RB:We have the great opportunity today of having a discussion today with one of the major contributors to our understanding of renal pathology and nephrology, Dr. Jacob Churg. Welcome Dr. Churg.
JC: Thank you very much Dr. Blantz. Itís nice to be here. Nice to see this wonderful equipment here and Iím sure weíre going to have a nice day.
RB: Before we get into the many, many contributions in your career, why donít we just get to know each other by telling us a little bit about where you grew up, where you were born?
JC: Well, yes indeed. Well I was born in what was Russia at that time. That was in 1910. I donít know too much far back but I only know my great grandparents and a little bit about my grandparents. It is an interesting thing. My grandfather on my fatherís side was a rather successful businessman who imported tea from China to Russia. Perhaps you know, Russia is the tea drinking nation, second only to England perhaps but the only kind of tea they would drink is one that was brought by a caravan of camels because they always claimed that the sea voyage ruined the taste of tea, which of course took three months at that time. So he imported it and quite successfully and my grandfather was a chemist who worked for his father, which was all right except when he got involved in anti-Czarist politics and landed in jail and when he was released he promptly left Russia for America. That was towards the end of the 1880s. Well, here he had to start all over again and he worked on any kind of jobs. Among them there was a Hotel Astor in Times Square in New York and he was one of the electricians in there. And you know it was a long arm of coincidence because we were married in the very same hotel which by now is torn down. Anyhow, he saved enough money to put himself through dental school and to bring over his family. His family consisted of his wife and three children, of whom my father was the eldest. My father was left behind with his uncle to finish the gymnasium and right after that he was admitted to medical and it was decided to wait until he finished at medical school. Well, it didnít work out that way because right after that the Russian-Japanese War broke out and he was drafted and became an army physician way out in the Far East. For a while he was stationed in Harbin in Manchuria and on my visit to China I had an opportunity to see Harbin. In his time it was a little village - maybe 5,000 people. Now itís a city of 3 million people. Of course nothing is left of the old Russian influence. Harbin was important to the Russians because it was a shortcut for the TransSiberian railway to Vladivostock in the Far East. Now of course they go all the way around in Manchuria. Well, he spent three years in army and when he got out he felt it was too late to change countries so he settled down in a small town and began practice and thatís where he got married and started raising a family. Again, another war broke out, i.e., World War I and again he was called back to the army and spent another four years in the army. So much of his early life was devoted to military activities.
Well, I was born in that part of Russia that eventually became Poland. So the first 12 years of life I lived in Russia and then it became Poland so I had to learn Polish and went to Polish schools - the gymnasium, the medical school and for graduate training for the next 14 years to 1936. My interest in medicine was always there because I really started reading my fatherís books at the age of 8 or so. I always pestered him with questions. So it was natural for me. My brother on the contrary had much abilities as an engineer and became an engineer in France. That part of the family eventually landed in America.
On my motherís side, my great grandfather was a rather well known rabbi, who was well-known for his knowledge of Jewish laws and interpretations of Jewish laws. He had people coming to him from all over the area. His son, my grandfather, was a businessman, a small town businessman - not very successful but he appreciated learning and he sent my mother, his eldest daughter to the big city to study in the gymnasium and after that in a dental school which was quite unusual for that time - to promote women. She finished dental school and began to practice in the same small town as my father and you can see that in no time she acquired a husband in addition to her practice.
So, this background perhaps is of some importance. I hope that I inherited something from either side of the family.
RB: Well, there are many choices in medicine - surgery, internal medicine, pediatrics. How was it that you eventually chose as a career the study of pathology.
JC: I tried everything. I had a regular rotating internship. After that I worked in the department of internal medicine and I was not very successful with patients. I didnít know how to approach them. Whereas, I did fairly well with tissues. What interested me in pathology was a minor thing. We had to do our own sections, frozen sections - stain them. Of course it was normal tissue but I was very much impressed by the beautiful colors and I decided that this is something that is maybe worthwhile.
Then, when I got here - to the United States - I had the same choice again. My uncle, who brought me over, was a dermatologist and he offered me a place in his office. Again, I tried it for a while and again it didnít work out well. So I decided that I might as well go into the laboratory work which as it turned out would be much better. Thatís how I started and the next 5 or 6 years I spent studying pathology - anatomic pathology, clinical pathology, passing the Boards. Eventually, I became a full time pathologist.
RB: Aside from your many experimental observations and clinical formulations, one of the major contributions from a practical standpoint in clinical medicine that you have contributed to is the analysis of renal biopsy materials. What do you feel that the impact of that development has been upon our current state of knowledge of renal disease?
JC: Well, I think it contributed considerably. Maybe that influence is waning now but for 20 or 30 years it was very important because treatment depends to a great degree on the diagnosis. Prognosis depends on the diagnosis and renal pathology was able to supply the diagnosis. This is because we had tissue from living patients.
Actually, I started studying renal pathology on autopsy tissue. All pathologists did at that time. There are two books: one by Bell, who published a small book but it had very carefully observed autopsy reports and the second one by Arthur Allen?. Again based mainly upon autopsies and we started working on autopsy material. Perhaps we found a few more things but real development of renal pathology started with biopsies. Because: (1) you could see much more, and correlate it with the actual patient physiology, and (2) you could contribute to the clinical treatment of the patient. So I think we collected something like 8000 biopsies. By present day standards, it might not be very much. I know people have 30,000 biopsies but if you study them carefully you can learn a good deal.
