Source: https://www.cybernephrology.ualberta.ca/ISN/VLP/Trans/Pirani.htm
Timestamp: 2019-04-21 00:51:46+00:00

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VD:	Good morning, I’m Vivette D’Agati, Director of Renal Pathology at Columbia Presbyterian Medical Center, and I have been given the honor of interviewing Dr. Conrad Pirani for this Video Legacy series of the International Society of Nephrology.
Dr. Pirani, I’ve known you since 1980 now, when I came as a second year resident to your laboratory here at Columbia. I know quite a bit about your career, but many of our viewers may not be as familiar with the early history of your life and career. Maybe you can start by telling us a little bit about something of your early days in Italy and how it was you came to study medicine.
CP:	I come from what I could call an academic family, my father being a Professor of Chemical Engineering at the Polytechnic Institute in Milano, Italy and I always thought, through my days in High School and Junior College that I would study engineering because of my father being in the field. However, at the last moment I got a bit afraid because my mathematics was kind of weak and I was afraid to be a student in the same institution where my father taught and not doing well so I changed my mind and I decided to go for medicine. In other words, I was not a born physician. It was a decision taken at the last minute really. From then on I followed my medical studies mainly with major interests in research.
VD:	How was it that you came to leave Milano and come to the United States? Can you tell us a little bit about that background.
CP:	Well, I went through my medical studies and did some research work as a medical student, as well as for my thesis which is required for graduation from Italian Universities. Then around 1938 in Italy the fascist government passed racial laws similar to those which had been introduced in Germany a few years before. In other words, people of Jewish background could not enter the professions, could not work. So, although I was able to finish my studies, within a year after graduation, which was in 1938, I realized I could not do anything in Italy and had to get out of the country. So, I opted for the United States, a decision which I think was the right one.
VD:	Did you know anyone in the United States at that time?
CP:	No, I didn’t know anybody, although I had some letters of introduction which ended up not being of much help actually. At any rate, I was able to meet some people shortly after I arrived and then I had some people whom I knew but not in the medical field.
VD:	When you first came, did you go directly to Chicago?
CP:	No, I was in New York. The first year I was in New York and at that time, New York was crowded with medical doctors escaping from Europe and it was very difficult to find a job so my first job was when I replaced an intern who had become ill, while I was looking for an internship which I was able to find in Chicago.
VD:	When you first went to Chicago, you worked for sometime, as I recall, in the U.S. Army Medical Research Laboratory.
CP:	Before that I had several years in Chicago, actually. I had two years rotating clinical internship and at that time I was still undecided whether to go into internal medicine or into pathology. My thesis in Milano to graduate from medical school had been in pathology, so perhaps that was a field in which I had a little more experience coming out of medical school. After the rotating clinical internship I was able to secure a residency in pathology at the Michael Reese Hospital, where at that time the Department of Pathology was directed by Dr. Otto Saphir, a renowned pathologist, especially in the field of cardiovascular pathology.
VD:	I’ve heard you speak of him many times. He was a big influence on your career at that time.
CP:	Well, he was a superb morphologist, very precise in the training of his residents. Every morning we had to have studied the surgical pathology slides and be ready to answer any questions Dr. Saphir should ask.
VD:	I don’t know that today’s residents are so ready in the morning.
CP:	He would ask what I thought of this or that and he was pretty strict in what he required of us.
VD:	So you spent two years then in a rotating residency.
CP:	I spent a three year residency in pathology at the Michael Reese Hospital which was exclusively anatomic pathology. I did not want to take any training in clinical pathology and at that time, most of my work was in cardiovascular disease which was the great specialty of Dr. Saphir and I worked mainly with the assistants and residents in the section of cardiovascular diseases of the Department of Medicine and I published several papers on heart disease at that time as a resident, one of which on the heart in uremia, was with Dr. Langendorf, who became a renowned cardiologist. Also one on endocardial infarcts. So my interest was, and I still thought I would become a cardiovascular pathologist or perhaps a clinical cardiologist. I was still a bit uncertain whether to stay in pathology or go into medicine.
VD:	What influenced your decision to enter pathology. What was the deciding factor?
CP:	Well, I liked the field and Dr. Saphir had been very nice to me and so I remained in pathology. However, for a moment, as I mentioned, I had some doubts. Actually, for a period of a couple of months I attended a clinic on renal diseases which was directed by Dr. Sternheimer of Sternheimer cell fame and he was, again, very precise. He required that every clinician working at that clinical should first look at the sediment of a freshly voided urine specimen of the patient before examining the patient which I still think is a very good idea although I don’t think it is done any longer.
VD:	I don’t think the art of urinalysis is done well anymore. So you first started doing urinalyses before you looked at renal biopsies?
CP:	Yes, because really if you think about it, the urinary sediment, as Sternheimer said many years ago, is much more likely to give you an inkling of the type of disease which affects the kidneys. In other words, if you see red blood cells, the chances are the disease is in the glomeruli, if you see white blood cells, the chances are the disease is in the interstitium and if it is tubular cells that means there is degeneration of tubular cells that you may see at times in the nephrotic syndrome, there are oval fat bodies at times in acute tubular necrosis there are severely damaged tubular cells. Now renal functional tests will not tell you anything about the type of disease. They’ll tell you about the overall function but qualitatively these tests are not very helpful.
VD:	Now, it’s my understanding that you have some experience in renal physiology from the work that you did at the U.S. Army Medical Research Laboratory during the Korean War.
CP:	After I completed my residency, I was able to secure a position as Instructor in Pathology at the University of Illinois College of Medicine in Chicago. That was the first academic step and at the time the Department was directed by Dr. Granville Bennett, who was mainly a bone and joint man - very good in his field - and the Associate Director of the Department was Cecil Karkower, who had done some excellent work on sodium and cardiac hypertrophy and more especially on the isolation of glomeruli and identification of nephritogenic antigen in the basement membrane. So, it was a good Department at that time, a strong Department. Dr. Bennett had promised me that he would find some money for my research. However, he was never able to do so and I got a bit discouraged until Dr. Bennett called me and said, "Look, I realize I promised to find some money for your rabbits but I cannot find any money. However, I have been contacted by someone saying that they need an experimental pathologist in the U.S. Army Medical Research Laboratory right here in Chicago. Go and see what they have to offer and if you should accept that position, you can still remain on the staff here to help us teach in the course at the second year level." So I did this and there was a lot of money available in the Army and this was a laboratory which was very well organized. It was directed by a physiologist, Dr. Johnson, who was perhaps one of the few remaining human physiologists in the United States, who knew what the significance of fatigue is in man, not in rats and the other remarkable man in the Laboratory was Dr. Robert Kark, who was the Director of Clinical Investigation and he was particularly interested in malnutrition and he was studying this problems in troops at the Veterans Hospitals and so forth. A third very capable and competent man was Stanley Levenson, who was a metabolism expert. He was a surgeon originally, trained at Harvard who had originally studied the famous Coconut Grove Fire nutrition problems of people who had been burned, who had lost a lot of proteins and had serious nutritional problems. Anyhow, this was a very important period in my scientific life because the laboratory was not a large institution. I was then in close contact with physiologists, with a man interested in metabolism and with a man interested in clinical medicine. Whenever we had a project to carry out, we consulted each other and criticized each other and I learned a great deal. Now, in that period (I remained in that lab for about five years) that was the time of the Korean War, I did a lot of work on wound healing with Stanley Levenson, particularly with vitamin C and then vitamin C in stress phenomena, and vitamin C in relation to the adrenal cortex. I think the experimental work I did there was of considerable help to me in my medical career.
