We have previously shown that in the case of PKD1, renal cyst development is likely to require somatic inactivation of the normal allele coupled to a germline PKD1 mutation.
Unsupervised analysis revealed that rHU-EPO free patients had a specific clinical/biological profile (presence of renal cyst, longer dialysis vintage, lower ferritin, and EPO and hepcidin levels compared to the control group).
These results suggest that PEP-1-FK506BP delayed cyst formation and could be a new therapeutic strategy for renal cyst formation in PKD.[BMB Reports 2017; 50(9): 460-465].
These results suggest that PEP-1-FK506BP delayed cyst formation and could be a new therapeutic strategy for renal cyst formation in PKD.[BMB Reports 2017; 50(9): 460-465].
These results suggest that PEP-1-FK506BP delayed cyst formation and could be a new therapeutic strategy for renal cyst formation in PKD.[BMB Reports 2017; 50(9): 460-465].
These results suggest that PEP-1-FK506BP delayed cyst formation and could be a new therapeutic strategy for renal cyst formation in PKD.[BMB Reports 2017; 50(9): 460-465].
The role of serum E-selectin level and E-selectin gene S128R polymorphism on the enlargement of renal cyst in patients with polycystic kidney disease: Genetic background of renal cyst growth .
The SPARC level in the renal cyst fluid of patients with ADPKD was greater than that in patients with simple renal cyst (SRC), and also greater than that found in the plasma and urine of patients with either ADPKD or SRC and normal subjects.
In this report we have used a spontaneous mouse mutant of type 3 nephronophthisis to examine whether the doxycycline-inducible synthesis of Timp-2, a natural inhibitor of matrix metalloproteinases, can influence renal cyst growth in transgenic mice.
Genetic analysis of PKD genes from peripheral blood lymphocytes and renal cyst epithelium identified a constitutional PKD1 germline mutation, p.Trp1582Ser, predicted to be pathogenic.
Genetic analysis of PKD genes from peripheral blood lymphocytes and renal cyst epithelium identified a constitutional PKD1 germline mutation, p.Trp1582Ser, predicted to be pathogenic.
Compared with PCK, the FHH.Pkhd1 strain had significantly decreased renal cyst formation that coincided with a threefold reduction in mean kidney weights.Further analysis revealed that the FHH.