Abdul waris khan
Dept: internal medicine
• Subjective: a 44 years old male married working in a factory
presented to ER with complains of haematuria, polyuria and
• 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
• Objective: History taking appropriate to the symptoms and physical
• Evaluation: UTI, DM, hypercalcemia, nephrocalcinosis
• Plan: CBC, U&E, CT, X-ray, urine culture
• Elaboration: Appropriate management according to the diagnosis.
• Nephrocalcinosis is a condition in which calcium levels in the
kidneys are increased.
• Hypercalcemia is also a well-established cause of renal failure, through
direct renal vasoconstriction and volume depletion induced by
• 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.
Calcium is a cation that is transported,
along with sodium, potassium, and
water, in a complex and regulated
manner along the renal tubular
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
• Calcium nodules may rupture through the papillary epithelium into the
calyceal system to become urinary stones and elicit the clinical presentations
Passage of urinary stones
Urinary tract infection
• 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
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
Measurement of serum calcium, phosphate, and albumin levels is
necessary to establish whether nephrocalcinosis is associated with
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.
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
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
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
Steroids (to decrease intestinal calcium absorption and vitamin-D
Calcitonin or bisphosphonates (to inhibit bone resorption)
Thiazide diuretics and dietary salt restriction will reduce renal calcium
excretion e,g Hydrochlorothiazide. The usual dose range is 12.5-25
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.
• Kumar and clark 7th edition