Kidney Stone Disease

KIDNEY STONE DISEASE. Contents: Composition and structure of kidney stones.......643 Etiology and pathogenesis...............644 Symptomatology and course.............650 Diagnosis.......................652 Prognosis........................653 Prevention...................6 54 Treatment.......................65 4 Kidney stone disease (nephrolithiasis) is a chronic condition, the main characteristic feature of which is the presence of concretions or stones in the cavities of the kidney or in its parenchyma, formed from components of urine. In contrast to gallstone disease, which usually proceeds hidden and is often discovered only at autopsy, kidney stone disease is primarily detected during the patient's life by a whole series of characteristic clinical symptoms, which constitute the so-called renal colic. In modern surgical-urological practice, kidney stone disease accounts for 30% to 40% all kidney surgical conditions. Despite the significant frequency of kidney stone disease, its etiology and pathogenesis remain insufficiently clarified to this day. The difficulty in understanding the nature of kidney stone disease as a whole is explained by the fact that stone formation in the kidney is the result of a complex metabolic disorder in the body, an expression of a special 'diathesis' which is still not fully studied at present. Historical data concerning the general concept of 'urinary stone disease' (urolithiasis) date back to antiquity. It is sufficient to mention Hippocrates, Galen, Persian and Arab physicians, who were familiar with the clinical picture of the condition and contributed their share of assumptions and conjectures regarding the conditions of origin of urinary stones depending on geographical features of the locality, climatic conditions, drinking water, etc. The extreme antiquity of the condition is evidenced by the finding of a urinary stone in an Egyptian mummy, which is estimated to be 7,000 years old. In the development of the clinical picture of kidney stone disease, X-rays played an enormous role as the main means of detecting the presence of stones in one or another part of the urinary system. To appreciate the enormous progress made in the diagnosis of kidney stones since the introduction of X-ray examination into clinical practice, it is sufficient to recall the previous number of diagnostic errors in kidney stones, when for example one Morris made 42 nephrotomies to find a non-existent stone in the kidney. At present, the number of so-called 'invisible stones' that escape X-ray detection is measured by a negligible figure of 2-3%. In Russia, the first operation for kidney stones was performed in 1883 by Prof. N. V. Sklifosovsky. Composition and structure of kidney stones are extremely diverse. From a physicochemical standpoint, two main groups of kidney stones can be distinguished. The first, largest and most widespread group should include dense, crystalline stones consisting of various combinations of inorganic and organic salts (urates, oxalates, phosphates, carbonates, cystine and xanthine stones). The second, smaller group of kidney stones, which has little clinical significance, consists of soft, elastic stones composed mainly of protein substance - protein stones, which include stones from bacteria, stones from fibrin and from amyloid. These protein stones usually consist of a crystalline nucleus (calcium phosphate) and concentric layers of fibrin mesh and bacterial accumulations partially impregnated with lime salts. According to the literature, 21 such protein stones have been described (Fedorov). According to Israel, protein stones are often found in large numbers in the cavity of pyonephrosis in the form of gray-yellow, white or brownish formations, ranging in size from a pea to a cherry. The main site of origin, growth and residence of kidney stones is the renal pelvis, then the renal calyx and less frequently the convoluted tubules of the cortex or the tip of the renal papillae. In both of the latter cases, they are referred to as parenchymatous stones. The size of stones (see separate tables, p. 647 - 643) varies from a hemp seed to several kilograms in weight. The average weight of a kidney stone is 20-50 g. Oxalates and urates are rarely larger than a walnut and grow very slowly. On the contrary, phosphates and carbonates with a nucleus of oxalic lime and uric acid grow very quickly and can reach enormous sizes. An example of the extreme rapidity of growth of phosphate stones is the observation by Israel, who, 16 months after an operation to remove numerous stones, had to remove again 57 very large concretions consisting of calcium carbonate with traces of ammonium magnesium phosphate. Wildbolz saw how within one year a phosphate the size of a pea grew to the size of a chicken egg. Kidney stones weighing several kilograms (4½, 2½ kg) have been repeatedly found at autopsy. Large stones removed during operation are known, for example, in Fedorov the maximum weight of a stone was 192 g, in Grave 340 g, etc. For the most part, kidney stones that are the subject of clinical observation are single. Gottstein, based on his material (162 cases), data of Küster (709 cases) and the Mayo Clinic (850 cases), believes that in 50-56% there is a single stone. Multiple pelvic stones or combinations of a pelvic stone with a calyceal or parenchymatous stone are encountered. The maximum number of stones found in a kidney was in Israel-36, in Fedorov-69. Despite the great external diversity of kidney stones, their structure is characterized by the presence of a nucleus and a shell or body of different composition. As for the sex of patients with kidney stone disease, in 242 cases of Fedorov there were 152 men, or 62.7%, in Gottstein's 213 kidney stones there were 133 men, i.e. 62.4%. Thus, almost ²/₃ ^{of all} kidney stones occur in men. Kidney stones can be observed at any age, but they become the subject of surgical intervention predominantly between the ages of 20 and 40 years. As for the localization of stones, stones in the right kidney occur somewhat more frequently, which is explained by the predisposition of the right kidney to displacement, stagnation phenomena, etc. Based on large personal statistics of authors (Israel, Fedorov, Mayo Clinic), bilateral kidney stones occur in 11-17% of cases. Etiology and pathogenesis. Urinary stones are quite widespread in the animal kingdom and are found in pigs, horses, cattle, dogs, hares, fish, toads, turtles and rats. The fact of finding urinary stones in various representatives of the animal kingdom would seem to facilitate the discovery of the causes of stone formation in humans by including in animal experiments all the smallest conceivable and favorable conditions for their appearance in the human body. Unfortunately, it turned out that the experimental reproduction of stones in animals has very limited possibilities, hardly approaching the conditions of stone development in humans. Thus, despite the significant frequency of kidney stone disease, its cause remains to this day unsolved. Based on two sharply defined clinical types of stone carriers - those in whom a single stone formation in the kidney is a random episode in their life, and others in whom a persistent tendency to repeated stone formation runs like a red thread through their entire life - it should be said that there is no single cause for the formation of any stones and cannot be. It would be more correct to speak not of the causes of stone formation, which we essentially do not know, but only of factors and moments favorable to this process. The most substantiated theories of urinary stone formation, based on clinic and experiment, date back to 1856, since the appearance of Meckel v. Hemsbach's doctrine 'On the stone-forming catarrh'. According to this doctrine, a slight degree of catarrhal inflammation of the kidneys leads to the deposition of elements of exudate with some urinary salts and thus the beginning of stone formation is laid. In 1857, Rainey obtained atypical crystals from various salts (calcium carbonicum, oxalicum) by precipitating them from a medium containing colloidal substances - gelatin, protein, acacia gum, mucus. Rainey expressed the assumption of a connection between such atypical crystals and urinary concretions. Somewhat later, Ord (1875) confirmed and expanded the ideas of Rainey, showing that calcium oxalate from aqueous solutions crystallizes in the form of octahedrons, and from a colloidal medium it can be obtained in the form of tablets, weights and in spherical form, especially easily merging into a crystalline mass. Ord's study of the microscopic structure of stones led him to the conclusion that colloids of urine participate in the formation of stones from oxalic lime and uric acid. Ord's work is thus chronologically the first to definitely establish in the mechanism of stone formation the importance of two factors - urinary colloids and atypical crystallization of urinary salts. By feeding animals with oxamide - a derivative of oxalic acid - it was possible to obtain artificial urinary stones ranging in size from a sand grain to a dense mass 1 cm in diameter.

Chemical analysis of these stones showed the presence in them, in addition to oxalate, of an organic protein substance. According to Ebstein, the desquamative catarrh and epithelial debris, formed as a result of the toxic effect of oxalate on the renal epithelium, provide the colloidal material, thanks to which the precipitation of stone-forming crystals occurs. An indispensable condition for stone formation, according to Ebstein, must thus be the central protein substance, the organic core of the stone, around which the precipitation and layering of the crystalline elements of urine occur. Moritz, Mendelsohn and others subsequently proved that an organic, protein core is not necessary for stone formation, since organic substance is also found in the primary single crystal. According to Rosenbach, one of the indispensable conditions for the formation of primary kidney stones from uric acid and urates, and the combination of these salts with oxalates, phosphates, and cystine stones, must be considered the excessive content of these salts in the blood—the presence of diathesis. However, one diathesis is not sufficient, since uric acid diathesis in gout, oxaluria, phosphaturia do not necessarily lead to the formation of stones. The cause of urolithiasis ultimately, in Rosenbach's opinion, lies in the disturbance or change in the ratios between uric acid and other salts and colloids of urine. Linwood-Keyser studied the formation of stones in animals (rabbits and dogs) by introducing under the skin the ester of oxalic acid—butyloxalate—and simultaneously calcium chloride. The study of the experimental stone formation process showed that the typical octahedral form of calcium oxalate crystals gradually disappears as oxaluria intensifies, being replaced by a plate-like form—the form of gymnastic dumbbells and finally a spheroidal (spherical) form. With the appearance of the latter form of individual crystals, their fusion and gluing into a more compact mass begins. The main conclusion of Linwood-Keyser's work is the indication of the most important role in stone formation, in addition to the excessive stone-forming material delivered to the kidneys, of so-called protective colloids. A discrepancy in the qualitative or quantitative relationship between these latter and the crystalline components of urine serves as a factor favoring the precipitation of salts and stone formation. Any kind of infection, especially focal infection, by changing the protective colloids in a qualitative manner, can, with increased excretion of crystalline salts, cause lithiasis (Rosenow).-The enormous significance attributed to vitamins in the normal functions of the organism could not but lead to attempts to explain stone formation in some cases by the state of avitaminosis in one form or another. Experimenting on rats receiving a diet deficient in vitamin A, Osborne and Mendel found on 857 autopsies in 81 animals stones in the kidneys and urinary tract. Japanese authors have demonstrated the possibility of obtaining urinary stones in white rats and dogs under the influence of food deprived of vitamin A, which was confirmed by a whole series of other authors, including Gasparian and Ovchinnikov, and in all cases with positive results. The predominant spread of urolithiasis in one locality or another has long given rise to a desire to seek the cause of this phenomenon in the climatic, geographical peculiarities of the locality, socio-domestic conditions of the population, but all attempts to establish a causal relationship here, the known regularity of the appearance of urolithiasis, proved and prove to be extremely shaky, little substantiated, since urolithiasis is encountered in all climates, among representatives of all races and nationalities, and, most importantly, the zones of its spread and frequency prove to be extremely unstable, changing during individual decades. With regard to individual countries where urolithiasis occurs on a large scale, endemically (e.g., Syria, countries of Asia Minor), attempts were made to establish the dependence of this phenomenon on the properties of the soil and the hardness of drinking water. Abderhalden and Hanslian conducted research in the indicated regions on the character and properties of drinking water and came to the conclusion that the cause of kidney stone disease in Asia Minor can be hard water. However, there are many countries where urolithiasis is very widespread, and the water and soil do not have a calcareous character. Research by Pereshchikin showed frequent morbidity from urolithiasis among the indigenous population of Tashkent (out of 104 cases of stone disease, only 4 cases occur in Europeans), and yet in the native part of the city the water is softer, while the same part of Tashkent inhabited by Europeans has very hard water. Most likely, the peculiar geographical distribution of urolithiasis is connected with the peculiarities of the domestic life and nutrition of the population. The influence of nutrition is most clearly manifested in the origin of lithiasis in childhood. In this respect, the research of Kuttner and Weil on the frequency of urolithiasis in connection with the nutritional conditions of difficult children in Württemberg is instructive. The local custom of early and exclusive feeding of children with cereals and all kinds of flour dishes, besides the enormous morbidity and mortality of infants, also gave rise to a significant frequency of urolithiasis. Only with the elimination of nutritional defects, improvement of nutrition by introducing large quantities of milk into the diet, did the morbidity and mortality of children decrease and at the same time the suffering from urinary stones sharply decreased. Some authors attribute the formation of uric acid stones to excessive protein nutrition. As proof of the untenability of the expressed assumption, one can cite the poor population of the foothills of Sicily, who feed exclusively on polenta (a thick porridge from cornmeal) and nevertheless often suffer from uric acid stones. Kidney stones occur endemically both in countries with vegetarian nutrition and in those exclusively consuming meat or mixed food. Perhaps here it is not the one or another character of nutrition, but the quantity and quality of drinking water that plays a role, but the entire way of life of the population, the level of its cultural needs and functions. Heredity of kidney stone disease is not proven for most cases, however, in its favor speak individual pedigrees, as well as the fact that metabolic disorders, so-called gouty or uric acid diathesis, can be inherited, sometimes in combination with obesity, gallstones. In addition, various anomalies of the kidney, pelvis, and ureter, which play a significant role in the origin of kidney stones not only by the mechanical conditions of impaired urine outflow, can be inherited.-A local factor lying in the kidney itself, in its cellular parenchymal elements, plays a significant role in primary aseptic stone formation, because without it, under conditions of excessive content of stone-forming material in the blood, stones should develop in both kidneys. Meanwhile, bilateral calculosis, as already indicated, is observed comparatively rarely. Adler sees the cause of stone formation in the discrepancy between the flow of urine and the structure of the urinary tubules, in the existence of 'dead corners' of a congenital nature in the renal tubules in the form of abnormal bends, curvatures, constrictions and dilutions of the latter due to protruding vessels, partitions, diverticula, etc. The significance for stone formation of the local factor lying in the kidney itself is most easily taken into account in its clear form in trauma and infection. Especially demonstrative for the influence of kidney trauma on stone formation are those cases where in the center of the core of a kidney blood clots or elements of old blood were found. Bleeding from the kidneys itself does not play an exclusive role in stone formation, since then we would have more frequent development of stones after kidney hemorrhages of various origins.-The general influence on the origin of nephrolithiasis of trauma not directly affecting the kidney is noted with outstanding frequency and constancy in damage to the spine. For every ten injuries of the latter, Müller found on autopsy eight times bilateral kidney stones. The cause of stone formation in spinal injuries is a complex chain of conditions, which includes, in addition to possible and simultaneous trauma to the kidney itself, the subsequent development in it of inflammatory and stagnant phenomena under the influence of spinal paralysis and the paralysis of urine-expelling forces caused by it, whether it be paralysis of the bladder or also paralysis of the renal pelvis cups, and perhaps also of the ureter, as Hollander assumes. Infection, entering the kidney by one way or another, plays an even greater role in stone formation than trauma. With a clear picture of the presence of infection in the kidney, the appearance of stones in it can be called secondary stone formation. In other cases, infection causes in the cell-tubular apparatus of the kidney the finest imperceptible changes of a necrobiotic nature, however sufficient to lay the beginning of the formation of a colloid-crystalloid core with the subsequent development of a real stone around it. A number of authors observed in kidney stone patients in the past the most diverse infectious processes.