RB: Earlier in your career you had interactions with a variety of clinical nephrologists, even though nephrology wasnít a defined subspecialty possibly at that time. Are there any particular figures in that area that were important to your interactions, or are there people that you remember from the clinical nephrology arena that helped advance the field?
JC: Well, to some degree but, as you mention, there was considerable disparity between renal physiologists and renal pathologists. The Chief of the Renal Division at that time at Mount Sinai was Dr. Marvin Levitt? I donít know if you know his name. He was a pupil of Homer Smith and he was not interested in pathology at all. He was an excellent clinician but his idea was that you can divided renal diseases into those that respond to steroids and those that donít respond to steroids. If they donít respond to steroids, eventually it ends in dialysis and transplantation. So he didnít care too much. So we had to do our studies mainly for people on the outside of the medical school. Of course, they were much more interested and people who influenced it were mostly renal pathologists: Dr. Arthur Allen, Dr. Benjamin Spargo, who was probably one of the earliest in the field. I tried to follow what they did and we tried to do the same thing.
RB: It seems like weíve covered the full circle. Some of the observations of the original renal pathologists of the 40s, 50s and 60s are now being re-analyzed and some of their wisdom is being perceived, like the importance of scarring in the kidney, the factors that cause progression, and more important, what the interstitium looks like in particular disease. Could you comment on some of those types of observations that we may have temporarily forgotten?
JC: Well, as you know, anything in medicine comes back in a slightly different form and there is no doubt about it that it is much more obvious if you look at the tubules and interstitium what the prognosis might be in the case because glomeruli may recover or may go on to sclerosis but it does not necessarily determine the outcome. However, the question nowadays is are the changes we see in the interstitium primary changes or are they secondary to glomerular diseases. My own impression was that whatever follows glomerular disease is caused by glomerular disease, even if the glomeruli themselves recover. But thatís an important indicator of the status. The main thing we donít know is why glomeruli progress to sclerosis, why interstitium tissue progresses to sclerosis. We are only now beginning to see a hint from molecular studies. So I think that this is going to give us a hand in understanding and preventing sclerosis. Thatís probably the most important thing in the kidney now because Dr. Levitz? said, "If they donít respond to steroids, you have nothing else to offer." Nowadays, likely? we have something more to offer.
RB: Well, Iím going to try to put you on the spot here a little bit by saying youíve made a wonderful number of disparate contributions to pathology in general during your life and in particular to renal disease but are there particular contributions that you made experimentally or observationally during your career that you feel are most important or most satisfying to you personally?
JC: Well we did some experimental work. Actually, I started in research doing experimental work. After finishing the medical school and internship, I became an assistant in the Department of Pathology at the University of Vilna/. We had two Departments of Pathology - one was devoted to anatomical pathology and the other to experimental pathology and thatís why I started and I had an idea to follow the effect of hormones on the status of complement in blood. How I came about it I donít even remember. May be it was suggested by my teacher at that time. That was a new idea at that time. Nobody thought about it and, yes, I was able to show that hormones do affect the level of complement. We used gonadotropic hormones and it increased the level of complement and we experimented with females rabbits and if the ovaries were removed the effects were abolished. So obviously there was some kind of a hormonal connection. We published the observation in one of the German medical journals and it came to the attention of JAMA and they commented. It was an editorial comment and thatís when it became known that they work that way. Nowadays, we know that so many things influence the system. So itís not that unusual but at that time it was an interesting observation.
RB: What about some of your contributions to our understanding of vasculitis in the kidney and elsewhere. Youíre certainly known, obviously, for Churg-Strauss syndrome but you also had interests prior to that on other forms of generalized vasculopathy.
JC: That is correct. You know, itís a matter of luck. We had a patient at the Barnett? Hospital who came in with lymphadenopathy. When he was worked up we found out that he also had a history of asthma and he had a high eosinophil count, something like 30 or 40%. So a biopsy of lymph nodes was done and it looked quite strange to me. I took it to an experienced pathologist, he looked at it. He said, "I really donít know what it is but it may be Hodgkinís. Well, there was eosinophilic infiltration, early granulomas - it could be Hodgkinís - but the patient started to improve in the sense that lymph nodes disappeared which of course was against a diagnosis of Hodgkinís. Then he died of brain hemorrhage and at autopsy there was vasculitis of the brain arteries. That was the cause of hemorrhage but also many granulomas in various tissues. Any that is something unusual which I hadnít seen before. Later, of course, we found such cases had been reported previously but what happened and at the same time Dr. Strauss, Dr. Michael Strauss at Mount Sinai, also had a similar case. You know, if you have one unusual case you say, "Well, thatís an unusual case." If you have two, you say, "Oh, it must be a new disease!" So we worked up those cases and then started looking through the material in the files at Mount Sinai. We found 13 or 14 such cases. This was due to the fact that one of the men in .................................., Dr. ............................., an allergist, he noted this unusual combination of vasculitis and eosinophilia. It was known before him too but he started collecting these cases and I think half of our cases came from him alone. So we had also a number of cases without such histories of eosinophilia and asthma and compared them and they did not have these granulomas. Then we decided it must be a new disease.
