Hypercalcemia & Hypocalcemia Dr. Nora Khreba - Assistant Lecturer of Nephrology Mansoura Nephrology and Dialysis Unit (MNDU) Course

1. Hypercalcemia & Hypocalcemia
by Nora Khreba

2. Ca2+ Homeostasis

3. Ca2+ Homeostasis

4. Factors affecting Ca concentration:

5. Factors which Influence the Concentration of Ionised Calcium

6. Effect of acid base abnormality

7. Ca2+ Homeostasis

8. PTH

9. Regulation of PTH by plasma Ca concentration

10. Actions on bone:

11. Vitamin D

12. Actions of Vit D :

13. calcitonin

14. Ca2+-Sensing
Receptor
(CaSR)
On parathyroid gland
(1) PTH synthesis
(2) PTH secretion
(3) parathyroid cellular proliferation.

15. Ca2+-Sensing
Receptor
(CaSR)
In the kidney, activation of CaSR in the thick ascending limb
of Henle’s loop inhibits paracellular transport of Ca2+,
resulting in hypercalciuria.
In the inner medullary collecting duct, CaSR is localized in
the endosomes that contain vasopressin-regulated water
channel, aquaporin
Activation of CaSR causes: reduction in vasopressin-
stimulated water absorption, resulting in defective uri- nary
concentration. This results in polyuria, particularly in
conditions of hypercalcemia due to which the development
of nephrocalcinosis and nephrolithiasis is prevented.

16. Renal handling of Ca

17. PCT

18. Thick
ascending
limb of loop
of henle

19. distal
convulted
tubule

20. Renal handling of Ca
• No calcium reabsorption is taking place in this segment, which
totally depends on the calcium load delivered by the CNT. Apical
CaSR-like proteins sense urine calcium concentration. This leads to
inhibition of water reabsorption and stimulates urine acidification,
decreasing the risk of stone formation

21. Effect of various factors on Ca2+ reabsorption in the nephron

23. Factors that increase and decrease TRPV5 activity

25. Hypocalcemia
•Plasma [Ca2+] <8.5 mg/dL
•For each gram decrease of albumin from
normal (i.e., 4.0 g/dL), [Ca2+] decreases
by 0.8 mg/dL.

26. Role of Ca

27. Clinical manifestations of hypocalcemia

28. ECG manifestation of hypocalcemia

29. corrected QT interval

31. Causes of hypocalcemia

32. Causes of hypocalcemia

33. Causes of hypocalcemia

34. Causes of hypocalcemia

35. Causes of hypocalcemia

36. Causes of hypocalcemia

37. Diagnostic
approach to a
patient with
hypocalcemia

38. Treatment of
Acute
Hypocalcemia
IV preparation :
Intravenous calcium gluconate (1 g available
as 10% in a 10 mL ampule) is the treatment
of choice for symptomatic hypocalcemia.
One gram of calcium chloride (10%) contains
273 mg of elemental Ca2+; however, it is not
always preferred because of its unbearable
irritation to veins..

39. Treatment Acute Hypocalcemia
• Initially, one to two ampules of calcium gluconate in 50 mL of
5% dextrose should be given over a period of 10–20 min,
• followed by 0.3–1 mg of elemental Ca2+/kg/h, if necessary.
Once symptoms improve, the patient can be started on oral
Ca2+ tablets
• In order to increase total serum Ca2+ by 2–3 mg/dL, a 70 kg
patient requires 1 g of elemental Ca2+ (approximately ten
ampules of calcium gluconate).

40. precautions
Solution may be diluted in NS, D5W (mix in up to 1000 mL),
Do not mix in same bag or line with carbonates, and Ringer, to avoid precipitation
For intermittent IV infusion, maximum rate is 200 mg/min (2 mL/min)
May administer IV push at rate of 50-100 mg/min (0.5-1 mL/min); rapid IV
administration may produce arrhythmias, hypotension, myocardial infarction, or
vasodilation
Central line
If hypomagnesemia is the underlying cause for hypocalcemia, IV magnesium
sulfate (8 mEq) should be given.

41. Oral calcium preparations

42. Treatment chronic Hypocalcemia
• Treatment is aimed at correcting the cause, if possible.
• Oral calcium supplementation (500–1,500 mg elemental Ca2+)
• calcitriol 0.5–1 μg/day are generally used for patients with hypoparathyroidism or PTH
resistance, chronic kidney disease, and osteomalacia.
• A few patients with hypoparathyroidism may benefit from thiazide diuretics.
• For patients with nutritional vitamin D deficiency, either cholecalciferol
• (effective dose 400–1,000 U/day) or ergocalciferol (effective dose 25,000–
• 50,000 U three times/week) can be used. For many patients,

43. Empirical Ca administration prior to
dialysis in ESRD patient , first discovered ,
presented with emergency in need for
urgent dialysis?????

45. Hypercalcemia
•serum [Ca2+] >10.2 mg/dL in an individual with normal
serum albumin concentration.
•severe hypercalcemia is considered when
serum [Ca2+] is above 14 mg/dL.

46. Clinical manifestations of hypercalcemia

47. Clinical manifestations of hypercalcemia

48. ECG manifestation of hypocalcemia

49. Causes of hypercalcemia

50. Causes of
hypercalcemia

51. Causes of hypercalcemia

53. Diagnostic
approach to a
patient with
hypocalcemia

54. Treatment of acute hypercalcemia
• 1. Hydration with normal saline and then administration of
furosemide for volume overload. Note that furosemide-
induced volume depletion may increase reabsorption of Ca2+
by the proximal tubule
• 2. Inhibition of bone resorption of Ca2+.
• 3. Decrease intestinal absorption of Ca2+.
• 4. Removal of Ca2+ by hemodialysis using a dialysate bath
containing low Ca2+.

55. Treatment of acute hypercalcemia

56. Treatment of acute hypercalcemia

57. Treatment of
chronic
hypercalcemia
1. Correction of the underlying cause:
parathyroidectomy and chemotherapy. Use cinacalcet
(30–120 mg/day) for secondary hyperparathyroidism
2. Maintenance of euvolemia: prescribe adequate
amount of water that should be equal or slightly more
than urine output and insensible loss.
3. Decrease the production of 1,25(OH)2D3: low-
calcium diet, avoid vitamin D intake, steroids,
chloroquine (250 mg/day) and ketoconazole (100–200
mg/day).
4. Decrease intestinal absorption of Ca2+: low-calcium
diet, steroids, and avoidance of vitamin D
preparations.

58. Treatment of
chronic
hypercalcemia
5. Decrease bone resorption: steroids, lower
PTH levels, avoid vitamin D use,
bisphosphonates, and receptor activator of
nuclear factor-kB ligand (RANKL) inhibitor,
and denosumab.
6. Bisphosphonates are used to treat
hypercalcemia in patients with
malignancy.they inhibit osteoclast-induced
bone resorption.
7. Denosumab is a humanized monoclonal
antibody that inhibits osteoclastic activity
and thereby bone resorption.