Rovsing observed bilateral nephrolithiasis after typhus. Israel, in his patients, was able to establish preceding stone-forming diseases in the form of typhus, erysipelas, osteomyelitis, phlegmonous toad, suppurative appendicitis, etc. Mir-Kasimov attributes the endemic development of urolithiasis in Azerbaijan to the widespread malaria in that region. Among specific types of infection, the role of streptococcus as a causative factor in stone formation is particularly emphasized by Rose-now and Meisser. For some cases of stone formation, the role of staphylococcal infection is more convincing, as the staphylococcus directly affects the reaction of urine in the kidney itself and causes the appearance of precipitates by changing the acidic reaction to alkaline through the bacterial transformation of urea into uric acid ammonium. Hellstrom observed a series of kidney stones, the nucleus of which consisted of colonies of staphylococci stuck together. Some significance in kidney stone formation can also be attributed to intestinal bacteria. Piccininni and Lombardi isolated in pure culture from the human intestine a bacterium similar to Bact. coli communis, but unlike the latter, it did not produce indole. By means of cultures on nutrient media, the authors were able to prove the ability of this bacterium to produce oxalic acid lime. The oral administration of cultures of this bacterium caused the appearance of oxaluria in healthy people, depending on the excessive formation of oxalates in the intestine, their absorption and excretion with urine. The whole range of the above factors favoring kidney stone formation, with constancy, reveals its action in the presence of so-called lithogenic diathesis in patients. Under this term should be understood a special metabolic disorder, expressed in the excessive production of various salts, which creates supersaturation of urine with salts and promotes the formation of precipitates in it, which are freely excreted outward or settle in various parts of the urinary basin. The clinical course of nephrolithiasis in the presence of lithogenic diathesis is distinguished by the early onset of the disease, its persistent existence, or the persistent return of stones after various methods of their removal. It is extremely difficult to prove the constant presence of stone-forming substances in excess in the blood in lithogenic diathesis, since the presence of excess salts may be temporary, associated with certain phases of the vital activity of the whole organism or its individual organs (state of rest or enhanced muscular activity, disturbance of the neuropsychic system, phases of hunger or digestion, etc.), and yet it can be the cause of the appearance of the first salt precipitates, the first elements of the future growth and development of kidney stones. According to modern concepts, urine is a saturated aqueous solution of inorganic and organic salts (crystalloids), maintained in a dissolved, suspended state by favorable conditions—temperature, acidity, ratio of salts, and mainly due to the presence in it of so-called protective colloids. The role of the latter is to maintain salts in a dissolved state, to protect them from precipitation or sedimentation. How important colloids are for the dissolution of salts is shown by uric acid, which in plain water dissolves in the ratio of 1:39,000. Protective colloids are the finest particles of organic substance suspended in urine and consist of urinary pigments, nucleoalbumins, mucin, albumin, chondroitin sulfuric acid and nucleic acids. The amount of colloids in daily urine is approximately 1 g. The decisive factor for the protective effect is not the amount of existing colloids, but the specific type of colloid. Part of the protective colloids of urine is in a ready form in the blood itself and can pass unchanged through the kidney, while another is modified and formed in the kidneys themselves under the influence of the vital activity of kidney cells. The process of stone formation in the kidney can be considered partly as a result of the insufficient quantitative or qualitative formation of protective colloids by kidney elements, as a special disease of the kidney cell, similar to what is now recognized in relation to the liver cell in gallstone formation. The most important point in stone formation is the appearance of the stone nucleus. The still existing dispute between biochemists (Lichtwitz, Schade) as to which of the indicated elements—only the colloid or also the crystalloid—should be attributed the main importance in the formation of the initial stone nucleus must be resolved in favor of Schade, who proved the possibility of the formation of a nucleus and stones from pure uric acid without any participation of colloids. Any disturbance of the equilibrium between colloids and crystalloids gives impetus to the primary precipitation of one or the other elements of urine with the formation of an initial nucleus, which in turn becomes the center of absorption of various components of urine and creates conditions for the further growth and development of the stone. Any pathological impurities to urine—mucus, pus, blood clots, tissue fragments, worm eggs, etc.—can serve as centers for the absorption of colloids and crystalloids of urine, the nucleus of stone formation. The normal surface of the urinary pathways is as necessary for the stability of urine as the unchanged wall of blood vessels for flowing blood. Diseases of the mucous membrane of the urinary pathways reduce the stability of urine, promoting the formation of precipitates in it, just as in the disease of the endothelium of blood vessels, the clotting of fibrinogen occurs. Whether in the formation of the nucleus, the precipitation of the colloid occurred first, followed by the settling of the crystalloid on it, or vice versa, it is important to know that the resulting precipitate of colloid and crystalloid can be in a 'reversible' state, i.e., not completely and finally lose its ability to subsequent dissolution by the flow of urine, or in an 'irreversible' state—not to be subject to dissolution under any conditions of natural presence in the cavities of the kidney. Incidentally, such an irreversible colloid is considered fibrin and all compounds of crystalloids with it. Symptomatology and course.