risk of hyperphosphatemia compared to paricalcitol, but lower hypercalcemia risk than calcitriol
- SEs: Hypercalcemia
- Cinacalcet (Sensipar): 30 mg PO QD (Max 180 mg QD)
- Binds Ca receptor on PT gland and decreases PTH secretion directly
- CI: Hypocalcemia (< 7.5 mg/dL) hold until Ca > 8 mg/dL
Monitoring
Parameter |
CKD3 |
CKD4 |
CKD5 |
Goal |
Ca |
Q6-12mo |
Q3-6mo |
Q1-3mo |
8.5-105 mg/dL |
Phos |
Q6-12mo |
Q3-6mo |
Q1-3mo |
2.5-4.5 mg/dL |
Calcitriol |
Baseline |
Individualized |
Individualized |
30 ng/mL |
iPTH |
Baseline |
Q6-12mo |
Q3-6mo |
11-54 pg/mL HD: 100-500 pg/mL |
Anemia in CKD
See the Anemia for DDx of anemia. Common causes of anemia in CKD patients are iron deficiency and EPO deficiency.
Monitoring
- Hgb annualy in CKD3, twice yearly in CKD4, and Q3mo in ESRD
- TSAT and Ferritin Q3mo
- Iron repletion indicated if TSAT < 30% and Ferritin < 500 ng/mL
Treatment
- PO Iron: 200mg elemental iron QD
- Not commonly enough to manage ESRD pts
- Heme Iron (Proferrin ES): 2-3 tba (1mg elem Fe / tab) QD
- Better absorbed, does not follow the 200mg rule and is less irritating
- SEs: Nausea
- Separate from Ca and drugs raising gastric pH by 2hr
|Agent|Load|Maintenance|Monitoring|Notes|
|Iron Dextran (InFed, Dexferrum)|25mg Test
100mg q HD session x10 doses|25-100mg weekly|HR, BP, RR q15min|Can cause anaphylaxis, especially dexferrum (high mol. wt)|
|Na Ferric Gluconate (Ferrlicit)|125mg q HD session x8-10 doses|31.25-125 mg weekly|HR, BP, RR q15min||
|Iron Sucrose (Venofer)|100mg q HD session x10 doses
OR
200mg IVPB x5d (ND-CKD)|25-100 mg weekly|HR, BP, RR q15min||
|Ferric Carboxymaltose (Injectafer)|750mg q7d x2||Hr, BP, RR q15min||
|Ferumoytol (Feraheme)|510mg q3-8d x2||HR, BP, RR q15min|Interferes w/ MRI up to 3mo after last infusion|
*Monitor Ferritin and TSAT q3mo w/ all IV iron
- EPO Agents
- Initiate if Hgb < 10 and falling fast, OR if ESRD and Hgb 9-10
- Hgb NTE 11.5 via EPO agents
- rErythropoetin (rHuEPO, Epoetin, Epogen, Procrit, EPO)
- 120-180 U/kg/wk IV in 3 divided doses
- 80-120 U/kg/wk SubQ in 2-3 divided doses
- Darbepoetin alfa (Aranesp)
- 0.45 mcg/kg IV or SubQ weekly titrated to Hgb 12
- SEs: Pure red Cell Aplasia (Igs develop to EPO; D/C drug permenantely), High Hgb => HF, stroke, Sz, MI, HTN, or cardiac arrest
Weekly EPO Dose (units) |
Weekly Darbepoetin Dose (mcg) |
< 1500 |
6.25 |
1500-2499 |
6.25 |
2500-4999 |
12.5 |
5000-10999 |
25 |
11000-17999 |
40 |
18000-33999 |
60 |
34000-89999 |
100 |
> 90000 |
200 |
Monitor Hgb weekly, adjust q4wks or longer, goal Hgb rise of 1-2 g/dL monthly, decrease by 25% when approaching 11-11.5 g/dL OR w/ increase ≥ 2 g/dL in 4 wks.
Dialysis Efficiency
- Kt/V
- K: Urea Clearance
- t: Time on Dialysis
- V: Urea Volume of Distribution
- Goal ≥ 1.4
- Urea Reduction Ratio (URR): ≥ 70%
AKI
- FENa ≤ 1% => Intrinsic Renal Failure
- FENa > 1% => Prerenal or Functional Renal Failure
Common Nephrotoxic Agents
- NSAIDs: Inhibition of vasodilatory prostaglandins in afferent arteriol leading to constriction and decreased filtration pressure
- APAP: Acute Tubular Necrosis
- Aminoglycosides: Proximal Tubular Injury, usually 5-10d after initiation
- ACEIs / ARBs: Vasodilation of efferent arteriols leading to drop in filtration pressure
- Amphotericin B: Direct Tubular Damage via pore creation along with afferent arteriol vasoconstriction
- Contrast: Direct tubular toxicity
- Cisplatin / Caroplatin: PCT Damage
- Cyclosporine / Tacrolimus: Interstitial fibrosis and vasoconstriction of afferent and efferent arteriols
- Li: Acute tubular necrosis and nephrogenic diabetes insipidus
- PPIs: Acute intersitial nephritis
References
- KDOQI
- KDIGO