VD:	You had to do careful histopathologic grading, isn’t that right, of the lesions in wound healing?
CP:	The function and significance of lesions, the factors involved in lesions and perhaps one thing I should mention in addition is that as I was studying wound healing, and we took specimens at regular intervals after we had inducted wounds in the experimental animal, we took specimens at day 2, day 4, day 7, day 10, and day 14. And there were different microscopic findings in these wounds depending on the state of nutrition and in order to compare, to reconstruct the evolution of the healing process under normal conditions or under a condition of nutritional deficiency, we had to quantitate the different changes that one saw in the wound area and compare day 2 to day 4, day 4 to day 7 and so on and so forth, and this gave us something that you could actually put on a curve and give you a much clearer understanding of what was going on. Incidentally, that was one of the reasons why several years later I instituted the same method in the examination of renal biopsies.
VD:	Although we didn’t do so many serial biopsies did we?
CP:	When they used to take serial biopsy, yes. But also in order to compare semi-quantitatively the histologic findings with the renal functional data.
VD:	Yes, it taught you to be very precise with your observations and to correlate them.
CP:	Yes, it helped you to be more precise and to try to quantitate or to semi-quantitate in order to have a better understanding of the functional significance of the lesions.
VD:	Well, let’s turn a bit to those early days at the University of Illinois. I know in 1952 Kark and Muercke were perfecting the technique of percutaneous renal biopsy that Iversen and Brun had introduced in Denmark and that you became a very integral part of that team. How was it that you came to work with them originally and that these renal biopsies became entrusted to you?
CP:	I went to the U.S. Army Lab at the end of 1947 and in the spring of 1952 the character of the Laboratory changed completely. Actually the Laboratory shortly thereafter was moved to Denver, Colorado and I didn’t want to move from Chicago and Dr. Bennett in whose Department I was still working part time, offered me an Associate Professorship. By that time, I had published quite a bit - mainly experimental work and so I went back full time to the University of Illinois in 1952. Shortly thereafter, Bob Kark, Dr. Robert Kark, had become interested in renal diseases although originally he was interested in liver disease and nutrition. One of the reasons he became interested in it, as he and others have written, is that once in awhile, when he was taking a liver biopsy, he got kidney tissue instead and absolutely nothing untoward resulted - no functional damage kidney or anything. So he felt a renal biopsy could be taken. At about the same time Dr. Iversen and Dr. Claus Brun in Copenhagen, Denmark had developed a method to take renal biopsies and the reason that they developed the method was for the same reason that Dr. Kark had become interested. They also once in awhile , Iversen, instead of taking a liver biopsy, because he was originally a liver man, got renal tissue. So they felt the method could be applied to the kidney and it was Kark and Muehrcke, who was then a young resident, modified the method and imparted to it ideas from Perez Ara, who was a Cuban pathologist, and the renal biopsy then was taken with the patient lying down instead of being in a sitting position. The method became much safer with a much better yield of biopsy specimens. So essentially Kark and Muehrcke modified some methods and developed their own method. Then somehow the renal biopsy came to me for study.
VD:	Why were you selected from among the pathology team there? Did you express an interest?
CP:	Well, still I’m not sure I have an answer to that. Dr. Krakower, who was Director of Surgical Pathology at that time, was a very busy man, involved in other studies. Surgical Pathology was a very busy service. He felt renal biopsies were too much for him to handle. Bennett called me up and said, "I’m sorry." He practically apologized! He said, "I have to give you this responsibility because Dr. Krakower does not have enough time to take care of it." So the renal biopsy came to me by accident really. Now it may be that Bennett knew that I had worked in the past with Dr. Kark before and that I had a little experience of renal functional tests because I had worked on a project at the Army Laboratory in relation to dextran and renal function. What is interesting, looking back, is that when I got these biopsies, I thought it was an imposition. I did not realize at all what I was getting except additional work that I did not have much time either to take care of. I certainly did not realize the opportunity that was being given. I don’t think Dr. Bennett either realized the possible future of renal biopsy. So, I had to take it. You know, Dr. Bennett was the Chief, I had to take this responsibility and do the best I could in my spare time. I was very busy with the autopsy service. At that time the staff pathologists also rotated in the cytology service and also in surgical pathology from time to time. So that was something extra. It took me several years before I began understand what I was looking at.
VD:	In the beginning there was tremendous skepticism about first of all the safety of doing renal biopsies and secondly the value of doing these biopsies in terms of diagnosis. Can you tell us a bit about this?
CP:	There was some criticism and some opposition. The urologists didn’t like the idea because they felt the internists were entering their field. Also they did not like to be called if some accident should happen.
VD:	I am reminded of a story that you once told me about Kark’s reply to an editorial that appeared in Lancet around 1955. The editorial said something to the point that it is of as much value to treat a patient with nephrotic syndrome initially with cortisone as it is to do a renal biopsy and probably of far less detriment to the patient because you will get the same amount of information and it won’t do the patient any harm. Kark wrote a rebuttal to that, I remember at that time. Really there was tremendous skepticism about the safety and value of renal biopsy.
CP:	You are absolutely right. There was a very critical editorial that appeared in Lancet but I think a few months later Kark answered also in Lancet in which he pointed out that renal biopsy contributed a significant manner to the understanding of renal disease. Now the two major objections to biopsy were that: (1) it was felt that the information that the pathologist would get was only of academic interest and (2) in any case, there was no therapy anyhow, so what was the sense of understanding better. If we follow this type of reasoning, no problems would ever be solved in medicine. Just like not searching for antibiotics because a bacterium had been isolated or something. So new methods have to be evaluated but certainly at that time, I did not realize what future renal biopsy would have. It took awhile.
VD:	I think there was also a tremendous degree of skepticism about how one could draw conclusions from examination of so few glomeruli or so little renal tissue. How could it be representative because the pathology up to that point had all been autopsy based?
CP:	The specimen was so small, being a needle specimen, that many people felt it was totally inadequate to draw conclusions from. We made a very simple study on that by comparing the needle specimen with the larger areas from the same kidney obtained at autopsy and found there was an excellent correlation, not only in type of lesion that you would see but also in the degree or severity of the disease. However, you had to have, in our opinion at that time, at least five glomeruli and adjacent cortex. The study was repeated with many more cases by Dr. Chomet and others at the West Side Veterans Hospital in Chicago and this confirmed those results so in other words, you could obtain very good information in practically all diffuse renal diseases. We knew that in pyelonephritis the needle biopsy may be inadequate but then even a larger specimen may be inadequate in pyelonephritis and more seriously in focal segmental glomerulosclerosis.