-Asymptomatic course of kidney stone disease is a rare exception. In the vast majority of cases, kidney stone disease is expressed by a whole range of clinical symptoms of a subjective and objective nature, which include as the main elements of the disease: 1) pain, 2) passage of stones, 3) hematuria. 1. Pain in nephrolithiasis can be more or less constant, dull, aching in character or occur suddenly and acutely in the form of periodic attacks, so-called renal colic. Dull pain sensations are observed with parenchymal or calyceal stones and with large immobile pelvic stones and depend on mild forms of the inflammatory process in the pelvis, in the kidney itself and in the surrounding parts of the capsule and connective tissue. Renal colic as an acute attack of pain is encountered in many kidney diseases, e.g., in the obstruction of the ureter by a blood clot, a purulent plug, in bends of the ureter, compression from outside or inside, etc., but it is most often observed with kidney stones. Cabot and Israel define the frequency of renal colic with stones at 66%. The pains are usually localized in the area of the kidneys and are felt as cramping, cutting or stabbing pain; the pain attack can last for several minutes, hours and even days. These pains arise suddenly, sometimes during sleep. Starting in the lumbar region, deeply below the XII rib, the pains descend along the ureter to the groin, with radiation to the penis, testicle, to the labia majora in women or to the anus. Much less frequently, the pains radiate to the epigastric region, to the scapula, shoulder, neck or head. Simultaneously with the pain attack, sometimes prevailing over it or somewhat obscuring it, there may be manifestations from the abdomen and intestines—bloating, tension of the abdominal walls, constipation or diarrhea. An attack of renal colic usually begins suddenly and is accompanied by chills or a shaking chill, to which an increase in temperature is added. Why, in a completely aseptic condition of the kidneys with stones, an increase in temperature appears has not yet been clarified. Most likely, here there is a periodic entry of bacteria into the blood under the influence of trauma to the pelvis or kidney by a stone—a state of transient bacteremia, similar to the appearance of the latter in so-called catheterization fever. To the increase in temperature are added nausea, vomiting, bloating of the abdomen, frequent urges to urinate. Urine may be excreted in small amounts due to reflex suppression of the other kidney, the presence of vomiting, the excretion of sweat. With complete obstruction of the ureter by a stone on the side of infected nephrolithiasis, urine, which was previously turbid from pus, may become clear. Among the general phenomena, headache, general weakness, malaise, dryness in the mouth, thirst are noted. An attack of renal colic can suddenly stop together with the passage of a stone, it can resume again (after the lapse of varying time depending on the new formation or passage of the stone).

Simultaneously with purely local radiating pains, reflex phenomena may be observed from the other kidney, bladder, and sexual organs in the form of pains of various characters, burning, frequent urges, etc. The mechanism of the origin of renal colic consists in the increase in intrarenal pressure depending on the stagnation of urine in the pelvis in case of its obstruction and of the ureter by a displaced or newly formed stone. At the same time, other factors also play a role, such as the increased tension of the renal capsule due to acute inflammatory swelling, venous congestion of the kidney. To this is added the influence of the swelling of the mucous membrane of the pelvis or ureter. Spasmodic contractions of the pelvis and ureter play a significant role in the appearance of acute colicky pains, by means of which they seek to eliminate the mechanical obstacle (sand or stones) that interferes with the free outflow of urine. The independent role of the ureter in the origin of colic is proved by the fact that after removal of the kidney, the remaining or stone seen in the ureter can give an attack of colic. The acuteness of the attacks of renal colic is explained by the passage of sand or small stones through the ureter, i.e., of the movable elements of nephrolithiasis. 2. The passage of stones, being the most characteristic symptom of K. b., is not always observed in this disease. Not every acute attack of renal colic ends with the passage of a stone. The stone may pass back into the pelvis or remain lying in the ureter, obstructing it. A stone that has descended into the bladder may either be expelled outward or in turn serve as a nucleus for a bladder stone. The passage of stones is not always accompanied by painful attacks. Chopart reports two cases where during several days patients expelled 300 and 400 stones without any pain.-3. Hematuria may be detected in macroscopic or microscopic admixtures of blood in the urine. According to the data of Mayo and Israel, macroscopic hematuria is observed in 50-56%. Arising periodically, it is not pathognomonic, since it is also observed in other renal and ureteral diseases. This hematuria usually does not create a danger to life. Microscopic hematuria in kidney stones occurs much more frequently (according to the data of the Mayo clinic in 91%) and constitutes an almost constant symptom of this disease. Appearing with movements, walking, disappearing at rest, microscopic hematuria is an important diagnostic symptom. The examination for microscopic content of blood in urine should be done before cystoscopy, and in women urine should be taken for examination from the bladder with a soft catheter, to avoid the appearance of traumatic hematuria. Pyuria in kidney stones, especially infected ones, occurs frequently (according to the data of Brasch in 93%), although it is not specifically characteristic of K. b. Consequences and complications of K. b. In aseptic stones, due to chronic retention of urine, dilation of the renal pelvis, large and small renal calyces often develops, followed by atrophy of the renal parenchyma and the picture of partial hydronephrosis [see separate table (art. 719-720), fig. 2]. More destructive processes in the kidney in stone disease develop when infection is secondarily added. On the basis of the combined conditions of mechanical obstacle to the outflow of urine and infection, pyelitis, pyelonephritis, pyonephrosis