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Parenchymal Calculosis of the Kidneys1
PARENCHYMAL CALCULOSIS OF THE KIDNEYS 1 M. MUSCHAT
AND
L. KOOLPE
From the Department of Urology, Mt. Sinai Hospital, Philadelphia, Pa.
The name "renal calculosis" is used here in lieu of a better term to denote a certain rare pathological condition in which the kidneys are literally riddled and studded with concretions ranging from the size of a red blood cell to that of a cherry. The microscopic concretions are found in the parenchyma while the macroscopic ones are in the calices and pelvis. We followed this patient over a period of years and were fortunate to be permitted to study the kidneys at autopsy. Case report. Mt. Sinai Hospital No. 93187, H. W., a milk dealer aged 59, entered the service of Dr. A. I. Rubenstone July 5, 1935. He had a chili 2 days before admission, accompanied by fever, vomiting and a sudden severe pain in the abdomen. He had had frequency and nocturia 10 to 12 times for a number of years. A diagnosis of renal calculi had been made elsewhere. Except for marked distension and tenderness in the abdomen, the physical examination was negative. An x-ray showed innumerable calcareous deposits in both kidneys, ranging in size from a small barley grain to a large pea, and also 2 small concretions at the left ureterovesical juncture. An x-ray of the lungs showed an old healed tuberculosis of both apices (fig. 1). Laboratory data: Urine: specific gravity 1007, alkaline, moderate trace of albumin, 50 to 75 white blood cells, and an occasional red blood cell and bacteria. Blood examination: hemoglobin 88, red blood cells 4,710,000, white blood cells 9,950, polymorphonuclears 84 per cent. Blood chemistry: blood urea nitrogen 40, sugar 132, creatinine 2.4, calcium 8.4, phosphorus 2. 7. Wassermann reaction negative. Functional tests: urea clearance 25.6, P. S. P. 14 per cent (repeated). A study of five 24 hour specimens of urine revealed no acid fast bacilli. Urine and blood cultures were negative. Cystoscopy revealed a normal bladder and ureteral orifices. A No. 7 catheter passed to the left kidney without meeting any obstruction. The kidney was found to be filled with creamy pus. Lavage of the kidney was carried out and the catheter left in place. Two days after cystoscopy the patient passed 2 small calculi, chemical analysis of which showed magnesium and calcium phosphate. The patient's temperature was 103. 1 Read before the Philadelphia Urological Society, February 28, 1938, and the Mount Sinai Clinical Society, May 17, 1938. 293
294
M. MUSCHAT AND L. KOOLPE
Two days after the calculi were passed, the patient developed chills, accompanied by pain in the left loin and vomiting. Urine obtained by catheterization of the left kidney wa.s clear. A retrograde left pyelogram disclosed a huge hydronephorisis with innumerable calcareous deposits in the parenchyma; very little normal kidney tissue remained (fig. 2). The next day the temperature was 101. The patient complained of burning and difficulty on urination, which necessitated catheterization. For 2 weeks his temperature had ranged from 100 to 102. He was discharged from the hospital on August 7, a month after admission. He returned to the hospital on August 23 in a semi-stuporous state. He complained of pain in the right loin, which began 3 days before admission, and which was accompanied by vomiting for 1 day, and hematuria.
FIG. 1
FIG. 2
FIG. 1. Flat film showing innumerous calcareous shadows in region of both kidneys. FIG. 2. Left pyelogram showing small amount of remaining renal tissue studded with calcareous shadows.
