Opinion
28930/2001
03-21-2019
PUBLIC ADMINISTRATOR OF KINGS COUNTY as Administrator of the Estate and of the Goods, Chattels, and Credits which were of Marietta Avetisian, Surain Avetisian, Individually and Anida Avetisian, Individually, Plaintiffs, v. NEW YORK PRESBYTERIAN HOSPITAL-NEW YORK WEILL CORNELL CENTER, as Successor to New York Hospital, William T. Stubenbord, M.D., Susan Boolbol, M.D., Sandip Kapur, M.D., Saint Vincent's Catholic Medical Center of New York, and James Pacholka, M.D., John Doe M.D., No. 1—4, Jane Doe M.D. # 1—4, Defendants.
Frank A. Delle Donne, Esq. Monoco & Monoco, LLP Attorney for Plaintiffs7610-7612 13th Avenue, Second Floor Brooklyn, New York 11228 William Brady., Esq. Martin Clearwater and Bell Attorney for Defendants New York Presbyterian Hospital- New York Weill Cornell Center as successor to New York Hospital, William T. Stubenbord, M.D., Susan Boolbol, M.D. and Sandip Kapur, M.D.,220 East 42 Street New York, New York 10017-5842 Steven E. Garry, Esq. Attorney for Defendants Saint Vincent's Catholic Medical Center of New York and James Pacholka, M.D., 44 Wall Street New York, New York 10005
Frank A. Delle Donne, Esq.
Monoco & Monoco, LLP
Attorney for Plaintiffs7610-7612 13th Avenue, Second Floor
Brooklyn, New York 11228
William Brady., Esq.
Martin Clearwater and Bell
Attorney for Defendants
New York Presbyterian Hospital
New York Weill Cornell Center as
successor to New York Hospital,
William T. Stubenbord, M.D., Susan
Boolbol, M.D. and Sandip Kapur, M.D.,220 East 42 Street
New York, New York 10017-5842
Steven E. Garry, Esq.
Attorney for Defendants Saint Vincent's Catholic Medical Center of New York
and James Pacholka, M.D.,
44 Wall Street
New York, New York 10005
Lara J. Genovesi, J.
Recitation, as required by CPLR § 2219(a), of the papers considered in the review of this motion:
Papers Numbered
Notice of Motion/Cross Motion/Order to Show Cause and Affidavits (Affirmations) Annexed 1, 2
Opposing Affidavits (Affirmations)
Reply Affidavits (Affirmations) 3, 4
Other Papers: Supplemental Affirmations, Hearing Exhibits 5-7
Introduction
Defendants, New York Presbyterian Hospital-New York Weill Cornell Center as successor to New York Hospital, William T. Stubenbord, M.D., Susan Boolbol, M.D. and Sandip Kapur, M.D., move by order to show cause, sequence number 16, seeking an order (1) pursuant to Frye v. United States and/or Parker v. Mobil Oil Corp . precluding plaintiff's expert from offering any evidence at trial that the plaintiff decedent Marietta Avetisian was caused to develop amyloidosis as a result of the extravasation of urine into the peritoneum following a kidney transplant, on the ground that such a theory of causation has no basis in the medical literature and it otherwise lacking in foundation; (2) or in the alternative directing a hearing in accordance with Frye and Parker; (3) and any such other relief as the court deems just and proper.
Plaintiffs oppose this application and cross move by motion, sequence number 17, seeking an order precluding defendants from offering expert testimony that the decedent's amyloidosis was pre-existing prior to the February 9, 1999, renal transplant surgery and for such other and further relief as this Court deems just and proper.
Defendants Saint Vincent's Catholic Medical Center of New York and James Pacholka, M.D. take no position.
Procedural History
Defendants moved on February 22, 2018. Plaintiffs cross moved on March 7, 2018. A hearing was scheduled for June 12, 2018. On or about May 16, 2018, this Court was advised that plaintiff's expert, Dr. Gershwin, who submitted an affidavit in opposition to defendant's motion with articles to support his position, was no longer available to testify. As a result, the matter was scheduled for a conference on June 1, 2018. Counsel for plaintiffs stated that their new expert was adopting the literature submitted by Dr. Gershwin. Thereafter, the June 12, 2018, hearing date was vacated, and the parties entered into a briefing schedule for supplemental opposition and reply. After oral argument on September 20, 2018, the matter was scheduled for a hearing. A hearing took place on December 13, 2018 and December 14, 2018 and the matter was submitted on January 22, 2019.
Background
This is a medical malpractice action to recover damages for personal injuries and the wrongful death of plaintiff Marietta Avetisian. The decedent was 38 years of age when she was admitted as a patient at New York Presbyterian Hospital-New York Weill Cornell Center as successor to New York Hospital (NY Presbyterian Hospital). It is undisputed that she had an extensive medical history including psoriatic arthritis, a bilateral total knee replacement, end stage renal disease, dialysis, and an enlarged spleen.
