Table 2.
Modifiable CKD progression risk factors and potential treatment targets evaluated in the CRIC Study
| Risk Factor | Potential Treatment Target |
|---|---|
| Behavioral | Smoking |
| Healthy dietary patterns | |
| ↑ Urine sodium and potassium intake | |
| Fragmented sleep | |
| Hard illicit drug use (heroin) | |
| Poor self-management behaviors | |
| Medication nonadherence | |
| Genetic | APOL1 gene variants |
| SNPs in LINC00923 (RNA gene expressed in the kidney) | |
| RAAS genes | |
| Cardiovascular | ↑ Systolic BP |
| Treatment-resistant hypertension | |
| Aortic stiffness | |
| Heart failure | |
| Atrial fibrillation | |
| Metabolic | ↑ FGF23 |
| ↓ Serum bicarbonate | |
| ↓ Net acid excretion | |
| ↑ Urinary oxalate | |
| ↑ Serum uric acid | |
| Novel factors | 20-HETE (AA metabolite) |
| Inflammation (fibrinogen, TNF-α, albumin) | |
| Urine NGAL | |
| AKI |
CRIC, Chronic Renal Insufficiency Cohort; SNP, single-nucleotide polymorphism; RAAS, renin-angiotensin-aldosterone system; FGF23, fibroblast growth factor 23; 20-HETE, 20-hydroxyeicosatetraenoic acid; AA, amino acid; NGAL, neutrophil gelatinase-associated lipocalin.