Cystoscopy disclosed a small calculus protruding from the right ureteral orifice, and which was dislodged by manipulation and removed. A No. 8 ureteral catheter was maneuvered into the orifice and inspissated pus then exuded. The catheter met an obstruction about 3 cm. above the orifice, but finally passed to the pelvis. About 100 cc. pyonephrotic fluid was removed. The catheter was left in place. The patient was given 2 ampoules of glucose, 250 cc. Fisher's and 150 cc. saline intravenously. He was rational and oriented at intervals. There was tenderness over the right upper quadrant and loin, but no rigidity or mass was palpable. Owing to his unsatisfactory condition, a rectal examination was not done. Laboratory data: Urine: specific gravity 1.010, alkaline, a trace of albumin and acetone, white blood cells 40,000 to 50,000, red blood cells 1,000,000 to 2,000,000, and bacteria. No acid fast bacilli were found. Culture of urine
P ARENCHYMAL CALCULOSIS OF KIDNEYS
295
yielded Bacillus pyocyaneus. Blood examination: hemoglobin 77 per cent, white blood cells 19,400, red blood cells 3,980,000, polymorphonuclears 87 per cent. Blood chemistry: blood urea nitrogen 50.8, sugar 130, alkali reserve 36 volume per cent. Three hours after cystoscopy the patient had a violent chill, accompanied by dyspnoea and cyanosis, which lasted about 20 minutes, after which his temperature went to 106.8. His pulse was 128. The next morning (August 24) the temperature was down to 101. Saline solution was injected into the kidney through the right ureteral catheter (which had been left in place) after which urine began to drain from the kidney. The patient complained of right lumbar pain and was somewhat distended. The catheter was removed. On August 25 the temperature was 103, but the patient felt better. He was given intravenous injections of Fisher's solution, normal saline solution and glucose. Two days later (August 27) the intravenous injections of saline and Fisher's solution were repeated. The patient looked much better. His temperature, pulse and respirations were normal. On August 29 the patient passed a calculus without pain. He was discharged from the hospital the next day. Dilatation of both ureters with a No. 10 F. bougie was carried out at the office on three occasions. The patient returned to the hospital on December 15, 1935 (1 month after the last bilateral ureteral dilatation) complaining of pain in the right side. His temperature was 104. After cystoscopic dilatation he passed a calculus. He was readmitted to the hospital on July 5, 1936 (7 months later) with high temperature, toxemia and pain in the left side. A catheter was left in place in the left kidney for 48 hours. He passed a calculus 2 days later. On July 27 the patient had an attack of pain in the right side, and passed a stone without instrumentation. Both ureters were dilated. Bilateral ureteral dilatation was carried out on September 3, and again on March 17, 1937 and May 20. On this latter date the patient had an attack of pain in his right loin. Cystoscopy disclosed a vesical calculus which was washed out. On July 14, 1937 the patient complained of a severe attack of pain on the left side, accompanied by fever and vomiting. A No. 12 F. bougie was passed, after which the symptoms disappeared. Three days later the patient returned to the hospital in a semi-comatose condition. He complained of gradually increasing pain in the left abdomen, associated with vomiting and general weakness. The temperature was 106.2. The abdomen was rigid, especially over the left flank. On cystoscopy, no catheter would pass to the left kidney. It met an ob-
296
M. MUSCHAT AND L. KOOLPE
struction about 25 cm. above the bladder. A nephrostomy was performed. The kidney, which was huge, was filled with over a quart of pus. It was necessary to remove several calculi in order to insert the nephrostomy tube. The patient stood the operation well, and within 4 hours his temperature was normal. With the aid of hypoclysis and glucose, the urine output mounted rapidly, and the blood urea dropped from 110 to 57 within 5 days. Ten days after operation the patient developed a left sided parotitis, the toxemia returned, and the urinary output began to diminish. Hartman solution with glucose was administered intravenously twice a day because of the low CO2~24
FIG. 3. Autopsy specimen of both kidneys. has a brown-black nucleus.
Nephrostomy tube still in situ.
