HOMEPRODUCTSCOMPANYCONTACTFAQResearchDictionaryPharmaSign Up FREE or Login

Calcium citrate ameliorates the progression of chronic renal injury.

AbstractBACKGROUND:
Metabolic acidosis is a consequence of chronic renal failure and it may produce bone demineralization, muscle proteolysis, and progression of chronic renal failure. The aim of this study was to evaluate the effects of correction of metabolic acidosis with calcium citrate in an experimental model of renal mass ablation.
METHODS:
Wistar rats were subjected to 5/6 nephrectomy and were randomly assigned to one of 4 groups: nontreated (NFX); treated with calcium citrate (1.45 g/100 g feed) (NFX-CIT); treated with captopril (500 mg/L water) (NFX-CAP); or treated with both (NFX-CAP-CIT) during 1, 10, or 20 weeks. Body weight, systolic blood pressure, proteinuria, arterial bicarbonate concentration, urine citrate excretion, plasma calcium, and inulin clearance were measured. Histologic glomerular and tubulointerstitial damage scores were measured at 1, 10, and 20 weeks, and glomerular and tubular proliferating cell nuclear antigen (PCNA)-positive cells, alpha-smooth muscle actin, and desmin staining were studied by immunohistochemistry at 1 and 10 weeks.
RESULTS:
The treated groups showed significantly less glomerular and tubulointerstitial cellular proliferation in the first week (P < 0.05), less glomerular cell transdifferentiation and higher plasma bicarbonate at 10 weeks (P < 0.05), as well as diminished histologic glomerular and tubulointerstitial damage scores at 20 weeks (P < 0.05). Inulin clearances were higher (P < 0.05), and urine protein excretion rates were lower (P < 0.05) than in the NFX non-treated group, but arterial blood pressure was not significantly different in the NFX-CIT group.
CONCLUSION:
Calcium citrate slows the progression of chronic renal injury in the 5/6 NFX model. It improves metabolic acidosis and diminishes cell proliferation and transdifferentiation without changes in systolic blood pressure.
AuthorsLiliana Gadola, Oscar Noboa, María Natalia Márquez, María José Rodriguez, Nicolás Nin, José Boggia, Alejandro Ferreiro, Silvia García, Virginia Ortega, María Luisa Musto, Paolo Ponte, Pablo Sesser, Carlos Pizarrosa, Silvana Ravaglio, Ana Vallega
JournalKidney international (Kidney Int) Vol. 65 Issue 4 Pg. 1224-30 (Apr 2004) ISSN: 0085-2538 [Print] United States
PMID15086461 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Alkalies
  • Bicarbonates
  • Drug Combinations
  • Inulin
  • Captopril
  • Calcium Citrate
Topics
  • Alkalies (pharmacology)
  • Animals
  • Bicarbonates (blood)
  • Calcium Citrate (pharmacology)
  • Captopril (pharmacology)
  • Cell Division
  • Disease Progression
  • Drug Combinations
  • Immunohistochemistry
  • Inulin (metabolism)
  • Kidney (metabolism, pathology)
  • Kidney Failure, Chronic (metabolism, pathology, physiopathology, urine)
  • Kidney Glomerulus (pathology)
  • Kidney Tubules (pathology)
  • Male
  • Nephrectomy
  • Proteinuria (etiology, urine)
  • Random Allocation
  • Rats
  • Rats, Wistar

Join CureHunter, for free Research Interface BASIC access!

Take advantage of free CureHunter research engine access to explore the best drug and treatment options for any disease. Find out why thousands of doctors, pharma researchers and patient activists around the world use CureHunter every day.
Realize the full power of the drug-disease research graph!


Choose Username:
Email:
Password:
Verify Password:
Enter Code Shown: