Table 2.
High-dose IL-2–associated nephrotoxicity from selected series
| Reference and Patients (n) | Systemic Manifestations | Kidney Syndrome | Outcome Data |
|---|---|---|---|
| Shalmi et al.22 | |||
| 10 | Capillary leak syndrome, hypotension, weight gain, edema, ascites, pleural effusions | Nine of 10 developed increase in sCr (mean 1.9 mg/dl); nine of 10 developed trace/1+proteinuria | Measured GFR decreased in nine of 10; of these, five had <30% decrease in ERPF, whereas four had increase in ERPF (suggesting intrinsic kidney injury) |
| Guleria et al.23 | |||
| 199 | Capillary leak syndrome, hypotension, edema, weight gain | Oliguria, AKI (13%), proteinuria (11%), hematuria, pyuria, granular casts (30%) | More severe AKI with NSAID coadministration, discontinued IL-2 for AKI, partial or complete kidney recovery after discontinued IL-2 |
| Belldegrun et al.24 | |||
| 99; IL-2 (n=23); IL-2 + LAK cells (n=76) | Capillary leak syndrome, hypotension, abdominal distension, weight gain | 90% Developed increased sCr (mean 3.44 mg/dl), oliguria (77.5%), mean FeNa =0.07% | Complete recovery of kidney function: 84% at 2 wk, 95% at 1 mo; faster kidney recovery in patients with baseline sCr <1.5 mg/dl |
| Memoli et al.25 | |||
| Nine: all received concomitant NSAID | Not mentioned | Increased sCr, decreased urine output and FeNa over 5 d of IL-2 without renal dose dopamine | Complete recovery of kidney function after discontinued IL-2; renal dose dopamine on day 3 of IL-2 prevented increase in sCr and decrease in urine output and FeNa |
sCr, serum creatinine; ERPF, effective renal plasma flow; NSAID, nonsteroidal anti-inflammatory drug; LAK, lymphokine-activated killer cell; FeNa, fractional excretion of sodium.