VD:	I was always very impressed as a resident by the story you told me about a paper that you once submitted demonstrating the foot process effacement in a patient with minimal change disease and how on repeat biopsy there was restoration of normal foot processes. I believe you had something like seven glomeruli to look at by electron microscopy in the first biopsy and five or so in the second, but when this paper was submitted for review, the reviewers criticized it for the small number of glomeruli that had been studied and said certainly no conclusion could be drawn based on a study of so few.
CP:	Yes, that was a sort of famous episode. The problem of adequacy - we thought we had resolved that problem with our studies by light microscopy and then it emerged again when electron microscopy was introduced. The little bits of tissue left often contained only a few glomeruli and the case you mentioned was a case in point. Actually, we were much aware of that. We studied in that particular case, all the glomeruli or seven in the first biopsy, five in second biopsy, and we found very consistent lesions so there was no question that the interpretation adequacy was demonstrated but the journal felt still that the sampling was inadequate and the paper was rejected by the journal. However, this was accepted by another journal later. The first author is now a prominent cardiologist in Rome, Italy. His name is Guiseppe Folli and we actually demonstrated what perhaps was most important in the paper, that the lesion of minimal change disease is completely reversible and the glomeruli may return to entirely normal structure after therapy with cortisone and that was what these two biopsies represented: one was before therapy and the other was two or three months later, after therapy, after the proteinuria had decreased to practically nothing. So, perhaps one of the great merits of Kark and Muehrcke was that they insisted, at that time, on the importance of sequential biopsies. They were the first to use sequential biopsies> We demonstrated reversibility of lesions not only in minimal change disease, but in pre-eclampsia, and later with John Lewy in post-streptococcal glomerulonephritis. Really repeat biopsies are essential, not only because of the possibility that the lesion may reverse completely, but also to see the effects of therapy, to evaluate the effects of therapy. This is something that has now become more difficult to pursue because of ethical considerations. It’s very difficult to repeat a biopsy when the patient is better. Repeat biopsies, as a rule, are done in a number of diseases, including lupus nephritis only when the patient gets worse but not when he or she gets better and if you think about it, it’s still one of the avenues of future research. For example, in acute post-streptococcal glomerulonephritis you have an increased cellularity of the glomeruli in the acute phase with increased amounts of mesangial matrix being produced. Within months the hypercellularity in the great majority of cases has disappeared and also the mesangial matrix, which had increased in a significant manner, disappears. So it is not true, necessarily, that mesangial matrix increases or thickening of basement membrane are truly an irreversible lesion. Apparently, if the cause is removed such lesions to some degree can be reversed. Now what causes the reversion of this lesion - that is the question one should ask. Are there perhaps enzymes coming from inflammatory cells? I think it has to be something more than just the degree of immune complexes in the circulation. This may cause the increase in mesangial matrix but not the disappearance. It is difficult to visualize this. So, again, although I understand the ethical reason why repeat biopsies are not practiced today as they used to be, I still think it would be very important to understand the evolution of renal disease to repeat the biopsy in appropriate cases in a proper situation.
VD:	I’m rather interested to hear from you a little bit more about how the team of Kark, Muehrcke and Pirani developed in those early days and later Vic Pollak became a player. Can you tell us a little bit about how you developed your association and what each individual brought that was unique to the partnership and made it so successful?
CP:	Well, once the biopsy was given to me for "interpretation", which I’m sure was often wrong in the first year or two years, obviously contact with Kark and Muehrcke became very close and actually that is one of the most satisfactory things in renal biopsy work - that the contact with the clinician is very close. I’ve found that the clinical nephrologist still today have an active interest in renal pathology - something which I’m not sure is true in many other fields of pathology.
VD:	I agree with you and I think they have more knowledge of renal pathology than the average surgical pathologist by far.
CP:	That’s correct, absolutely. They have more knowledge of renal pathology than what other pathologists know.
Once I saw a young man with the nephrotic syndrome and I looked at the slides by the light microscopy. This was before electron microscopy. I couldn’t see any changes whatsoever. I reported, mistakenly, that it was essentially normal renal tissue. The following day I heard the booming voice of Bob Kark - he was a big man, he still is a big man - down the corridor saying, "Where is Dr. Pirani?" And he came into my office and said, "Don’t give me that stuff that this is essentially normal renal tissue. That tissue cannot be normal. The patient is losing 10 grams of protein everyday. There has to be something wrong with those glomeruli." I said, "I don’t see anything." He looked at the slides and he couldn’t see anything either and at that time I said, "Well, perhaps an electron microscope might be of help here." And sure enough, from then on, we started discussing this and eventually we came up with a little money to use an electron microscope. That of course revealed the widespread fusion or effacement of foot processes in all glomeruli but that’s the way it went. There was a continuous exchange between clinician and pathologist. If my observations did not make sense to them, they did not hesitate to tell me, believe me!
VD:	When did Vic Pollak join the team?
CP:	Pollak came two or three years later. So the first biopsy came out late in 1952 and Pollak came on board in about 1955 or late ’54. Bob Kark had a lot of connections, not only in South Africa, from where he came originally, but also in England, where he had done postgraduate studies and for a period we had a large number of research fellows all from the British Commonwealth, either from Canada or England or Australia, just name them, and they had the clipped British accent or South African accent or Australian accent. I learned how to recognize the different intonations of the English language plus my Italian accent. So many students kidded us about our accents.
VD:	Well, how was it that you came to choose the areas of study that you concentrated on. I’m thinking, for example, of your main interest in lupus and toxemia.
CP:	The first major interest was suggested by Dr. Kark, I believe, I ‘m not entirely sure about this but I think he had a major interest in the nephrotic syndrome, originally because of the nutritional problems of the big loss of proteins in the urine in the nephrotic syndrome. So the nutritional problem of the nephrotic syndrome intrigued him a lot and so we studied a large number of patients with nephrotic syndrome and actually wrote a big paper about the multiple causes, multiple different diseases of the nephrotic syndrome. Obviously, it was not a single disease. That became quite clear and actually the paper, I believe, fully confirmed this. There were no clinical studies alone, even detailed laboratory studies alone, that could identify the different diseases and still today we have problems I think in this although I think clinical nephrologist have become much smarter and perhaps not as many renal biopsies are taken today as they used to. But pathologists have become smarter too. So they know how to interpret the biopsy better perhaps.
