Nephrocalcinosis
| Nephrocalcinosis | |
|---|---|
| Classification and external resources | |
| Specialty | urology |
| ICD-10 | E83.5†N29.8* |
| ICD-9-CM | 275.49 |
| DiseasesDB | 8902 |
| MedlinePlus | 000492 |
| eMedicine | article/243911 |
| Patient UK | Nephrocalcinosis |
Nephrocalcinosis, once known as Albright's calcinosis after Fuller Albright, or Anderson-Carr kidneys, is a term originally used to describe deposition of calcium salts in the renal parenchyma due to hyperparathyroidism. It is now more commonly used to describe diffuse, fine, renal parenchymal calcification on radiology.[1] During its early stages, nephrocalcinosis is visible on x-ray, and appears as a fine granular mottling over the renal outlines. These outlines eventually come together to form a dense mass.[2] It is most commonly seen as an incidental finding with medullary sponge kidney on an abdominal x-ray. However, it may be severe enough to cause (as well as be caused by) renal tubular acidosis or even end stage renal failure, due to disruption of the renal tissue by the deposited calcium.
Stages of nephrocalcinosis
- Chemical nephrocalcinosis
- Microscopic nephrocalcinosis
- Macroscopic nephrocalcinosis
Symptoms of nephrocalcinosis
Though this condition is usually asymptomatic, if symptoms are present they are usually related to the causative process, (e.g. hypercalcemia).[3] These include renal colic, polyuria and polydipsia:[3]
- Renal colic is usually caused by pre-existing nephrolithiasis, as may occur in patients with chronic hypercalciuria.[3] Less commonly, it can result from calcified bodies moving into the calyceal system.[3]
- Nocturia, polyuria, and polydipsia from reduced urinary concentrating capacity (i.e. nephrogenic diabetes insipidus) as can be seen in hypercalcemia, medullary nephrocalcinosis of any cause, or in children with Bartter syndrome in whom essential tubular salt reabsorption is compromised.[3]
There are several causes of nephrocalcinosis that are typically acute and present only with renal failure.[3] These include tumor lysis syndrome, acute phosphate nephropathy, and occasional cases of enteric hyperoxaluria.[3]
Etiologies
Causes of cortical nephrocalcinosis
- Acute cortical necrosis. May be caused by:
- Chronic glomerulonephritis
- Alport syndrome
- Prolonged hypercalcemia and/or hypercalciuria
- Renal transplant rejection
- Sickle cell disease (rare)
- Vitamin B6 (pyridoxine) deficiency (rare)
Causes of medullary nephrocalcinosis
- Medullary sponge kidney
- Hyperparathyroidism
- Hypoparathyroidism[4]
- Renal tubular acidosis (specifically distal RTA)
- Renal tuberculosis
- Renal papillary necrosis
- Hyperoxaluria
And other causes of hypercalcemia (and thus hypercalciuria)
- Immobilization (leading to hypercalcemia and hypercalciuria)
- Milk-alkali syndrome
- Hypervitaminosis D
- Sarcoidosis
References
- ↑ "Nephrocalcinosis". eMedicine. 2003-09-09. Retrieved 2007-03-10.
- ↑ "Albright's Nephrocalcinosis". e-radiology. Retrieved 2007-03-10.
- 1 2 3 4 5 6 7 "Nephrocalcinosis, Clinical presentation". UpToDate Online. January 2010. Retrieved 2010-05-29.
- ↑ Mitchell DM, Regan S, Cooley MR, Lauter KB, Vrla MC, Becker CB, Burnett-Bowie SA, Mannstadt M (2012). "Long-Term Follow-Up of Patients with Hypoparathyroidism". J Clin Endocrinol Metab. pp. 4507–4514. doi:10.1210/jc.2012-1808. PMC 3513540
. PMID 23043192.