develop. The latter disease can be complicated by the development of paranephritis in the purulent or sclerotic form, can give perforation of the stones into the perirenal space or into adjacent cavities, accompanied by severe septic phenomena threatening the life of the patient. The most formidable complication in K. b. is calculous anuria: secretory, when the other kidney, previously supposed healthy, ceases to excrete urine by reflex, and excretory, when the lumen of both ureters in bilateral lithiasis is obstructed by a concrement. The diagnosis of kidney stone disease with its cardinal symptoms, when it is possible to use modern methods of examination of kidney patients (cystoscopy, ureteral catheterization, radiography) in most cases presents no difficulties. The differentiation of renal colic in stones from renal colic in other kidney diseases (tuberculosis, neoplasms, painful nephritis) is carried out on the basis of the strength, duration of the painful attack, passage of sand or small stones with positive radiological data. In hepatic colic, in contrast to renal colic, the pains are felt in the depth of the right hypochondrium with irradiation upward and backward to the right shoulder, under the right scapula; rarely hepatic pains irradiate to the left, even more rarely the pains radiate downward to the lumbar or iliac region. Jaundice speaks for hepatic colic, but even in renal colic with simultaneous septic phenomena, slight jaundice may be observed. It is necessary to remember that renal and hepatic stones can exist simultaneously. In lead colic, more often observed in men, the pains are localized in the middle of the abdomen, are diffuse. The abdomen is usually drawn in, tense, blood pressure is elevated, on the gums a typical lead line. Renal crises in tabes dorsalis can give pains along the ureter to the bladder, urethra with tenesmus, but the pains in them are of lesser strength, vomiting is more prolonged and abundant, there is no rise in temperature and, most importantly, the symptoms of the disease of the central nervous system are present. If the difference between renal colic and hepatic colic is easy to establish, it is often much more difficult to differentiate acute renal colic from acute appendicitis. The phenomena accompanying acute renal colic and acute appendicitis-meteorism, constipation, tension of the abdominal walls, sensation of chilliness-may be observed in both diseases. True, in kidney stones the most intense sensation of pain is noted in the costovertebral angle, in appendicitis the pains are lower, in the iliac region, but here too pains can be felt in case of incarceration of a stone in the ureter. Ortner described as typically painful for a ureteral stone the point lying at the junction of the horizontal line drawn through the navel with the vertical one going along the outer edge of the right rectus muscle. The differentiation of renal colic from acute attack of appendicitis is made on the basis of the strength and duration of the painful attack (more significant in renal colic), the characteristic irradiation of the pains, changes in urination and the urine itself-frequent urges, high specific gravity of urine, blood macroscopically and microscopically in the urine, presence of salts or even more important the passage of sand or gravel with the urine. Macroscopic and microscopic hematuria is not conclusive in an absolute sense for renal colic, since it can be observed in acute appendicitis, especially with retrocecal position of the appendix, 663

KIDNEY STONE DISEASE

651 most difficult for differential diagnosis. A characteristic difference is observed in the behavior of patients with the conditions in question. In renal colic, patients cannot find a comfortable position in bed, toss and turn, jump up, and assume various positions in an attempt to alleviate the severity of their pain. Patients with acute appendicitis lie on their back or right side as if paralyzed, avoiding any unnecessary movement. In the final analysis, in case of doubt, if the case does not tolerate delay and cystoscopy, ureteral catheterization, and radiography cannot be performed, it is better to operate as for acute appendicitis to avoid the threat and risk of the patient's death from peritonitis. Similarly difficult conditions for diagnosis arise when renal colic is accompanied by symptoms of ileus. There have been numerous cases where the abdominal cavity was opened with a diagnosis of ileus, when in fact the condition was due to kidney and ureteral stones (Ortner). No matter how clear the clinical picture of kidney stone disease may be, only positive findings from radiography can provide complete certainty in the diagnosis of kidney stones. X-rays should be taken of both kidneys and ureters due to the possible existence of bilateral stones. Even with the most advanced equipment, flawless radiographic technique, and strict adherence to all rules for careful patient preparation, a certain number of kidney stones still escape detection by radiographic examination to this day. The main reason for this is their chemical composition and structure, which prevent the stones from blocking X-rays. Stones made of pure uric acid, protein stones, and xanthine stones are considered to be those that allow X-rays to pass through and do not leave any noticeable shadows on X-ray plates. However, cases have been described where stones that allowed X-rays to pass through and did not appear on the plates were found to consist of calcium oxalate and calcium phosphate, magnesium-phosphate salts, i.e., elements that do cast a shadow on the X-ray. To detect such invisible stones, it is necessary to use filling of the renal pelvis with bromine or insufflation of air into it, or preliminary staining of the stones with a 10-20% solution of collargol. The prognosis in kidney stone disease should be strictly individualized and depends on the location of the stone, its size, and the number of stones. Infected stones, phosphate stones, bilateral stones, which indicate infection and a severe disturbance of metabolism in the body, carry a poor prognosis: relapses after surgical removal of such stones are inevitable, and patients usually soon die from kidney failure. An attack of renal colic usually ends favorably in terms of cessation of all painful sensations. Sometimes during this, sand, fine gravel, or a small stone