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Renal failure/Oliguria (General guidelines)
(1) Avoid magnesium containing products (Maalox etc), NSAID’s, and nephrotoxins.

(2) Consider fluid challenge to rule out pre-renal azotemia if not fluid overloaded.

(3) Lasix: IV bolus 10-200 mg (usually every 2 hours). Doses > 200mg should be infused at 4 to 10 mg/min (usually 4 mg/min) to minimize ototoxicity. IV infusion of 0.25 to 0.4 mg/kg/hour titrated to urine output.

(4) Metolazone (Zaroxylyn ® ) 5-10 mg po qd (max 20 mg/day)

(5) Bumetanide (Bumex ®): IV bolus 0.5 to 4mg over 1-2min prn (usually q2-3 hr). IV infusion: usually 0.5 to 1 mg/hr. T1/2= 1 to 1.5hr Duration of action: 2-4hrs.

(6) Torsemide (Demadex ®): IV bolus: 5 to 100 mg over 1-2 minutes. IV infusion: 5 to 20 mg/hr. [1 mg Bumex] = [10-20 mg Demadex] = [40 mg Lasix]

(7) Mannitol: When instituting treatment with mannitol in patients with marked oliguria, a test dose should be used. Infusion of 0.2 grams/kg over 3 to 5 min should produce a diuresis of at least 30 to 50 ml/hr. A second test dose may be given if no response is seen—if no response with second dose—do not use. To treat oliguria: 12.5 to 25 grams IV every 2 to 4 hours. A 15 to 20% solution may be used. Rate should be adjusted to maintain urinary output at 30-50 ml/hr. (Usual test dose= 12.5 grams over 3 to 5 minutes. )

When the Ca x PO4 product exceeds 70, there is a possibility of dangerous precipitation of Ca in non-osseous tissues. Use of Ca based PO4 binders may transiently exacerbate the problem. Use of aluminum hydroxide (300 to 600 mg p.o. tid with meals) for periods not to exceed 7-10 days (to avoid Al3+ toxicity) may be necessary. When the Ca x PO4 product falls below this dangerous level, calcium-carbonate or calcium-acetate may be started. RenaGel®, a new polymeric resin that does not contain Ca++ may be used.

Aluminum hydroxide  -  alternagel ®,  alu-cap ®

 Hyperphosphatemia: Oral: Initial: 300-600 mg 3 times/day with meals. (Not to exceed 7-10 days (to avoid Al3+ toxicity).

Hyperacidity: Oral: 600-1200 mg between meals and at bedtime.

Aluminum antacids may cause constipation, phosphate depletion, and bezoar or fecalith formation. In patients with renal failure, aluminum may accumulate to toxic levels.

Supplied: Suspension, oral: 320 mg/5 mL (473 mL)
AlternaGel®: 600 mg/5 mL (360 mL)

Calcium acetate  -  phoslo ®

Hyperphosphatemia: Start 2 tablets (1334 mg) with each meal. Range: 2 to 4 tablets with each meal. Can be increased gradually to bring the serum phosphate value <6 mg/dl as long as hypercalcemia does not develop.

Usual dose: (3 to 4 tablets) 2001-2868 mg with each meal.

[Supplied: 667mg tablet, Gelcap]

Calcitriol   - calcijex ®; rocaltrol ®

Man's natural supply of vitamin D depends mainly on exposure to the ultraviolet rays of the sun for conversion of 7-dehydrocholesterol in the skin to vitamin D3 (cholecalciferol). Vitamin D3 must be metabolically activated in the liver and the kidney before it is fully active as a regulator of calcium and phosphorus metabolism at target tissues. The initial transformation of vitamin D3 is catalyzed by a vitamin D3-25-hydroxylase enzyme (25-OHase) present in the liver, and the product of this reaction is 25-hydroxyvitamin D3 [25-(OH)D3]. Hydroxylation of 25-(OH)D3 occurs in the mitochondria of kidney tissue, activated by the renal 25-hydroxyvitamin D3-1 alpha-hydroxylase (alpha-OHase), to produce 1,25-(OH)2D3 (calcitriol), the active form of vitamin D3. Endogenous synthesis and catabolism of calcitriol, as well as physiological control mechanisms affecting these processes, play a critical role regulating the serum level of calcitriol. Physiological daily production is normally 0.5 to 1 mcg and is somewhat higher during periods of increased bone synthesis (eg, growth or pregnancy).

