MONOCYTIC LEUKEMIA, AN UNCOMMON CAUSE OF RENAL FAILURE *

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1 CASE REPORTS 1197 MONOCYTIC LEUKEMIA, AN UNCOMMON CAUSE OF RENAL FAILURE * By R. D. TAYLOR, M.D., Cleveland, ROBERT BIRCH ALL, M.D., New Orleans, La., and IRVINE H. PAGE, M.D., F.A.C.P., Cleveland, Ohio MOST causes of renal failure are easily recognized. However, the record of the patient reported here presents an example of death due to renal insufficiency, the mechanism of which was not clear until autopsy had been performed. The kidneys were found to be almost completely replaced by leukemic tissue. Such infiltration of kidneys to a degree great enough to cause uremia is uncommon. CASE REPORT A 50 year old Jewess was admitted to the Research Division of Cleveland Clinic Hospital because of progressive anasarca and weakness of short duration. She had been examined as an out-patient in the Clinic three years previously, when her arterial blood pressure was found to be 155/105 mm. Hg; urinalysis normal; blood urea 30 mg. per 100 c.c.; blood hemoglobin 13 gm. per 100 c.c, and the white blood count 8,300 per cu. mm. Except for obesity and associated dyspnea she remained well until the onset of her final illness. Two weeks before the last admission she consulted her physician because of generalized weakness, pain in the calves of her legs and mild hot flashes. Her complaints were thought to be due to menopause and she was treated with intramuscular * Received for publication April 4, 1947.

2 CHART

3 CASE REPORTS 1199 theelin. Within 48 hours anasarca developed. Seven days later she again received an injection of theelin in oil. Edema promptly became more severe and she was referred to Cleveland Clinic Hospital. The patient was 61 inches in height and weighed pounds. The conjunctivae, face and extremities were edematous. Temperature was 99 F.; pulse rate 80 and blood pressure 210/100 mm. Hg. The optic discs and retinae were normal. The retinal arterioles showed grade 2 narrowing. The red blood cell count was 4,370,000 per cu. mm.; blood hemoglobin 10.5 gm. per 100 c.c; white blood count 15,700 per cu. mm.; urea clearance 45 per cent of average normal and blood urea 39 mg. per FIG. 1. The cut surfaces of the left kidney (328 gm.) show thickening of the capsule, the bulging parenchymal tissue and the alteration of normal markings. The cortex was 1.3 cm. in thickness. 100 c.c. The maximal ability to concentrate urine, as measured by the Addis test, was represented by a specific gravity of There was 1.0 gm. of proteinuria per 24 hours. The Addis count of the urinary sediment showed 500,000 casts and a normal number of red and white cells. Intravenous and retrograde pyelograms were normal. Urine cultures were repeatedly negative. The electrocardiogram was within normal limits. Teleroentgenogram snowed a cardiac shadow, the transverse diameter of which deviated plus 5 per cent from the predicted normal (Ungerleider and Clark 1 ). The course of her illness is summarized in chart 1. The outstanding features were rapid renal failure and mounting leukocytosis. No clear explanation of either could be established. Significant anemia, lymphadenopathy, splenic or hepatic enlargement were not found. Gross hematuria due to acute hemorrhagic cystitis occurred once following cystoscopy. Urine specimens taken at this time were sterile.

4 1200 R. D. TAYLOR, ROBERT BIRCHALL AND IRVINE H. PAGE The total white blood cell count gradually rose from the admission level of 15,700 per cu. mm. to 33,150, 10 days before death. Five days later it was 93,000 and after another 48 hours 192,000 per cu. mm. of blood. Of these, 55 per cent were atypical mononuclear cells, half of which gave a positive peroxidase reaction. There were 36 per cent neutrophiles, 3.6 per cent nonfilamented neutrophiles, 2.5 per cent lymphocytes, 2 per cent monocytes and 1 per cent myelocytes. Aspiration and surgical biopsies of the sternal marrow taken ante mortem were examined by Dr. L. W. Diggs.* Both showed moderately increased cellularity with normal myeloid and erythroid distribution. There was slight increase of reticuloendothelial and large mononuclear cells; however, none was considered pathognomonic of neoplastic disease. Dr. Diggs FIG. 2. Infiltration of glomeruli, tubular and interstitial tissue with monocytes is illustrated by this section. The tubular tissue is hardly discernible. felt that the absence of pathological cells of the type noted in peripheral blood was against a diagnosis of leukemia. He suggested that there was probably a reticulum cell sarcoma with a leukemoid reaction of the bone marrow. She became anuric three days before death and died on the twenty-fifth hospital day. Pathological Report: Only the kidneys, spleen, sections of the liver and pancreas could be obtained for postmortem study. The kidneys were twice normal size, the right weighing 308 gm. and the left 328 gm. (normal gm.). There was moderate thickening of the capsules which stripped with increased difficulty. The external surfaces were pale, yellowish-brown and granular. The cut surfaces bulged and the cortices, which appeared swollen, measured as much as 1.3 cm. in thickness (figure 1). The pyramids were indistinctly demarcated from the cortices and were deep yellowish-brown color. Microscopic examination (figure 2) showed that the entire kidney was diffusely and heavily infiltrated by monocytic cells. The tubules were dilated and lined by degenerated epithelium. * Clinical Pathologist, Cleveland Clinic Foundation.

