Analysis Tools
renal/urinary system
| N |
• male homozygotes show no signs of renal tubule cell injury or Randall's plaques, no glomerular or vascular changes, and no evidence of autoimmune glomerulonephritis
• also, neither calculi nor calcifications are found in the renal parenchyma, pyelocaliceal system or ureter of any mutant male mice
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• male homozygotes display a significantly higher kidney weight than age- and body weight-matched wild-type males (220 6 mg vs 201 6 mg, respectively)
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• male homozygotes display a ~2-fold increase in urine calcium levels relative to wild-type males, along with microscopic crystals and heterogeneous material; in contrast, serum calcium levels remain unaffected
• hypercalciuria appears to be secondary to mislocalization and possibly malfunction of PMCA, an important calcium pump protein in the mouse distal nephron
• notably, female homozygotes show urine calcium levels comparable to those of wild-type females
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• male homozygotes display impaired Ca++ active reabsorption from urine
• however, renal function, as assessed by creatinine clearance, remains normal
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urolithiasis
(
J:82490
)
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• starting at 2 months of age, male homozygotes display a higher incidence of urinary bladder calculi that increases with age
• at 4 months of age, calculi are evident as either early urinary calculi with relatively abundant matrix debris or as frank solid stones
• at 5 months of age, 80% of male homozygotes display overall urinary calculi formation within the bladder vs only 19% of wild-type males
• at 5 months of age, early urinary bladder calculi are detected in 67% of male homozygotes vs 19% of wild-type males, while frank urinary stones are noted in 13% of male homozygotes vs none of wild-type males
• 4 of 7 urinary solid stones contained calcium phosphate and/or calcium oxalate while 6 contained nonspecific cellular/organic material
• at 5 months, 31% of mutant urinary calculi show positive Von Kossa staining indicating calcium deposition, whereas all wild-type calculi show negative staining
• no urinary calculi or stones are observed in female mutant or wild-type mice at any age examined
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homeostasis/metabolism
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• male homozygotes display a ~2-fold increase in urine calcium levels relative to wild-type males, along with microscopic crystals and heterogeneous material; in contrast, serum calcium levels remain unaffected
• hypercalciuria appears to be secondary to mislocalization and possibly malfunction of PMCA, an important calcium pump protein in the mouse distal nephron
• notably, female homozygotes show urine calcium levels comparable to those of wild-type females
|
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• male homozygotes display impaired Ca++ active reabsorption from urine
• however, renal function, as assessed by creatinine clearance, remains normal
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growth/size/body
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• male homozygotes display a significantly higher kidney weight than age- and body weight-matched wild-type males (220 6 mg vs 201 6 mg, respectively)
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