Well, that was the first major area and the second major area was lupus and the reason for that was that lupus, because of the finding of LE cell, the disease was being recognized much more frequently now with a much greater degree of accuracy and obviously the renal involvement was a very serious problem in lupus and perhaps one of the major causes after infection, perhaps for the mortality in lupus patients. So, it was felt for that reason plus the possibility of using cortisone, and although Muehrcke started the work on lupus, Pollak took it over eventually. And we wrote a number of papers and Pollak was really the man who realized that in order to, so to speak, "break the back" of lupus nephritis you needed high doses of cortisone and also we realized something that unfortunately is not done anymore - that the earlier you treat, the better off you are. You should start treating lupus from the time of the earliest lesion. In other words, you should perhaps biopsy all patients with lupus, as long as they have minimal urinary findings because that’s the time to treat and perhaps prevent evolution to serious renal disease. There is evidence that this should be done. If you wait until the disease is very severe, treatment may slow down the evolution but eventually all glomeruli will become sclerosed and the patient will end up in chronic renal failure. There is evidence in the experimental animal certainly that you can control the disease if you treat early.
VD:	For those of us studying renal pathology as novices today, we take for granted right away the WHO Classification of lupus nephritis as a "fait accompli" and it’s hard to imagine, I think, the confusion that existed in those early days about the classification of lupus. In your view, when were the different forms first classified and what role did you play there. I am speaking in particular about the mesangial form and the membranous form. There is a lot of confusion about this.
CP:	This came on very gradually, as I looked at more and more biopsies from lupus patients. The presentation of the patient with renal disease was based on a variety of renal lesions. In other words, the renal lesions were very pleomorphic so we saw patients with minimal mesangial changes, patients with membranous nephropathy, patients with focal segmental glomerulonephritis. One of the first cases I had was a focal segmental necrotizing glomerulonephritis and I knew the patient had lupus but I felt it possibly due to bacterial endocarditis. It looked to me like focal embolic glomerulonephritis and I felt that perhaps this was a bacterial endocarditis, perhaps superimposed on Liebman-Sachs endocarditis.
VD:	I guess this was one of the most difficult things about renal pathology. The idea that one lesion can have many possible etiologies was really a new concept.
CP:	In other words, it’s not only that different diseases cause different lesions but the same disease can cause different lesions.
VD:	Or one lesion can be caused by many different diseases!
CP:	That’s right. That’s a very important concept that evolved from those studies but in fact it took many years of my work plus the work of many others to gradually unravel the complexity of lupus nephritis and to recognize that there were certain patterns and these patterns actually tended to persist as such. Others did not persist, they changed character, especially after therapy. So gradually a classification evolved and this really was only part of my work. Many others contributed to this and eventually a classification evolved that is now widely used. Together with that we clarified the fact - I believe others did too - that there were lesions which were active, that were potentially reversible and potentially reversible under therapy and other lesions which were very slowly progressive and were not reversible - chronic lesions, inactive lesions. This is very important to guide therapy because obviously it is hopeless if glomeruli are sclerotic and therapy - present day therapy at least - is not going to do much.
VD:	Yes, I think it was understood intuitively, even at that time, that there were reversible and irreversible lesions for every condition.
CP:	And again serial biopsy was very important here to clarify some of these concepts.
VD:	Now, as I look back at that period, in dividing your career from the early period into the middle period, I think a defining moment was the Ciba Symposium of 1961 which really was a monumental meeting in terms of putting renal biopsy on the world map and convincing the medical population that renal biopsy had a value diagnostically and therapeutically which led to its acceptance around the world. What are your recollections of that meeting and who were the players?
CP:	Well, that was probably the best meeting I have ever attended in my life and the reason it was so excellent is there was a limited number of people in attendance. I think the total number was less than 30 and there were 6 or 7 pathologists and the rest were clinicians - clinical nephrologists. The meeting was conducted at a leisurely pace. There was plenty of time for discussion. In other words, 3 or 4 papers were presented a day and there were no 10 minute papers. Each paper was presented in half an hour, 40 minutes. There was half an hour for discussion and also it was clear that the clinicians and the pathologists for that time were very well informed in the field. They were knowledgeable. The clinicians asked very intelligent pathology questions and perhaps vice versa.
VD:	Who were the pathology representatives? I know there was Jennings?
CP:	The pathologists were Heptinstall, who talked on focal glomerulonephritis, McCluskey, who talked on acute post-streptococcal glomerulonephritis. There was Movat who talked a bit on membranous. André Movat was the one from Toronto. Who else was there? Renée Habib, who talked on the nephrotic syndrome and membrano-proliferative glomerulonephritis. Among the clinicians there was Kark, Hamburger and Brun, of course. Iversen unfortunately had been ill so he could not attend. And then the people from Sweden and so on and so forth. There were several people from England as well - Black, among others. It was a very good meeting.
Now the Chairman of the meeting was the man from Hopkins, the Chairman of Pathology, Arnold Rich and he was not too enthused about the future of renal biopsy. But many others were enthused including myself and I believe the end result was that this meeting which was essentially based on the experience of many people over a period of almost ten years, perhaps 5,000 biopsies had been seen, really that was the meeting that launched renal biopsy and made it realized. Even today, with much better clinical diagnostic methods and so forth, still renal biopsy is essential in many cases.
VD:	And in English style, I think it helped to have a little sherry in the morning and a cup of tea in the afternoon. It certainly helped the discussion! A very civilized meeting!
CP:	Yes, it was very friendly and very helpful and very civilized! That’s right. The meetings today where there is a 10 minute presentation followed by 3 minutes of discussion, one after the other, are not very productive I think.
VD:	It’s not the same pace.
CP:	No, you should take your time discussing things.
VD:	What was it that made the Chicago area such an important focal point for renal biopsy.
CP:	Well, we were lucky in Chicago, I guess. At the same time as Kark and Muehrcke and Pollak and myself did our work at Illinois, Dr. Earle and Dr. Jennings in Northwestern were doing some very good work. They particularly studied post-streptococcal glomerulonephritis and membranous glomerulonephropathy and they did excellent, very good quality work I think and Ban Spargo at the University of Chicago also was very active at the same time. Actually, for a short period we met once a month to exchange views and this was very useful in many ways, both from the technical aspects to improve our technology as well as for the interpretative problems.
VD:	Was there a feeling of competition between you or was there a certain collegiality?
CP:	There was certainly a feeling of competition - who had seen the most biopsies. It was a bit of a joke actually but the fact is that we were competing against each other in the field. There is no question about that and at the same time there were other groups who were also very active. Renée Habib in Paris was very active. Claus Brun and his group in Copenhagen, after a few years, became somewhat less active but still he had produced a number of histopathological studies on renal biopsy.
VD:	As you look back, Dr. Pirani, which of the renal pathologists who were prominent in that period do you think had the biggest impact on you in terms of your thinking?
