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Treating complications of hyperphosphatemia in diabetic kidney disease
Summary Data Summary
Applicant Rieg, Timo
E-Mail Address trieg@health.usf.edu
Project Title Treating complications of hyperphosphatemia in diabetic kidney disease
CBU ID 21AU4195
External SubContract ID 36305-2
Diabetic Complication Nephropathy
Funding Program Group Pilot & Feasibility [PF2021]
Abstract Half of diabetic patients ultimately develop diabetic kidney disease (DKD),
which is the leading cause of chronic kidney disease (CKD). In CKD patients,
heart failure is highly prevalent and strongly associated with mortality.
Elevated plasma phosphate levels (hyperphosphatemia) are common in CKD and are a
serious risk factor in the progression of cardiovascular disease (CVD) and
vascular calcification (VC). Of note, an increase in fibroblast growth factor 23
has been shown to reduce plasma phosphate in the early stages of CKD at the
expense of developing left ventricular hypertrophy. Due to the kidney’s ability
to increase phosphate excretion in response to elevated parathyroid hormone
levels, hyperphosphatemia only develops in later stages of CKD. In the proximal
tubule of the kidney, the sodium/phosphate cotransporter 2a (Npt2a) plays an
important role in reabsorbing 70% of the filtered phosphate. Currently,
treatment of hyperphosphatemia is limited to dietary phosphate restriction,
phosphate binders and nicotinamide, which unfortunately often are ineffective.
We recently described a new approach to manage hyperphosphatemia by inhibiting
Npt2a with a newly developed Npt2a inhibitor (Npt2a-I, PF-06869206). We observed
a significant reduction in plasma phosphate levels as well as parathyroid
hormone levels in normal and CKD mice after an acute treatment with Npt2a-I.
Therefore, we hypothesize that chronic treatment of Npt2a-I in DKD mice will
decrease the progression of hyperphosphatemia associated complications. Our
specific aims will study the therapeutic effect of Npt2a-I in the progression of
hyperphosphatemia associated CVD and VC. Studies will be carried out in db/db or
db/db uninephrectomized (Nx) or db/db Npt2a-/- Nx mice. The latter will serve as
a proof-of-concept experiment. This study will investigate a new therapeutic
approach towards hyperphosphatemia and its associated progression of CVD and VC
in the context of diabetes. These experiments will be instrumental to determine
if Npt2a inhibition is a valuable therapeutic intervention for diabetic
complications.
Application PDF Application Research Plan
Status Contract Executed
Key Personnel Dr. Linto Thomas, Postdoctoral Fellow, University of South Florida
Salary Total Costs 42732
Supply Total Costs 22000
Equipment Total Costs 0
Travel/Other Total Costs 2000
Direct Costs 66732
Indirect Costs Proposed 33032
Total Costs Proposed 99764
Total Costs Approved 99764
Start Date 7/1/2021
End Date 6/30/2023
IFO Name Kern, Eric
IFO E-Mail Address ericmkern@usf.edu
IACUC/IRB No. IS00007525
IACUC/IRB Institution University of South Florida
Entity ID No. D16-00589 (A4100-01)
Report Request Date 6/30/2023
T1D NO
TypeCount
Invoices 7
Progress Reports 1
Data Submission


Invoices
UrlCBU IDExternal IDInstitutionDateDirectIndirectInvoiceBalancePDF
  View  21AU419536305-2University of South Florida8/23/2023$7,625.81$3,774.77$11,400.58$17,531.33View PDF
  View  21AU419536305-2University of South Florida7/12/2022$8,011.61$3,965.75$11,977.36$17,531.33View PDF
  View  21AU419536305-2University of South Florida5/25/2022$9,482.79$4,693.98$14,176.77$17,531.33View PDF
  View  21AU419536305-2University of South Florida4/28/2022$10,759.33$5,325.87$16,085.20$17,531.33View PDF
  View  21AU419536305-2University of South Florida4/19/2023$2,178.57$1,078.40$3,256.97$17,531.33View PDF
  View  21AU419536305-2University of South Florida12/2/2022$5,739.19$2,840.90$8,580.09$17,531.33View PDF
  View  21AU419536305-2University of South Florida10/27/2022$11,207.83$5,547.87$16,755.70$17,531.33View PDF


Reports
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