Urinary osmolality remained low at approximately 130 140 mOsm/Kg H2O and urinary electrolyte concentrations done on several samples averaged 30 mm/L for sodium, 20 mm/L for potassium and 40 mm/L for chloride.
To exclude the possibility that epinephrine infusion (in one case, Tables 1) increased urinary excretion, in a subsequent analysis we excluded that case, but urinary epinephrine remained different between AKI and controls (19.99 ± 2.62 vs. 7.48 ± 1.07 ng/mg creatinine; ANOVA p = 0.001).
In the normoalbuminuria group, the urinary NAPCR remained significantly associated with a decline in eGFR (r = 0.261, P = 0.002) in the final model, whereas urinary CCR did not (r = 0.097, P = 0.199).
In spite of these potentially helpful effects, renal arterial blood flow and urinary output remained as low as in the IAH control group.
In contrast, the deoxypyridinoline/creatinine urinary level remained stable in normal controls but increased significantly in AIA controls.
The increased levels of both urinary CCR and NAPCR remained significantly associated with progression to CKD stage 3 or greater after adjusting for several clinical factors in each multivariate model.
Overall, urinary symptoms remained higher after 1 year in the 74 Gy group (P=0.02), but this reduced on longer term follow-up (Table 6).
In the survival study, all treated animals survived PDT for at least 2 weeks and the intestinal and urinary tract remained functional.
In multiple regression analyses, urinary NAG/Cr remained as a significant risk factor after adjusting for other variables (unstandardized coefficient, 95% CI; -4.5, -8.6 to −0.5, P = 0.03).
At 2 years of age, an ammonium chloride challenge suggested that the child has incomplete dRTA; in the 7 hours of the test, the blood bicarbonates decreased to 15.6 mM, but urinary pH remained above 5.90.