Predialysis Patients
Calcitriol Capsules are indicated in the management of secondary hyperparathyroidism and resultant metabolic bone disease in patients with moderate to severe chronic renal failure (Ccr 15 to 55 mL/min) not yet on dialysis. In children, the creatinine clearance value must be corrected for a surface area of 1.73 square meters. A serum iPTH level of ≥100 pg/mL is strongly suggestive of secondary hyperparathyroidism.

Dialysis Patients
Calcitriol Capsules are indicated in the management of hypocalcemia and the resultant metabolic bone disease in patients undergoing chronic renal dialysis. In these patients, calcitriol administration enhances calcium absorption, reduces serum alkaline phosphatase levels, and may reduce elevated parathyroid hormone levels and the histological manifestations of osteitis fibrosa cystica and defective mineralization.

Hypoparathyroidism Patients
Calcitriol Capsules are also indicated in the management of hypocalcemia and its clinical manifestations in patients with postsurgical hypoparathyroidism, idiopathic hypoparathyroidism, and pseudohypoparathyroidism.

Calcitriol Capsules should not be given to patients with hypercalcemia or evidence of vitamin D toxicity. Use of Calcitriol Capsules in patients with known hypersensitivity to Calcitriol Capsules (or drugs of the same class) or any of the inactive ingredients is contraindicated.

Dosing (Adults):
Renal failure:
Oral: 0.25 mcg/day or every other day (may require 0.5-1 mcg/day).
IV: 0.5 mcg (0.01 mcg/kg) 3 times/week; most doses in the range of 0.5-3 mcg (0.01-0.05 mcg/kg) 3 times/week.

Hypoparathyroidism/pseudohypoparathyroidism: Oral: 0.5-2 mcg/day.
Vitamin D-dependent rickets: Oral: 1 mcg qd.

Kidney failure disrupts systemic calcium and phosphate homeostasis and affects the bone, gut, and parathyroid glands via limited exretion of phosphate, diminished hydroxylation of 25-hydroxyvitamin D to calcitriol (1,25-dihydroxyvitamin D) and resulting hypocalcemia. Circulating calcitriol levels begin to fall when the glomerular filtration rate is less than 40 mL/min and are typically markedly reduced in subjects with end-stage renal failure. Both the loss of functioning renal tissue and, in early renal failure, physiologic suppression by hyperphosphatemia participate in the decline in calcitriol synthesis.

Supplied: Capsule (Rocaltrol®): 0.25 mcg, 0.5 mcg.
Injection, solution: 1 mcg/mL (1 mL); 2 mcg/mL (2 mL). Calcijex®: 1 mcg/mL (1 mL). Oral soln: (Rocaltrol®): 1 mcg/mL (15 mL).

Doxercalciferol  -  hectorol ® 

Vitamin D levels in humans depend on two sources: (1) exposure to the ultraviolet rays of the sun for conversion of 7-dehydrocholesterol in the skin to vitamin D3 (cholecalciferol) and (2) dietary intake of either vitamin D2 (ergocalciferol) or vitamin D3. Vitamin D2 and vitamin D3 must be metabolically activated in the liver and the kidney before becoming fully active on target tissues. The initial step in the activation process is the introduction of a hydroxyl group in the side chain at C-25 by the hepatic enzyme, CYP 27 (a vitamin D-25-hydroxylase). The products of this reaction are 25-(OH)D2 and 25-(OH)D3, respectively. Further hydroxylation of these metabolites occurs in the mitochondria of kidney tissue, catalyzed by renal 25-hydroxyvitamin D-1-α-hydroxylase to produce 1α,25-(OH)2D2, the primary biologically active form of vitamin D2, and 1α,25-(OH)2D3 (calcitriol), the biologically active form of vitamin D3.

