Nephrocalcinosis

Soepel: 4

Abdul waris khan

Dept: internal medicine

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

• 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.

Definition• 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 excessive diuresis.

• 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.

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.

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

• 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

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.

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.

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)

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.

References • Emedicine.medscape.com

• Kumar and clark 7th edition