- What is Hypercalcaemic Nephropathy
- Statistics on Hypercalcaemic Nephropathy
- Risk Factors for Hypercalcaemic Nephropathy
- Progression of Hypercalcaemic Nephropathy
- Symptoms of Hypercalcaemic Nephropathy
- Clinical Examination of Hypercalcaemic Nephropathy
- How is Hypercalcaemic Nephropathy Diagnosed?
- Prognosis of Hypercalcaemic Nephropathy
- How is Hypercalcaemic Nephropathy Treated?
- Hypercalcaemic Nephropathy References
What is Hypercalcaemic Nephropathy
Hypercalcaemic nephropathy involves the kidney and urinary tract, and also encompasses kidney damage related to excessive amounts of calcium in the blood.
Statistics on Hypercalcaemic Nephropathy
Hypercalcaemic nephropathy occurs in conditions that cause prolonged elevation of plasma calcium levels. Its incidence is therefore related to the incidence of the causative conditions. As a result of early detection of high serum calcium, less than 20% of patients experience hypercalcaemic-associated renal disease.
Risk Factors for Hypercalcaemic Nephropathy
Hypercalcaemic nephropathy is associated with any causes of prolonged calcium levels in the blood. The causes of hypercalcaemia range from primary hyperparathyroidism and malignant disease to excess action of vitamin D, excessive calcium intake, endocrine disorders, medications and other problems such as long-term immobility and inherited disease.
Primary hyperparathyroidism and malignant disease account for greater than 90% of the cases of hypercalcaemia. It most frequently occurs in patients with breast cancer and multiple myeloma, although other cancers also at risk include squamous cell carcinoma of the lung, ovarian cancer, prostate cancer lymphoma, leukaemia, renal cancer and cancers of the head and neck.
Progression of Hypercalcaemic Nephropathy
With prolonged elevation of blood calcium levels, the calcium salts may come out of solution (precipitate) both within the kidney (called nephrocalcinosis) or within the urinary tract resulting in urinary stone formation. If the deposits grow large enough, or remain in place for long periods, the urinary tract may become obstructed or infected as the normal flow of urine to the bladder and eventual excretion is disturbed.
How is Hypercalcaemic Nephropathy Diagnosed?
Hypercalcaemia is diagnosed by the laboratory demonstration of increased corrected serum calcium level. The use of the corrected serum calcium level considers the effect of the altered albumin concentration.
The normal range is: 2.15 – 2.55 mmol/L. Serum calcium and albumin should therefore both be measured.
Prognosis of Hypercalcaemic Nephropathy
The prognosis of hypercalcaemic nephropathy depends on its severity and the type of nephropathy present – nephrocalcinosis or urinary stone disease. As high blood calcium affects other organ systems simultaneously, it is important to consider their contribution to the morbidity and mortality of patients. These complications include nerve (neurological), gastrointestinal, cardiovascular and musculoskeletal effects.
Without treatment, uncontrolled hypercalcaemia will result in the deterioration of nephropathy and development of renal failure. With early diagnosis, the cause of hypercalcaemia is usually identified and treated to avoid long-term complications.
How is Hypercalcaemic Nephropathy Treated?
The treatment of hypercalcaemia is determined by the underlying disease, the level of hypercalcaemia and the patient’s clinical presentation. The aim of treatment is directed at decreasing serum calcium levels by increasing urinary excretion of calcium and decreasing bone resorption of calcium.
Key features include:
- Rehydration with intravenous saline
- Intravenous bisphosphonates – inhibits the activity of cells that break down bone (osteoclasts)
- Avoid immobilisation – increases bone resorption of calcium
- Review patient medications for any drugs that inhibit urinary calcium excretion, decrease renal blood flow or increase intake of calcium
Hypercalcaemic Nephropathy References Braunwald, Fauci, Kasper, Hauser, Longo, Jameson. Harrison’s Principles of Internal Medicine. 15th Edition. McGraw-Hill. 2001
 Cotran, Kumar, Collins 6th edition. Robbins Pathologic Basis of Disease. WB Saunders Company. 1999.
 Kumar P, Clark M. CLINICAL MEDICINE. WB Saunders 2002 Pg 545-549.
 Longmore M, Wilkinson I, Torok E. OXFORD HANDBOOK OF CLINICAL MEDICINE. Oxford University Press. 2001