is passed. More often the attack recurs, as the stone moves downward, getting stuck at points of physiological narrowing of the ureter, to advance further during the next attack of renal colic. In other cases, the stone that caused the acute attack of colic returns back to the renal pelvis; more rarely, the attack ends with complete obstruction of the ureter or perforation of the renal pelvis, resulting in the first case in obstructive phenomena (hydroureter, pyelectasis, hydronephrosis), and in the second case in an inflammatory process in the cellular tissue (paranephritis) or false hydronephrosis. Prevention of kidney stone disease consists in diluting concentrated urine, reducing the salt content in it, and eliminating stagnation and infection in the kidney. Preventive measures are difficult to implement, as they involve changing the hereditary constitutional gouty or lithogenic diathesis. However, a rational diet, general hygiene, medications, and the use of mineral waters are beneficial. Diet (see below - treatment) is prescribed according to the properties of the precipitating or excreted salts or gravel (urates, oxalates, phosphates). It is all the more difficult (to say impossible) to prevent an attack of renal colic, as it usually occurs without warning, unexpectedly, sometimes at night during sleep. As a general measure, nervous and physical rest can be recommended; furthermore, careful regulation of the bowels, abundant drinking of indifferent liquids--plain water, liquid tea--and adherence to a diet that prevents the concentration of uric acid, calcium oxalate, and phosphates are recommended. Treatment of established kidney stone disease can be purely medicinal or surgical. Renal sand, gravel, or small stones consisting of uric acid, urates, or phosphates and periodically passed with the picture of renal colic are best treated with glycerin and increased fluid intake, with the aim of washing out the renal pelvis and calyces and simultaneously reducing the content of solid constituents in the urine. Casper recommends the following prescription for glycerin: Glycerini purissimi 150.0, T-rae Corticis Aurantii, T-rae Amarae aa 5.0, to be taken by the tablespoonful every three hours, two doses weekly. To avoid the possible development of hemoglobinuria, glycerin should not be taken for more than 4-6 weeks (Wildbolz). Of diuretic agents, lemon tea, linden tea, tea from grape leaves, and horsetail tea are used. Other diuretics are also suitable. They reduce the concentration of urine and by the volume of urine excreted, they help to push the salts or small stone into the bladder. To relax the spasm of the ureteral musculature, belladonna extract or atropine is administered orally, in suppositories, or subcutaneously. For uric acid stones, alkaline waters are recommended--Borjomi, Essentuki, Izhevsk water, or ordinary spring water with the addition of soda. The alkaline water should be taken until the urine shows an amphoteric, but not alkaline, reaction, to avoid the precipitation of phosphates. For oxalates and phosphates, indifferent or carbonated mineral waters (Narzan, Izhevsk) or teas from horsetail, valerian, and chamomile are prescribed. They should be taken hot. Visits to resorts are not mandatory if the home environment and living conditions are suitable for carrying out treatment. In the dietetics of patients with kidney lithiasis, general strict moderation in eating is of essential importance. For uric acid stones, the task of the diet is to prevent excessive formation of uric acid in the body and to promote its dissolution and excretion. For this purpose, all substances containing an excess of purine bases are excluded from the diet, namely: liver, kidneys, brains, stewed, fried, and roasted meat, salted fish, meat soups. Alcohol and spices are forbidden only when there is an inflammatory condition of the urinary tract. The basic diet for uric acid diathesis should be vegetarian. Bread, fats, butter, coffee in moderate amounts, and plenty of greens and fruits are allowed. For oxalate stones, which appear in both acidic and alkaline urine, a mixed, easily digestible diet is prescribed, avoiding all foods that contain oxalic acid salts in ready form or a large amount of lime. Thus, strong tea, cocoa, chocolate, spinach, rhubarb, beets, sorrel, wine berries, asparagus, radishes, tomatoes, and mushrooms are forbidden. The consumption of milk, eggs, and fresh greens should be limited due to their high lime content and the danger of alkalinizing the urine. To increase the solubility of oxalates in urine, the immediate intake after meals of calcined magnesia or magnesium carbonate, one teaspoonful, is recommended. In primary phosphaturic diathesis, which depends on functional disorders of the nervous system and is accompanied by disturbances of gastrointestinal digestion, a meat diet is prescribed to acidify the urine, and foods containing calcium salts (for example eggs, milk), potatoes, vegetables, all kinds of alkalis and alkaline waters are forbidden. To acidify the urine and keep phosphates in suspension, phosphoric or hydrochloric acid is administered internally (in drops or mixture). In secondary phosphaturia, which is a consequence of infection of the upper urinary tract, the main attention should be directed to combating infection and stagnation in the kidney and pelvis by administering internal disinfectants (salol, urotropin) or irrigating the pelvis with antiseptic, astringent solutions (silver nitrate, collargol). From a purely practical standpoint, the idea of finding a means to dissolve urinary stones has always been attractive. Unfortunately, such means have not yet been found. Treatment of renal colic itself consists in the energetic use of morphine or pantopone subcutaneously, along with the application of local heat in various forms--a heating compress, a hot water bottle on the lumbar region or abdomen, or a warm bath. In recent times, Marion has opposed the use of morphine in renal colic, as he believes that although morphine relieves pain, it also immobilizes the ureter, hindering the further passage of the stone into the bladder. On this basis, he recommends belladonna in pills up to 0.08 daily. For prolonged, less acute, or dull pains, aspirin in combination with codeine 0.5:0.03 or pyramidone in a dose of 0.3 is recommended. Surgical treatment of kidney stone disease.

