Nephrocalcinosis

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- r ay, 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 :- microscopic crystalline calcium precipitates in the form of oxalate or phosphate. M acroscopic nephrocalcinosis :- observed on visual or radiologic examination without further magnification.

7. Pathophysiology

8. 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 H ematuria P assage of urinary stones U rinary tract infection

9. 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

10. 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.

11. 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.

12. 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)

13. 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.

14. References Emedicine.medscape.com Kumar and clark 7 th edition