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Dietary potassium citrate does not harm the pcy mouse
Judith A Tanner1, George A Tanner
1Department of Cellular and Integrative Physiology, Indiana University School of Medicine, 635 Barnhill Drive, Indianapolis, Indiana 46202, USA.
Experimental Biology and Medicine (Maywood, N.J.)
|December 25, 2004
Summary
Potassium citrate in feed did not worsen kidney disease in pcy mice, a model for human nephronophthisis (NPHP3). This finding suggests citrate therapy may still be viable for autosomal-dominant polycystic kidney disease (ADPKD).
Area of Science:
- Nephrology
- Genetics
- Pharmacology
Background:
- Inherited kidney diseases causing multiple cysts often lead to kidney failure.
- Current therapies lack definitive treatments to slow cystic kidney disease progression.
- Animal models are crucial for investigating potential therapeutic interventions.
Purpose of the Study:
- To evaluate the effect of potassium citrate supplementation in feed on renal cystic disease progression in pcy mice.
- To determine if citrate treatment, previously shown to benefit some models, adversely affects the pcy mouse model of nephronophthisis (NPHP3).
Main Methods:
- Male homozygous pcy mice were administered either regular feed or feed supplemented with 6% potassium citrate.
- Mice had ad libitum access to water and treatment began at 3 weeks of age.
- Survival rates of treated and untreated groups were compared to assess disease progression.
Main Results:
- Ingesting potassium citrate via feed did not significantly alter the survival curves of pcy mice.
- The progression of renal cystic disease in the pcy mouse model was not affected by dietary potassium citrate.
- This indicates citrate treatment is not detrimental to this specific model of cystic kidney disease.
Conclusions:
- Dietary potassium citrate does not impact renal cystic disease progression in the pcy mouse model, which resembles human nephronophthisis type 3 (NPHP3).
- Citrate treatment is not recommended for NPHP3 based on these findings.
- The lack of adverse effects removes a barrier for considering citrate therapy in autosomal-dominant polycystic kidney disease (ADPKD).