HYPERPHOSPHATEMIA

AND HYPOPHOSPHATEMIA

Dr.Hariprasad
Intern
 HYPERPHOSPHATEMIA

• Hyperphosphatemia is a serum phosphate

concentration > 4.5 mg/dL (> 1.46 mmol/L)
 ETIOLOGY AND PATHOPHYSIOLOGY

• Renal insufficiency is the most common cause of hyperphosphatemia

• When kidney function is <30% of normal, hyperphosphatemia usually
develops
 CAUSES OF HYPERPHOSPHATEMIA
Transcellular Shifts:
• Tumor lysis syndrome
• Rhabdomyolysis
• Acute hemolysis
• Diabetic ketoacidosis and lactic acidosis
Increased Intake:
• Enemas and laxatives
• Cow's milk in infants
• Treatment of hypophosphatemia
• Vitamin D intoxication
Decreased Excretion:
• Renal failure
• Hypoparathyroidism or pseudohypoparathyroidism
• Acromegaly
 CLINICAL MANIFESTATIONS

• The principal clinical consequences of hyperphosphatemia

are hypocalcemia and systemic calcification.
• hypocalcemia is caused by tissue deposition of calcium-
phosphorus salt, inhibition of 1,25-D production, and
decreased bone resorption.
• Systemic calcification occurs because the solubility of
phosphorus and calcium in the plasma is exceeded.
• this condition is often apparent in the conjunctiva, where it
manifests as a foreign body feeling, erythema, and injection
 DIAGNOSIS

• Plasma creatinine and BUN levels should be assessed

• Measurement of K+ ,uric acid, calcium, LDH, bilirubin,
hemoglobin, and CPK may be indicated if rhabdomyolysis,
tumor lysis, or hemolysis is suspected
• measurement of the serum PTH level distinguishes
between hypoparathyroidism and
pseudohypoparathyroidism
TREATMENT
 HYPOPHOSPHATEMIA

• Hypophosphatemia is a serum phosphate

concentration < 2.5 mg/dL (0.81 mmol/L)
 CAUSES OF HYPOPHOSPHATEMIA

Transcellular Shifts:
• Glucose infusion
• Insulin
• Refeeding
• Total parenteral nutrition
• Respiratory alkalosis
• Tumor growth
• Bone marrow transplantation
• Hungry bone syndrom
Decreased Intake:
• Nutritional
• Premature infants
• Low phosphorus formula
• Antacids and other phosphate binders
Renal Losses:
• Hyperparathyroidism
• Parathyroid hormone–related peptide
• X-linked hypophosphatemic rickets
• Overproduction of fibroblast growth factor-23
• Dent disease
• Metabolic acidosis
• Diuretics
• Glycosuria
Multifactorial:
• Vitamin D deficiency
• Vitamin D–dependent rickets type 1
• Vitamin D–dependent rickets type 2
• Alcoholism
• Sepsis
• Dialysis
CLINICAL MANIFESTATIONS
THANK YOU