Even to this day, pathologists divide inflammation into two types, as you know. Acute inflammation, which is mostly polymorphs, maybe neutrophils and eosinophils, and chronic inflammation which is mononuclear cells - lymphocytes, monocytes, etc. To me though there is a difference between inflammation that contains neutrophils and inflammation that contains many eosinophils. Eosinophils are quite different in appearance and probably in function.
While at Mount Sinai I worked also for a while in hematology and if there had been a position for me, I would have stayed in hematology but at that time there were very few positions in the hospital. I think Pathology had 3 pathologists for a 600 bed hospital, with a very active surgical service and there was nothing I could use for myself. But to this day, I always feel that eosinophils are different from neutrophils and this hemorrhagic granulomatosis is characterized by eosinophils and - ...................... regular granulomatosis by neutrophils. Itís not always acknowledged to this day but I think itís a valid distinction. Incidentally, in that case there was quite a diffuse infiltration of the renal pelvis, ureters, veins in the liver with eosinophils, which you could see grossly as brown color. Eosinophils, I believe, contain metal or enzymes, perhaps zinc, and that gives them the color, which is quite different from neutrophils. Well, there may be minor differences but it impressed the two of us and thatís why we went ahead and published it.
RB: Well, also since your career in renal pathology has essentially spanned the time where it has become a science, as well as an observational art, you must have run into a lot of contemporaries over the years that you think might have made significant contributions. Are there any memorable friends or contemporaries in that area?
JC: Well, one of them of course is Dr. Heptinstall. You know Dr. Heptinstall. He is quite a character! And very bright indeed. His book is really the standard text of renal pathology. There is some competition now but I think he is now preparing the fifth edition. So this seems to be some indication of its value. He had his own views on everything including renal pathology. Everyone could learn quite a bit from because he could really review the literature and pick up all the important contributions. If you look at his book I think he missed nothing. He has a very special ability.
The other person of course is Dr. Benjamin Spargo. He was the one who first started applying electron microscopy to renal biopsies and, of course, he made very many contributions. He is different from Dr. Heptinstall. He was a very mild person who never tried to push himself but I think his contributions were probably of equal importance.
Then there are various other people, many of them my own collaborators, particularly Dr. Edith Grishman?, who did a tremendous amount of work - a very good pathologist. You know why I became interested in renal diseases? Well, there were two things: while at medical school I read a book by a professor in Berlin by the name of Rosenberg. At that time the German literature was the most outstanding in medicine and in Poland we had very little original contributions but German contributions were important. So there was this little book which discussed glomerulonephritis in such clear terms, it stayed we me to this very day. Dr. Grishman says that Dr. Rosenberg was a very boring teacher but the book was very clear.
What he said was that there are two types of glomerulonephritis which was well known before him. One is characterized mainly by proteinuria, edema, nephrotic syndrome and the other mainly by hematuria and hypertension. However, he said, "Now that you know there are two types, the main difficulty is to realize that many patients have a combination of the two. Thatís what makes for such a great variety of presentation and seems to make it difficult to understand it. Bear in mind the two basic features. You can discern them either separately or together and understand how glomerulonephritis progresses. I think this principle applies to many things in medicine. We have to establish basic principles but also there are many combinations.
The second period that influence my interest in renal diseases was during my residency in Europe? with Dr. William Anta? He worked on the effects of poorly soluble sulfonamides on the kidney. At that time they were the only type of sulfonamides that were effective against infection but they tend to precipitate in the kidney and in experimental work you could show that they obstruct in the .................. of the kidney, the kidney became functionless and the animal died - it was rats where we worked. But also at the time, many of these animals developed changes in the aorta and major branches consisting of necrosis of smooth muscle secondary calcification and I think endstage it would be and thatís why I was interested in the kidney and in vascular diseases. In due time I studied it again, trying to see how this type of large vessel disease compared with so called fibrinoid necrosis. Classic arteritis of course is fibrinoid necrosis which is necrosis of the smooth muscle and entire media but there is a difference between the two: (1) fibrinoid necrosis is truly infiltration of the wall but unusual protein which contains a lot of fibrin and looks like fibrin; whereas that due to, when we started with sulfonamide, was very clear. It could be seen as due to necrosis of just the smooth muscle, not infiltration and that was followed by destruction of the wall, fragmentation of elastica, calcification, etc. So these two types are different.
Actually, I canít remember his name, but there was a man in South America who showed that rats after nephrectomy will develop degeneration of smooth muscle in aorta but he didnít follow it because the rats died within a couple of days. When we repeated it we could see a similar degeneration of muscle as a principal change in the aorta and large vessels and that was different from fibrinoid necrosis. So we presented a study on renal vasculitis due to hypertension caused by obstruction of one artery or wrapping of kidneys in silk and renal primary hypertension. In primary disease of vessels due to obstruction and perhaps destruction of the function of the kidney. Unfortunately we couldnít follow because very soon the poorly soluble sulfonamides were replaced by well soluble sulfonamides and the manufacturer stopped making them. So it is still a mystery to me exactly how it works.
