Opinion ID: 657211
Heading Depth: 2
Heading Rank: 1

Heading: facts

Text: 3 On October 3, 1986, Manual Porter fractured his left great toe at work. He sought treatment first from Dr. Diane Wells, an internist, who referred Mr. Porter to Bloomington Hospital. At the hospital, Mr. Porter was treated by Dr. Jones. Dr. Jones set a surgery date of October 10, 1986 to reset Mr. Porter's toe. Dr. Jones also prescribed Tylenol # 3, a pain reliever, until the surgery. 4 Because of his continuing pain, Mr. Porter called Dr. Wells on October 4, 1986. Dr. Wells' nurse practitioner gave Mr. Porter samples of Motrin, a prescription form of ibuprofen, and Vicoden, an acetaminophen. Dr. Wells did not recall reviewing the message and response to Mr. Porter's call; however, she knew of no medical condition that would preclude Mr. Porter's taking ibuprofen. 2 Mr. Porter took fourteen Motrin tablets between October 13, 1986 and November 7, 1986. Mr. Porter took approximately fifteen Advil tablets between November 7 and November 18, 1986. 5 Other than his injured toe, Mr. Porter had no significant health problems prior to November 19, 1986. On that day, he returned to Dr. Wells' office with complaints of headache, vomiting, and blurred vision. Dr. Wells examined Mr. Porter and found that he was suffering from high blood pressure, significant papilledema (swelling of the fundi of the eyes), and puffiness of the face. Based on these symptoms, Dr. Wells had Mr. Porter transferred by ambulance to Bloomington Hospital for treatment by Dr. Richard Combs, a nephrologist. Dr. Combs conducted a series of tests which revealed that Mr. Porter was experiencing kidney failure from which he would not recover. Dr. Comb's diagnosis of Mr. Porter's condition at that time was acute tubular necrosis secondary to ibuprofen; specifically, upon Mr. Porter's discharge on December 5, Dr. Combs wrote: The patient's ... Ibuprofen reactions have both an interstitial and glomerular reaction and I believe this can explain all of his problems. Loose Pleadings VI, ex. 2. 6 In January 1987, Mr. Porter was readmitted to Bloomington Hospital for a renal biopsy. That biopsy revealed rapidly progressive glomerulonephritis (RPGN). Glomerulonephritis is an inflammation and disease of the filtering unit in the kidney that causes decreased renal function. RPGN describes how rapidly the kidney function decreases when inflamed by glomerulonephritis. RPGN is a rare and serious disease which leads to end-stage renal failure in a significant number of cases without any ibuprofen or other drug use. Mr. Porter suffered from the types of RPGN known as anti-glomerular basement membrane glomerulonephritis (anti-GBM) and membranoproliferative glomerulonephritis (MPGN). Ibuprofen is not known to be a cause of these or any other types of RPGN. 7 Mr. Porter's biopsy also indicated that he suffered from interstitial nephritis which often occurs as a secondary result of glomerulonephritis. There is no scientific evidence that the opposite is true--that interstitial nephritis will progress to RPGN. Studies have linked the use of ibuprofen with interstitial nephritis. 8 The experts examining Mr. Porter's records have explained Mr. Porter's kidney failure in two ways. Dr. Fred Ferris, who participated in the transplant, and Dr. William Dick, Mr. Porter's treating nephrologist at Bloomington Hospital, testified that Mr. Porter's kidney failure was caused by anti-GBM RPGN. The other experts testified that Mr. Porter's failure was caused by RPGN, but did not identify which type of RPGN disease process, anti-GBM or MPGN, caused the failure. 9 In their motion for summary judgment, defendants contended that the record failed to establish a genuine issue of fact that ibuprofen is capable of causing anti-GBM, MPGN, or any other type of RPGN, or that ibuprofen caused Mr. Porter's RPGN. Furthermore, they argued that the record failed to establish that a genuine issue of fact existed with regard to ibuprofen causing a change from interstitial nephritis to RPGN.