Each stone
per cent. Ten days later (20 days after operation) the patient's condition improved after several incisions into the suppurating parotid, and blood transfusions. The CO2 mounted to 43 per cent, the blood urea nitrogen dropped to 44, the hemoglobin to 70 per cent, the red blood cells 3,560,000 and white blood cells 16,500. The patient insisted that he be sent home, and that he be taken care of by his family physician. He grew weaker and expired 2 weeks later. Autopsy (partial): We were permitted to remove only the kidneys. They were small in size, 12 x 7 x 3 cm. The consistency was hard and one could feel the concretions through the cortex. On opening them from the pelvic side innumerable white concretions were found in the pelvis and in the recesses
P ARENCHYMAL CALCULOSIS OF KIDNEYS
297
of the former calices. All concretions were irregular and bizarre in appearance, taking the form of their lodging beds. It was impossible to find a single round or oval shaped concretion. All were white with a brown nucleus uncovered on one aspect (fig. 3). The parenchyma was dirty grayish red with much gray fibrotic tissue interspersed. About 80 per cent of the parenchyma appeared to have been destroyed by an inflammatory process of long duration. The pelvic mucosa was livid red and granular in appearance with hyperplastic areas here and there. On cutting the kidneys one was impressed with the hardness and grittiness of the tissues, like cutting through soft cement. Close inspection and palpation revealed myriads of small and tiny concretions embedded within the
FIG. 4. X-ray of kidneys as found at autopsy. Note small concretions within parenchyma
parenchyma like particles of glass dust. An x-ray of both kidneys revealed various sized concretions throughout the parenchyma. Histological study: The parenchyma presented a rather uniform appearance of normal renal architecture interspersed with areas of small cell infiltration and tubuli filled with hyaline masses. Figure 5 shows recognizable renal tissue on the right with an area of alteration on the left. One can see the tubules filled with hyaline of varied consistency, some staining light and others very dark. In Figure 6 one notes the concentric appearance of these tubular masses, some of them shaped like an onion, but most of them formed to fit the lumen of the particular tubule. Throughout the kidney were greatly dilated tubules (fig. 7) with a very marked hyperplasia of their epithelial lining. In many instances the hyper-
298
M. MUSCHAT AND L. KOOLPE
plasia had produced 10 to 20 new layers of epithelial cells. Frequently one noted a complete obliteration of the tubular lumen, filled tightly with the hyperplastic epithelial cells. In others, one half of the lumen of the tubule was filled with hyperplastic cells; the other half showed the progress of a disintegrating process of hyaline degeneration of these epithelial cells. One then found tubules filled with a varied amount of living cells and others with the product of their complete disintegration, having the appearance of pure hyaline without evidence of cellular structure whatsoever.
FIG. 5 FIG. 6 FIG. 5. Photomicrograph of parenchyma of right kidney showing normal structure on right side of field and calcareous deposits on left. FIG. 6. Parenchyma of left kidney studded with deposits. Some deposits have concentric onion-like appearance.
These large hyaline masses filling the tubules grew to immense proportions. We designated them as "pearls". Many of these pearls were found in the parenchyma, others in the center and some on the caliceal side of the papillae, ready to drop into the caliceal urine (figs. 8, 9). One found these yellow round "pearls", filled with a hyaline substance, freely in the pelvis and calices (fig. 10). Throughout the parenchyma one saw evidence of a very marked pyelonephritis involving the glomeruli, tubules and mucosa of the pelvis. Areas of round cell infiltration were common and one could not find a section without them.
PARENCHYMAL CALCULOSIS OF KIDNEYS
FIG.
7
299
FIG. 8
Fm. 7. Hyperplasia of lining of tubule encroaching and beginning complete obliteration of lumen, Below tubule filled ·with soft homogeneous material. FIG. 8. Renal papilla with pearl in center
-~
FIG. FIG.
9
FIG.10
9. Renal papilla with pearl on lateral ,val! about to drop into pelvis FIG. 10. Pearls found freely movable in pelvis
In theorizing upon the etiology of this condition, one is fascinated with the wealth of possibilities. In order not to be misled in the interpretation one fact must clearly be borne in mind, namely, that this patho-
300
M. J\!IUSCHAT AND L. KOOLPE
logical state, while closely resembling renal calculi, in actuality has no relationship to the latter. It is a state of soft intrarenal concretions which became hard as they came in contact with the tubular or pelvic unne. Tuberculosis was eliminated by careful ante- and post-mortem studies. The presence of parasites like the Pentostoma denticulata was questioned but none were found on repeated examinations. The blood chemistry showed no remarkable alteration. Except for the anemia and an increase of urea-nitrogen in the later stages the blood presented a perfectly normal picture. Studies were undertaken in order to assemble more data for interpretation.