Mechanism of Action
Calcitriol (1α,25-(OH)2D3) and 1α,25-(OH)2D2 regulate blood calcium at levels required for essential body functions. Specifically, the biologically active vitamin D metabolites control the intestinal absorption of dietary calcium, the tubular reabsorption of calcium by the kidney and, in conjunction with parathyroid hormone (PTH), the mobilization of calcium from the skeleton. They act directly on bone cells (osteoblasts) to stimulate skeletal growth, and on the parathyroid glands to suppress PTH synthesis and secretion. These functions are mediated by the interaction of these biologically active metabolites with specific receptor proteins in the various target tissues. In patients with chronic kidney disease (CKD), deficient production of biologically active vitamin D metabolites (due to lack of or insufficient 25-hydroxyvitamin D-1-alpha-hydroxylase activity) leads to secondary hyperparathyroidism, which contributes to the development of metabolic bone disease


Dialysis Patients:
Hectorol is indicated for the treatment of secondary hyperparathyroidism in patients with chronic kidney disease on dialysis.

Pre-Dialysis Patients:
Hectorol is indicated for the treatment of secondary hyperparathyroidism in patients with Stage 3 or Stage 4 chronic kidney disease.

Hectorol should not be given to patients with a tendency towards hypercalcemia or current evidence of vitamin D toxicity.

Dosing (Adults):
Initial dose of doxercalciferol is 10 mcg administered three times weekly at dialysis. The maximum recommended dose of doxercalciferol is 20 mcg administered three times a week at dialysis for a total of 60 mcg/week

Etelcalcetide - parsabiv ™ injection 

Drug UPDATES:  PARSABIV ™ (etelcalcetide) injection, for intravenous use
PACKAGE INSERT -Dosing:  Click (+) next to Dosage and Administration section (drug info link)

Initial U.S. Approval:  2017

Mechanism of Action:
Etelcalcetide is a calcimimetic agent that allosterically modulates the calcium-sensing receptor (CaSR). Etelcalcetide binds to the CaSR and enhances activation of the receptor by extracellular calcium. Activation of the CaSR on parathyroid chief cells decreases PTH secretion.

PARSABIV is a calcium-sensing receptor agonist indicated for:
Secondary hyperparathyroidism (HPT) in adult patients with chronic kidney disease (CKD) on hemodialysis. (1)

Limitations of Use:
PARSABIV has not been studied in adult patients with parathyroid carcinoma, primary hyperparathyroidism, or with CKD who are not on hemodialysis and is not recommended for use in these populations.

Ensure corrected serum calcium is at or above the lower limit of normal prior to initiation, dose increase, or re-initiation. (2.1)

The recommended starting dose is 5 mg administered by intravenous bolus injection three times per week at the end of hemodialysis treatment. (2.1)

The maintenance dose is individualized and determined by titration based on parathyroid hormone (PTH) and corrected serum calcium response. The dose range is 2.5 to 15 mg three times per week. (2.1)

The dose may be increased in 2.5 mg or 5 mg increments no more frequently than every 4 weeks. (2.2)

Measure serum calcium within 1 week after initiation or dose adjustment and every 4 weeks for maintenance. (2.2)
Measure PTH after 4 weeks from initiation or dose adjustment. (2.2)
Decrease or temporarily discontinue PARSABIV in individuals with PTH levels below the target range. (2.2)

Consider decreasing or temporarily discontinuing PARSABIV or use concomitant therapies to increase corrected serum calcium in patients with a corrected serum calcium below the lower limit of normal but at or above 7.5 mg/dL without symptoms of hypocalcemia. (2.2)

Stop PARSABIV and treat hypocalcemia if the corrected serum calcium falls below 7.5 mg/dL or patients report symptoms of hypocalcemia. (2.2)
Do not mix or dilute prior to administration. (2.3)

Administer by intravenous bolus injection into the venous line of the dialysis circuit at the end of the hemodialysis treatment during rinse back or intravenously after rinse back. (2.3)

Injection: 2.5 mg/0.5 mL solution in a single-dose vial
Injection: 5 mg/mL solution in a single-dose vial
Injection: 10 mg/2 mL solution in a single-dose vial

Ferric sodium gluconate  - ferrlecit ®  

Indicated for the treatment of iron deficiency anemia in patients undergoing chronic hemodialysis who are receiving supplemental erythropoietin therapy.

