Inability of vultures to digest diclofenac
Via: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1618889/


  Post-mortem examination revealed extensive visceral gout in all diclofenac-treated birds (see electronic supplementary material). Histological examination revealed significant lesions in the kidneys, liver and spleen with extensive uric acid crystal deposition.


Via: https://repository.up.ac.za/bitstream/handle/2263/26027/Complete.pdf?sequence=7


  From the mechanistic studies both diclofenac and meloxicam were directly toxic to chicken and vulture renal tubular epithelial cells following 48h of incubation. It was later shown that this toxicity was associated with an increased production of reactive oxygen species (ROS), which could be temporarily ameliorated by pre-incubation with uric acid due to its anti-oxidant activity. When cultures were incubated with either drug for only two hours, meloxicam showed no toxicity in contrast to the cellular toxicity present for diclofenac. In both cases no increase in ROS production was evident. In addition, diclofenac influenced the excretion of uric acid by interfering with p-amino-hippuric acid channels. The effect on uric acid excretion persisted after the removal of the diclofenac. It was therefore concluded that vulture susceptibility to diclofenac results from a combination of an increase in cellular ROS, a depletion of intracellular uric acid concentration and most importantly the drug’s long half-life in the vulture. 


The second link posits three mechanisms for the cause of renal failure in vultures (ref., pg. 26):


Ischaemic nephropathy with secondary visceral gout 
Organic Anion Transporter antagonism
Secondary renal toxicity with or without toxic activation