RB: Even though your most famous contributions have been probably in the area of vascular and renal pathology, if I were a pulmonologist I would say that one of your major contributions relate to the role of asbestos in both pleural diseases and malignancy. Can you make some comments about how you ended up making those observations?
JC: Well, thatís an interesting story indeed. Actually, the person who did most of the work in that field is Dr. Irving Selico..... We both worked in Paterson, New Jersey and during the Second World War there was a factory in Paterson that produced insulation for the navy. The insulation consisted mainly of asbestos. The x-ray man on the staff of Barnett? Hospital used to visit this factory and he said he couldnít seen around more than 6 feet , it was so dusty. The men were told to where masks but they didnít and so within the next 15-20 years, we began to see cases of asbestosis, pulmonary cancer and mesothelioma. He saw them clinically and I saw them at autopsy. He is the one who was able to persuade the union, who were very resistant, to revealing their information. He persuaded them that it was to their benefit if they give him the data. Then he could pursue it, learn something about it, and get the manufacturers to change their ways. He was very skillful in that because he did persuade them to give him the information and he was clearly able to establish a relation between asbestos exposure and cancer. I think that was a major contribution, and then to study a new area, which is mesothelioma. because until that time, mesothelioma was considered to be a very rare disease and then we started to see a large number of cases or mesothelioma. So he and I formed a mesothelioma panel, letting pathologists know that we would make an effort to diagnose the disease for them and indeed we started receiving cases. There were a large number of cases -several hundred in a matter of 10 years. Some of them were not mesothelioma but many were truly mesothelioma and obviously there was a clear-cut relation between asbestos and mesothelioma. I think that was an important contribution. Of course mesothelioma comes in several varieties and between myself and my associate, Dr. Caniston? we found a new variety, i.e., desmoplastic mesothelioma, which fortunately proved to be most difficult to diagnose because it is so similar to pulmonary pleural fibrosis. Anyhow it was a worthwhile contribution. We published a fascicle for AFIP and now its in the second edition, "Tumors of Serosal Surfaces". It is a separate field anyway.
You see my point - in addition to renal pathology, I was a general pathologist. I ran the laboratory at Barnett Hospital in Paterson. Of course I saw all the cases, all the slides, all the difficult cases, so I maintained my interest in general pathology. In the laboratories, I was the one who introduced blood banking at Paterson. We also had the School of Medical Technology. Al of that of course was part of my job as a pathologist and director of laboratories and it did take 8 hours a day including various meetings, committees, God only knows! Still, I was able to work for more than 8 hours. As somebody said, "You cannot accomplish very much working 40 hours a week. It take more than that." I used to work usually 12 hours a day and as long as I was young enough it didnít bother me.
RB: If we can switch gears slightly, youíve received many awards and many visiting professorships throughout your career. You also have had a strong interaction with the International Society of Nephrology. What kind of interactions can you recall? I guess youíve attended those meetings.
JC: I was never active in the Society as such. There simply was not enough time to do that. Whatever we could report at the international meetings we did. Right now, my associate Dr. ............, is going to Australia for meeting. We made a small observation which may be interesting - diffuse mesangial sclerosis in children. Well, we looked at the casts in the disease. Purely by chance, looking for glomeruli, we noticed there were also unusual casts. Usual casts under the electron microscope consist of granular material and short fibrils. These casts were different in the sense that they consisted only of fibrils - long fibrils with very well defined periodicity. Then we looked again under the light microscope and these casts were indeed unusual. They were not usual round casts, they were angulated, they seemed to be easily fractured, like myeloma casts but they stained differently from myeloma casts. So there is something in that disease possibly ........................ protein in the blood. At least we have histological observations. So far we are not able to show any kind of physiological alteration or immunological changes in the serum but hopefully there may be something.
RB: Youíve also, during your career, been a member of various grant review study sections for the National Institutes of Health and other places. There is obviously concern now about how we spend our research dollars and there is convincing evidence that billions of dollars are being spent on renal disease, probably $12 billion this year, for all elements of endstage renal disease. Given the limited dollars to spend on research, what is your opinion about the research directions that the nephrology and immunopathology community have right now? Do you think we are going in the right direction?
JC: Maybe not anymore. Of course, I donít know enough about molecular physiology to express an opinion but I think thatís where we should be going. Eventually we will have to go that way. Like everything else, when renal biopsy came it was something new and it contributed a good deal over the next 20-30 years, just like Virchows contributed with ?surgical pathology. Everything takes a new point of view.
My teacher, Dr. Paul Klemper, who really established systemic connective tissue disease as a separate entity, always felt that what we do now is only a small part of what can be done. We need to do more and always look for a new approach. You know the old saying, "The more we know, the more we see how little we know" and how much more work there is to be done. As far as Iím concerned, very good. It will keep young physicians and scientists busy for the next hundred years. When this is finished, there will be something new. The whole world is a very interesting place.