On February 9, 1999, while a patient at NY Presbyterian Hospital, the decedent underwent renal transplant surgery. Post operatively, a renal biopsy was performed on February 17, 1999, and was described within normal limits. Although the decedent had low urine output, she was discharged. On February 22, 1999, the decedent was seen in the Rogosin Institute clinic for her post-transplant outpatient treatment. On March 1, 1999, she was readmitted to NY Presbyterian Hospital with a probable urine leak. Corrective surgery was completed on March 3, 1999, by defendant Dr. Sandip Kapur. The corrective surgery operative note written by Dr. Nicholas Garcia, a junior resident, states that "ureter sewn to peritoneum not bladder" (see Cross Motion, Operative Note, Exhibit B).
Post-operatively, the decedent developed heart failure. By March 16, 1999, she was much improved and was discharged on March 17, 1999. Her renal function improved to a normal creatine of 1.4. On March 19, 1999, the decedent missed a scheduled appointment at the Rogosin Institute clinic. On March 23, 1999, hospital staff contacted the decedent and she presented the following day "pale, dyspneic, cachetic, and unable to walk without assistance" (Order to Show Cause, Affirmation in Support at ¶ 21). Her lungs were filled with fluid. She had a white coating on her tongue. The decedent refused to be admitted and was not taking her cardiac medication (see id. at ¶ 22).
On March 29, 1999, the decedent was admitted to NYU Medical Center. She presented with shortness of breath, a distended abdomen and abdominal pain. The impression, after examination in the emergency department, was ascites or a small bowel obstruction (see id. at ¶ 23). "An abdominal CT scan revealed ‘huge ascites — hypodense,’ not suggestive of a hemorrhage. The CT scan was also significant for splenomegaly and an atrophic native kidney. The peritoneal fluid tests were determined not to be suggestive of a urinary leak" (see id. at ¶ 26). A progress note dated March 30, 1999, stated that "[s]he developed leak of urine through wound. She was reexplored & by report her ureter was anastomised [sic ] to peritoneum-ureter was reanastomised [sic ] to her bladder & she began to make urine" (Cross Motion, Delle Donne Affirmation at ¶ 9). Amyloid was first noted in plaintiff's medical records on April 1, 1999. By April 1, 1999, "the impression was that the decedent was suffering from ascites of unclear etiology" (id. at ¶ 28). On April 6, 1999, the ascites tested positive for candida (see id. at ¶ 29). On April 19, 1999, "the transplant physician documented ‘[n]o urine leak into the peritoneum,’ but also noted that a rise in creatine levels was likely due to rejection." (id. at ¶ 30).
As the decedent's hospitalization at NYU progressed, it became increasingly likely that she would reject the donor kidney because her immunosuppressants were being held in order to treat the Candida infection. The remainder of the decedent's two month hospitalization at NYU was spent attempting to determine a cause of her ascites and treating her infection. It was determined that she had a urinary tract infection (UTI), and her uretal stents were removed. (id. at ¶ 31).
She was discharged in June 3, 1999 but returned on July 8th. A sonogram revealed "a highly resistive index, consistent with acute rejection, and bloody ascites. The decedent was given antibiotics for presumptive sepsis. In addition, she required emergent dialysis, and was diagnosed with acute renal failure" (id. at ¶ 33). "On July 9th, the Transplant Attending stated that the decedent had undergone a renal transplant that was complicated by ‘placement [of the] ureter to [the] peritoneum resulting in fungal peritonitis ’ (Id.). There was no indication as to the source of this information" (id. at ¶ 35). Paracentesis was performed, and the results were consistent with spontaneous bacterial peritonitis. "The decedent was given antibiotics, although peritoneum and blood cultures were negative. Accordingly, it was thought that her presentation was not related to infection, but to acute rejection. All antibiotics except bactrim were eventually discontinued on July 16th" (id. at ¶ 36). The hospital staff was unable to determine the cause of the ascites. After expressing her desire to leave on July 20th, the decedent was released against medical advice on July 22, 1999. (see id. at ¶ 39).
Nearly six months later, the decedent was admitted to Saint Vincent's Medical Center on January 8, 2000. On May 26, 2000, a contraindicated splenectomy was performed by Dr. James Pacholka. Plaintiff died at St. Vincent's Medical Center six months later on July 8, 2000 (see id. at ¶ 12). At his deposition, Dr. Pacholka stated that the splenectomy was difficult because the decedent had a "frozen abdomen" meaning that all of the organs were "fixed", sticking to each other, and not easily movable (see id. ). Dr. Pacholka opined that this frozen abdomen was due to her amyloidosis (see id. ).
After autopsy, it was discovered that the decedent had severe amyloid deposits in all her organs, including her native kidney. However, no amyloid was found in the donor kidney (see Order to Show Cause, Goldberg Affirmation at ¶ 3; see also Exhibit R, Autopsy Report). The amyloid deposits were not tested at the time of autopsy. As such, the specific type of amyloid found is unknown. According to the autopsy report, the decedent suffered from, inter alia , "renal amyloidosis complicated by dehiscence of ureter to bladder anastomosis", "candida albicans peritonitis", "hepatic amyloidosis", "cardiac amyloidosis" and "thyroid amyloidosis" (Order to Show Cause [1], Exhibit R, Autopsy Report). The cause of death is listed as "multiple complications following renal transplant for treatment of renal failure due to reactive systemic amyloidosis due to psoriatic arthritis" (id. ).
