Nephrocalcinosis symptoms can range from asymptomatic and discovered incidentally on ultrasounds or abdominal X-ray to life-threatening. Symptoms may include polyuria (excess urination), polydipsia (excessive drinking) and hematuria (blood in urine). Other symptoms of nephrocalcinosis are hypertension, urinary tract infections and recurrent urinary stones.
Symptoms depend on the underlying cause of the calcium deposition. Some causes include premature infants, renal tubular acidosis, medullary sponge kidney and primary hyperparathyroidism. Others are induced by drugs, such as amphotericin B and triamterene. Other conditions that can lead to nephrocalcinosis are sarcoidosis, chronic glomerulonephritis, transplant rejection and tuberculosis.
Common Nephrocalcinosis Symptoms
Medullary nephrocalcinosis is the most common form of the condition and is associated with increased levels of urinary calcium, phosphate, and oxalate, and/or alkaline urine pH (Box 57.1). This type of nephrocalcinosis is also called chemical nephrocalcinosis and is found most commonly in patients with oxalosis, such as those with primary hyperoxaluria or end-stage kidney disease.
In medullary nephrocalcinosis, small parenchymal calcifications occur in the kidney medulla and are more symmetric than those found in cortical nephrocalcinosis. This type of nephrocalcinosis can be caused by a number of conditions, including oxalosis and inflammatory diseases such as sarcoidosis and tuberculosis.
Another type of nephrocalcinosis, known as macroscopic nephrocalcinosis, occurs when calcium crystals form in the glomerular and tubular epithelial cells. These calcifications can form within the glomeruli, in the interstitial fluid, or in the tubular fluid. These calcifications can form into plaques or nidus, or rupture into the tubular fluid, resulting in nephrolithiasis.
Other types of nephrocalcinosis, such as those associated with hypocitraturia, can also result in the development of nephrolithiasis and may occur in preterm infants and/or children who have a history of metabolic acidosis. Other types of nephrocalcinosis, including those that result from kidney diseases or HIV-related disorders, are less common and may not be detected on physical examination or imaging.
The diagnosis of nephrocalcinosis must be made by an experienced urologist. There are various methods of diagnosing the condition, including blood and biochemical tests and radiographic evaluation with X-ray, CT, or ultrasound.
Medications and dietary supplements can also contribute to the formation of nephrocalcinosis. A diet rich in phosphorus, potassium and vitamin D can help to minimize the buildup of calcified materials and reduce the risk of nephrocalcinosis. Other medications such as acetazolamide, amphotericin B, and triamterene can also increase the risk of nephrocalcinosis.
Infectious diseases can also cause nephrocalcinosis, especially in children and infants with inflammatory or kidney disorders. Several infectious causes of nephrocalcinosis have been reported, including atypical mycobacterial infection and AIDS-related diseases.
Some rare genetic conditions can also contribute to nephrocalcinosis, but these are not common. X-linked hypercalciuric nephrolithiasis, X-linked hypophosphatemic rickets and Bartter syndrome can all be related to nephrocalcinosis.
The most severe forms of nephrocalcinosis, resulting in kidney failure and nephrolithiasis, are associated with autoimmune disorders, such as hereditary nonpolyglandular myopathy and autoantibody-induced nephropathy. The presence of nephrocalcinosis in these cases may be more difficult to detect, and patients often require a kidney biopsy.