RB: Well, the other aspect of that is that renal pathology has contributed a great deal to our understanding of the pathogenesis and classification of renal diseases and may be the limitation in therapy relates to the fact that we donít know really what proper therapy should be applied to which of these diseases. This brings up the big debate of should we fund these large and expensive clinical trials and if so, would they be of value and who should supply the money. Should it be governmental agencies, should it be pharmaceutical companies and if so, how do we coordinate these things?
JC: You can only do what you know. Thatís all we know at the moment and I guess we have to pursue it and see what we really can accomplish with what we have in hand. May be our therapies are too limited to begin with? May be gene therapy will be something that will be of great importance in the next 20, 30, 50 years - we donít know - but you cannot say, "Well, we donít know enough so better do nothing." I think it is always much better to do something because something new will emerge from whatever we are doing.
RB: Letís see. Well, I think it was the guy that wrote Bridge at San Louis Rey, not John ............... Post.......
JC: Unfortunately, young people nowadays donít look back. They realize of course that there was not much accomplished until recently. Do you remember Dr. Engelfinger, who was the editor of NEJM?
RB: I didnít know him. I knew his daughter.
JC: While he still was the editor he wrote an editorial: "The Contribution of Medicine to the Welfare of the Patient". He said that until this century the encounter between the physician and the patient was generally to the detriment of the patient. Only in this century things have changed and really we do make a contribution - may be in 15-20% of cases medicine really helps. However, in 10% or maybe more, medicine produces complications in disease. So the net gain is something like 5-10%. Still, itís much better than it was before. So knowing history, one at least becomes more modest and says, "Well we only know so much."
Always follow the suggestion of Hippocrates, do not harm the patient!
RB: Your interests in medicine are not merely confined to, letís say clinical nephrology, medicine and renal pathology/ It is a little bit broader than that.
JC: Yes. I worked in various areas and published papers in various areas. But still the main areas are what we mentioned, namely pulmonary and pleural diseases, vascular diseases and renal diseases. The field is too big now. You look at textbooks on nephrology and they run to 3000 pages. There is too more information - not even information - data, which may be valuable. It may not be valuable. Still, we have to do whatever we can because while we work, we may have new ideas, if we donít work, we donít have the ideas.
RB: At your own institutions, you also established societies or lectureships related to the history of medicine. What contribution do you think that makes to our capabilities as physicians?
JC: Well, you see, my teacher, Dr. Klemper, was very much interested in the history of medicine. He was the one who established or at least help create the Rare Book Division at the New York Academy of Medicine. You know how he came across his idea of diffuse collagen diseases? He looked carefully at autopsies and lupus cases. It was Dr. Bayer who collected them. He was known for that and they had many cases of lupus and had many autopsies. What he found is there were changes in the interstitial connective tissue, rather few changes in the cells themselves. Usually itís the cells that suffer and then you have secondary changes in the interstitial tissue. He remembered from the history of medicine that before Virchows concentrated on the cell, pathologists defined diseases by changes in the fibers. Well, of course, it was only what they saw grossly - with the naked eye - but presumably they had in mind tissue outside of the cells and so it suggested to him, maybe what he saw in lupus is not a disease of the cell itself, but a disease of interstitial connective .tissue. In a way he is right but still it starts with the cell, but eventually you have connective tissue changes. That has always interested me - the history of medicine, how people viewed various diseases and how they tried to approach them. You know very well that medicine always changes its standing with people. In some periods physicians were respected, like say from the discovery of antibiotics to recent times, and other times they were not and theyíd just suck the blood from the patient and do nothing for them! Well, not true! Because, physicians did know how to help patients. Nowadays, young people may not even know it. I remember very well that a surgeon came to me with a complaint and he had infection of the finger and he had this antibiotic and that antibiotic and it was still there. I asked him, "Did you try to soak your finger in hot water?" and immediately it helped. So thatís what physicians knew - how to help the patient, not how to cure the disease but how to help the patient. Nowadays it is too often forgotten and physicians have no time to listen to the patients. Who said that most of the diagnoses are made from good history? Itís still probably true.
RB: Also, I think that we found over the last couple of decades that itís may be increasingly difficult to convince our brightest medical students that an academic career either in clinical teaching or in laboratory investigation is their best alternative. Do you think if they had a little bit better knowledge of the history of medicine, that might be different?
JC: Maybe but after all who selects the future medical students? The directors of admissions and they tend to select the same people who do very well in business, with the same abilities and so we tend toward the business of medicine rather than the science of medicine.
RB: You have not officially retired from your position.
JC: No I am still on the staff. I am emeritus staff. This April I will go back to teach and may be Iíll do it next year but I donít think its going to last much longer. If you are not in a daily contact with medicine, pretty soon you begin to forget some of the essentials.
RB: But youíve seen the departmental structures and school of medicine structures change over the years and youíve contributed to the governance of those programs in places like Mount Sinai. Do you think that even time academicians now have to become businessmen?
JC: Well they are being pushed that way because they have no money.
RB: Tell us a little bit about you life here now. You moved to California. That was a choice to be close to your children but are you maintaining your interest in whatís happening?