Amyloidosis
While there are 36 different types of amyloidosis, the disease is mainly distinguished as either primary or secondary amyloidosis. Primary or AL amyloidosis is characterized by amyloid deposits in the blood. "AL amyloidosis means amyloid light-chain. The light chain refers to the light chain of an immunoglobulin or antibody molecule. Light-chain amyloidosis is the most common type of amyloid we see in a referral center" (Hearing transcript at p 138). AL amyloid is treated as a type of cancer and has a poor prognosis (see id. at p 138).
Secondary or AA amyloidosis is characterized by amyloid deposits in the organs (see Hearing Transcript at p 49). "AA amyloidosis is a systemic disease that almost invariably affects and compromises the kidneys, more rarely the digestive tract, liver or heart. It occurs along with chronic infectious or inflammatory diseases such as psoriatic arthritis" (Gorevic Affidavit dated January 18, 2018 at ¶ 11). AA amyloidosis "is characterized by the tissue deposition of fibrils of amyloid, and they are seen where there is an elevation of something called the SAA protein" (see Hearing Transcript at p 56). AA amyloidosis is most commonly, approximately 60% of the time, associated with rheumatic diseases such as rheumatoid arthritis ; 10-20% of the time it is associated with inflammatory bowel disease ; 10% of the time it is associated with chronic infection; a small percentage of patients are predisposed to this amyloidosis based on their ethnicities or history of Familial Mediterranean fever ; and approximately 3-4% of the time, it may be associated with psoriasis, psoriatic arthritis or spondylarthropathy (see Hearing Transcript at pp 135-137). Approximately 10% of the time, the cause is unknown (see id. at p 137). DRA or dialysis related amyloidosis is a distinct form of amyloid related to the dialysis process. The incidence of this type of amyloid is decreasing, but it is a complication of chronic ambulatory peritoneal dialysis and hemodialysis (see id. at 139).
Plaintiff's Expert
Dr. Mark Poznansky specializes in general infectious disease medicine, specifically in immune compromised or transplant patients. He is not specialized in Rheumatology or Hematology, and it is not part of his practice to research amyloidosis or diagnose and treat patients of amyloidosis (see Hearing Transcript at pp 44-45, 47). Dr. Poznansky submitted an affidavit dated July 2, 2018. Annexed thereto was the affidavit of plaintiff's prior expert, whose opinion and accompanying medical literature was adopted by Dr. Poznansky, as well as an additional 15 medical articles (see Plaintiff's Supplemental Affirmation [5], Exhibit D). Further, plaintiffs provided a supplemental exchange with three additional articles at the hearing, which was marked into evidence as plaintiff's exhibit 1.
Annexed as exhibit A to Dr. Poznansky's affidavit is the affidavit of plaintiffs' prior expert, whose name is redacted, dated February 15, 2018, as well as 14 articles, separated therein as M1 through M14. Exhibit B to Dr. Poznansky's affidavit includes an additional 15 articles and one page of the decedent's medical records. Exhibit C is the decedent's death certificate and autopsy report.
This submission includes the full article entitled "Systematic amyloidosis involving the diaphragm and acute massive hydrothorax during peritoneal dialysis". The abstract of this article was included in Poznansky's original submission.
Plaintiffs allege that the decedent suffered from a urine leak as a result of the surgeon mistakenly sewing the ureter to the peritoneal lining instead of the bladder. Dr. Mark Pozansky opines that the cause of plaintiff's amyloidosis is "chemical peritonitis established by the leaking urine as a result of the misplaced ureter during the renal transplant, and the subsequent fungal peritonitis that continued after the repair of the ureteric anastomosis" (Hearing Transcript at p 10; see also id. at p 8). With respect to the decedent, Dr. Poznansky opines that,
In this particular patient, in this particular incident, the urine leaking into the abdomen, into the peritoneal cavity, at the point of which the anastomosis was not present between the grafted kidney and bladder, the naked bladder of the patient initiated that inflammatory process, set this patient up for amyloidosis, secondary amyloidosis subsequently developed.
And I think that the point that has to be made, is to understand the severity of the chemical irritation that urine pouring into the abdomen of an individual represents; and, in particular, that, where we can go about our daily lives thinking of urine as a benign substance that we excrete out of our body multiple times a day without event, mostly, actually, it contains multiple waste products that we are actually trying to get rid of, drugs that we might be taking, as well as other chemical irritants, which is the reason we actually have to expel the urine because it represents a toxic threat to us.
So, the fact that urine leaks back into our body, in this particular case, the patient's body, into their abdomen, is a very significant chemical irritation to that anatomic site.
...
So, consequently, when you start pouring a chemical irritant into the belly, the response is very, very significant inflammation; and, essentially, peritonitis, which is a serious clinical condition, which in this patient actually went from the point of which the operation was performed, all the way until both in combination with the infection and the chemical component, all the way until the patient's death on the 8th of July. So, there was this continuous inflammatory process.
