Calcification is the abnormal accumulation of calcium salts in body tissue. This abnormal accumulation of calcium in the kidney is referred to as nephrocalcinosis, which means a generalized increase in the kidney’s calcium content rather than a localized increase seen in calcified renal infarction and tuberculosis.
Nephrocalcinosis can be associated with renal stones, however, it is more likely to be due to an underlying metabolic disorder. It may be divided into three categories although there is a substantial degree of overlap between them.
These categories are chemical, microscopic, and macroscopic nephrocalcinosis. It can also be differentiated into medullar and cortical nephrocalcinosis.
In chemical nephrocalcinosis, there is predominantly an increase of calcium in renal cells. This increase is seen particularly in the tubular epithelium and results in significant compromise to renal function and structure, leading to increased water, potassium, sodium, magnesium, and calcium excretion.
Microscopic nephrocalcinosis is only seen with a magnifying instrument and presents with calcium precipitates in crystalline form as phosphate and/or oxalate. Macroscopic nephrocalcinosis presents with large areas of calcifications that do not require magnifying in order to be seen.
The most frequent form of nephrocalcinosis is medullary nephrocalcinosis. It is characterized by the involvement of the renal medullary pyramids. Moreover, it usually is associated with dysregulation of calcium homeostasis (balance or equilibrium).
Cortical nephrocalcinosis is a much rarer form of nephrocalcinosis and it typically involves the entire renal parenchyma. Serious metabolic derangements like end-stage kidney disease, hyperoxaluria (excess oxalate excretion in the urine), hemolytic uremic syndrome, and polycystic kidney disease are frequently implicated in cortical nephrocalcinosis.
Histopathology Kidney--Nephrocalcinosis
Etiology and Pathophysiology
The most common cause of nephrocalcinosis is primary hyperparathyroidism, which causes hypercalcemia. Nephrocalcinosis as a complication of hyperparathyroidism, however, is relatively rare.
Other causes of hypercalcemia include vitamin D excess, diet and bone loss from conditions such as osteoporosis and chronic immobilization.
Hypercalciuria (excess urinary calcium) is another cause of nephrocalcinosis and is a complication of distal renal tubular acidosis (second most common cause of nephrocalcinosis), hypothyroidism, and familial disorders such as Bartter’s syndrome (defect in the thick ascending limb of the loop of Henle).
Calcium is tightly regulated and kept at very low levels under physiological conditions. It is transported along the renal tubular epithelium together with potassium, sodium, and water. Increase in calcium, in chemical nephrocalcinosis, disrupts the calcium transporting system and leads to impairment of the renal tubules.
Stone formation with the blockage of the collecting tubules and resultant inflammatory response are implicated in microscopic nephrocalcinosis.
It is believed that in macroscopic nephrocalcinosis intraluminal tubular calcium crystals serve as nidi for subsequent buildup of calcium and renal calculi-forming (stone-forming) substances such as uric acid and oxalate.
Clinical Presentation, Diagnosis, Treatment and Prognosis Nephrocalcinosis
The clinical presentation and prognosis of nephrocalcinosis depends mainly on the underlying cause of the calcium accumulation in the kidneys. Moreover, the clinical presentation may range from asymptomatic and discovered incidentally on ultrasounds or abdominal X-rays to life-threatening.
Symptoms associated with hypercalcemia include polydipsia (excessive thirst), polyuria (excessive urination), nausea, and vomiting. Furthermore, these patients may have hypertension, hematuria (blood in urine), and recurrent urinary tract infections.
Investigations for nephrocalcinosis include routine blood and biochemical tests, urine analysis and radiographic assessments with X-ray, CT, or ultrasounds.
Treatment involves ensuring adequate fluid intake and treating the underlying cause, if applicable, in order to prevent renal failure. Surgical therapy may be required in cases where there is significant stone formation in the renal tract, particularly if the stone causes obstruction and/or recurrent infections.
Further Reading
Low magnesium intake identified as a key factor in cardiovascular disease