CP:	Well, it is very difficult to say who had the most impact. I would say that the man who straightened out my ideas, came a bit later and was Robert Heptinstall. When he published his book in 1962, the first edition, was a one volume book, all written by Dr. Heptinstall, no multiple authors. It was beautifully written. He had clarified many ideas including those originally expressed by some other authors. In other words, he clarified what other people had written in a perhaps somewhat confused manner, including some of my own papers. This book became the bible, if you will. It was the original modern source of accurate renal pathology. However, at that time, don’t forget that immunofluorescence and electron microscopy had been in use for almost five years already, perhaps even longer. So until electron microscopy was used, the structure of the kidney was not really completely understood and perhaps even today there is something to be learned through ultrastructural studies, immunopathology, which was mainly headed by Dr. McCluskey in the United States also clarified a number of problems which would have been impossible to clarify by other methods obviously. So, at that time, the Heptinstall’s book really played a major role in stabilizing and clearly expressing our knowledge of renal pathology.
VD:	When I think of it, even in 1980, when I first started my studies, it was my bible.
CP:	So he played a major role.
VD:	Did you have much contact with Renée Habib?
CP:	Yes, we have had much contact. It started at the Ciba meeting and then I went to the l’Hôpital des Enfants Malades in Paris, where I met her and Dr. Hamburger in 1961 and she is a very accurate observer, very precise, detailed observer of the pathology of renal disease and published very important papers based on a very large number of cases which is also very important to establish the reliability of results. So, Renée Habib certainly played a major role. And also others from different parts of the world: Priscilla Kincaid-Smith played a role, especially in relation to analgesic nephropathy.
VD:	You went to study with her for some period of time didn’t you or your visited Australia at one point in your career?
CP:	It was a very common disease in Australia. That is one of the mysteries that has not really been clarified to the best of my knowledge. Why the disease was so much more common in certain countries.
VD:	You visited her in Australia didn’t you?
CP:	Yes, Priscilla asked me to come down for a few weeks to work in her Department. That was in 1970 and I spent a month there reviewing biopsies. She is obviously a clinician but she also does her own renal pathology. So she wanted to check with a renal pathologist who is not a clinician if what she was looking at was accurate or not and I’m not sure I helped her a lot frankly but it certainly was a very pleasant period of work. It kept me busy, it kept me hopping, giving lectures from Adelaide to Brisbane to Sydney. I visited most of Australia. I visited with Dr. Jim Lawrence, who is retiring this year, who became one of the most important clinical nephrologists in Australia and who had been a research fellow of ours in Chicago. He was in Adelaide originally, so I visited him in Adelaide.
VD:	Certainly there was a large network that was growing for exchange between renal pathologists but up to that point there really was not a common source of dissemination of knowledge I imagine. There were not annual meetings that you could go to in those early days to exchange views.
In the early 1960’s before the International Society of Nephrology and the American Society of Nephrology came into existence there were not annual meetings where you could exchange views, so you had to maintain personal contact.
CP:	You are absolutely right. The International Society of Nephrology actually was founded before the American Society of Nephrology, I believe. Hamburger was the first President and the first meeting was held in Evian and the second one was in Prague in 1963. The first one was in 1960 or ‘61.
The American Society I think was founded about the same time.
VD:	Yes, in ’66 or ’67; Neil Bricker was the first President, I believe.
Tell me Dr. Pirani, as you look back, what do you think has given you your biggest satisfaction in your career?
CP:	There are a number of things. It is difficult to say which one is more important. I think one thing I enjoyed the most really is the close contact with the clinician. As I mentioned before, clinicians even to this day still come down and want to look at the biopsy themselves. This is vital incidentally because, as most people know, today diagnosis of renal disease is a combined diagnosis - a clinicopathologic diagnosis. So, you feel you are doing something for the patient. You really are a physician after all, you are not just somebody buried in a small room in the laboratories. That gave me great satisfaction.
Of course other things were that I love to teach so I taught a lot of pathology. I gave short courses for the International Academy for many years, I participated in the long courses, I gave the big slide seminar of the American Society of Clinical Pathology together with Robert McCluskey which was a very satisfactory experience in many ways, although perhaps it was a bit too complicated for most pathologists! Then we established a course here at Columbia that you are in charge of now. It is now in its 20th year, I believe.
VD:	That’s right, this year.
CP:	Also, a similar course was established at my suggestion in Bergamo, Italy, where Dr. Bertani has been a pupil of mine. He is now in charge of that course. Dr. Remuzzi is the Director of the Institute there.
Now it is difficult to put these things in order so teaching gave me great satisfaction and another major source of satisfaction was the number of excellent fellows , both men and women, that I have been lucky enough to have in my Laboratory over the years. Many of them have had excellent careers. There are several Chairs of Pathology from Jerusalem to Prague to Oklahoma.
VD:	Can you name a few for us?
CP:	Well, Dr. Rosenmann is Head of Pathology at the Hadassah Medical School in Jerusalem. He spent a year with me in Michael Reese Hospital and he did much work on renal vein thrombosis. Dr. Joseph Stejskal from Prague spent a year with me and did what I think is a very important piece of work that perhaps should have got him more recognition. He is retired now but he was Head of Pathology at one of the two medical schools in Prague. He did work on discontinuities or gaps or perforations, call them what you like, of the glomerular basement membrane in glomerular diseases. There is no question that some diseases have perforations and other do not and the exact clinical significance of this in terms of hematuria and leukocyturia and other progressive damage is still not perfectly clear and this is a problem that still should be investigated.
Dr. Silva is Chairman of Pathology in Oklahoma, you are Director of Renal Pathology at Columbia, and several others, for example, Dr. Manaligod, originally from the Philippines, who perhaps was the first to help me out with some work on lupus. He is now Acting Chairman of Pathology at Illinois. Seymour Rosen was a resident at Illinois. We worked together on a couple of projects on renal biopsies I believe he is now Associate Professor at Harvard, and Head of Surgical Pathology at Beth Israel Hospital in Boston. He has done some excellent work after he left my Lab, especially on tubular function. Most of my work was on glomerular diseases, much less on the tubules and the interstitium.
think some of the most important work - renal clinicopathologic correlative work - was done by people like Dr. Craig Tisher and others who worked on the fine structure of the tubules in different renal functional states. I still believe that ultrastructural study can yield some important information.
VD:	It seems to me that for renal pathologists in general, the glomerulus has always been far more glamorous than the tubulointerstitital or the vascular compartment, and it really is only in the last decade that they have been studied in depth by people like Craig Tisher.
Let me ask you, Dr. Pirani, before we close, just a few more questions about looking back on your career and the body of work that you have accomplished. I would be curious to know in you own estimation what you consider to be your most valuable contribution to the field overall or if there are several that you would want to name?
CP:	Well, it is difficult for me to choose, perhaps I’m partial myself. I think my work with Bob Kark and Victor Pollack and Robert Muercke on lupus nephritis probably stands out. However, there are other studies which I think are important in my estimation. For example, a study we did with Michael Koss, who is now Professor of Pathology at the University of Southern California on experimental myeloma kidney in which we tested several light chain proteins and found out that only one of the three light chain proteins tested was able to reproduce the disease. I think that was an important contribution that eventually may lead hopefully to more specific therapy for multiple myeloma. In other words, depending on the type of light chain protein toxicity to the kidney may vary considerably and that was an important study in my mind.