Now, how does the body react to inflammation? You basically produce proteins that are a response to the inflammation that end up being deposited on these membranes that over a long period of time turning what was saran wrap into that thick, leathery, sticky material that causes this freezing of the abdomen, all of the consequence symptoms the patient would experience, the fever, pain, the discomfort and so forth. None of that, none of that was evident previously, prior to the transplant being done.
I think that the course of the disease, with the length of the time where urine was leaking in between the transplant and redo when the ureter re-established connection to the bladder and then the subsequent infection led to this chronic inflammatory process — the chronic type of infection and inflammation that is well known, it's an established, documented cause of secondary amyloidosis, which is essentially the description of the proteins being deposited on membranes and tissues.
So, the factor [sic ] when they go in and at a certain point they see the description postmortem of this frozen abdomen, it is entirely consistent with the magnitude of the injury previously related to urine leaking into the abdomen and the subsequent infection with candida. (Hearing Transcript at pp 11-14).
Dr. Poznansky represents that approximately a liter of urine leaked into the peritoneum each day, and "fluid is crossing back into the circulation and being recycled in a continuous process. So, she was effectively experiencing peritoneal dialysis with urine, meaning that the toxins ultimately are building and building in that belly and potentially causing more inflammation" (id. at p 15).
Peritoneal dialysis involves the introduction of a salt water solution through a catheter into the peritoneum, the catheter is capped, the solution absorbs and flushes out the toxins in the peritoneum (Exhibit B Bates pg 189) and the solution containing the toxins is then drained where fresh solution again is introduced through the catheter and then capped again for another cycle. Ms. Avetisian's presentation is much more severe than a presentation of peritoneal dialysis in that Ms. Avetisian['s] toxins from the allograft kidney urine including the urine itself and the toxins the body tissues forced to the peritoneum collected there from the renal transplant on February 9, 1999 to the corrective surgery on March 3, 1999. The infection was developing on March 8, 1999 as a sonogram demonstrates the septation of ascites and non-simple transudate (Exhibit B Bates pg 200). This buildup of urine and toxins without being drained daily and the body response to this massive insult is an extraordinary cause of severe inflammation and infection (Poznansky Affidavit, July 2, 2018 at ¶¶ 5-6).
Dr. Poznansky further opines that "[t]hough pyelonephritis is kidney related due to urine buildup, in cases where the kidneys are not functioning properly, the peritoneum acquires some of the function of the kidney which supports peritoneal dialysis procedures In Ms. Avetisian's presentation for these purposes, there is no significant difference in her presentation and presentations of pyelonephritis or peritoneal dialysis as relates [sic ] to secondary amyloidosis..." (Poznansky Affidavit at ¶ 9). Based on the articles provided,
acute pyelonephritis is a sudden and severe kidney infection. It causes the kidneys to swell and may permanently damage them When repeated or persistent attacks occur, the condition is called chronic pyelonephritis. The chronic form is rare but it happens more often in children or people with urinary obstructions The infection usually starts in the lower urinary tract as a urinary tract infection (UTI). Bacteria enter the body through the urethra and begin to multiply and spread up to the bladder. From there, the bacteria travel through the ureters to the kidneys. Bacteria such as E. Coli often cause the infection. However, any serious infection in the bloodstream can also spread to the kidneys and cause acute pyelonephritis. (id. , Exhibit B, Healthline, https://www.healthline.com/health/pyelonephritis, p 133).
He opines that the inflammation did not just last for the two-week period that the urine was leaking; "we are talking about a chronic inflammatory and infectious process that went, by my calculations, over a year in this patient's abdomen" (see id. at 16). Poznansky theorizes that the decedent "suffered from both a chronic chemical induced inflammation due to persistent urine from the renal allograft leaking directly into [her] peritoneal cavity and a persistent chronic candida infection as a result of infected urine draining out of the open orifice in the bladder which had been established to receive the donor allograft associated ureter" (Poznansky Affidavit, July 2, 2018 at ¶ 5). A candida infection noted in the decedent's medical records in April 1999, which Poznansky opines, caused a bacterial or fungal peritonitis. "In Ms. Avetisian's case she had both, the inflammatory process and infectious process as well" (id. at 23). Dr. Poznansky testified that he did not provide any articles to support his assertion that candida can cause amyloidosis, but that he has seen it in his own experience with a patient (see id. at 53).
Dr. Poznansky describes an acute disease as one week to 10-day illness, and a chronic disease as "two weeks or more" (id. ).
Upon autopsy, amyloid was found in plaintiff's native kidney but not in the transplanted kidney. Dr. Poznansky opined that "it's common in a patient that develops amyloidosis in grafted kidneys that is unrelated to the patient does not develop amyloidosis in grafted kidneys in the overall majority of transplant cases" (see id. at p 25).
