RENAL TUBERCULOSIS1 HANS WILDBOLZ Berne, Switzerland
I fully appreciate the honor done me by your President when he asked me to speak at your meeting on tuberculosis of the kidney. I accepted the invitation still more gladly because it has been my good fortune to have had a rather unusual number of such cases come under my observation. As a matter of fact, I have followed up the various phases in more than a thousand patients and of every case I have at my disposal an accurate written record. My nephrectomies for renal tuberculosis have now reached a total of 660. I have made frequent reports of my operative results-the last having appeared in the Handbuch der Urologie. At the present time I would like to supplement these reports by data gained from a recent investigation concerning the end-results after nephrectomy for tuberculosis of the kidney; and by the end-results I mean the condition of patients upon whom the operation was performed at least more than ten years ago. By way of introduction, I should like to state that the operative mortality of nephrectomy for tuberculosis in my patients has always been low- 2.2 to 2.5 per cent. (The mortality figure may vary by a few decimals according as it deals with a large series of favorable cases or whether it is reckoned just after the occurrence of a few sporadic deaths.) At the present time I am able to look back upon a series of 140 consecutive nephrectomies for renal tuberculosis without a death, and previously I had had a series of 182 similar operations without a fatality. But, after that, this series of successful operations was broken by 3 deaths that 1 Read at the Annual Meeting of the American Urological Association, Chicago, Ill., June, 1928.
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followed one shortly after the other. In 2 of these instances, the patient died from miliary tuberculosis six weeks after operation, and in the other, of pulmonary tuberculosis five weeks after operation. But far more interesting for you than a confirmation of the low mortality would be to know how many patients are permanently cured of their urinary tuberculosis by extirpation of the diseased kidney. It is, of course, well known to all of you that nephrectomy gives excellent temporary results and that two or three years after such operative intervention, approximately 60 per cent are well and appear to be completely cured. But since we know relatively little about the final fate of such patients, ten, fifteen or more years after nephrectomy, it is just this question that deserves our interest. By nephrectomy we aim to do more than to rid-the tuberculous patient temporarily of his urinary complaints or bring about an amelioration of symptoms; we hope rather that the removal of the tuberculous kidney combined with general treatment may bring about not only a healing in the urinary apparatus, but may also afford the patient the best possible protection against the further spread of tuberculosis in other organs and even influence a cicatrizing process in tuberculous foci already present. For the evaluation of these curative efforts an unusually favorable type of material is at my disposal. I work in a small country with a relatively unchanging population. Consequently, it has been possible for me to follow a large number of my patients, not only for a few years after operation but for a decade later and even more. In 1921, I reported the end-results in my first series of 125 nephrectomies for tuberculosis in patients operated upon between 1901 and 1911. I have tried to obtain in the past few months reports concerning all patients operated upon by me for tuberculosis of the kidney prior to 1918. This means all cases in which the operation had been done at least ten, in many of them twenty to twenty-five, years, previously. The series now comprises a total of 341 patients. Not all of these patients were located, but I have obtained accurate reports of more than three-fourths of the whole
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number, about 270 in all, and in a considerable proportion I was able to make a personal examination. The results of this inquiry have shown that the percentage of ·Cures in this substantially large operative series is essentially the same as in the first series reported in 1921. In this total of patients operated upon by me more than ten years ago, 40 per cent are dead. Of this number more than half of the deaths were due to tuberculosis of the remaining kidney or to pulmonary tuberculosis. The third most common cause of death I found to be miliary tuberculosis. Isolated deaths were due to peritoneal tuberculosis, solitary tubercle in the brain, bowel tuberculosis and spondylitis. Not less than 15 per cent of the deaths were due to intercurrent diseases-influenza, apoplexy, perforated gastric ulcer, pneumonia and other causes, and quite often in patients whose urogenital tuberculosis was apparently ,cured. Of the patients who were operated upon, 59 per cent are alive .a nd with the exception of 3 they have remained cured of their urogenital tuberculosis. What I should particularly like to €mphasize is that, even outside of the urogenital tract, they show no signs of active tuberculosis. In several of these patients, at various intervals following the nephrectomy, fresh tuberculous foci outside of the urogenital organs had made their appearance, €specially pulmonary tuberculosis and spondylitis. At the time ,of my inquiry, however, these lesions had all become cicatrized and the cure was complete. In the 3 patients mentioned as not yet cured, despite the fact that nephrectomy was done so long ago, the patients suffer from a small tuberculous focus in the bladder, although the remaining kidney in none of the three shows any sign of tuberculous disease. None shows any other active tuberculous focus outside of the urinary tract. There are only these 3 rare exceptions of persistence of the tuberculous cystitis without the involvement of the remaining kidney. Otherwise, I found uniformly that the tuberculosis of the bladder had healed completely within two to five years after