I can mention others. For example, the work of Stejskal on the discontinuities of basement membrane is still work which has not been fully evaluated in its functional significance really but still may lead to more significant results.
So there are several papers but I cannot say I am more attached to one than another really.
VD:	Is there one that you think has made a bigger impact on the nephrology community?
CP:	Well, lupus made a big impact. I think the work with John Louis on post-streptococcal glomerulonephritis and Luis Salinas-Madrigal, who is now Professor at the University of St. Louis, was an important piece of work primarily because of the series of observations in sequential biopsies in the study of the resolution the rapidity of the resolution of the disease. I think this was important. It may explain a number of clinical features of post-streptococcal nephritis.
VD:	You’ve received a number of major awards in your career. I’m thinking of the John Peters Award in particular in 1987 and this past year an award from the Renal Pathology Society. Which one of these or are there others that have been a particular source of pride to you?
CP:	Well, certainly the John Peters Award is the major award I was lucky to receive, being awarded by a society which is primarily made up of clinicians. After all the work of pathologists has to get recognition by clinicians at a certain moment, if it is felt the work is useful to the patient as having some importance in therapy.
But I’m very attached to a smaller award that I received way back in 1955 in which the second year class in the Medical School at the University of Illinois awarded me the Best Teacher of the Year Award and gave me a small golden apple and I was really moved by that and after all for a teacher, there is nothing that can beat the recognition by one’s students as a teacher. Believe me, it is much more difficult to get recognition from students than it is from your peers. That’s really is something that is still very close to my heart.
VD:	As you look back, Dr. Pirani, is there anything that you would do differently if you had a chance to relive your life? Are there any regrets you have in terms of the particular twists and turns your career has taken?
CP:	Well, it’s impossible to answer that. The only thing that my life probably demonstrates is that life is an adventure. You cannot really predict what is going to happen to you and you can guide your destiny only to a very limited extent. I certainly could not have predicted when I lived in Milano, that I would come to the United States and that I would become a Professor, first at the University of Illinois and then at Columbia. Certainly, I could not have predicted what came out of renal biopsy either. So, much of my life was dictated by chance and I was lucky overall, I think, to be able to work with very good people over the years, who left an imprint on my way of thinking and guided some of my activities.
VD:	Well, I can certainly re-echo that sentiment personally because I think has been no more fortuitous event in my own career than having had the opportunity to work with you, as I did in 1980 and again in 1983.
CP:	Well, I was lucky to have you first as a Research Fellow and then as an Assistant and then as a successor. Thank you very much for your help.
VD:	Thank you very much for the opportunity to interview you today, Dr. Pirani. It’s been a pleasure, as always. Although I’ve heard many of these stories before, they remain endlessly fascinating. It's been a pleasure for me. Thank you.
Rosen S. Pirani CL. Muehrcke RC. Renal interstitial foam cells. A light and electron microscopic study. American Journal of Clinical Pathology. 45(1):32-41, 1966 Jan.
Abrahams C. Pirani CL. Pollak VE. Ultrastructure of the kidney in a patient with multiple myeloma. Journal of Pathology & Bacteriology. 92(1):220-5, 1966 Jul.
Schewitz LJ. Pirani CL. Pollak VE. Observations of a case or pre-eclampsia with respect to hypertensive vascular disease as a sequel. Obstetrics & Gynecology. 27(5):626-36, 1966 May.
Pollak VE. Pirani CL. Seskind C. Griffel B. Bilateral renal vein thrombosis. Clinical and electron microscopic studies of a case with complete recovery after anticoagulant therapy. Annals of Internal Medicine. 65(5):1056-71, 1966 Nov.
Friederici HH. Taylor H. Rose R. Pirani CL. The fine structure of capillaries in experimental scurvy. Laboratory Investigation. 15(9):1442-58, 1966 Sep.
Reiss E. Pirani CL. Hypertension and muscle spasms; a clinical pathologic conference. Chicago Medical School Quarterly. 26(1):39-52, 1966 Spring.
Kaplan BM. Pick A. Pirani CL. Clinical pathologic conference (coronary disease). American Heart Journal. 73(2):245-60, 1967 Feb.
Mombelloni P. Pirani CL. Catchpole HR. Serum glycoproteins in experimental scurvy and carageenan granuloma. Archives of Pathology. 83(5):429-33, 1967 May.
Muehrcke RC. Pirani CL. Arsine-induced anuria. A correlative clinicopathological study with electron microscopic observations. Annals of Internal Medicine. 68(4):853-66, 1968 Apr.
Pollak VE. Rosen S. Pirani CL. Muehrcke RC. Kark RM. Natural history of lipoid nephrosis and of membranous glomerulonephritis. Annals of Internal Medicine. 69(6):1171-96, 1968 Dec.
Rosenmann E. Pollak VE. Pirani CL. Renal vein thrombosis in the adult: a clinical and pathologic study based on renal biopsies. [Review] [154 refs] Medicine. 47(4):269-335, 1968 Jul.
Bacani RA. Velasquez F. Kanter A. Pirani CL. Pollak VE. Rapidly progressive (nonstreptococcal) glomerulonephritis. Annals of Internal Medicine. 69(3):463-85, 1968 Sep.
Ort M. Salinas ML. Metcoff J. Pirani CL. Some clinical and morphological features of the acute phase of acute glomerulonephritis in children. Acta Universitatis Carolinae - Medica. 15(3):207-25, 1969.
Rosenmann E. Kanter A. Bacani RA. Pirani CL. Pollak VE. Fatal late postpartum intravascular coagulation with acute renal failure. American Journal of the Medical Sciences. 257(4):259-73, 1969 Apr.
Pirani CL. The morphologic basis of proteinuria. Proceedings of the Institute of Medicine of Chicago. 27(10):271-2, 1969 Jul.
Lewy JE. Salinas-Madrigal L. Pirani C. Metcoff J. Clinical and morphological correlates in acute glomerulonephritis. Proceedings of the Institute of Medicine of Chicago. 27(8):211-2, 1969 Mar.
Pollak VE. Pirani CL. Renal histologic findings in systemic lupus erythematosus. Mayo Clinic Proceedings. 44(9):630-44, 1969 Sep.
Salinas-Madrigal L. Pirani CL. Pollak VE. Glomerular and vascular "insudative" lesions of diabetic nephropathy: electron microscopic observations. American Journal of Pathology. 59(3):369-97, 1970 Jun.
Zarnow H. Pirani CL. Sodium depletion proteinuria: experimental and electron microscopic studies. Proceedings of the Society for Experimental Biology & Medicine. 135(2):275-84, 1970 Nov.
Mandalenakis N. Mendoza N. Pirani CL. Pollak VE. Lobular glomerulonephritis and membranoproliferative glomerulonephritis: a clinical and pathologic study based on renal biopsies. Medicine. 50(4):319-55, 1971 Jul.