Defendant's Expert
Peter Gorevic, M.D., a board-certified physician who specializes in rheumatology, allergy and immunology, provided two affirmations in support of defendant's motion and in opposition to the plaintiff's cross motion (see Notice of Motion [1], Exhibit A, Gorevic Affirmation dated 1/18/18; see also Supplemental Reply Affirmation [6], Exhibit A, Gorevic Affirmation dated 7/26/18). Dr. Gorevic opines that the decedent's amyloidosis was caused by her history of psoriatic arthritis. In this case, the decedent's amyloid was suspected by Dr. Pacholka on May 26, 2000 and diagnosed at the autopsy. The medical records show that no test was conducted to "type" the amyloid. However, Dr. Gorevic opines, based on her presentation, her history of psoriatic arthritis, and the amyloid found in her organs that the decedent suffered from AA or secondary amyloidosis.
Dr. Gorevic opines that patients generally have inflammatory disease for several years before amyloid is recognized (see Hearing Transcript at p 141). Dr. Gorevic testified that the average onset of AA amyloidosis is between 11 and 18 years (see id. at p 155). However, Dr. Gorevic testified that the shortest development of AL amyloidosis he has seen was 3-4 months (see id. at p 178). Based on the decedent's long-standing psoriatic arthritis, Dr. Gorevic opines that the decedent likely had amyloid deposits in her organs long before her kidney transplant on February 9, 1999 (see id. at ¶ 12). Although amyloidosis is predominantly associated with rheumatoid arthritis, it is associated with psoriatic arthritis in approximately 3-4% of cases (see Hearing Transcript at p 137; see also id. at p 170). Gorevic further stated that "the amyloid deposits predated the kidney transplant because if the consequences of the transplant had caused the decedent to develop amyloidosis, amyloid deposits would have also been present in the transplanted kidney" (Gorevic Affidavit 1/18/18 at ¶ 14). However, Dr. Gorevic testified that in his own practice, he has seen transplanted kidneys develop amyloidosis (see Hearing Transcript, at p 152). He testified that the literature shows varying degrees of recurrence and amyloid may not recur in the transplanted kidney up to 30 percent of the time (see id. at 174).
Dr. Gorevic opines that the decedent's enlarged spleen and eventual splenic infarction were a result of "the presence of amyloid deposits in the patient's tissues over many years preceding her kidney transplant" (Gorevic Affidavit 1/18/18 at ¶ 15). In addition, Dr. Gorevic opines that the decedent is predisposed to amyloidosis because of her Armenian background. One in five individuals from Armenia and the Armenian population in Georgia carry a gene "known to be associated with periodic fevers and thus predisposed to the development of AA Amyloidosis" (id. at ¶ 16).
Dr. Gorevic, in his over 40 years of practice dealing with amyloidosis, is unaware of any instance where systematic amyloidosis was caused by extravasation of urine into the peritoneum following a kidney transplant.
"To the contrary the medical literature establishes that amyloid deposits and the development of amyloidosis are caused by a long-term inflammatory process such as the decedent's psoriatic arthritis, and that as such, it is not generally accepted in the relevant scientific community that the extravasation of urine following a kidney transplant can cause amyloid deposits and the development of amyloidosis" (id. at ¶ 18).
Dr. Gorevic provided numerous articles to support his position (see Notice of Motion [1], Exhibit B; see also Supplemental Reply Affirmation [6], Exhibit A, Exhibits 1-3).
Discussion
"At issue in this case is the admissibility of the plaintiff's experts' opinions relating to the plaintiff's novel theory of medical causation" ( Ratner v. McNeil-PPC, Inc. , 91 AD3d 63, 933 N.Y.S.2d 323 [2 Dept., 2011] ). "New York courts permit expert testimony based on scientific principles or procedures only after the principle, procedure, or theory has gained general acceptance in the relevant scientific field Under the Frye standard, the burden of proving general acceptance rests upon the party offering the disputed expert testimony [internal citations omitted]" ( State v. Hilton C. , 158 AD3d 707, 70 N.Y.S.3d 565 [2 Dept., 2018], appeal withdrawn , 31 NY3d 1077, 103 N.E.3d 1245 [2018], citing Frye v. United States, 293 F. 1013, 54 App.D.C. 46 [1923] ).
"As Justice Catterson of the Appellate Division, First Department, stated in his concurrence in Styles v. General Motors Corp., 20 AD3d 338, 799 N.Y.S.2d 38, ‘[t]he Frye general acceptance test is intended to protect [ ] juries from being misled by expert opinions that may be couched in formidable scientific terminology but that are based on fanciful theories’ [internal quotation marks omitted]" ( Lugo v. New York City Health & Hosps. Corp. , 89 AD3d 42, 929 N.Y.S.2d 264 [2 Dept., 2011] ). "General acceptance can be demonstrated through scientific or legal writings, judicial opinions, or expert opinions other than that of the proffered expert" ( Shah v. Rahman , 167 AD3d 671, 88 N.Y.S.3d 228 [2 Dept., 2018], quoting Dovberg v. Laubach, 154 AD3d 810, 63 N.Y.S.3d 417 [2 Dept., 2017] ).
