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 ::  Introduction
 ::  Case report
 ::  Discussion
 ::  References

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Year : 1984  |  Volume : 30  |  Issue : 3  |  Page : 193-5

Leukaemia in chronic uraemia (a case report).

How to cite this article:
Baldwa V S, Gupta B S, Bhansali A A, Purohit S S. Leukaemia in chronic uraemia (a case report). J Postgrad Med 1984;30:193

How to cite this URL:
Baldwa V S, Gupta B S, Bhansali A A, Purohit S S. Leukaemia in chronic uraemia (a case report). J Postgrad Med [serial online] 1984 [cited 2023 Jun 6];30:193. Available from:

  ::   Introduction Top

Patients with chronic uraemia not only have to suffer the consequences of their renal failure, but also have an increased rate of arteriosclerosis,[4] infection[2] and an increased incidence of malignancies.[3]
Matas et al[6] reported 21 tumours in 896 patients (with mean age of 43 years) who came to the hospital for dialysis. This incidence was seven times greater than that in the age-matched, general population. Miach et al[7] reported 6 out of 47 patients (13%) (with mean age of 53 years) who had malignancies that did not directly cause their renal failure. Kjellestrand[3] reviewed the whole profile and observed chronic leukaemia in 3 (8.5%) out of 35 patients.
The leukaemia may be asymptomatic or its symptoms are masked by manifestations of chronic uraemia. We had such a case which was complicated by renal failure. The case is reported in order to highlight increased incidence of malignancy in general and leukaemia in particular, in patients with chronic renal failure.

  ::   Case report Top

A 56 year old Hindu male was admitted in the S.M.S. Medical College and Hospital, Jaipur, with complaints of acute onset breathlessness of gradually increasing severity, accompanied by epigastric pain of 10 days' duration. The patient had uneventful past history except for mild dysuria 5 years earlier. There was no history of chest pain, cough, diabetes mellitus and hypertension. Clinical examination revealed that he was drowsy, dyspnoeic and moderately anaemic. His pulse was 104/per minute and regular, B.P. 140/90 mm Hg, respiratory rate 44 per minute and temperature 99.6F, There was no evidence of lymphoreticular proliferation, bony tenderness or congestive cardiac failure. His systemic examination disclosed no abnormality except bilateral basal crepitations.
His investigations revealed haemoglobin of 8.6 gm%, total RBC count of 3 million per cmm, and total leucocyte count of 55800 per cmm. Peripheral blood film examination showed 80% immature cells of myeloid series-mainly myeloblasts and promyelocytes, inadequate platelets and normocytic normochronic anaemia. [Fig. 1]. Urine examination showed trace albuminuria, microscopic haematuria, 5-6 pus cells and no growth on culture. His biochemical studies depicted blood urea of 370 mg%, serum creatinine 8.5 mg%, creatinine clearance 6 mg/ml/24 hours and uric acid 14.1 mg%. Other tests were in the normal range, e.g. blood sugar 109 mg%, serum calcium 10 mg% and serum cholesterol 184 mg%. Skiagram of the chest revealed bilateral perihilar haziness and I.V.P. showed bilaterally contracted kidneys without any evidence of obstructive uropathy. E.C.G. was normal. Fundi showed bilateral multiple haemorrhages and exudates without papilloedema, periodic acid-Schiff staining of the peripheral blood film confirmed immature cells to be of myeloid series.
After establishing acute myeloblastic leukaemia, the patient was put on vincristine 1 mg I. V. weekly, prednisolone 100 mg/day, allopurinal 100 mg three times a day, and blood transfusion. With this treatment, leucocyte count dropped to 48,000/cmm, serum uric acid to 8.4 mg% without any change in blood urea and serum creatinine.
On the 7th day of admission, the patient died of massive gastro-intestinal bleeding. Autopsy could not be done due to reluctancy of his relatives.

  ::   Discussion Top

Mitotic activity in renal failure is usually due to nitrogenous waste products or some undefined substances as suspected by Penn.[8] Quadracci et al[9] demonstrated that uraemic serum had a profound effect on T cell mitogenic response. Yet it is difficult to establish the cause-effect relationship between acute myeloblastic leukaemia and uraemia.
The findings of (a) marked deterioration of the renal function, (b) course of the disease and (c) bilaterally contracted kidneys in our case probably point out that uraemia might have been an initiating event. However in leukaemia, kidneys are invariably enlarged due to infiltration of the renal parenchyma and is rather a rare cause of renal failure.[5] With the control of the disease, renal size and function rapidly return to normal; However in our patient, serum uric acid and immature cells declined without any appreciable change in the renal function. Absence of massive proteinuria points out that the kidneys had escaped leukaemic infiltration.
Often, renal failure and hyperuricemia can be the presenting manifestation of occult haematological malignancies. However, in advanced stages of renal failure the cause and/or result relationship cannot be ascertained. Hypertension is usually present in patients with hyperuricemia due to renal dysfunction. Absence of hypertension in our case probably negates uric acid nephropathy. Obstructive uropathy (urate stones) quite frequently presents as an acute renal shutdown which was not seen in our patient.
The most common cancer sites are the kidney and the skin; the most common clinical diagnosis of such uraemic patients is polycystic kidney disease and/or chronic pyelonephritis.[10] Slow progression of uraemia and defective immune defense system[1] in chronic renal disease are probably the attributes of increased incidence of malignancies.

  ::   References Top

1.Birkeland, S. A.: Uraemia as a state of immune deficiency. Scand. J. Immunol.. 5: 107-115, 1976.  Back to cited text no. 1    
2.Kjellestrand, C. M.: Editorial-The Achilles heel of the hemodialysis patient. Arch. Intern. Med., 138: 1063-1054, 1978.  Back to cited text no. 2    
3.Kjellestrand, C. M.: Editorial - Are malignancies increased in uraemia? Nephron, 23: 159-161, 1979.  Back to cited text no. 3    
4.Linder, A., Charra, B., Sherrard, D. J., and Scribner, B. H.: Accelerated atherosclerosis in prolonged maintenance hemodialysis. New Engl. J. Med., 290: 697-701, 1974.  Back to cited text no. 4    
5.Lundberg, W. B., Cadman, E. D. and Finch, S. C.: Renal failure secondary to leukaemic infiltration of the kidneys. Amer. J. Med., 62: 636-642, 1977.  Back to cited text no. 5    
6.Matas, A. J., Simmons, R. L., Kjellestrand, C. M., Buselmeier, T. J. and Najarian, J. S.: Increased incidence of malignancy during chronic renal failure. Lancet, 1: 883-886, 1975.  Back to cited text no. 6    
7.Miach, P. J., Dawborn, J. K. and Xipell, J.: Neoplasia in patients with chronic renal failure on long term dialysis. Clin. Nephrol., 5: 101-104, 1976.  Back to cited text no. 7    
8.Penn, I. and Starzl, T. E.: Malignant tumors arising de novo immunosuppressed organ transplant recipients. Transplant, 14: 407-417, 1972.  Back to cited text no. 8    
9.Quadracci, L. J., Ringden, O. and Krzymanski, M.: The effect of uremia and transplantation on lymphocyte subpopulation. Kidney Int., 10: 179-184, 1976.  Back to cited text no. 9    
10.Sutherland, G. A., Glass J. and Gabriel, R.: Increased incidence of malignancy in chronic renal failure. Nephron, 18: 132-184, 1977.  Back to cited text no. 10    

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Online since 12th February '04
2004 - Journal of Postgraduate Medicine
Official Publication of the Staff Society of the Seth GS Medical College and KEM Hospital, Mumbai, India
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