FIG. 11. Composite drawing illustrating theoretical genesis of stones and their chemical composition. It shows pearls made up of pure fibrin within papilla, becoming incrustated with calcium and magnesium phosphate and calcium oxalate upon leaving papilla and dropping into pelvic urine. F.-fibrin.
The microscopic sections were made with great difficulty, ruining many knife edges because of the hard intraparenchymal concretions (figs. 5, 6). Summarizing the histological findings, one obtains the following picture: For an unknown reason the tubular epithelium begins to multiply, producing many new epithelial cells in layers (fig. 7). This process goes on indefinitely until the tubular lumen is completely occluded. This mass of cells then undergoes degeneration and complete disintegration until a homogenous mass is formed completely filling the tubular lumen (figs. 8, 9). Some of these intratubular masses are very large and round and, because many of them were found lying freely in the pelvis, we called them "pearls" (fig. 10). They are round, smooth, transparent and yellow in color.
PARENCHYMAL CALCULOSIS OF KIDNEYS
301
In order to determine their chemical composition we not only analyzed the "free pearls" found in the pelvis but also removed the "intrarenal pearls" by microscopic dissection. These pearls were found to be composed of pure fibrin without any other organic or inorganic admixture (fig. 11). The only time these pearls showed evidence of inorganic admixture of calcium or magnesium phosphate was when the examined pearl was removed from a section where it came in contact with urine. In such an instance it also showed evidence of layer deposit, much like an onion. We feel certain that the reason for the small number of "free pearls" in the renal pelvis was their rapid incrustations with urinary salts and transformation into stone. This is further supported by the finding of a brown nucleus in every pelvic stone. The brown nucleus and white coating of the pelvic stones were found to have approximately the same chemical composition, the brown color of the nucleus being probably due to the residual staining of the intraparenchymal "pearl." The process of gradual stone formation from an intraparenchymal "pearl" is theoretically and graphically depicted in figure 2.
Medical Arts Bldg., Philadelphia, Pa.
AND
L. KOOLPE
From the Department of Urology, Mt. Sinai Hospital, Philadelphia, Pa.
The name "renal calculosis" is used here in lieu of a better term to denote a certain rare pathological condition in which the kidneys are literally riddled and studded with concretions ranging from the size of a red blood cell to that of a cherry. The microscopic concretions are found in the parenchyma while the macroscopic ones are in the calices and pelvis. We followed this patient over a period of years and were fortunate to be permitted to study the kidneys at autopsy. Case report. Mt. Sinai Hospital No. 93187, H. W., a milk dealer aged 59, entered the service of Dr. A. I. Rubenstone July 5, 1935. He had a chili 2 days before admission, accompanied by fever, vomiting and a sudden severe pain in the abdomen. He had had frequency and nocturia 10 to 12 times for a number of years. A diagnosis of renal calculi had been made elsewhere. Except for marked distension and tenderness in the abdomen, the physical examination was negative. An x-ray showed innumerable calcareous deposits in both kidneys, ranging in size from a small barley grain to a large pea, and also 2 small concretions at the left ureterovesical juncture. An x-ray of the lungs showed an old healed tuberculosis of both apices (fig. 1). Laboratory data: Urine: specific gravity 1007, alkaline, moderate trace of albumin, 50 to 75 white blood cells, and an occasional red blood cell and bacteria. Blood examination: hemoglobin 88, red blood cells 4,710,000, white blood cells 9,950, polymorphonuclears 84 per cent. Blood chemistry: blood urea nitrogen 40, sugar 132, creatinine 2.4, calcium 8.4, phosphorus 2. 7. Wassermann reaction negative. Functional tests: urea clearance 25.6, P. S. P. 14 per cent (repeated). A study of five 24 hour specimens of urine revealed no acid fast bacilli. Urine and blood cultures were negative. Cystoscopy revealed a normal bladder and ureteral orifices. A No. 7 catheter passed to the left kidney without meeting any obstruction. The kidney was found to be filled with creamy pus. Lavage of the kidney was carried out and the catheter left in place. Two days after cystoscopy the patient passed 2 small calculi, chemical analysis of which showed magnesium and calcium phosphate. The patient's temperature was 103. 1 Read before the Philadelphia Urological Society, February 28, 1938, and the Mount Sinai Clinical Society, May 17, 1938. 293
294
M. MUSCHAT AND L. KOOLPE
Two days after the calculi were passed, the patient developed chills, accompanied by pain in the left loin and vomiting. Urine obtained by catheterization of the left kidney wa.s clear. A retrograde left pyelogram disclosed a huge hydronephorisis with innumerable calcareous deposits in the parenchyma; very little normal kidney tissue remained (fig. 2). The next day the temperature was 101. The patient complained of burning and difficulty on urination, which necessitated catheterization. For 2 weeks his temperature had ranged from 100 to 102. He was discharged from the hospital on August 7, a month after admission. He returned to the hospital on August 23 in a semi-stuporous state. He complained of pain in the right loin, which began 3 days before admission, and which was accompanied by vomiting for 1 day, and hematuria.