"[G]eneral acceptance does not necessarily mean that a majority of the scientists involved subscribe to the conclusion. Rather it means that those espousing the theory or opinion have followed generally accepted scientific principles and methodology in evaluating clinical data to reach their conclusions" ( Zito v. Zabarsky, 28 AD3d 42, 44, 812 N.Y.S.2d 535 [internal quotation marks omitted], and Ratner v. McNeil—PPC, Inc., 91 AD3d 63, 71, 933 N.Y.S.2d 323 [internal quotation marks omitted] ). "Broad statements of general scientific acceptance, without accompanying support, are insufficient to meet the burden of establishing such acceptance" ( Saulpaugh v. Krafte, 5 AD3d 934, 935—936, 774 N.Y.S.2d 194 ). Furthermore, even if the proffered expert opinion is based on accepted methods, it must satisfy "the admissibility question applied to all evidence-whether there is a proper foundation-to determine whether the accepted methods were appropriately employed in a particular case" ( Parker v. Mobile Oil Corp., 7 NY3d at 447, 824 N.Y.S.2d 584, 857 N.E.2d 1114 ). ( Dovberg v. Laubach , 154 AD3d 810, supra ).
"Frye is not concerned with the reliability of a certain expert's conclusions, but instead with whether the [expert's] deductions are based on principles that are sufficiently established to have gained general acceptance as reliable" ( State v. Hilton C. , 158 AD3d 707, supra , citing Lipschitz v. Stein , 65 AD3d 573, 884 N.Y.S.2d 442 [2 Dept., 2009] ). "Put another way, ‘[t]he court's job is not to decide who is right and who is wrong, but rather to decide whether or not there is sufficient scientific support for the expert's theory’ " ( Lugo v. New York City Health & Hosps. Corp. , 89 AD3d 42, supra , quoting Gallegos v. Elite Model Mgt. Corp., 195 Misc 2d 223, 758 N.Y.S.2d 777 [Sup. Ct., 2003] ).
New York courts have also applied the Frye test to assess the reliability of an expert's theory of causation in a particular case. For this category of expert opinion testimony, "it is not necessary ‘that the underlying support for the theory of causation consist of cases or studies considering circumstances exactly parallel to those under consideration in the litigation. It is sufficient if a synthesis of various studies or cases reasonably permits the conclusion reached by the plaintiff's expert’ " ( Zito v. Zabarsky, 28 AD3d at 44, 812 N.Y.S.2d 535 ( Lugo v. New York City Health & Hosps. Corp. , 89 AD3d 42, supra ).
"It is well-established that an opinion on causation should set forth a plaintiff's exposure to a toxin, that the toxin is capable of causing the particular illness (general causation) and that plaintiff was exposed to sufficient levels of the toxin to cause the illness (specific causation)" ( Parker v. Mobil Oil Corp. , 7 NY3d 434, supra ). "Parker explains that ‘precise quantification’ or a ‘dose-response relationship’ or ‘an exact numerical value’ is not required to make a showing of specific causation Parker by no means, though, dispensed with a plaintiffs burden to establish sufficient exposure to a substance to cause the claimed adverse health effect [internal citations omitted]" ( Cornell v. 360 W. 51st St. Realty, LLC , 22 NY3d 762, 986 N.Y.S.2d 389 [2014] ).
As plaintiffs are the parties offering this disputed expert testimony, the burden of proving general acceptance rests on them (see , State v. Hilton C. , 158 AD3d 707, supra ). It is undisputed that there are no scientific or legal writings, judicial opinions, or expert opinions which demonstrate the general theory of causation herein; that a urine leak into the peritoneum can cause a patient to develop amyloidosis. However, Frye does not require an expert's opinion to be subscribed to by a majority of scientists (see Dovberg v. Laubach, 154 AD3d 810, supra ). "The fact that there [is] no textual authority directly on point to support the [expert's] opinion is relevant only to the weight to be given the testimony but does not preclude its admissibility" ( Lugo v. New York City Health & Hosps. Corp., 89 AD3d 42, supra , quoting Zito v. Zabarsky , 28 AD3d 42, supra ). Rather, Frye and Parker require that the principles relied upon by plaintiff's expert have gained general acceptance in the medical field. Therefore, to meet their burden, the plaintiffs must provide medical support to establish that Dr. Poznansky's underlying reasoning herein is based on a generally accepted medical principles.
In the case at bar, plaintiffs failed to meet their burden. Plaintiffs failed to provide medical literature, legal writings or judicial opinions, or other expert opinions which support Dr. Poznansky's broader theory of causation herein, which, stated succinctly, is that the decedent developed amyloidosis from: (1) peritonitis, caused by both chronic inflammation and bacterial or fungal infection ; (2) the urine leak acting akin to peritoneal dialysis ; and (3) the inflammation in the peritoneum acting akin to pyelonephritis (see generally, Poznansky Affidavit). Most of the articles submitted by the plaintiffs' experts generally address different types of amyloidosis within the context of renal transplant patients. The remaining articles, fail to support the expert's theories as to the cause of the decedent's amyloidosis, as discussed more fully, below.
