Proteinuria or albuminuria?

has themajor role inwater absorption in collecting duct principal cells. Cyclophosphamide-induced hyponatraemia may correspond to type D (nephrogenic syndrome of inappropriate antidiuresis) among the four subtypes of syndrome of inappropriate antidiuresis proposed by Robertson [3]. It is interesting that cyclophosphamide can suppress the production of interleukin-1 (IL-1) and tumour necrosis factor (TNF) from human monocytes through its metabolites. Nuclear factor kappa B (NF-κB) and pro-inflammatory cytokines may downregulate V2R and AQP2 in acute inflammatory conditions, and the authors proposed a hypothesis that cyclophosphamide-induced suppression of IL-1 and TNF-α may upregulate V2R and AQP2 in the kidney. According to Hasler et al., NF-κB is a negative regulator of AQP2 transcription at a post-V2R level [4]. However, it is not clear whether the expression of V2R may be altered by pro-inflammatory cytokines in other conditions than sepsis animal models. Studies are required to provide direct evidences showing that the vasopressin–V2R–AQP2–cAMP pathway in the renal collecting duct is affected by cyclophosphamide administration or cyclophosphamide metabolites and which level (V2R or post-receptor) is the major determinant.