Nephrocalcinosis

1. Nephrocalcinosis
Soepel: 4
Abdul waris khan
Dept: internal medicine

2. SOEPEL
• Subjective: a 44 years old male married working in a factory
presented to ER with complains of haematuria, polyuria and
polydipsia.
• H/O presenting illness: the symptoms have been there for past 8
days and are progressing. The blood in the urine is mixed. He is
known to be hypertensive for a year.
• No past medical history
• No family history

3. • Objective: History taking appropriate to the symptoms and physical
examination.
• Evaluation: UTI, DM, hypercalcemia, nephrocalcinosis
• Plan: CBC, U&E, CT, X-ray, urine culture
• Elaboration: Appropriate management according to the diagnosis.

4. Definition
• Nephrocalcinosis is a condition in which calcium levels in the
kidneys are increased.

5. • Hypercalcemia is also a well-established cause of renal failure, through
direct renal vasoconstriction and volume depletion induced by
excessive diuresis.

6. • Microscopic nephrocalcinosis:-
o microscopic crystalline calcium precipitates in the form of oxalate or phosphate.
• Macroscopic nephrocalcinosis:-
o observed on visual or radiologic examination without further magnification.

7. Pathophysiology
Calcium is a cation that is transported,
along with sodium, potassium, and
water, in a complex and regulated
manner along the renal tubular
epithelium.
Increased extracellular calcium leads to
impairment of the calcium messenger
system with gross tubular impairment.
Hypercalcemia results in renal
vasoconstriction and a reduced GFR. It
also interferes with renal tubular
functions. Impaired renal concentration
ability and resistance to vasopressin are
the most common defects observed
with hypercalcemia.

9. Clinical presentation
• Calcium nodules may rupture through the papillary epithelium into the
calyceal system to become urinary stones and elicit the clinical presentations
of:
 Renal colic
 Hematuria
 Passage of urinary stones
 Urinary tract infection

10. • The following may be noted:
 Polyuria and polydipsia may be prominent because of the excess of free water diuresis with
reduced renal concentrating ability.
 Microscopic pyuria is common and represents a chronic inflammatory response to medullary
calcification.
 Distal tubular dysfunction is common with a mild salt-losing defect; it may become obvious
only with profound decrease of oral intake (anorexia) or when another source of salt-water
loss (eg, diarrhea or vomiting) emerges.
 Medullary nephrocalcinosis of any etiology can cause secondary distal tubular acidosis
related to distal tubular calcium deposition and chronic inflammation in the medulla.
 Patients may present with renal failure or with features of their underlying disease

11. Workup
 Measurement of serum calcium, phosphate, and albumin levels is
necessary to establish whether nephrocalcinosis is associated with
hypercalcemia.
 The serum phosphate level is low in primary hyperparathyroidism with
normal renal function, however, it is typically elevated in
nephrocalcinosis associated with renal insufficiency.
 Blood urea nitrogen (BUN) and serum creatinine levels are elevated
when nephrocalcinosis is associated with renal insufficiency.

12.  The serum potassium concentration may be low when
nephrocalcinosis is caused by certain conditions, such as distal renal
tubular acidosis (RTA)
 Urinalysis and urine culture should always be performed to look for
evidence of chronic infection. Elevated urinary pH may suggest
distal RTA
 Assessment of 24-hour urinary excretion of calcium, oxalate, citrate,
and uric acid, with simultaneous determination of BUN, creatinine,
and protein excretion, can be very helpful in calculating measured
renal function.

15. Management
 Adequate hydration with an isotonic sodium chloride solution is the
single most effective measure for reversing hypercalcemia and
protecting the kidneys.
 Calcium-sensing receptor stimulant cinacalcet (for correction of
hyperparathyroidism)
 Steroids (to decrease intestinal calcium absorption and vitamin-D
activity)
 Calcitonin or bisphosphonates (to inhibit bone resorption)

16.  Thiazide diuretics and dietary salt restriction will reduce renal calcium
excretion e,g Hydrochlorothiazide. The usual dose range is 12.5-25
mg/day
 Potassium and magnesium supplementation will increase the
solubility of urinary calcium.
 Citrate supplementation (preferably as potassium citrate) can be
used in idiopathic hypercalciuria and in distal RTA because it
increases urinary citrate and decreases urinary calcium excretion.

17. References
• Emedicine.medscape.com
• Kumar and clark 7th edition