JC: Well only in the sense that I am still participating in books that are being written. Otherwise, no I havenít. In a way it is a pity but also I cannot contribute much more. I know what I knew before but new things escape me. I really donít know much about molecular physiology, or molecular pathology. Unless you know something about it, you are not contributing,
RB: We mentioned other memorable people in experimental pathology. Were there other people in your interactions internationally that you had either clinical nephrologists you must have known, Habib and Hamberger.
JC: Oh sure. Habib and I worked together on many issues, particularly the international study of renal disease in children. That was a major study. She had a very sharp eye. Itís too bad that she was sick, as you probably know and she couldnít work much. She was a most energetic person and a very deserving pathologist.
RB: The other area of renal biopsy to which you contributed so much is now being used very greatly in the area of renal transplant evaluation. Thatís done frequently. Thatís probably the most common biopsy we do per patient. Is that, do you think, going to be helpful in our therapy?
JC: I think it is because it would help you to distinguish between an acute process which can be affected by therapy and a chronic process that really doesnít respond much to therapy. So I think itís important to know - how much, how severe and what can you do about it. Yes, I think itís helpful.
RB: You also mention that when you were a young physician in training that the dominant experimental knowledge and observational knowledge seemed to be coming out middle Europe, letís say Germany. That seems to have changed a bit - not that theyíre not making contributions but do you have any feelings about why that change occurred?
JC: I think they were badly hit by the War. Everything was destroyed. No, they are coming back. There are some very valuable contributions from Germany but every country in Europe - Italy is contributing a good deal nowadays. France to some degree, England is pretty good. No, I think most countries now have recovered enough to make a contribution. They still donít have the personnel or the money that we have here and for the last 50 years this was a dominant medical center - the United States. But everybody is trying and I think they are succeeding to a great degree. Take Stewart Cameron. He did a lot in nephrology.
RB: Youíve had a lot of trainees yourself in your Department. Any particular personal experiences with trainees or some that you are very proud of?
JC: It is interesting that most fellows came from Asia - China, Taiwan, Philippines and they did quite well. Many of them went back, some of them stayed here, some were very, very bright, as bright as anybody else can be. They just have fewer opportunities but that is going to develop. Even in China I think theyíre going to. Somebody said renal biopsy must be akin to acupuncture in some ways!
RB: You were also involved in teaching medical student, also in your affiliations with Mount Sinai. Itís some of our perceptions that the way we teach pathology has changed over the last several years, probably because of the knowledge expansion. Do you feel thatís for the better or for the worse.
JC: I think maybe we have too many specialists nowadays and medical students are not interested in such a special field as pathology. They would like to have a report that tells them what the patient has but they donít want to look at slides because itís not being taught. You cannot teach understanding of slides in a few sessions. Nowadays, at Mount Sinai, we don't even show them slides. We only show kodachromes in relation to cases. If you have a clinical case of this or that and clinical information is such and such. In addition, the renal biopsy shows this and this - so they can put it all together. Thatís what they really want and thatís what they like. People donít go into pathology as a basic science because itís really not a basic science anymore. Itís an applied science and I think itís part of the clinical picture rather than basic science. My impression that basic science nowadays is done mainly by Ph.Dís and not M.Dís and those who go into also go into basic science rather than applied science. So, may be itís to the better and maybe its not because students only want certain information and donít want to know anymore than is necessary, than what they think is enough to take care of the patient. Probably itís too limited.
RB: How we spend time with, letís say medical students, in this country in the second year has changed radically too because it seems now that pathology is taught as pathophysiology in lectures with slides as you mention, and even 30-40 years ago I remember it being taught in small group sessions, where you had buckets in the morning and you had gross anatomic changes, slides in the afternoon. That must have an impact on what kind of product weíre are producing as a medical student.
JC: Yes, thereís no questions about it. Again, we live in an age of specialists. Do you remember that this is not the first time that we have so many specialists in the world? The first time it was in Roman times, around the time of Galen, when there was a specialist for every known disease at that time. You say, "What did they know? Why did they specialize?" Yet they specialized and then they disappeared and came back again in the Middle Ages - I think in the time of Paracelsus. Again, there were specialists for every known disease. Now we have specialists for every known disease and Iím sure it is going to disappear. And we wonder what they really tried to specialize about. Well, that is called progress. As you said, everything recurs and this whole thing has recurred. Perhaps to the detriment of medicine. There is too much information, as I said, and too much data. Itís just impossible for anybody to know more than a limited field. What do we have now? There is something like 30,000 known diseases. If a physicians knows a few hundred of them, he is doing quite well.
RB: But itís also disappointing in that if we do not expose medical students to the process of being a pathologist, then we will never create a pathologist.
JC: No. Perhaps you notice too that may be 1 or 2 per cent of students who go into pathology.
RB: But even for the internist and surgeon, it is valuable to have had that exposure. Many of ours have only observed and never performed an autopsy.
JC: That is quite right. So you have nephrologists. Nephrologists do look at kidney slides and they learn that much pathology that is helpful in their own field. Same thing for the surgeons. They do surgery, letís say orthopedic surgery. They learn a lot about bones and joints and nothing else. Again, too much data.
RB: From your perspective, taking the last 10 or 15 years, could you point out to us some of the observations that you think have been most important in the last decade or so?