5 CASE REPORTS 1201 The spleen weighed 430 gm. and was covered by a thickened tense capsule. On the cut surface the lymphoid follicles were prominent as pale gray circular areas measuring up to 1 mm. in diameter. Microscopically there was diffuse infiltration of monocytes. The mononuclear cells throughout the tissues examined contained oval or indented nuclei filled with irregularly distributed chromatin. The nuclei were surrounded by a scanty amount of faintly basophilic cytoplasm. No definite grooving could be seen. The peroxidase reaction showed that numerous cells contained granules, and staining by the Kingsley method demonstrated many of the abnormal cells to be mononuclear resembling immature myelocytes. The pathological diagnosis was monocytic leukemia (Naegeli type). 2 COMMENT Extensive studies conducted during the first two weeks of hospitalization demonstrated no cause for rapid renal failure or anasarca. There was no evidence of congestive heart failure, acute nephritis, hypoproteinemia (plasma albumin was 3.26 gm. per 100 c.c.) or appreciable anemia. Excessive retention of sodium and water was the only explanation that seemed tenable. This could have come about if there was glomerulo-tubular imbalance with a disproportionately great reabsorption of filtrate. That this might have existed was suggested by the Addis test done 14 days before death. The 12 hour volume was only 285 c.c. (normal 150 to 400 c.c.) and the maximum specific gravity was while the urea clearance was depressed to 15 per cent of normal. Further, the cast count of the urinary sediment was 1.5 million per 12 hours with but 0.7 gm. of proteinuria per 24 hours. This might indicate sluggish flow of urine through tubules. Such glomerulo-tubular imbalance is seen in patients with toxemia of pregnancy and acute nephritis. It has been suggested that increased interstitial pressure within the kidneys might reduce glomerular filtration pressure while tubular reabsorption is comparatively unaffected. The excessive leukocytosis which appeared terminally suggested some type of leukemia; however, neither the peripheral blood, lymph nodes nor bone marrow were typical of any given type. It was assumed that the rapidly rising white cell count represented a leukemoid response to a neoplastic process which probably was infiltrating the kidneys to cause increased intracapsular pressure which effectively reduced filtration pressure and resulted in glomerulo-tubular imbalance, and eventually renal failure and death. Postmortem examination demonstrated extensive infiltration of both kidneys by monocytes. The liver and spleen were similarly infiltrated. The spleen weighed 430 gm. as compared with the normal values of 120 to 180 gm. It is probable that this enlargement was masked by obesity and ascites during life. Had the extreme leukocytosis occurred earlier the possibility of monocytic infiltration of the kidneys might have been considered, at which time a liver biopsy would have been helpful. SUMMARY A 50 year old woman developed anasarca and died of rapid renal failure of somewhat obscure origin. The explanation proposed for the generalized edema was sodium and fluid retention due to glomerulo-tubular imbalance. Extreme terminal leukocytosis suggested that infiltration of the kidneys by monocytes

6 1202 S. F. HORNE, A. C. CURTIS, AND E. A. KAHN might have increased intracapsular pressure enough to produce this syndrome. Examination of the bone marrow and peripheral blood did not allow for exact diagnosis but it seemed probable that a reticulum cell sarcoma was infiltrating the kidneys and inducing a leukemoid reaction of the bone marrow. At postmortem examination the kidneys, liver and spleen were found infiltrated with the cells of acute monocytic leukemia. The diagnosis could have been made antemortem had peritoneoscopy and biopsy of the liver or spleen been done. BIBLIOGRAPHY 1. Ungerleider, H. E., and Clark, C. P.: A study of the transverse diameter of the heart silhouette with prediction table based on the teleroentgenogram, Am. Heart J. 17: , Watkins, C. H., and Hall, B. E.: Monocytic leukemia of the Naegeli and Schilling types, Am. J. Clin. Path. 10: 387, 1940.

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