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nephrectomy, if a tuberculosis of the remaining kidney did not prevent it. Nearly all of my other patients whom I have found alive more than ten years after nephrectomy, have lost their bladder symptoms and have normal micturition. Only four patients still complain of bladder trouble in spite of a complete healing of the tuberculous lesions. These bladder symptoms are evidently purely nervous in 2 cases. Slight frequency is noticeable only when the patients go into society or when they have some other excitement; the capacity of the bladder is 250 to 300 cc. In 2 other cases the bladder trouble is more serious. A lady of seventy-six years for whom I did a nephrectomy twelve years ago has to empty her bladder every one and one-quarter to one and one-half hours in spite of a normal urine. Another lady, sixty-three years old, upon whom I operated eleven years ago is also still suffering from a pollakiuria of about the same degree. In these 2 cases, both in ladies of very advanced age, a certain degree of contraction of the bladder has persisted. Otherwise I have not seen a contracted bladder following tuberculous cystitis provided that the tuberculosis of the urinary tract had really been cured. Several of my patients complained of urgency for two or three years even though the tuberculous lesions had disappeared from the urinary tract. All of them, however, with the exceptions mentioned, finally attained a normal frequency. In these respects my results are better than those of Rafin and Suter, who observed bladder troubles in many of their patients ten and more years after nephrectomy. How this comes about I do not know. I only wish to point out that nearly all my patients, in whom the cystitis did not spontaneously subside and completely disappear a short time after nephrectomy, were treated for months and months with methylene blue and with intravesical injections of iodoform, guaiac oil or gomenol and sometimes also with tuberculin and roentgen rays. Otherwise Rafi.n's and Suter's statistics of nephrectomy in connection with the remote end-results coincide fairly well with mine, so that we might say that approximately 55 to 60 per cent of all cases of unilateral renal tuberculosis have a prospect of permanent cure.
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These unmistakably favorable results of operative treatment of caseo-cavernous tuberculosis of the kidney give a clearly cut indication for operative removal of the tuberculous kidney, provided only that the disease is unilateral. At first sight this indication would seem markedly plain, but as a matter of fact it is by no means always easy to follow it. In the first place, it is not always easy to determine in a patient in whom tuberculosis of the urinary tract has been demonstrated, whether a caseo-cavernous or any other form of renal tuberculosis exists, nor is it always easy to find out whether the caseous tuberculo::iis is unilateral or bilateral. You are probably surprised that I touch on these elementary questions on renal diagnosis which apparently were solved long ago, but I wish to emphasize the fact that the diagnosis of caseous chronic renal tuberculosis appears more difficult today than it did a few years ago. We know that tuberculous infection of the kidney produces not rarely, instead of the caseous form, the fibrotic type of renal tuberculosis or a tuberculous nephritis without formation of tubercles. How can these different forms of renal tuberculosis be differentiated clinically? In the literature the statement occurs quite frequently that the finding of tubercle bacilli in the renal secretion is to be taken as evidence of a caseous tuberculosis of the corresponding kidney, and that as soon as tubercle bacilli are demonstrated in the secretion of a kidney, that organ should be removed, provided that the other is healthy. This conception must be energetically combated. The demonstration of tubercle bacilli in the renal secretion by no means signifies that the corresponding kidney must be removed, nor does it prove that this kidney is the seat of specific tuberculous tissue changes. The presence of the bacilli in the kidney secretion may be due to so-called tuberculous bacilluria. That an excretory bacilluria may occur, especially in patients with pulmonary foci of advanced nature, without there being any tuberculous changes in the kidney from which the bacilli-containing urine comes, can no longer be doubted. Whether such a bacillary excretion may