Lewy JE. Salinas-Madrigal L. Herdson PB. Pirani CL. Metcoff J. Clinico-pathologic correlations in acute poststreptococcal glomerulonephritis. A correlation between renal functions, morphologic damage and clinical course of 46 children with acute poststreptococcal glomerulonephritis. [Review] [71 refs] Medicine. 50(6):453-501, 1971 Nov.
Jao W. Pirani CL. Renal amyloidosis: electron microscopic observations. Acta Pathologica et Microbiologica Scandinavica - Section A, Pathology. 233:217-27, 1972.
Dujovne I. Pollak VE. Pirani CL. Dillard MG. The distribution and character of glomerular deposits in systemic lupus erythematosus. Kidney International. 2(1):33-50, 1972 Jul.
Dillard MG. Dujovne I. Pollak VE. Pirani CL. The effect of treatment with prednisone and nitrogen mustard on the renal lesions and life span of patients with lupus glomerulonephritis. Nephron. 10(5):273-91, 1973.
Finkel PN. Kronenberg K. Pesce AJ. Pollak VE. Pirani CL. Adult Fanconi syndrome, amyloidosis and marked kappa-light chain proteinuria. Nephron. 10(1):1-24, 1973.
Jao W. Lewy P. Norris SH. Pollak VE. Pirani CL. Lipoid nephrosis: a reassessment. [Review] [26 refs] Perspectives in Nephrology & Hypertension. 1 Pt 1:183-98, 1973.
Pollak VE. Pirani CL. Dujovne I. Dillard MG. The clinical course of lupus nephritis: relationship to the renal histologic findings. Perspectives in Nephrology & Hypertension. 1 Pt 2(0):1167-81, 1973.
Pollak VE. Mendoza N. Pirani CL. Immunohistologic observations in mesangio-proliferative glomerulonephritis. Perspectives in Nephrology & Hypertension. 1 Pt 1:633-40, 1973.
Pollak VE. Pirani CL. Clyne DH. The natural history of membranous glomerulo-nephropathy. [Review] [37 refs] Perspectives in Nephrology & Hypertension. 1 Pt 1:429-42, 1973.
Stejskal J. Pirani CL. Okada M. Mandelanakis N. Pollak VE. Discontinuities (gaps) of the glomerular capillary wall and basement membrane in renal diseases. Laboratory Investigation. 28(2):149-69, 1973 Feb.
Simon N. Cohen H. Glick G. Kanter A. Levin B. Pirani CL. Clinical pathologic conference. American Heart Journal. 86(4):539-52, 1973 Oct.
Jao W. Pollak VE. Norris SH. Lewy P. Pirani CL. Lipoid nephrosis: an approach to the clinicopathologic analysis and dismemberment of idiopathic nephrotic syndrome with minimal glomerular changes. Medicine. 52(5):445-68, 1973 Sep.
Clyne DH. Brendstrup L. First MR. Pesce AJ. Finkel PN. Pollak VE. Pirani CL. Renal effects of intraperitoneal kappa chain injection. Induction of crystals in renal tubular cells. Laboratory Investigation. 31(2):131-42, 1974 Aug.
Mendoza N. Mandalenakis N. Kanter A. Pirani CL. Pollak VE. Chronic membranoproliferative glomerulonephritis. A patient with recurrent episodes simulating rheumatic fever and acute nephritis. American Journal of Medicine. 59(2):251-61, 1975 Aug.
Derosena R. Koss MN. Pirani CL. Demonstration of amyloid fibrils in urinary sediment. New England Journal of Medicine. 293(22):1131-3, 1975 Nov 27.
Beach JE. Pirani CL. Letter to the editor: Proliferative arteriopathy in macaques and vascular neurofibromatosis. Experimental & Molecular Pathology. 24(1):126-7, 1976 Feb.
Koss MN. Pirani CL. Osserman EF. Experimental Bence Jones cast nephropathy. Laboratory Investigation. 34(6):579-91, 1976 Jun.
Abitbol MM. Gallo GR. Pirani CL. Ober WB. Production of experimental toxemia in the pregnant rabbit. American Journal of Obstetrics & Gynecology. 124(5):460-70, 1976 Mar 1.
Abitbol MM. Pirani CL. Ober WB. Driscoll SG. Cohen MW. Production of experimental toxemia in the pregnant dog. Obstetrics & Gynecology. 48(5):537-48, 1976 Nov.
Buda JA. Baer L. Parra-Carrillo JZ. Kashef MM. McAllister FF. Voorhees AB. Pirani CL. Predictability of surgical response in renovascular hypertension. Archives of Surgery. 111(11):1243-8, 1976 Nov.
Appel GB. Williams GS. Meltzer JI. Pirani CL. Renal vein thrombosis, nephrotic syndrome, and systemic lupus erythematosus: an association in four cases. Annals of Internal Medicine. 85(3):310-7, 1976 Sep.
Abitbol MM. Ober MB. Gallo GR. Driscoll SG. Pirani CL. Experimental toxemia of pregnancy in the monkey, with a preliminary report on renin and aldosterone. American Journal of Pathology. 86(3):573-90, 1977 Mar.
Salomon MI. Silva F. Tchertkoff V. Ayuthia I. Pirani CL. Renal lesions in chronic pancreatitis. Nephron. 22(4-6):409-17, 1978.
Appel GB. Woda BA. Neu HC. Parry MF. Silva F. Pirani CL. Acute interstitial nephritis associated with carbenicillin therapy. Archives of Internal Medicine. 138(8):1265-7, 1978 Aug.
Appel GB. Silva FG. Pirani CL. Meltzer JI. Estes D. Renal involvement in systemic lupud erythematosus (SLE): a study of 56 patients emphasizing histologic classification. Medicine. 57(5):371-410, 1978 Sep.
Pirani CL. Silva FG. The kidneys in systemic lupus erythematosus and other collagen diseases: recent progress. [Review] [137 refs] Monographs in Pathology. 20:98-139, 1979.
Chander PN. Nurse HM. Pirani CL. Renal involvement in adult Gaucher's disease after splenectomy. Archives of Pathology & Laboratory Medicine. 103(9):440-5, 1979 Aug.
Scholes J. Derosena R. Appel GB. Jao W. Boyd MT. Pirani CL. Amyloidosis in chronic heroin addicts with the nephrotic syndrome. Annals of Internal Medicine. 91(1):26-9, 1979 Jul.
Silva FG. Weber CJ. Pirani CL. Hardy MA. Reemtsma K. Blood glucose levels and proteinuria [letter]. New England Journal of Medicine. 301(3):160, 1979 Jul 19.
Weber CJ. Silva FG. Hardy MA. Pirani CL. Reemtsma K. Effects of islet transplantation on renal function and morphology of short- and long-term diabetic rats. Transplantation Proceedings. 11(1):549-56, 1979 Mar.
