Table 2.
Risk factors for developing severe COVID-19 disease
| Variables | Low risk | Intermediate risk | High risk |
|---|---|---|---|
| Age (years) | ≤65 | 65–≤75 | ≥75 |
| CKD | eGFR ≥60 mL/min/1.73 m2 and/or no/low-grade proteinuria | eGFR ≥30 mL/min/1.73 m2 and <60 ml/min/1.73 m2 and/or proteinuria <3.5 g/day | eGFR <30 mL/min/1.73 m2 and/or proteinuria ≥3.5 g/day |
| Chronic lung disease | No | No | Yes |
| Hypertension/CVD | No | Yes | Yes |
| Diabetes mellitus | No | No | Yes |
| Disease activity | Remission/low activity | - | Moderate/high/severe |
| Immunosuppression | Monotherapy (non-glucocorticoid-based IS and no RTX, CYC or MMF | - | Any use of glucocorticoids, RTX, or CYC, multiple IS therapies |
| Vaccine response (humoral) | Yes (with high antibody titres) | Yes (with low antibody titres) | No |
| Previous COVID-19 severity | Mild | Moderate | Severe |
| Previous severe infections (especially viral) | No | No | Yes |
Risk stratification might help prioritize the need for booster vaccinations. Some of these are based on no/very limited evidence, mainly due to a lack of good studies focusing on patients with immune-mediated kidney diseases. For example, we don't know if patients with nephrotic-range proteinuria have a higher risk of contracting severe COVID-19. Similarly, a severe disease course might protect from future severe COVID-19, but it seems plausible that these patients will not mount very effective protection (i.e. antibodies) because they usually have more comorbidities and might have received medication impairing immune response. CVD, cardiovascular disease; CYC, cyclophosphamide; IS, immunosuppression; RTX, rituximab