Dosing (Adults):
The recommended dosage of ferric sodium gluconate for the repletion treatment of iron deficiency in hemodialysis patients is 10 ml of ferric sodium gluconate (125 mg of elemental iron) diluted in 100 ml of 0.9% sodium chloride solution administered intravenously over 1 hour. Most patients will require a minimum cumulative dose of 1 gram of elemental iron, administered over eight sessions at sequential dialysis treatments to achieve favorable hemoglobin or hematocrit response.

Paricalcitol  -  zemplar ®  

Secondary hyperparathyroidism is characterized by an elevation in parathyroid hormone (PTH) associated with inadequate levels of active vitamin D hormone. The source of vitamin D in the body is from synthesis in the skin and from dietary intake. Vitamin D requires two sequential hydroxylations in the liver and the kidney to bind to and to activate the vitamin D receptor (VDR). The endogenous VDR activator, calcitriol [1,25(OH)2 D3], is a hormone that binds to VDRs that are present in the parathyroid gland, intestine, kidney, and bone to maintain parathyroid function and calcium and phosphorus homeostasis, and to VDRs found in many other tissues, including prostate, endothelium and immune cells. VDR activation is essential for the proper formation and maintenance of normal bone. In the diseased kidney, the activation of vitamin D is diminished, resulting in a rise of PTH, subsequently leading to secondary hyperparathyroidism, and disturbances in the calcium and phosphorus homeostasis.1 The decreased levels of 1,25(OH)2 D3 and resultant elevated PTH levels, both of which often precede abnormalities in serum calcium and phosphorus, affect bone turnover rate and may result in renal osteodystrophy.

Mechanism of Action
Paricalcitol is a synthetic, biologically active vitamin D analog of calcitriol with modifications to the side chain (D2) and the A (19-nor) ring. Preclinical and in vitro studies have demonstrated that paricalcitol's biological actions are mediated through binding of the VDR, which results in the selective activation of vitamin D responsive pathways. Vitamin D and paricalcitol have been shown to reduce parathyroid hormone levels by inhibiting PTH synthesis and secretion.

Zemplar is indicated for the prevention and treatment of secondary hyperparathyroidism associated with chronic kidney disease Stage 5.

Zemplar should not be given to patients with evidence of vitamin D toxicity, hypercalcemia, or hypersensitivity to any ingredient in this product (see WARNINGS).

Acute overdose of Zemplar may cause hypercalcemia, and require emergency attention. During dose adjustment, serum calcium and phosphorus levels should be monitored closely (e.g., twice weekly). If clinically significant hypercalcemia develops, the dose should be reduced or interrupted. Chronic administration of Zemplar may place patients at risk of hypercalcemia, elevated Ca × P product, and metastatic calcification.

Treatment of patients with clinically significant hypercalcemia consists of immediate dose reduction or interruption of Zemplar therapy and includes a low calcium diet, withdrawal of calcium supplements, patient mobilization, attention to fluid and electrolyte imbalances, assessment of electrocardiographic abnormalities (critical in patients receiving digitalis), hemodialysis or peritoneal dialysis against a calcium-free dialysate, as warranted. Serum calcium levels should be monitored frequently until normocalcemia ensues.

Phosphate or vitamin D-related compounds should not be taken concomitantly with Zemplar.

Dosing: 0.04 to 0.1 mcg/kg (2.8 to 7.0 mcg) IV 3 times/week at dialysis. Max dose 0.24 mcg/kg (16.8 mcg).

