Table 2.
Gaps in data requiring additional research
| End Point | CKD Population (Stage) | Gaps in Data |
|---|---|---|
| Kidney stones | 1–3b | Standards for definition of clinical stone event do not exist |
| Standards for radiographic assessment of stone burden are not available | ||
| Quantitative methods for stone assessments which avoid ionizing radiation not available | ||
| 4–5a | No reported studies | |
| Slope of GFR | 1–4 | Changes in rate of decline by CKD stage are not well defined |
| Patient-patient variability is not well understood | ||
| Discontinuity in eGFR formula performance as children transition to adulthood (52) | ||
| Urine oxalate excretion | 1–3a | Correlation between spot urine oxalate/creatinine and 24-h urine oxalate excretion not established |
| Confirmation of the relationship of urine oxalate excretion and incident ESKD in a validation cohort | ||
| Relationship of urine oxalate and plasma oxalate over the range of GFR not well described | ||
| Interplay between urine oxalate and plasma oxalate and the development of intrarenal calcium oxalate crystals and kidney damage are poorly understood | ||
| Quantitative effect of reduction of urine oxalate on GFR and stone burden is not known | ||
| 3b–5a | Effect of low GFR on urine oxalate has not been described; urine oxalate expected to decrease at low GFR due to declining kidney function. | |
| Plasma oxalate concentration | 1–3aa | Not widely used in clinical practice; minimal data available |
| Biologic variation not characterized | ||
| Association with later irreversible morbidity and mortality not studied | ||
| 3b–5 | Biologic variation not well characterized | |
| Standards for sample collection, processing, and measurement are lacking | ||
| Interpretation requires correction for GFR due to kidney clearance | ||
| Dynamic equilibrium between plasma oxalate and tissue oxalate stores is poorly understood | ||
| Predictive value of elevated plasma oxalate on clinical end points including risk for ESKD not defined | ||
| Magnitude of decrease in plasma oxalate needed to achieve a meaningful clinical benefit not known | ||
| Quantitative effect of plasma oxalate on systemic oxalosis is not known |
Evidence supporting the association of potential end points with disease progression differs by CKD stage. Urine oxalate is a more useful biomarker when kidney function is preserved but is expected to decrease as GFR falls to low levels. Plasma oxalate becomes the biomarker of choice when the failing kidney is no longer able to adequately excrete oxalate into the urine (CDK stages 3b–5). Additional study is needed to determine whether plasma or urine oxalate performs better as a biomarker in CKD stage 3.
a
Minimal data available.