From: Renal failure during chemotherapy: renal biopsy for assessing subacute nephrotoxicity of pemetrexed
Orientation | Clinical situation | Importance of renal biopsy | Drugs involved |
---|---|---|---|
Prerenal failure | Weigh loss, dizziness, skin dryness, low blood pressure, tachycardia, oliguria. | No biopsy | All drugs associated with dehydration, vomiting or diarrhea |
Obstructive renal failure | Pelvic cancer localization Suspicion or demonstration of ureteral dilation No ureteral stenting in presence of peritoneal carcinosis Oliguria, anuria Hypogastric pain or in the lumbar fossa Hematuria with clots | No biopsy | All drugs inducing a lysis syndrome or renal stones |
Glomerular disease | Hypertension, edema Proteinuria composed mostly with albumin, hematuria without clots Nephrotic syndrome (plasma albumin below 30Â g/L and nephrotic range proteinuria) | Perform immediate renal biopsy | - Interferon: podocytopathy inducing clinically minimal change disease, focal segmental glomerulosclerosis [22] - Anti-VEGF agents: hypertrophy of glomerular endothelial cells, widening of the subendothelial space [23, 24] - Tyrosine kinase inhibitors: Gefitinib: minimal changes [25, 26] Sorafenib [27] - Anthracyclines: Doxorubicin: focal segmental glomerulosclerosis [28] |
Tubular disease | Proteinuria composed mostly with low weight proteins Leukocyturia No hematuria | Perform delayed renal biopsy if - If no resolution after 2 to 4Â weeks - If clinical and biological picture is not clearly in favor of tubular disease | - Antimetabolites: Methotrexate: precipitation on renal tubules and tubule cells apoptosis [29] Pemetrexed: renal tubular cells apoptosis - Alkylating agents: Platinum salts: renal tubular cells apoptosis [3, 18] Ifosfamide: acute proximal tubular injury inducing Fanconi syndrome, diabetes insipidus [30] - Hormone therapy: Androgen deprivation therapy: acute tubular injury [31] - Anti-EGFR agents: Cetuximab: hypomagnesemia due to magnesium transport channel alteration in the loop of Henle [32] - mTOR inhibitors: Everolimus: antiproliferative effects and induction of tubular cells autophagy [33] |
Interstitial disease | Cutaneous rash, liver enzymes increase, hypereosinophilia, urinary eosinophils | Essential and with no delay | - Acute interstitial disease: bevacizumab [34, 35], sunitinib [36, 37, 38], ifosfamide [39, 40], carboplatin [41], gemcitabin [38], methotrexate [38], interferon [42], Bcg therapy [43,44,45] - Chronic interstitial disease [24]: ifosfamide, carboplatin, doxorubicin |
Vascular disease | Presence of schizocytes, drop in platelet count, undetectable haptoglobin or low level in an inflammatory context Cutaneous vasculitis | Perform biopsy if platelet level compatible | VEGF inhibitors: bevacizumab [46, 47], sorafenib [48], gemcitabine [12, 13, 49, 50], sirolimus [51], afilbercept [52, 47] Antitumor antibiotic: mitomycin C [53] Interferon [54] Tyrosine kinase inhibitors: |