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Because in actual practice renal failure will prolong rocuronium and if you plan on extubating the patient you aren’t doing yourself any favors by using it in a patient was with renal failure when you have an option that doesn’t undergo renal clearance.
That isn't really true; even if it was, it wouldn't be a problem if you reversed everybody with sugammadex or neostigmine. The data is pretty solid that residual NMB is a real thing and that nearly everyone should get at least some reversal treatment. I contend that in actual practice rocuronium is just fine for patients with renal failure, and that avoidance of its use in ESRD is a lesser crime of academic dogma that ought to die alongside greater crimes like proving ventilation before giving relaxant.
Again, from the package insert: "When compared to patients with normal renal and hepatic function, the mean clinical duration is similar in patients with end-stage renal disease"
Its effect is only prolonged in patients with hepatic disease, which is unsurprising because rocuronium is metabolized in the liver and excreted in bile. There is a small portion excreted in urine, but not much. There is a much much less active metabolite that "has been rarely observed in the plasma or urine of humans" (also per the package insert). In any case, the end of its clinical effect is primarily brought about by redistribution, not metabolism or excretion.
The half-life of a dose of rocuronium in a normal patient and in a kidney transplant patient is exactly the same:

Cis-atracurium is inferior to rocuronium in clinically relevant ways - you have to go to the fridge to get it, it has a much slower onset time, and there's no sugammadex equivalent for reversal, necessitating the use of neostigmine, a dirty drug.