Silva FG. Meyrier A. Morel-Maroger L. Pirani CL. Proliferative glomerulonephropathy in multiple myeloma. Journal of Pathology. 130(4):229-36, 1980 Apr.
Silva FG. Chander P. Pirani CL. Hardy MA. Disappearance of glomerular mesangial IgA deposits after renal allograft transplantation [letter]. Transplantation. 33(2):241-6, 1982 Feb.
Pirani CL. Olesnicky L. Role of electronmicroscopy in the classification of lupus nephritis. American Journal of Kidney Diseases. 2(1 Suppl 1):150-63, 1982 Jul.
Nash MA. Bakare MA. D'Agati V. Pirani CL. Late development of chronic renal failure in steroid-responsive nephrotic syndrome. Journal of Pediatrics. 101(3):411-4, 1982 Sep.
Bertani T. Olesnicky L. Abu-Regiaba S. Glasberg S. Pirani CL. Concomitant presence of three different glomerular diseases in the same patient. Report of a case and review of the literature. [Review] [42 refs]. Nephron. 34(4):260-6, 1983.
Appel GB. D'Agati V. Bergman M. Pirani CL. Nephrotic syndrome and immune complex glomerulonephritis associated with chlorpropamide therapy. American Journal of Medicine. 74(2):337-42, 1983 Feb.
Bertani T. Appel GB. D'Agati V. Nash MA. Pirani CL. Focal segmental membranous glomerulonephropathy associated with other glomerular diseases. American Journal of Kidney Diseases. 2(4):439-48, 1983 Jan.
Cramer CR. Hagler HK. Silva FG. Eigenbrodt EH. Meltzer JI. Pirani CL. Chronic interstitial nephritis associated with gold therapy. Archives of Pathology & Laboratory Medicine. 107(5):258-63, 1983 May.
Ramsay AG. D'Agati V. Dietz PA. Svahn DS. Pirani CL. Renal functional recovery 47 days after renal artery occlusion. American Journal of Nephrology. 3(6):325-8, 1983 Nov-Dec.
Feinfeld DA. Olesnicky L. Pirani CL. Appel GB. Nephrotic syndrome associated with use of the nonsteroidal anti-inflammatory drugs. Case report and review of the literature. Nephron. 37(3):174-9, 1984.
Olesnicky L. Doty SB. Bertani T. Pirani CL. Tubular microfibrils in the glomeruli of membranous nephropathy. Archives of Pathology & Laboratory Medicine. 108(11):902-5, 1984 Nov.
Silva FG. Hoyer JR. Pirani CL. Sequential studies of glomerular crescent formation in rats with antiglomerular basement membrane-induced glomerulonephritis and the role of coagulation factors. Laboratory Investigation. 51(4):404-15, 1984 Oct.
Pirani CL. Clinicopathologic correlations in lupus nephritis. Contributions to Nephrology. 45:185-99, 1985.
Manaligod JR. Pirani CL. Renal biopsy in 1985. Seminars in Nephrology. 5(4):237-9, 1985 Dec.
Ramsay AG. Olesnicky L. Pirani CL. Acute tubulo-interstitial nephritis from candida albicans with oliguric renal failure. Clinical Nephrology. 24(6):310-4, 1985 Dec.
Truong L. Kopelman RG. Williams GS. Pirani CL. Temporal arteritis and renal disease. Case report and review of the literature. [Review] [32 refs] American Journal of Medicine. 78(1):171-5, 1985 Jan.
Gelfand J. Truong L. Stern L. Pirani CL. Appel GB. Thrombotic thrombocytopenic purpura syndrome in systemic lupus erythematosus: treatment with plasma infusion. American Journal of Kidney Diseases. 6(3):154-60, 1985 Sep.
Park MH. D'Agati V. Appel GB. Pirani CL. Tubulointerstitial disease in lupus nephritis: relationship to immune deposits, interstitial inflammation, glomerular changes, renal function, and prognosis. Nephron. 44(4):309-19, 1986.
D'Agati VD. Appel GB. Estes D. Knowles DM 2d. Pirani CL. Monoclonal antibody identification of infiltrating mononuclear leukocytes in lupus nephritis. Kidney International. 30(4):573-81, 1986 Oct.
Pirani CL. Valeri A. D'Agati V. Appel GB. Renal toxicity of nonsteroidal anti-inflammatory drugs. [Review] [31 refs] Contributions to Nephrology. 55:159-75, 1987.
Appel GB. Cohen DJ. Pirani CL. Meltzer JI. Estes D. Long-term follow-up of patients with lupus nephritis. A study based on the classification of the World Health Organization. American Journal of Medicine. 83(5):877-85, 1987 Nov.
Pirani CL. Silva F. D'Agati V. Chander P. Striker LM. Renal lesions in plasma cell dyscrasias: ultrastructural observations. American Journal of Kidney Diseases. 10(3):208-21, 1987 Sep.
Silva FG. Pirani CL. Electron microscopic study of medical diseases of the kidney: update--1988. [Review] [224 refs] Modern Pathology. 1(4):292-315, 1988 Jul.
Start DA. Silva FG. Davis LD. D'Agati V. Pirani CL. Myeloma cast nephropathy: immunohistochemical and lectin studies. Modern Pathology. 1(5):336-47, 1988 Sep.
Truong L. Gelfand J. D'Agati V. Tomaszewski J. Appel G. Hardy M. Pirani CL. De novo membranous glomerulonephropathy in renal allografts: a report of ten cases and review of the literature. [Review] [59 refs] American Journal of Kidney Diseases. 14(2):131-44, 1989 Aug.
D'Agati VD. Theise ND. Pirani CL. Knowles DM. Appel GB. Interstitial nephritis related to nonsteroidal anti-inflammatory agents and beta-lactam antibiotics: a comparative study of the interstitial infiltrates using monoclonal antibodies. Modern Pathology. 2(4):390-6, 1989 Jul.
Pollak VE. Pirani CL. Schwartz FD. Clinical and experimental. The natural history of the renal manifestations of systemic lupus erythematosus. 1964 [classical article]. Journal of Laboratory & Clinical Medicine. 116(6):889-902, 1990 Dec.
Valeri A. Radhakrishnan J. Estes D. D'Agati V. Kopelman R. Pernis A. Flis R. Pirani C. Appel GB. Intravenous pulse cyclophosphamide treatment of severe lupus nephritis: a prospective five-year study. Clinical Nephrology. 42(2):71-8, 1994 Aug.
Appel GB. Pirani CL. D'Agati V. Renal vascular complications of systemic lupus erythematosus [editorial]. Journal of the American Society of Nephrology. 4(8):1499-515, 1994 Feb.
Pollak VE. Pirani CL. Schwartz FD. The natural history of the renal manifestations of systemic lupus erythematosus. 1964 [classical article]. Journal of the American Society of Nephrology. 8(7):1189-98; discussion 1189-95, 1997 Jul.

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