Hypophosphatemia Hyperphosphatemia

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MAJOR CAUSES OF HYPOPHOSPHATEMIA

FIGURE 7-11

Major causes of hypophosphatemia. (From Angus [1]; with permission.)

Internal redistribution

Decreased intestinal absorption

Increased urinary excretion

Increased insulin, particularly during refeeding Acute respiratory alkalosis Hungry bone syndrome

Inadequate intake Antacids containing aluminum or magnesium Steatorrhea and chronic diarrhea

Primary and secondary hyperparathyroidism Vitamin D deficiency or resistance Fanconi's syndrome Miscellaneous: osmotic diuresis, proximally acting diuretics, acute volume expansion

CAUSES OF MODERATE HYPOPHOSPHATEMIA

Pseudohypophosphatemia Mannitol Bilirubin Acute leukemia Decreased dietary intake Decreased intestinal absorption Vitamin D deficiency Malabsorption Steatorrhea Secretory diarrhea Vomiting

PO34-binding antacids Shift from serum into cells Respiratory alkalosis Sepsis Heat stroke

Neuroleptic malignant syndrome Hepatic coma Salicylate poisoning Gout

Panic attacks Psychiatric depression

Hormonal effects Insulin Glucagon Epinephrine Androgens Cortisol

Anovulatory hormones Nutrient effects Glucose Fructose Glycerol Lactate Amino acids Xylitol

Cellular uptake syndromes Recovery from hypothermia Burkitt's lymphoma Histiocytic lymphoma Acute myelomonocytic leukemia Acute myelogenous leukemia Chronic myelogenous leukemia in blast crisis Treatment of pernicious anemia Erythropoietin therapy Erythrodermic psoriasis Hungry bone syndrome After parathyroidectomy Acute leukemia

Increased excretion into urine Hyperparathyroidism Renal tubule defects Fanconi's syndrome X-linked hypophosphatemic rickets Hereditary hypophosphatemic rickets with hypercalciuria Polyostotic fibrous dysphasia Panostotic fibrous dysphasia Neurofibromatosis Kidney transplantation Oncogenic osteomalacia Recovery from hemolytic-uremic syndrome Aldosteronism Licorice ingestion Volume expansion

Inappropriate secretion of antidiuretic hormone

Mineralocorticoid administration Corticosteroid therapy Diuretics

Aminophylline therapy

FIGURE 7-12

Causes of moderate hypophosphatemia. (From Popovtzer, et al. [6]; with permission.)

CAUSES OF SEVERE HYPOPHOSPHATEMIA

Acute renal failure: excessive P binders

Reye's syndrome

Chronic alcoholism and alcohol

After major surgery

withdrawal

Periodic paralysis

Dietary deficiency and PO34-binding

Acute malaria

antacids

Drug therapy

Hyperalimentation

Ifosfamide

Neuroleptic malignant syndrome

Cisplatin

Recovery from diabetic ketoacidosis

Acetaminophen intoxication

Recovery from exhaustive exercise

Cytokine infusions

Kidney transplantation

Tumor necrosis factor

Respiratory alkalosis

Interleukin-2

Severe thermal burns

Therapeutic hypothermia

CAUSES OF HYPOPHOSPHATEMIA IN PATIENTS WITH NONKETOTIC HYPERGLYCEMIA OR DIABETIC KETOACIDOSIS

Decreased net

Acute movement of

intestinal phosphate

Increased urinary

extracellular phos-

absorption

phosphate excretion

phate into the cells

Decreased phosphate

Glucosuria-induced

Insulin therapy

intake

osmotic diuresis

Acidosis

Causes of hypophosphatemia in patients with nonketotic hyper-glycemia or diabetic ketoacidosis.

FIGURE 7-13

Causes of severe hypophosphatemia. (From Popovtzer, et al. [6]; with permission.)

CAUSES OF HYPOPHOSPHATEMIA IN PATIENTS WITH ALCOHOLISM

CAUSES OF HYPOPHOSPHATEMIA IN PATIENTS WITH RENAL TRANSPLANTATION

Decreased net intestinal phosphate absorption

Increased urinary phosphate excretion

Acute movement of extracellular phosphate into the cells

Increased urinary phosphate excretion

Poor dietary intake of phosphate and vitamin D Use of phosphate binders to treat recurring gastritis Chronic diarrhea

Alcohol-induced reversible proximal tubular defect Secondary hyperparathy-roidism induced by vitamin D deficiency

Insulin release induced by intravenous solutions containing dextrose Acute respiratory alkalosis caused by alcohol withdrawal, sepsis, or hepatic cirrhosis Refeeding of the patient who is malnourished

Persistent hyperparathyroidism (hyperplasia or adenoma)

Proximal tubular defect (possibly induced by glucocorticoids, cyclosporine, or both)

FIGURE 7-16

Causes of hypophosphatemia in patients with renal transplantation.

FIGURE 7-15

Causes of hypophosphatemia in patients with alcoholism.

FIGURE 7-17

MAJOR CONSEQUENCES OF HYPOPHOSPHATEMIA Major consequences of hypophosphatemia.