FIG. 1
FIG. 2
FIG. 1. Flat film showing innumerous calcareous shadows in region of both kidneys. FIG. 2. Left pyelogram showing small amount of remaining renal tissue studded with calcareous shadows.
Cystoscopy disclosed a small calculus protruding from the right ureteral orifice, and which was dislodged by manipulation and removed. A No. 8 ureteral catheter was maneuvered into the orifice and inspissated pus then exuded. The catheter met an obstruction about 3 cm. above the orifice, but finally passed to the pelvis. About 100 cc. pyonephrotic fluid was removed. The catheter was left in place. The patient was given 2 ampoules of glucose, 250 cc. Fisher's and 150 cc. saline intravenously. He was rational and oriented at intervals. There was tenderness over the right upper quadrant and loin, but no rigidity or mass was palpable. Owing to his unsatisfactory condition, a rectal examination was not done. Laboratory data: Urine: specific gravity 1.010, alkaline, a trace of albumin and acetone, white blood cells 40,000 to 50,000, red blood cells 1,000,000 to 2,000,000, and bacteria. No acid fast bacilli were found. Culture of urine
P ARENCHYMAL CALCULOSIS OF KIDNEYS
295
yielded Bacillus pyocyaneus. Blood examination: hemoglobin 77 per cent, white blood cells 19,400, red blood cells 3,980,000, polymorphonuclears 87 per cent. Blood chemistry: blood urea nitrogen 50.8, sugar 130, alkali reserve 36 volume per cent. Three hours after cystoscopy the patient had a violent chill, accompanied by dyspnoea and cyanosis, which lasted about 20 minutes, after which his temperature went to 106.8. His pulse was 128. The next morning (August 24) the temperature was down to 101. Saline solution was injected into the kidney through the right ureteral catheter (which had been left in place) after which urine began to drain from the kidney. The patient complained of right lumbar pain and was somewhat distended. The catheter was removed. On August 25 the temperature was 103, but the patient felt better. He was given intravenous injections of Fisher's solution, normal saline solution and glucose. Two days later (August 27) the intravenous injections of saline and Fisher's solution were repeated. The patient looked much better. His temperature, pulse and respirations were normal. On August 29 the patient passed a calculus without pain. He was discharged from the hospital the next day. Dilatation of both ureters with a No. 10 F. bougie was carried out at the office on three occasions. The patient returned to the hospital on December 15, 1935 (1 month after the last bilateral ureteral dilatation) complaining of pain in the right side. His temperature was 104. After cystoscopic dilatation he passed a calculus. He was readmitted to the hospital on July 5, 1936 (7 months later) with high temperature, toxemia and pain in the left side. A catheter was left in place in the left kidney for 48 hours. He passed a calculus 2 days later. On July 27 the patient had an attack of pain in the right side, and passed a stone without instrumentation. Both ureters were dilated. Bilateral ureteral dilatation was carried out on September 3, and again on March 17, 1937 and May 20. On this latter date the patient had an attack of pain in his right loin. Cystoscopy disclosed a vesical calculus which was washed out. On July 14, 1937 the patient complained of a severe attack of pain on the left side, accompanied by fever and vomiting. A No. 12 F. bougie was passed, after which the symptoms disappeared. Three days later the patient returned to the hospital in a semi-comatose condition. He complained of gradually increasing pain in the left abdomen, associated with vomiting and general weakness. The temperature was 106.2. The abdomen was rigid, especially over the left flank. On cystoscopy, no catheter would pass to the left kidney. It met an ob-
296
M. MUSCHAT AND L. KOOLPE