Peritonitis
Dr. Poznansky first theorizes that the urine leaking into the peritoneum caused the decedent to develop chemical peritonitis. Poznansky also theorizes that the urine leak and candida found after the renal transplant demonstrate that the decedent had developed a bacterial or fungal peritonitis. Furthermore, Poznansky opined that the decedent's peritonitis ultimately caused her to develop amyloidosis over the approximately 15 months between the first renal transplant surgery and her death.
With respect to chemical peritonitis, Dr. Poznansky theorizes that the urine leak caused chronic inflammation which led the decedent to develop peritonitis. The literature provided herein supports the position that chronic inflammatory diseases are the leading causes of amyloidosis. Here, the urine leaked for approximately one month into the peritoneum prior to the corrective surgery. As an initial matter, Dr. Poznansky failed to provide any medical articles which support the basic premise of this theory, which is that urine is a "chemical irritant" capable of causing peritonitis. Defendant's expert, Dr. Gorevic, testified that urine is a sterile and non-caustic substance (see Hearing Transcript at pp 166-167). Further, although Dr. Poznansky need not quantify the exact amount of urine necessary to cause peritonitis, he failed to provide support to establish his theory of specific causation, which is that the decedent was exposed to sufficient levels of urine to cause the illness (see generally, Parker v. Mobil Oil Corp. , 7 NY3d 434, supra ).
Dr. Poznansky further theorizes that the decedent suffered from a bacterial or fungal infection as a result of the urine leak. Poznansky posits that
the combination of both a chronic chemical peritonitis caused by sterile urine and chronic fungal peritonitis with urine infected with Candida together with the treatment and the related severe inflammation caused an overwhelming response which was a significant cause of decedent's death on July 8, 2000 as well as this severe infection and/or inflammation caused secondary amyloidosis, exacerbated and aggravated decedent's pre-existing conditions and was a significant cause of decedent's death whether considered individually or jointly. (id. at ¶ 7).
Here, Poznansky failed to provide any literature to support the theory that the decedent's candida infection could cause peritonitis. Further he testified that he did not provide any medical literature which supports the assertion that candida can cause amyloidosis (see Hearing Transcript at p 53). However, Poznansky testified that he has seen candida cause amyloidosis in his own experience with a patient, which may, in appropriate circumstances, be sufficient (see generally People v. Oddone, 22 NY3d 369, 980 N.Y.S.2d 912 [2013] ; see also People v. Brooks, 134 AD3d 574, 23 N.Y.S.3d 26 [1 Dept., 2015] ).
The crux of the above propositions is Dr. Poznansky's opinion that the decedent's peritonitis ultimately caused her to develop amyloidosis. Here, Dr. Poznansky provided medical support which demonstrates a link between peritonitis and amyloidosis. Familial Mediterranean Fever (FMF) is characterized by peritonitis and AA amyloidosis is one of the most severe complications of FMF (see Poznansky Affidavit, Exhibit A, p 10-13, Article M2: Familial Mediterranean fever (FMF) and renal AA amyloidosis — Phenotype-genotype correlation, treatment and prognosis by Eldad Ben-Chetrit; see also , Supplemental Frye Exchange, Plaintiff's Exhibit 1, Exhibit A, Periodic Peritonitis, Amyloidosis and Colchicine by Hobart A. Reimann, M.D., D.Sc.). Further, the articles submitted demonstrate a well-established link between certain chronic inflammatory diseases and amyloidosis (see id. ).
This Court notes that plaintiffs' expert did not establish a causal relationship between peritonitis and amyloidosis. Rather, through the articles submitted, Dr. Poznansky merely established that the two are linked or associated, specifically through Familial Mediterranean Fever (see generally , Cornell v. 360 W. 51st St. Realty, LLC , 22 NY3d 762, supra ).
However, these articles do not support Dr. Poznansky's hypothesis that the inflammation from this infection had a similar effect to a chronic inflammatory disease. Even assuming that the inflammation occurred for the entire month that the urine remained in the decedent's peritoneum, the articles submitted do not support the hypothesis that one month of inflammation can cause amyloidosis. The general articles about amyloidosis describe a list of well known causes, all of which are chronic, long term inflammatory diseases. Even if Dr. Poznansky is correct that the inflammation from this one month persisted for approximately 15 months as a result of the infection, the articles do not support the onset of amyloidosis in that period of time. Dr. Gorevic testified that the average onset of amyloidosis is between 11 and 18 years (see Hearing Transcript at p 155). Dr. Poznansky failed to provide medical literature to support his assertion that the decedent's amyloidosis could have an onset of only 15 months. The only article which could support this position is Systemic amyloidosis involving the diaphragm and acute massive hydrothorax during peritoneal dialysis, discussed below.
Peritoneal Dialysis
In addition, Dr. Poznansky theorized that plaintiff's urine leak acted akin to a type of peritoneal dialysis, except instead of the toxins being flushed out periodically, the toxins both from the urine itself and those present in the peritoneum, remained for one month until the corrective surgery took place. Dr. Poznansky provided no support for this theory, in and of itself.