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occur without the slightest involvement of the kidney, or whether, as Kielleuthner, Schonberg, Heyn and others suggest, small nonspecific foci of inflammation arise through the excretion of the bacteria, or whether, as Medlar thinks, this bacilluria is always followed by the formation of at least a few minute tubercles in the tissue of the kidney, is clinically of no importance. At any rate the indisputable fact is exceedingly significant that tubercle bacilli may pass through the kidney and appear in the urine without eliciting macroscopically demonstrable tuberculous tissue changes and without causing the admixture of pus in the kidney secretion. From a clinical standpoint, it is also highly significant that in such instances of bacilluria, which are certainly very unusual, the number of bacteria excreted is so small that they have never been demonstrated by microscopic examination but only culturally or by animal inoculation. It is quite easy to differentiate a tuberculous bacilluria from an early state of caseous renal tuberculosis by the paucity of bacilli. In this respect I am completely in accord with the opinion of Braasch and Scholl that, with a careful examination, tuberculous bacilluria seldom or never leads to diagnostic errors. If we find in a specimen of urine catheterized from the ureter tubercle bacilli, microscopically, without clumps of leucocytes, we cannot accept the diagnosis of tuberculous bacilluria in such an instance, but must rather interpret the finding as the result of a progression of the bacilli from the genital organs or the bladder, either by means of the catheter or through a reflux of the vesical contents. Even if in addition to tubercle bacilli pus cells are present in the renal secretion, a caseous tuberculous involvement of the corresponding kidney is not yet proven. Quite apart from the fact that the presence of leucocytes and bacilli in the ureter may have its explanation in a reflux of the bladder contents or in the existence of an ascending ureteral tuberculosis, it is always to be borne in mind that the excretion of tubercle bacilli and pus from a kidney is not a positive proof that the organ contains tubercles or caseous areas. To be sure, we know that such an excretion of pus and tubercle bacilli in the urine is -µsually the result of a caseo-cavernous disease of the kidney, but we must not forget
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that besides the caseo-cavernous renal tuberculosis the two other forms of renal tuberculosis,- the fibrotic form and the tuberculous nephritis without tubercles- must not be left out of consideration. These forms may also give rise to an admixture of pus and tubercle bacilli in the urine. Let us briefly review the pathology of these different forms of renal tuberculosis. It is well known that in a tuberculous kidney cavity formation may be totally absent, the tubercles becoming caseous but without breaking down. In this way the so-called nodular form of renal tuberculosis originates. In rare cases of chronic renal tuberculos.is not only cavity formation but also caseation may be absent, the tubercles showing an increased tendency to encapsulation. This fibroti~ or indurative form of renal tuberculosis is, from a pathologico-anatomical point of view, of extraordinary interest, because it constitutes a transitional form from chronic renal tuberculosis to the so-called tuberculous nephritis, which clinically probably plays a more important part than is usually accorded to it. In tuberculous nephritis not only are caseation and cavity formation lacking in the infected tissue but there is also no formation of tubercles. The renal parenchyma does not react in such cases to the invasion of the tubercle bacillus with specific tuberculous tissue changes. Neither giant cells nor epithelioid cells are present around the tubercle bacilli; there is only lymphocytic and leucocytic infiltration without specific evidences of tuberculosis. Formerly, one considered the nephritis without tuberculous tissue changes, observed in tuberculous patients and especially in phthisical subjects, to be caused by the tuberculous toxins in the blood-stream of such patients. Such a view seemed more plausible inasmuch as Arloing, Roux and several other authors had succeeded in producing nephritis, either with the injection of tuberculin or by the introduction of tubercle bacilli in collodion sacs (and therefore acting only through the toxins) . But later repeatedly suc_cessful demonstrations of tubercle bacilli in apparently non-specific inflammatory foci of the kidney by Heyn, d'Arrigo, Jousset and Liebermeister, and finally by Fedoroff, established the fact, that many of the so-called toxic
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nephritides are not the result of mere toxic action, but are the consequence of the penetration of the tubercle bacilli into the kidney tissue. These findings have shown that tubercle bacilli may invade the kidney and appear in the renal secretion without causing specific tuberculous tissue changes in the kidney; on the contrary, the bacilli may not infrequently produce only a nonspecific infiltration with a tendency to fibrosis of the kidney. In human pathology, except for the kidney, this reaction is not unusual. Similar non-specific reactions due to the invasion by tubercle bacilli occur in other organs of the body, especially in the liver; frequently, as one of my pupils (Jadassohn) showed, in the epididymis, also in the skin, lungs, pleura ·and probably in the joints, as Poncet first suggested. Why the