JC: Probably I have to go back to molecular pathology. You know the name of Dr.?Popper. He was Chief at Mount Sinai and worked in liver diseases and he was the one that suggested that when we study the cell, we should concentrate on cellular organelles. It is only an intermediate stop because the next one is the molecular change. That is going to contribute very significantly.
RB: Well it certainly requires some kind of interaction between the pathophysiologists and the molecular person because, obviously, of the limitations of molecular biology - itís not a kinetic science. Yet some people say that molecular biologists are accountants, pathophysiologists are economists. There is a difference.
JC: Thatís true. Again there are specialists and somebody has to come up who will be able to integrate it. This undoubtedly will happen.
RB: Iím getting a little far afield here but the way we do medicine has changed in the way we finance it. Iím sure in your time of training early in the United States you were basically seeing patients who had no bills or had either paid for it or didnít pay for it at all. We are now in a setting of managed care and obviously there are pressures to do less but may be more expensive procedures. Do you think thatís going to have an impact on the way medicine goes?
JC: We are back to the fact that probably 80% of patients recover by themselves. With treatment or without treatment, with individual physicians or HMOs. And I think the HMOs are taking advantage in the sense that, "Oh you donít have to do it. Either the patient is going to improve or the patient is going to die, so why do anything." I donít think itís a good attitude.
RB: And we also have a rather low autopsy rate in our academic institutions and a really very low rate in many of our private hospitals. Do you feel that thereís a long term impact of not having access to autopsy evaluations?
JC: To some degree thatís true because we will be missing something that can come up but we other methods of diagnosis, we usually do know most of the changes in the patient. Maybe 80%, maybe even more. So we are not missing as much as we were missing a hundred years ago. Thatís why autopsies were so important. Surely there are cases nowadays where the patient died of something else, not what the official diagnosis says. But I donít know that we are missing that much.
RB: But, for example, do you think in this day and age you would have been able to diagnose or describe the Churg-Strauss syndrome had you not had an anatomic file available?
JC: That is correct. And thatís why weíre missing something and weíre missing some new things that may emerge from that. But for practical purposes, we are probably not missing that much. How do you treat Churg-Strauss syndrome? With steroids!
RB: Well we also have to live unfortunately with the consequences of our therapy and one of the arguments that rheumatologists, nephrologists have constantly is that with the general success of renal transplantation, should we expose a young person to the potential horrors of heavy immunosuppressive therapy?
JC: No. But this is probably a matter of proper studies. Which approach is better? Because, after all, even transplantation, if successful, is very good but still there are so many rejections and so many re-transplantations. So, we need more accurate statistics.
RB: So if you had to pick some time in your life that was your favorite time in terms of your academic or personal development, what time seems to have been the best of times?
JC: Oh the best of times was probably the early years in training because I did have very good teachers and I think that so much depends upon your teacher. If you have a good teacher, you will enjoy it, and if your teacher is not interested in what you are doing, then you cannot develop it. When you are young, you do need help.
RB: It seems as if many of your teachers were, as I understand it, many people who had been may be only one or less generation removed from Europe as well.
JC: Thatís true. I donít know whether they were better teachers or that it meant only that they came here because they had more enterprise, more knowledge and some were able to succeed. Thatís always the question about immigrants. What distinguishes them from people who stayed behind.
RB: Well, as you said earlier in our conversation, to repeat a fact, is that if we do not learn the lesson of history, we are forced to relive it. Recently there are pressures to keep foreign physicians out of this country, either for academic or private medicine purposes. If we look back at the history of renal pathology or even nephrology, we would be certainly at a big loss had we not allowed people such as yourself into the United States.
JC: Well thatís true to some extent. It seems to me there are two problems. After all medical students in the United States are among the brightest young people and they indeed can accomplish a lot if they are not pushed to the business side. I think, fortunately, enough people do become interested in medicine for medicineís sake and so they do contribute considerably. In many countries outside of the United States getting into medical school is part ability and part knowing the right person. Some people who come here are in the second category and they do not contribute much.
RB: Also, thereís probably a screening process where only the most ambitious, possibly, are coming from other countries to come here for purposes that are for their own self development as well. Because I knew we were joking at the recent American Society of Nephrology meeting that among the 6000 abstracts or so, it was very hard to find an Anglo Saxon name.
JC: Well the Japanese names are dominant now.
RB: I suppose the other problem is that we are now the receptacle, for trainees from other countries. Youíve trained many people from Asia yourself. The question is: Should American tax dollars contribute to that or are we still the centre of training for all these countries to develop since now World War II is 50 years behind us?
JC: No. I think it is very important. After all, this is a leading nation in the world and also of course economically but I think also scientifically. I think that we should make an effort to spread our knowledge as far as possible, to improve the lot of people outside the United States. Some people say, "Well, letís be only concerned with ourselves." I donít think we should.
RB: Some of your family members - your children - are in medicine.
JC: My sons are in medicine, yes.
RB: And that was a choice they made because of their knowledge of looking at your books, just as you looked at your fathers?
JC: Well, thatís true of my younger son. My older son, Andrew in Vancouver, wanted to be a chemist and he went through college aiming for chemistry. Then I donít know what happened. He thought that may be he would do better in medicine than in chemistry, so he changes his mind.