Phoslyra® (calcium acetate oral solution)

PHOSLYRA is a phosphate binder indicated for the reduction of serum phosphorus in patients with end stage renal disease.

Starting dose is 10 mL with each meal.
Titrate the dose every 2 to 3 weeks until an acceptable serum phosphorus level is reached. Most patients require 15 to 20 mL with each meal.

Oral Solution: 667 mg calcium acetate per 5 mL.


PHOSLYRA for oral administration is a clear solution containing 667 mg calcium acetate per 5 mL. PHOSLYRA is supplied in amber-colored, multiple-dose bottles, packaged with a marked dosing cup in the following size:

473 mL (16 fl. oz) bottle (NDC 49230-643-31)

Sevelamer   - renagel ®. renvela®  

Patients with chronic kidney disease (CKD) retain phosphorus and can develop hyperphosphatemia. When the product of serum calcium and phosphorus concentrations (Ca x P) exceeds 55 mg2/dL2, there is an increased risk that ectopic calcification will occur. Hyperphosphatemia plays a role in the development of secondary hyperparathyroidism in renal insufficiency.

Treatment of hyperphosphatemia includes reduction in dietary intake of phosphate, inhibition of intestinal phosphate absorption with phosphate binders, and removal of phosphate with dialysis. Sevelamer carbonate taken with meals has been shown to control serum phosphorus concentrations in patients with CKD who are on dialysis.

Mechanism of Action
Renvela contains sevelamer carbonate, a non-absorbed phosphate binding crosslinked polymer, free of metal and calcium. It contains multiple amines separated by one carbon from the polymer backbone. These amines exist in a protonated form in the intestine and interact with phosphate molecules through ionic and hydrogen bonding. By binding phosphate in the gastrointestinal tract and decreasing absorption, sevelamer carbonate lowers the phosphate concentration in the serum (serum phosphorus).

Renvela® (sevelamer carbonate) is indicated for the control of serum phosphorus in patients with chronic kidney disease (CKD) on dialysis.

Because of the rapid reaction with the hydrochloric acid in the stomach, the dosing of Renvela powder or tablet is anticipated to be similar to that of the sevelamer hydrochloride salt or tablet.

General Dosing Information
Renvela should be given three times a day with meals.

Patients Not Taking a Phosphate Binder. The recommended starting dose of Renvela is 0.8 to 1.6 g with meals based on serum phosphorus level. Table1 provides recommended starting doses of Renvela for patients not taking a phosphate binder.

Table 1. Starting Dose for Dialysis Patients Not Taking a Phosphate Binder
Serum Phosphorus  Renvela® 800 mg Tablet  Renvela Powder 
 > 5.5 and < 7.5 mg/dL  1 tablet three times daily with meals  0.8 g three times daily with meals
≥ 7.5 mg/dL 2 tablets three times daily with meals 1.6 g three times daily with meals

Switching from Sevelamer Hydrochloride Tablets. For patients switching from sevelamer hydrochloride tablets to sevelamer carbonate tablets or powder, use the same dose in grams. Further titration may be necessary to achieve desired phosphorus levels. The highest daily dose of sevelamer carbonate studied was 14 grams in CKD patients on dialysis.

Switching between Sevelamer Carbonate Tablets and Powder. Use the same dose in grams. Further titration may be necessary to achieve desired phosphorus levels.

Switching from Calcium Acetate. In a study in 84 CKD patients on hemodialysis, a similar reduction in serum phosphorus was seen with equivalent doses (approximately mg for mg) of sevelamer hydrochloride and calcium acetate. Table 2 gives recommended starting doses of Renvela based on a patient’s current calcium acetate dose

Table 2. Starting Dose for Dialysis Patients Switching From Calcium Acetate to Renvela
 Calcium Acetate 667 mg
(Tablets per meal)
Renvela® 800 mg Tablet
(Tablets per meal) 
Renvela Powder 
1 tablet 1 tablet 0.8 g
2 tablets 2 tablets 1.6 g
3 tablets 3 tablets  2.4 g

Dose Titration for All Patients Taking Renvela. Titrate the Renvela dose by 0.8 g TID with meals at two-week intervals as necessary with the goal of controlling serum phosphorus within the target range.