struction about 25 cm. above the bladder. A nephrostomy was performed. The kidney, which was huge, was filled with over a quart of pus. It was necessary to remove several calculi in order to insert the nephrostomy tube. The patient stood the operation well, and within 4 hours his temperature was normal. With the aid of hypoclysis and glucose, the urine output mounted rapidly, and the blood urea dropped from 110 to 57 within 5 days. Ten days after operation the patient developed a left sided parotitis, the toxemia returned, and the urinary output began to diminish. Hartman solution with glucose was administered intravenously twice a day because of the low CO2~24
FIG. 3. Autopsy specimen of both kidneys. has a brown-black nucleus.
Nephrostomy tube still in situ.
Each stone
per cent. Ten days later (20 days after operation) the patient's condition improved after several incisions into the suppurating parotid, and blood transfusions. The CO2 mounted to 43 per cent, the blood urea nitrogen dropped to 44, the hemoglobin to 70 per cent, the red blood cells 3,560,000 and white blood cells 16,500. The patient insisted that he be sent home, and that he be taken care of by his family physician. He grew weaker and expired 2 weeks later. Autopsy (partial): We were permitted to remove only the kidneys. They were small in size, 12 x 7 x 3 cm. The consistency was hard and one could feel the concretions through the cortex. On opening them from the pelvic side innumerable white concretions were found in the pelvis and in the recesses
P ARENCHYMAL CALCULOSIS OF KIDNEYS
297
of the former calices. All concretions were irregular and bizarre in appearance, taking the form of their lodging beds. It was impossible to find a single round or oval shaped concretion. All were white with a brown nucleus uncovered on one aspect (fig. 3). The parenchyma was dirty grayish red with much gray fibrotic tissue interspersed. About 80 per cent of the parenchyma appeared to have been destroyed by an inflammatory process of long duration. The pelvic mucosa was livid red and granular in appearance with hyperplastic areas here and there. On cutting the kidneys one was impressed with the hardness and grittiness of the tissues, like cutting through soft cement. Close inspection and palpation revealed myriads of small and tiny concretions embedded within the
FIG. 4. X-ray of kidneys as found at autopsy. Note small concretions within parenchyma
parenchyma like particles of glass dust. An x-ray of both kidneys revealed various sized concretions throughout the parenchyma. Histological study: The parenchyma presented a rather uniform appearance of normal renal architecture interspersed with areas of small cell infiltration and tubuli filled with hyaline masses. Figure 5 shows recognizable renal tissue on the right with an area of alteration on the left. One can see the tubules filled with hyaline of varied consistency, some staining light and others very dark. In Figure 6 one notes the concentric appearance of these tubular masses, some of them shaped like an onion, but most of them formed to fit the lumen of the particular tubule. Throughout the kidney were greatly dilated tubules (fig. 7) with a very marked hyperplasia of their epithelial lining. In many instances the hyper-
298
M. MUSCHAT AND L. KOOLPE
plasia had produced 10 to 20 new layers of epithelial cells. Frequently one noted a complete obliteration of the tubular lumen, filled tightly with the hyperplastic epithelial cells. In others, one half of the lumen of the tubule was filled with hyperplastic cells; the other half showed the progress of a disintegrating process of hyaline degeneration of these epithelial cells. One then found tubules filled with a varied amount of living cells and others with the product of their complete disintegration, having the appearance of pure hyaline without evidence of cellular structure whatsoever.