Dr. Poznansky states in his affidavit that "[p]eritoneal dialysis is directly linked as a known cause of amyloidosis (Exhibit B Bates pg 178) even after only three days of peritoneal dialysis (Exhibit B Bates pg 187)" (Poznansky Affidavit, July 2, 2018 at ¶ 5). This article, cited by Poznansky, provides that "dialysis-related amyloidosis (DRA)" as "a serious complication of both long-term hemodialysis (HD) and peritoneal dialysis (PD)" (Poznansky Affidavit, July 2, 2018, Exhibit B, Dovepress, Dialysis related amyloidosis : challenges and solutions, Scarpioni R, p 178). Therefore, even assuming that Poznansky correctly theorized that the urine leak was akin to peritoneal dialysis, it is unclear whether one month of peritoneal dialysis could be considered "long-term" enough to cause amyloidosis. Furthermore, Dr. Poznansky clarified in his hearing testimony, that this article supports the proposition that peritoneal dialysis can "initiate" the process which can cause amyloidosis in three days, not that it can cause amyloidosis in as little as three days (see Hearing Transcript at p 72-78).
Further, Dr. Poznansky's assertion that peritoneal dialysis can cause amyloidosis after only three days is based upon his submission Systemic amyloidosis involving the diaphragm and acute massive hydrothorax during peritoneal dialysis (see Poznansky Affidavit, Exhibit B, p 187). In that case, a 54-year-old woman in renal failure from chemotherapy for ovarian cancer, developed a hydrothorax three days after onset of ambulatory peritoneal dialysis (see id. ). The abstract, provided by Poznansky, merely states that the patient underwent three days of peritoneal dialysis and was found, at autopsy, to have amyloidosis. The full article reveals that the subject underwent a kidney biopsy where no amyloid was detected. However, 6 months later, her autopsy revealed amyloidosis in many organs (see id. at p 477). The authors of this article were not able to determine whether their patient had developed primary, AL amyloidosis or secondary, AA amyloidosis.
As stated above, Poznansky originally provided only a one-page abstract of the case report, however he provided a full copy in his supplemental Frye exchange which was marked into evidence at the hearing as plaintiff's exhibit 1. This Court further notes that Dr. Gorevic also provided this Court with the full article (see Gorevic Affidavit 7/26/18, Exhibit 3).
The etiology of the amyloid in our patient is unclear. No association could be found in the literature between amyloid and endometriosis or the chemotherapy regimen of our patient. There is only one previous report of amyloid associated with ovarian cancer [Fernandez-Miranda et al. 1994]; in this case, the presence of amyloid AA antigens was consistent with secondary amyloidosis. In our case, the negative immunohistochemical studies for AA amyloid are compatible with primary amyloidosis although secondary causes are not ruled out. Unfortunately, histochemistry for AL amyloid was not available at the time of autopsy. The Congo red histochemistry stain was unaffected by pretreatment of the tissue sections with permanganate; despite the low specificity of this procedure, the absence of change is in favor of AL-type amyloid. Furthermore, the amyloid deposition in the diaphragm was restricted to the blood vessels in contrast to the heart where amyloid was observed extensively between the muscle fibers. A last point to note was the accelerated progression of amyloidosis which was not present in the kidney biopsy obtained 6 months earlier. (id. at p 478).
Here, Poznansky testified that the decedent developed AA or secondary amyloidosis. This article does not provide support for the assertion that the decedent herein could have developed AA amyloidosis in six months. Although unconfirmed, it appears that the patient in this article developed AL amyloidosis in the period of six months. However, this Court notes that although the experts opine that her presentation points to AA amyloidosis, the decedent's specific type of amyloidosis was never determined.
Pyelonephritis
Poznansky opines in his affidavit that "there is no significant difference in [the decedent's] presentation and presentations of pyelonephritis as it relates to secondary amyloidosis" (see Poznansky Affidavit at ¶ 9). Dr. Poznansky established through submission of medical literature that AA amyloidosis is linked with chronic pyelonephritis (see id., Exhibit B, NORD Amyloidosis, http://rarediseases.org/rare-diseases/amyloidosis /, p 117; see also Medscape, AA (Inflammatory) Amyloidosis Clinical Presentation, p 131-132). However, he failed to support his theory that there is no significant difference in the decedent's presentation and that caused by pyelonephritis. Poznansky testified that the decedent did not have these conditions (see Hearing Transcript at pp 68-69).
Based on the foregoing, the plaintiffs failed to demonstrate that the novel theory of causation offered herein is based on generally accepted scientific principles.
Conclusion
Defendants' motion to preclude plaintiff's expert from offering any evidence at the trial that the plaintiff decedent Marietta Avetisian was caused to develop amyloidosis as a result of the extravasation of urine into the peritoneum following a kidney transplant, on the ground that such a theory of causation has no basis in the medical literature and it otherwise lacking in foundation is granted. Based on the foregoing, plaintiffs' cross motion to preclude defendants from offering expert testimony that the decedent's amyloidosis was pre-existing prior to the February 9, 1999, renal transplant is denied.
The foregoing constitutes the decision and order of this Court.