Diagnostic Ultrasound - Abdomen and Pelvis

Nephrocalcinosis
Diagnoses: Urinary Tract
• Hyperuricemia: Gout, Lesch-Nyhan, glycogen storage
disease (hyperechoic medulla and cortex)
• Hypokalemia: Primary aldosteronism, pseudo-Bartter
syndrome
• Renal medullary fibrosis
• Abnormal protein deposition
PATHOLOGY
General Features
• Etiology
○ 3 primary mechanisms for calcium deposition
– Metastatic: Metabolic abnormality →calcium
deposition in medulla of morphologically normal
kidneys
– Urinary stasis: Calcium salts precipitate in dilated
collecting ducts containing static urine
– Dystrophic: Calcium deposition in damaged tissue
○ Causes of hypercalciuria
– Bone resorption: Hyperparathyroidism, bone
metastases, immobilization, multiple myeloma,
hyperthyroidism, Cushing syndrome
– Increased intestinal absorption of calcium: Sarcoidosis,
milk-alkali syndrome, hypervitaminosis D, idiopathic
hypercalciuria
– Decreased tubular reabsorption
○ Medullary nephrocalcinosis
– Hyperparathyroidism = most common cause; 5% of
patients with hyperparathyroidism have medullary NC
– Renal tubular acidosis type 1 (distal) = 2nd most
common cause
□ May be 1° or 2° to other systemic disease (Sjögren,
lupus, etc.)
□ Type 2 (proximal) RTA does not cause NC
– MSK: Common cause; congenitally abnormal dilation
of collecting ducts
□ Calcium in ectatic collecting ducts rather than renal
substance
□ Calcium deposits are larger and more sharply
defined
□ May be unilateral
– Renal papillary necrosis: Especially analgesic
nephropathy with calcified papillae; sickle cell disease
– Furosemide therapy in newborns; long-term
furosemide use in adults
– Tuberculosis
○ Cortical nephrocalcinosis
– Acute cortical necrosis (e.g., septic or hemorrhagic
shock, commonly in obstetrical complication)
– Chronic glomerulonephritis
– Alport syndrome: Hereditary nephritis and deafness
– Nephrotoxic drugs and poisoning: Amphotericin B,
methoxyflurane anesthesia, ethylene glycol
– Hemolytic uremic syndrome
– Chronic rejection of renal transplant
– Sickle cell disease
○ Combined medullary and cortical nephrocalcinosis
– Hyperoxaluria: Hereditary (altered bile metabolism)
and acquired (intestinal over absorption of oxalate;
small bowel pathology, e.g., IBD, surgery, or too much
oxalate in diet)
□ Hyperoxaluria → NC and urolithiasis → eventual
renal failure → oxalosis
□ Oxalosis = calcium oxalate crystal deposits in
vessels, bones, and organs
– AIDS-related infections: Described with
Mycobacterium avium-intracellulare, pneumocystis
carinii, Histoplasma, and cytomegalovirus
Microscopic Features
• Calcium deposition in interstitium, tubule epithelial cells,
along basement membranes
• Calcium deposition within lumen of tubules
CLINICAL ISSUES
Presentation
• Most common signs/symptoms
○ Most often asymptomatic
○ MSK may present with complication: UTI, hematuria,
urolithiasis
Demographics
• Age
○ Any
• Gender
○ M > F
• Epidemiology
○ Incidence: 0.1-6%
○ MSK: 0.5-1% general population
– ~ 18% female and 12% male calcium stone formers
DIAGNOSTIC CHECKLIST
Image Interpretation Pearls
• Unilateral, asymmetric, or segmental medullary
nephrocalcinosis → MSK
SELECTED REFERENCES
1. Koraishy FM et al: CT urography for the diagnosis of medullary sponge
kidney. Am J Nephrol. 39(2):165-70, 2014
2. Lee H: Nephrocalcinosis. In Kim S: Radiology Illustrated: Uroradiology. 2nd
ed. Berlin: Springer. 528-49, 2012
3. Aziz S et al: Rapidly developing nephrocalcinosis in a patient with end-stage
liver disease who received a domino liver transplant from a patient with
known congenital oxalosis. J Ultrasound Med. 24(10):1449-52, 2005
4. Kim YG et al: Medullary nephrocalcinosis associated with long-term
furosemide abuse in adults. Nephrol Dial Transplant. 16(12):2303-9, 2001
5. Schepens D et al: Images in nephrology. Renal cortical nephrocalcinosis.
Nephrol Dial Transplant. 15(7):1080-2, 2000
6. Dyer RB et al: Abnormal calcifications in the urinary tract. Radiographics.
18(6):1405-24, 1998
7. Toyoda K et al: Hyperechoic medulla of the kidneys. Radiology. 173(2):431-4,
1989
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