2.2 Sevelamer Carbonate Powder Preparation Instructions
The entire contents of each 0.8 or 2.4 g packet should be placed in a cup and mixed thoroughly with the amount of water described in Table 3.

Table 3. Sevelamer Carbonate Powder Preparation Instructions

Renvela Powder
Packet Strength
Minimum amount of water for dose preparation
(either ounces, mL or teaspoon/Tablespoon)
  ounces mL tsp/Tbsp
0.8 g 1 30 6 teaspoons/2 Tablespoons
2.4 g 2 60 4 Tablespoons

Multiple packets may be mixed together with the appropriate amount of water. Patients should be instructed to stir the mixture vigorously (it does not dissolve) and drink the entire preparation within 30 minutes or resuspend the preparation right before drinking.

Based on clinical studies, the average prescribed daily dose of sevelamer carbonate is approximately 7.2 g per day.

Tablets: 800 mg white oval, film-coated, compressed tablets imprinted with “RENVELA 800”

Powder: 0.8 g and 2.4 g pale yellow powder packaged in an opaque, foil lined, heat sealed packet

Sevelamer HCL:
ESRD (hyperphosphatemia): 2 to 4 (800-1600 mg) caps orally three times daily with meals.

Note: the dose may be based on serum phosphorous.
Initial phosphate level:
>6.0 mg/dl and <7.5 mg/dl: 800 mg 3 times/day
>7.5 mg/dl and <9.0 mg/dl: 1200-1600 mg 3 times/day
>9.0 mg/dl: 1600 mg 3 times/day

Adjustment: Dosage should be adjusted based on serum phosphorous concentration, with a goal of lowering to <6.0 mg/dl.

Supplied: 400 mg, 800 mg tablet

 sucroferric oxyhydroxide chewable tablet -velphoro® 

Drug UPDATES: VELPHORO® (sucroferric oxyhydroxide) chewable tablet for oral use
[Drug information  /  PDF]  
Dosing:  Click (+) next to Dosage and Administration section (drug info link)

Initial U.S. Approval:  2013

Mechanism of Action: In the aqueous environment of the GI tract, phosphate binding takes place by ligand exchange between hydroxyl groups and/or water in sucroferric oxyhydroxide and the phosphate in the diet. The bound phosphate is eliminated with feces.Both serum phosphorus levels and calcium-phosphorus product levels are reduced as a consequence of the reduced dietary phosphate absorption.

INDICATIONS AND USAGE:  Velphoro is a phosphate binder indicated for the control of serum phosphorus levels in patients with chronic kidney disease on dialysis.
osphorus levels in patients with chronic kidney disease on dialysis.
Velphoro tablets must be chewed and not swallowed whole. To aid with chewing and swallowing, the tablets may be crushed.

Starting Dose
The recommended starting dose of Velphoro is 3 tablets (1,500 mg) per day, administered as 1 tablet (500 mg) 3 times daily with meals.

Titration and Maintenance
Monitor serum phosphorus levels and titrate the dose of Velphoro in decrements or increments of 500 mg (1 tablet) per day as needed until an acceptable serum phosphorus level is reached, with regular monitoring afterwards. Titrate as often as weekly.

Based on clinical studies, on average patients required 3 to 4 tablets (1,500 mg to 2,000 mg) a day to control serum phosphorus levels.
The highest daily dose studied in a Phase 3 clinical trial in ESRD patients was 6 tablets (3,000 mg) per day.

Velphoro must be administered with meals. To maximize the dietary phosphate binding, distribute the total daily dose among meals. No additional fluid above the amount usually taken by the patient is required.
If one or more doses of Velphoro are missed, the medication should be resumed with the next meal. Do not attempt to replace a missed dose.

HOW SUPPLIED: Velphoro (sucroferric oxyhydroxide) chewable tablet 500 mg


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Renal Failure (agents)