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1 ding/trafficking defects that lead to type I cystinuria.
2 est that 4F2-lc6 is a new candidate gene for cystinuria.
3 al treatment, and follow-up of patients with cystinuria.
4 eutic strategy for the clinical treatment of cystinuria.
5 ove the diagnosis and clinical management of cystinuria.
6 fective in vivo in a knockout mouse model of cystinuria.
7 ughput, cost-effective diagnostic method for cystinuria, and for point-of-care clinical monitoring.
8 s, pediatric and adult urologists experts in cystinuria, and the Metabolic Nephropathy Joint Working
9  formation in the Slc3a1(-/-) mouse model of cystinuria by increasing the solubility of urinary cysti
10                                          The cystinuria gene SLC7A9 (n=19) was most frequently mutate
11 hree conditions (albinism, alkaptonuria, and cystinuria) have been identified, but the mutations resp
12 fluids such as urine and blood (detection of cystinuria, identification of penicillin anaphylaxis, ur
13  Bartter syndrome, primary hyperoxaluria and cystinuria, in patients attending kidney stone clinics i
14  management of both adults and children with cystinuria, including diagnosis, surgery, and medical tr
15                                              Cystinuria is an autosomal recessive hereditary disorder
16                                              Cystinuria is an incompletely dominant disorder characte
17                                              Cystinuria is an inherited defect in renal tubular and i
18                                              Cystinuria is discussed relative to mutations in SLC3A1
19                                              Cystinuria is linked to specific mutations in the rBAT s
20                                 Diagnosis of cystinuria is made typically by ion-exchange chromatogra
21                                              Cystinuria is the commonest inherited cause of nephrolit
22 acid transporter that is associated with the cystinuria-related type II membrane glycoprotein, rBAT (
23 studies of patients suffering from hypotonia-cystinuria syndrome (HCS) have revealed a deletion of a