Decreased erythrocyte 2,3-diphosphoglycerate levels, which result in increased affinity of hemoglobin for oxygen and reduced oxygen release at the tissue level Decreased intracellular adenosine triphosphate levels, which result in impairment of cell functions dependent on energy-rich phosphate compounds

SIGNS AND SYMPTOMS OF HYPOPHOSPHATEMIA

Central

Skeletal and

nervous system

Cardiac

Pulmonary

smooth muscle

Hematologic

Metabolic

dysfunction

dysfunction

dysfunction

dysfunction

dysfunction

Bone disease

Renal effects

effects

Metabolic

Impaired

Weakness of the

Proximal myopathy

Erythrocytes

Increased bone

Decreased

Low parathyroid

encephalopathy

myocardial

diaphragm

Dysphagia and ileus

Increased

resorption

glomerular

hormone levels

owing to tissue

contractility

Respiratory failure

Rhabdomyolysis

erythrocyte

Rickets and osteo-

filtration rate

Increased 1,25-dihy-

ischemia

Congestive heart

rigidity

malacia caused by

Decreased tubular

droxy-vitamin D3

Irritability

failure

Hemolysis

decreased bone

transport

levels

Paresthesias

Leukocytes

mineralization

maximum for

Increased creatinine

Confusion

Impaired phagocytosis

bicarbonate

phosphokinase

Delirium

Decreased renal

levels

Coma

Decreased

gluconeogenesis

Increased aldolase

granulocyte

Decreased titratable

levels

acid excretion

chemotaxis

Platelets

Hypercalciuria

Defective clot

Hypermagnesuria

retraction

Thrombocytopenia

Signs and symptoms of hypophosphatemia. (Adapted from Hruska and Slatopolsky [2] and Hruska and Gupta [7].)

FIGURE 7-19

Pseudofractures (Looser's transformation zones) at the margins of the scapula in a patient with oncogenic osteomalacia. Similar to the genetic X-linked hypophosphatemic rickets, a circulating phospha-turic factor is believed to be released by the tumor, causing phosphate wasting and reduced calcitriol formation by the kidney. Note the radiolucent ribbonlike decalcification extending into bone at a right angle to its axillary margin. Pseudofractures are pathogno-monic of osteomalacia with a low remodeling rate.

FIGURE 7-20 (see Color Plate)

Histologic appearance of trabecular bone from a patient with oncogenic osteomalacia. Undecalcified bone section with impaired mineralization and a wide osteoid (organic matrix) seam stained with von Kossa's stain is illustrated. Note the wide bands of osteoid around the mineralized bone. Absence of osteoblasts on the circumference of the trabecular bone portion indicates a low remodeling rate.

FIGURE 7-21 (see Color Plate)

Microscopic appearance of bone section from a patient with vitamin D deficiency caused by malabsorption. The bone section was stained with Masson trichrome stain. Hypophosphatemia and hypocalcemia were present. Note the trabecular bone consisting of very wide osteoid areas (red) characteristic of osteomalacia.

FIGURE 7-22

USUAL DOSAGES FOR PHOSPHORUS REPLETION Usual dosages for phosphorus repletion.

Severe symptomatic hypophosphatemia (plasma phosphate concentration < 1 mg/dL)

Phosphate depletion

Hypophosphatemic rickets

10 mg/kg/d, intravenously, until the

2-4 g/d (64 to 128 mmol/d), orally,

1-4 g/d (32 to 128 mmol/d), orally,

plasma phosphate concentration

in 3 to 4 divided doses

in 3 to 4 divided doses

reaches 2 mg/dL

PHOSPHATE PREPARATIONS FOR ORAL USE

FIGURE 7-23

Phosphate preparations for oral use.

Preparation

Phosphate, mg

Sodium, mEq

Potassium, mEq

K-Phos Neutral", tablet

250

13

1.1

(Beach Pharmaceuticals, Conestee, SC)

Neutra-Phos", capsule or 75-mL solution

250

7.1

7.1

(Baker Norton Pharmaceuticals, Miami, FL)

Neutra-Phos K", capsule or 75-mL solution

250

0

14.2

(Baker Norton Pharmaceuticals, Miami, FL)

PHOSPHATE PREPARATIONS FOR INTRAVENOUS USE Phosphate preparations for intravenous use.

Phosphate,

Sodium,

Potassium,

Phosphate preparation

Composition, mg/mL

mmol/mL

mEq/mL

mEq/mL

Potassium

236 mg K2HPO4

3.0

0

4.4

224 mg KH2 2PO44

Sodium

142 mg Na2HPO4

3.0

4.0

0

276 mg NaH2HPO4.H2O

Neutral sodium

10.0 mg Na2HPO

0.09

0.2

0

2.7 mg NaH2PO4.H2O

Neutral sodium, potassium

11.5 mg Na2HPO4

1.10

0.2

0.02

2.6 mg KH2PO4

3 mmol/mL of phosphate corresponds to 93 mg of phosphorus.