tubercle bacillus in rare instances causes only non-specific inflammatory changes in tissues, without tubercle formation or caseation, cannot be stated with certainty. In all probability the relation between the number and virulence of the bacilli invading the tissue and the type and quantity of opposing antibodies in the tissue is of first importance. When through the influence of the latter a sufficient quantity of tuberculopyrin has been liberated, and allowed to act on the tissue long enough, then and only then will specific tuberculous changes appear. Otherwise, apparently only non-specific tissue reactions occur. Whether the type of invading tubercle bacillus might influence the anatomical form of kidney tuberculosis has recently been made a matter of study, particularly through the investigation of Lowenstein. He maintains that renal tuberculosis frequently is caused by the avian tubercle bacillus instead of the human type. In the form of growth of the organisms, cultured on artificial media from the urine of patients with renal tuberculosis, and in its occasional lack of pathogenicity for guinea pigs, Lowenstein holds that human renal tuberculosis may not infrequently originate through infection with the avian type. This question has not been completely clarified. After the results of an investigation which was performed by one of my assistants, Dr. Vormann, I am unable to believe that the avian bacillus plays an essential role in human renal tuberculosis. In our investigations,
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the tubercle bacilli from urine almost always proved virulent for guinea pigs, which speaks against an avian tuberculosis; and furthermore, our cultures on artificial media showed no growth forms characteristic of avian tuberculosis. But, above all, the comparative skin allergy tests to which we submitted our patients spoke against an avian infection. Patients with renal tuberculosis reacted strongly against the human and bovine tuberculin, whereas the skin injection with the avian tuberculin gave no reaction or one much slighter than that produced by the other two. Only in 2 patients did the avian tuberculin elicit as marked a reaction as did the human tuberculin. We obtained the same results in cases of localized tuberculosis outside of the urogenital tract, namely, in the pulmonary and osseous forms. In my material I am unable to find any evidence to support the contention of Lowenstein that human tuberculosis may frequently be produced by the avian tubercle bacillus, or that such an explanation might account for the very mild course of renal tuberculosis. However that may be, clinically, at any rate, we have to deal with the fact that tubercle bacilli in the kidney sometimes produce only a non-specific inflammatory reaction and that we m ay find tubercle bacilli and leucocytes in the renal secretion without the existence of tubercle formations, caseous areas, or cavities in the kidney. The rare but undeniable occurrence of tuberculous nephritis must make us somewhat careful in deciding upon a nephrectomy for tuberculosis of the kidney. In our anxiety to remove a unilateral caseous tuberculous kidney as early as possible, we should not be misled into removing a kidney that contains bacilli, but that exhibits no typical tuberculous changes. In contrast with caseous renal tuberculosis it appears to me that a kidney that is the seat of a tuberculous nephritis may have the ability to heal by scar formation with at least partial retention of function. At any rate recently acquired knowledge concerning tuberculous nephritis should cause us to be somewhat more conservative than heretofore in our demand for early operation in unilateral renal tuberculosis. Unfortunately, we are still unable to differentiate with certainty between an early caseous renal tuberculosis and tuberculous
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nephritis. Nevertheless, there are a few really outstanding features of both forms of the disease by which we may be able to differentiate them clinically. In caseous tuberculosis of the kidney, the first lesions are almost always localized near the papillae and the calyces. I still maintain this assertion despite the communication of Medlar. I feel myself supported by the results of a continuation of my anatomical observations in early cases of caseous kidney tuberculosis, previously published in ,c onjunction with Prof. Wegelin. The observations of Wegelin :and myself, moreover, have been recently confirmed by the valuable investigations of the Japanese surgeon Koike. I am ,convinced that the first tuberculous lesions in the kidney develop about the papillae and calyces. Inasmuch as these foci caseate ,early and rupture into the renal pelvis, an early free admixture in the urine of pus cells is to be expected in excess of and at an ,e arlier date than that observed in tuberculous nephritis. In the latter condition no tendency to break down is manifested, but rather a tendency towards fibrosis. In case of doubt whether a patient is suffering from tuberculous nephritis or from an early .stage of caseous renal tuberculosis, the decision to operate should be delayed and the patient subjected to a few months' observation. In such cases repeated accurate determination of the renal function will help to distinguish between an early caseous tuberculosis and a tuberculous nephritis. The secretory function of the ,o rgan appears to be more rapidly reduced in caseous tuberculosis than in tuberculous nephritis. It appears that a much more intense toxic action on the entire organ is exerted by the caseous foci than by the fibrotic areas of tuberculous nephritis; for already in the earliest stages of caseous renal tuberculosis, even when only the smallest caseous foci are present, we can note a marked delay :and decrease in the excretion of indigo carmine as well as an appreciable diminution in the excretion of urea. For instance, I found in a patient, in whose kidney a single pea-sized caseous area was present, a delay of 3 to 4 minutes in the excretion of indigo ·carmine, without any demonstrable histological changes in the remainder of the extirpated kidney. However, I have no conclusive evidence that a consideration of
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the pus content of the urine and the diminution of renal function will serve to differentiate caseous renal tuberculosis from tuberculous nephritis. This much, however, I say in favor of the contention. I have never found a tuberculous nephritis where I had expected to find a caseous kidney at nephrectomy. On the other hand, in 8 patients in whom I made the diagnosis of tuberculous nephritis because of the slight disturbance in func-· tion of the kidney and the scanty pus content of the urine from which tubercle bacilli were cultured, after conservative treatment an apparent arrest in the disease was obtained and in Z cases an apparent cure. Not a single one of these patients has yet needed an operation, although in 4 of them the onset of the disease dates from many years back (fifteen, nine, six, five) . It is to be noted, however, that tuberculous nephritis after a long interval may also cause a marked disturbance of function due to a spread of the non-specific inflammatory areas and increased fibrosis. In such cases the operative removal of the badly damaged organ will occasion the patient no loss, even though it conceals no caseous area. These considerations again show how important it is to examine a patient suffering from tuberculosis of the urinary tract with extreme care, before we decide upon the treatment. Above all, they demonstrate how essential in all cases of tuberculosis in the urinary tract is the determination of renal function tests. During: the last few years, too many surgeons unfortunately have shown a tendency to substitute, for the renal function tests in tuberculosis of the urinary tract, radiography of the kidney, pyelography or even bilateral diagnostic lombotomy. This tendency cannot, be too strongly deprecated. Time does not permit me to set forth in detail the vital importance of the renal function tests in the diagnosis of tuberculosis of the kidney. Here I would only emphasize their great value in determining whether the renal tuberculosis is unilateral or bilateral. Medlar has recently denied the previously quite generally accepted opinion that chronic tuberculosis of the kidney is usually unilateral and involves the second kidney only after the disease has existed for a long time. He believes that because in
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88 per cent of his animal experiments the lesions appeared bilaterally, and because of the frequent bilateral occurrence of renal tuberculosis in patients with pulmonary tuberculosis, that the disease must usually be considered as a bilateral condition. These conclusions of Medlar, also accepted by Thomas and Kinsella, do not appear to me to be justified. The renal tuberculosis produced experimentally by Medlar does not correspond to a chronic renal tuberculosis, but to an acute miliary tuberculosis. Similarly, the tuberculous areas found by him in the kidneys of the bodies of patients who had died of pulmonary tuberculosis are often a manifestation of a local miliary tuberculosis, local miliary metastases from the pulmonary tuberculosis,, or they are signs of a fibrotic tuberculosis of the kidney. They seldom show the anatomical characteristics of a caseous renal tuberculosis. So far as my experience goes, clinical observation teaches with certainty that in only a minority of patients does chronic renal tuberculosis develop bilaterally from the start. Although patients usually present themselves for medical advice in a fairly advanced stage of renal tuberculosis, in a series of more than a thousand I found a definite bilateral involvement in only 12 per cent. Most authors give a similar incidence (10 to 14 per cent) for bilateral occurrence. To be sure, Braasch and Scholl may be correct in suggesting that clinical examination does not always permit us to recognize a very small tuberculous infection of the second kidney. Nevertheless, the large number of permanent cures following nephrectomy (59 per cent) indicates that renal tuberculosis certainly in more than half the cases is unilateral at the start, and that only after the disease has existed for a long while does the second kidney finally become involved. As opposed to Braasch and Scholl, I have the impression that at the present day the diagnosis of a bilateral infection is made rather too frequently. The consideration of the result of animal injections of the separate urines is given too much weight in the decision as to the diagnosis of bilaterality, and too little weight is placed on the microscopic findings of the secretions from the individual kidneys and on the