FIG. 5 FIG. 6 FIG. 5. Photomicrograph of parenchyma of right kidney showing normal structure on right side of field and calcareous deposits on left. FIG. 6. Parenchyma of left kidney studded with deposits. Some deposits have concentric onion-like appearance.
These large hyaline masses filling the tubules grew to immense proportions. We designated them as "pearls". Many of these pearls were found in the parenchyma, others in the center and some on the caliceal side of the papillae, ready to drop into the caliceal urine (figs. 8, 9). One found these yellow round "pearls", filled with a hyaline substance, freely in the pelvis and calices (fig. 10). Throughout the parenchyma one saw evidence of a very marked pyelonephritis involving the glomeruli, tubules and mucosa of the pelvis. Areas of round cell infiltration were common and one could not find a section without them.
PARENCHYMAL CALCULOSIS OF KIDNEYS
FIG.
7
299
FIG. 8
Fm. 7. Hyperplasia of lining of tubule encroaching and beginning complete obliteration of lumen, Below tubule filled ·with soft homogeneous material. FIG. 8. Renal papilla with pearl in center
-~
FIG. FIG.
9
FIG.10
9. Renal papilla with pearl on lateral ,val! about to drop into pelvis FIG. 10. Pearls found freely movable in pelvis
In theorizing upon the etiology of this condition, one is fascinated with the wealth of possibilities. In order not to be misled in the interpretation one fact must clearly be borne in mind, namely, that this patho-
300
M. J\!IUSCHAT AND L. KOOLPE
logical state, while closely resembling renal calculi, in actuality has no relationship to the latter. It is a state of soft intrarenal concretions which became hard as they came in contact with the tubular or pelvic unne. Tuberculosis was eliminated by careful ante- and post-mortem studies. The presence of parasites like the Pentostoma denticulata was questioned but none were found on repeated examinations. The blood chemistry showed no remarkable alteration. Except for the anemia and an increase of urea-nitrogen in the later stages the blood presented a perfectly normal picture. Studies were undertaken in order to assemble more data for interpretation.
FIG. 11. Composite drawing illustrating theoretical genesis of stones and their chemical composition. It shows pearls made up of pure fibrin within papilla, becoming incrustated with calcium and magnesium phosphate and calcium oxalate upon leaving papilla and dropping into pelvic urine. F.-fibrin.
The microscopic sections were made with great difficulty, ruining many knife edges because of the hard intraparenchymal concretions (figs. 5, 6). Summarizing the histological findings, one obtains the following picture: For an unknown reason the tubular epithelium begins to multiply, producing many new epithelial cells in layers (fig. 7). This process goes on indefinitely until the tubular lumen is completely occluded. This mass of cells then undergoes degeneration and complete disintegration until a homogenous mass is formed completely filling the tubular lumen (figs. 8, 9). Some of these intratubular masses are very large and round and, because many of them were found lying freely in the pelvis, we called them "pearls" (fig. 10). They are round, smooth, transparent and yellow in color.
PARENCHYMAL CALCULOSIS OF KIDNEYS
301
In order to determine their chemical composition we not only analyzed the "free pearls" found in the pelvis but also removed the "intrarenal pearls" by microscopic dissection. These pearls were found to be composed of pure fibrin without any other organic or inorganic admixture (fig. 11). The only time these pearls showed evidence of inorganic admixture of calcium or magnesium phosphate was when the examined pearl was removed from a section where it came in contact with urine. In such an instance it also showed evidence of layer deposit, much like an onion. We feel certain that the reason for the small number of "free pearls" in the renal pelvis was their rapid incrustations with urinary salts and transformation into stone. This is further supported by the finding of a brown nucleus in every pelvic stone. The brown nucleus and white coating of the pelvic stones were found to have approximately the same chemical composition, the brown color of the nucleus being probably due to the residual staining of the intraparenchymal "pearl." The process of gradual stone formation from an intraparenchymal "pearl" is theoretically and graphically depicted in figure 2.
Medical Arts Bldg., Philadelphia, Pa.