This is a 35 year old female who has been diagnosed with hyperparathyridism.
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19 comments:
Jessica,
This is a case of medullary nephrocalcinosis where there is markedly increase in the echogenicity of the renal medulla. common causes of nephrocalcinosis are hyperparathyroidism, renal tubular acidosis and medullary sponge kidney.
Irene, I agree with you 100%. If symptoms exist, they include nocturia, polyuria, and polydipsia from reduced urinary concentrating capacity; and possibly renal colic.
Nephrocalcinosis described originally the deposition of calcium salts in the renal parenchyma in hyperparathyroidism.
This appearance is different from that of calcification within the lumen of the collecting system, ureter, and bladder, which represents nephrolithiasis.
more addition of causes
•Renal papillary necrosis
•Immobilization
•Milk-alkali syndrome
•Sarcoidosis
•Hyperoxaluria
•Glucose-galactose malabsorption
In addition, a variety of conditions can cause bone destruction that is associated with hypercalcemia and hypercalciuria.
A variety of radiographic renal abnormalities have been associated with sickle cell disease, including renal enlargement, thickening of the renal cortex, focal hypertrophy, papillary necrosis, and changes associated with infection. However,it is rare cause of nephrocalcinosis.
also, usually most case of nephrocalcinosis is asymptomatic.
does anyone know how betweeen cortical and medullary nephrocalcinosis are different?
ZOULIATH SAID
Nephrocalcinosis, once known as Albright's calcinosis after Fuller Albright, 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.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. 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.
Great job! All of you are right. Please note the severe calcification of this patients renal pyramids. Do you think this patient will live a normal life?
"Parathyroidectomy to remove enlarged adenomas is very helpful in primary hyperparathyroidism and results in a low recurrence rate [of calcium nodules]."
http://emedicine.medscape.com/article/243911-treatment
"The goal of treatment is to reduce symptoms and prevent more calcium from being deposited in the kidneys.
Measures should be taken to reduce abnormal levels of calcium, phosphate, and oxalate in the blood. Medications that cause calcium loss will usually be stopped...
What to expect depends on the extent of complications and the cause of the disorder.
Although further deposits in the kidneys can be prevented with good treatment, deposits already formed usually cannot be eliminated. Extensive deposits of calcium in the kidneys does NOT always mean severe damage to the kidneys."
http://health.nytimes.com/health/guides/disease/nephrocalcinosis/overview.html
Here's an interesting study by NIH with regard to treatment and improved quality of life: "Nephrocalcinosis is accepted to contribute to the progression of renal failure. We have reviewed evidence that nephrocalcinosis is caused directly by the excess parathyroid hormone produced in renal disease. Evidence that hyperparathyroidism in uremic patients results from calcitriol deficiency and the mechanisms by which this comes about have been discussed. We have shown that renal secondary hyperparathyroidism can be eliminated or substantially reduced without increasing blood calcium using a low-dosage regimen of calcitriol. Decreasing PTH concentrations to or near normal alleviates this hormone's toxicity to many organs, including the kidneys. Potential benefits for the uremic patient include an increase in the quality and length of life. Calcitriol treatment provides a powerful means to reduce PTH concentration in uremic patients that may not be achieved with other methods. Further prospective clinical studies of uremic dogs and cats are warranted to document preservation of renal function and histology during calcitriol treatments."
http://www.ncbi.nlm.nih.gov/pubmed/1410853
Hyperparathyroidism is overactivity of the parathyroid glands resulting in excess production of parathyroid hormone (PTH). The parathyroid hormone regulates calcium and phosphate levels and helps to maintain these levels. Excessive PTH secretion may be due to problems in the glands themselves, in which case it is referred to as primary hyperparathryroidism and which leads to hypercalcemia (raised calcium levels). It may also occur in response to low calcium levels, as encountered in various situations such as vitamin D deficiency or chronic kidney disease; this is referred to as secondary hyperparathyroidism.http://en.wikipedia.org/wiki/Hyperparathyroidism
Nephrocalcinosis may be caused by a number of conditions:
Excess excretion of calcium by the kidney
Renal tubular acidosis
Medullary sponge kidney
Hypercalcemia (high calcium levels in the blood)
Renal cortical necrosis
Tuberculosis
Fragments of calcium oxalate or calcium phosphate may break free from the kidney and provide nuclei for formation of stones (nephrolithiasis). This may result in obstructive uropathy, possibly leading to eventual kidney failure if the obstructing stones are not passed in the urine or removed. This condition is relatively common in premature infants, partly from intrinsic kidney calcium losses and partly from enhanced calcium excretion when they are given loop diuretics.
www.steadyhealth.com
Nephrocalcinosis is associated with renal tubular acidosis in children with X-linked hypophosphatemia.
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