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result of the function tests. As an example of such a diagnostic error, I will mention only one out of many personal observations. In the spring of 1922 I examined a lady sent to Leysin with a diagnosis of bilateral renal tuberculosis. The urine of both kidneys inoculated into guinea pigs had produced tuberculous lesions. This result I was able to confirm, but two examinations done at an interval of a few weeks showed me that the left kidney had a perfectly normal function and secreted urine free from pus and albumin, whereas the right kidney was working badly and its urine contained bacilli and much pus. Confident as to the normal functioning and the normal urine of the left kidney, I removed the right cavernous kidney. The patient recovered completely. Her urine injected into guinea pigs failed to produce tuberculosis one year after the operation. The demonstration of tubercle bacilli in the urine from the second kidney by animal inoculation or by culture is certainly not pathognomonic of tuberulous involvement of this organ. Their presence is of ten due to the escape of tubercle bacilli from the lower urinary passages by way of the ureteral catheter or by a reflux from the bladder. Moreover, it is sometimes also the result of an ascending tuberculous ureteritis. That such a ureteritis may occur without the involvement of the corresponding kidney has been adequately demonstrated at the autopsy table. In addition to my own reported observations, I would cite the cases of Hottinger, Legueu, Papin and Verliac, Batzner, Pachoud and Zoepffel. The differentiation between an ascending ureteritis and a real kidney tuberculosis as a rule is rendered possible by inserting the ureteral catheter high up and combining this procedure with functional tests of the kidneys. This differentiation is very important. For naturally, when merely a tuberculous ureteritis without tuberculous involvement of the remaining kidney is present, nephrectomy on the other side is indicated. If the remaining kidney is also involved as well as its ureter, nephrectomy on the opposite side is not advisable. The suggestion which has recently become more popular that, despite the bilaterality of the disease, the more damaged kidney should be removed provided that the second kidney has a good
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function, is in my opinion to be rejected. The hope that the lesion in the remaining kidney will then heal is without foundation. At a.ny rate, proof of the occurrence of healing of the tuberculous process in the remaining kidney is lacking. Supposed cures of this nature are founded upon wrong diagnosis. The healing of a clinically demonstrable caseous renal tuberculosis, if it occurs at all, is certainly extraordinarilyrare. Of this there is no shadow of a doubt. Even the investigations of Medlar do not justify any favorable judgment on the possibilities of non-operative cure in caseous renal tuberculosis. To be sure, Medlar has recently brought forward evidence for the familiar fact that tuberculous areas in the kidney may become fibrosed. But it is not to be overlooked that the tuberculous areas examined and found healed by him were so small, that they had caused no symptoms during life and had given rise to no suspicion of renal tuberculosis. The observations of Medlar, therefore, have only a theoretical value. From a practical point of view one always has to deal with the fact that a clinically demonstrable caseous renal tuberculosis never becomes completely fibrosed or heals. Consequently, nephrectomy in demonstrated bilateral renal tuberculosis will never bring about a cure. The experience of many surgeons support this contention. Persson operated upon 8 patients with bilateral renal tuberculosis-all died within a year after the operation. Rafin operated upon 15 patients with bilateral renal tuberculosis- all died within a year's time with the exception of one who survived the operation for nine years. Judd and Scholl report similar results in 18 patients that were operated upon despite bilateral involvement. Of my 6 patients on whom I performed a nephrectomy in spite of a bilateral renal tuberculosis, all died within two years. Apparently, then, nephrectomy never brings about a cure in bilateral renal tuberculosis, nor does it appear to prolong the life of the patient and only in rare cases does it afford material relief. Experience then has clearly shown that a nephrectomy in bilateral cases of renal tuberculosis is hardly ever justified. If we limit . extirpation of the kidney to the unilateral case and
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endeavor constantly to attain greater accuracy in diagnosis in renal tuberculosis so that indications for operation may be based on a firmer foundation, we shall seldom expose our patients to futile or even harmful procedures and shall bring about a permanent cure for innumerable sufferers through nephrectomy. In the treatment of the bilateral cases of renal tuberculosis we must search earnestly for methods by which we may be able to enhance the slight natural tendency toward healing by chemical and physical means. Perhaps at some future time we may succeed in finding a way of healing tuberculosis of the urinary tract without sacrifice of the kidney. As yet this has not been accomplished.
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