3 mmol/mL of phosphate corresponds to 93 mg of phosphorus.

CAUSES OF HYPERPHOSPHATEMIA

Pseudohyperphosphatemia

Increased endogenous loads

Reduced urinary excretion

Miscellaneous

Multiple myeloma

Tumor lysis syndrome

Renal failure

Fluoride poisoning

Extreme hypertriglyceridemia

Rhabdomyolysis

Hypoparathyroidism

ß-Blocker therapy

In vitro hemolysis

Bowel infarction

Hereditary

Verapamil

Increased exogenous phosphorus

Malignant hyperthermia

Acquired

Hemorrhagic shock

load or absorption

Phosphorus-rich cow's milk in premature neonates Vitamin D intoxication PO34-containing enemas Intravenous phosphorus supplements White phosphorus burns Acute phosphorus poisoning

Heat stroke Acid-base disorders Organic acidosis Lactic acidosis Ketoacidosis Respiratory acidosis Chronic respiratory alkalosis

Pseudohypoparathyroidism Vitamin D intoxication Growth hormone Insulin-like growth factor-1 Glucocorticoid withdrawal Mg2+ deficiency Tumoral calcinosis Diphosphonate therapy Hyopophosphatasia

Sleep deprivation

FIGURE 7-25

Causes of hyperphosphatemia. (From Knochel and Agarwal [5]; with permission.)

CLINICAL MANIFESTATIONS OF HYPERPHOSPHATEMIA

TREATMENT OF HYPERPHOSPHATEMIA

Consequences of secondary changes in calcium, parathyroid hormone, vitamin D metabolism and hypocalcemia:

Neuromuscular irritability Tetany Hypotension Increased QT interval

Consequences of ectopic calcification:

Periarticular and soft tissue calcification

Vascular calcification

Ocular calcification

Conduction abnormalities

Pruritus

Acute hyperphosphatemia in Chronic hyperphosphatemia in patients with adequate renal patients with end-stage renal function disease

Saline diuresis that causes phosphaturia Dietary phosphate restriction

Phosphate binders to decrease gastrointestinal phosphate reabsorption

FIGURE 7-27

Treatment of hyperphosphatemia.

FIGURE 7-26

Clinical manifestations of hyperphosphatemia.

FIGURE 7-28

Periarticular calcium phosphate deposits in a patient with endstage renal disease who has severe hyperphosphatemia and a high level of the product of calcium and phosphorus. Note the partial

resolution of calcific masses after dietary phosphate restriction and oral phosphate binders. Left shoulder joint before (A) and after (B) treatment. (From Pinggera and Popovtzer [17]; with permission.)

FIGURE 7-29

FIGURE 7-29

Resolution of soft tissue calcifications. The palms of the hands of the patient in Figure 7-28 with end-stage renal disease are shown before (A) and after (B) treatment of hyperphosphatemia. The patient has a high level of the product of calcium and phosphorus. (From Pinggera and Popovtzer [17]; with permission.)

FIGURE 7-30

A, B, Bone sections from the same patient as in Figures 7-28 and 7-29, illustrating osteitis fibrosa cystica caused by renal secondary hyperparathyroidism with hyperphosphatemia.

FIGURE 7-31

Roentgenographs appearance of femoral arterial vascular calcification in a patient on dialysis who has severe hyperphosphatemia. The patient has a high level of the product of calcium and phosphorus.

FIGURE 7-32 (see Color Plate)

Microscopic appearance of a cross section of a calcified artery in a patient with end-stage renal disease undergoing chronic dialysis. The patient has severe hyperphosphatemia and a high level of the product of calcium and phosphorus. Note the intimal calcium phosphate deposit with a secondary occlusion of the arterial lumen.

FIGURE 7-33

Massive periarticular calcium phosphate deposit (around the hip joint) in a patient with genetic tumoral calcinosis. The patient exhibits hyperphosphatemia and increased renal tubular phosphate reabsorption. Normal parathyroid hormone levels and elevated calcitriol levels are present. The same disease affects two of the patient's brothers.

FIGURE 7-35 (see Color Plate)

FIGURE 7-34

Massive periarticular calcium phosphate deposit in the plantar joints in the same patient in Figure 7-33 who has genetic tumoral calcinosis.

FIGURE 7-35 (see Color Plate)

Complications of the use of aluminum-based phosphate binders to control hyperphosphatemia. Appearance of bone section from a patient with end-stage renal disease who was treated with oral aluminum gels to control severe hyperphosphatemia. A bone biopsy was obtained 6 months after a parathyroidectomy was performed. Note the wide areas of osteoid filling previously resorbed bone.

FIGURE 7-37 (see Color Plate)

FIGURE 7-36 (see Color Plate)

The same bone section as in Figure 7-35 but under polarizing lenses, illustrating the partially woven appearance of osteoid typical of chronic renal failure.

FIGURE 7-37 (see Color Plate)

The same bone section as in Figure 7-35 with positive aluminum stain of the trabecular surface. These findings are consistent with aluminum-related osteomalacia.

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