The macula densa of the nephron helps maintain tubular flow by adjusting dilation of the afferent arteriole of the nephron. When salt is low, its COX enzymes synthesize PGI2 which dilate the afferent arteriole. NSAIDs inhibit COX, blocking synthesis of PGI2 and so indirectly inhibiting afferent arteriole dilation. Two weeks ago our patient was put on ibuprofen, a non-selective COX inhibitor. This lead to all these effects, shutting off blood supply to the nephrons, creating an artifically induced drop in blood flow that looks has elevated BUN and creatinine, but maintains the 15:1 ratio.
so I was stuck on this because his BUN /creatinine ratio led me to think he had an intrinsic renal dysfunction. And a PGI2 inhibition would lead to a pre-renal azotemia, where the BUN/ creatinine ratio would be more than 20. I know that NSAIDs inhibit PGIS. But how are you supposed to cross out induction of distal tubular acidosis?