When a kidney contains such a large stone that its passage seems unlikely, the question arises whether it should be removed or not. A stone causing severe, often recurring attacks of pain, a stone causing urinary retention and stretching of the kidney with subsequent inflammatory phenomena in the pelvis and in the perirenal cellular tissue, must be removed surgically. In deciding this question, not only the clinical manifestations but also to a large extent the age of the patient and his general condition should be taken into account. The general tendency to set indications for surgical treatment of nephrolithiasis as strictly as possible is based on the extremely high frequency of stone recurrence after "operation." Therefore, for aseptic stones that give insignificant clinical manifestations, for stones located in the parenchyma or calyces, operation should not be insisted upon. The situation is different when a young, robust subject has a stone in the pelvis, especially an extrarenal pelvis: the possibility of applying here the relatively harmless pyelotomy with subsequent suture of the pelvis gives full grounds for offering the operation. Indications for removal of already infected stones are set more broadly. The main one is the desire to protect the kidney (which is often belated) from progressive death of the parenchyma under the influence of stasis and infection, to eliminate pains, fever, pyuria, which sharply affect the patient's condition and working capacity. Of operations on the kidney for removing stones, pyelotomy, nephrotomy, and nephrectomy are used. Each of these operations has its own indications, advantages, and disadvantages. The most effective and safe operation is pyelotomy. The most dangerous in terms of the appearance of severe bleeding either directly on the operating table or later, after several days, is nephrotomy. Nephrectomy is performed for multiple calyceal or coral-like stones, for infected stones with far advanced death of the renal parenchyma. (For the technique of nephrotomy, nephrectomy, and pyelotomy, see Kidney.) Out of a total of 9,328 operations for kidney stones collected by Gottstein, with an overall mortality of 7.3%, there are: 1) pyelotomies-2,511, which is 26.9% of the total number of operations, with a mortality of 1.9%, 2) nephrectomies-3,052, which is 32.8% of the total number of operations, with a mortality of 8.5%, 3) nephrotomies-3,761, which is 40.3%, with a mortality of 9.8%. The results of applying various operations for nephrolithiasis should be considered not cumulatively but separately, for aseptic and infected stones. The corresponding data of Gottstein are as follows: for aseptic stones, 2,567 operations were performed with an overall mortality of 4.8%. For each type of operation separately: 1) pyelotomies-1,197, mortality-1.8%, 2) nephrotomies-1,315, mortality-7.8%, 3) nephrectomies-53, mortality-6%. For infected stones, 3,120 operations were performed (same statistics) with an overall mortality of 10.2%. For each type of operation separately: 1) pyelotomies-217, mortality-5.9%, 2) nephrotomies-1,020, mortality-14.5%, 3) nephrectomies-1,881, mortality-8.4%. Whatever kidney-preserving operation for nephrolithiasis is performed, however smoothly it proceeds in the postoperative period, there is no guarantee that recurrent stones will not appear in the operated kidney. Fedorov calculates the percentage of stone recurrences as 20-25. In other surgeons it is even higher: in Rovsing (113 operations)-41%, in Barney-45%, in Cabot-50%. When speaking of recurrences of stones after operation, one means exclusively the so-called false recurrences, depending on overlooked small stones or fragments of stones in the kidney, which subsequently serve as material and nucleus for continued growth or new development of stones. There is no doubt that the operative trauma to the pelvis and kidney in removing stones, associated with the formation of small blood clots, particles of dead parenchyma, or layers of desquamated epithelium at the same time, can serve as a factor favorable to the resumption of stone formation. Finally, the lithogenic diathesis, which cannot be eliminated by any operation, the remaining phenomena of stasis and infection of urine in the kidney, all kinds of inflammatory processes in it cannot but have an influence in the sense of return of kidney stones. Some reduction in stone recurrences promises to be given by more careful technique in stone operations-more careful removal of them without leaving fragments, more careful examination of the kidney and pelvis with the aim of not missing and leaving any concrement overlooked. Particularly valuable results (so far only under American conditions) are given by intraoperative fluoroscopic control of the kidney extracted into the wound. The successes achieved in this direction can best be seen from the sharp drop in the percentage of recurrences in the Mayo Clinic. In 1915 the percentage of stone recurrences was calculated as 45 (Barney), after the introduction of fluoroscopy in 1922 it fell to 10.5%, and according to the latest data the percentage of recurrences is measured by the figure 4.93%. Thus, from all that has been said, it is clear that the problem of combating kidney stone disease in all its phases lies in the sphere of more thorough and deep study of the causes of its occurrence. Until we know in each individual case of nephrolithiasis the individual, causal factor of its appearance, all measures to combat this suffering along the lines of prevention and treatment are doomed to a certain extent to failure, since in both cases we can only have palliative means at our disposal.