RB: Heís in pathology and heís an expert in pulmonary pathology I believe?
JC: Yes. As you know, in Vancouver there are a lot of pulmonary diseases. Vancouver is a tourist place but also it is a big port with all kinds of diseases connected to transportation. Also, there are many mines around there and so they have diseases connected to mining. There are several pulmonary pathologists there, for that reason.
RB: Any other children in medicine?
JC: My younger son is right here in Los Angeles. He in fact is in charge of a training program in family medicine at one of the hospitals.
RB: Looking over your curriculum vitae, itís looks like youíve not only written many many hundreds of papers, but youíve also served on a variety of committees and received a number of awards, including the John Peters Award. Would you describe some of these activities that you thought were significant - may be some of the important international committees, that were most interesting to you?
JC: Yes. I think that many were very interesting. For example, the Mesothelioma Panel established by the International Union Against Cancer. You see something that is not common and you develop expertise. You know pathologists are interested in details and they were a very detailed studies that we did.
I think that in many other things I was fortunate. I served on many committees that required collaborators and my collaborators were generally able people. I think without them I couldnít have accomplished much. Each one of them contributed something and each one established new interesting areas. Dealing with people who are interested in the same area that you are is always stimulating. I presume that you have found it also the same way. Thatís why I participated in all these committees. You see Iím not a committee person by itself but to interact with people was very very helpful. Like the WHO Committee on Classification of Renal Diseases. It still stands because this classification turned out to be quite successful. Now we have a second edition of Glomerular Diseases and now we are working on a second edition of Tubulointerstitial and Vascular Diseases, all for the same reason.
RB: Well certainly progress in the classification and identification of renal disease has been ongoing and it is becoming highly complex but at least everything is compartmentalized into fairly neat categories. Yet Iím disappointed as a clinical person and as an experimentalist that something as seemingly straightforward as treatment of nephrotic syndrome has not in my view progressed very much in the last 27 years.
JC: You know, you look at the classification and it seems like a reasonable classification and perhaps a helpful classification and yet we learned that there is no one-to-one correspondence between the histological picture and the clinical picture. The same histological picture occurs in many clinical situations and vice versa. So classification is only useful, to my mind, if it helps the patient. If it doesnít help the patient, itís very nice, very interesting, but not necessarily important.
RB: Actually the importance of the renal biopsy that you made contributions in its utility is that sometimes we do not give credit for the temporal dimension of a disease process. In other words, something may look this ........................ at this stage following an insult but unless we know the natural history of that evolution - hence the biopsy.
JC: So really I think biopsy may be considered only a part of the information, taken together with everything else, not by itself. At first it seemed, "Ah well, now we have an answer to everything." But we donít.
RB: You are interested obviously greatly with childhood renal disease as well. Thatís an area where sometimes it seems like the treatment is worse than the cure. Youíve have interactions on those types of panels. Any comments in that area?
JC: Well, I we mentioned before, letís take the approach of pediatricians to, letís say, nephrotic syndrome in children. First treat and only then biopsy if the treatment is ineffective. Which may be perfectly all right. The same goes for poststreptococcal GN. If it resolved by itself, donít biopsy. In a way, we donít see ordinary cases like minimal change disease - we donít see it often anymore. On the other hand, we see many new diseases which although seem to be ordinary clinically, turns out to be something unusual pathologically. New diseases tend to proliferate. I just recently saw something about dermatology. A hundred years ago dermatologists recognized something like 100 different diseases and now they recognize over a thousand.
RB: Also, the other impact that has lessened or, letís say, undermined the utility of the renal biopsy has been medicolegal issues because I know that academic medical centres tend to do a very high percentage of renal biopsies, whereas the private arena in nephrology does far less, and probably because it takes time to do a renal biopsy.
JC: There is also another aspect to it and that is that the pathologist should know something about clinical medicine and understand what the clinician expects from a renal biopsy because just giving a histologic diagnosis by itself is not very helpful. I have done many biopsies from the various areas in Northern New Jersey and the clinicians were quite interested because I could tell them something of what I saw in other similar cases. How they behaved, how they responded to therapy, and I think pathologists who only look at slides and make histologic diagnoses are not very helpful.
RB: And obviously the question of follow-up, because we have patients who are changing doctors and there may not be continuity to their care that is required, that many years ago only academic medical centres could supply because they had a population of patients that were theirs for a continuous period.
JC: On the other hand, if a patient lives in a certain area, he is liable to go to only a limited number of places and since the number of renal pathologists is not increasing, the Renal Pathology Society has something like 120 or 130 members now, but most of them are general pathologists who also do renal biopsies. Only Dr. Habib does only renal pathology. I donít know many more people who are able to do that. But still, young pathologists have to have some understanding of clinical problems and that is unfortunately what is missing. When they are so intent on learning the histological diagnosis, they donít correlate it with the clinical information.
RB: Well, I want to thank Dr. Jacob Churg for having this discussion with us today and thank you again for all of your insights and I can see that you are an outstanding teacher, from the conversation and the insights you have supplied. Thank you very much.
JC: Thank you very much Dr. Blantz. Yes indeed. It was a very interesting conversation. I think Iíve learned something.