Abstract
Parameters of renal function were evaluated in severe malarial infection, using mice infected withPlasmodium berghei. When 7-week-old male BALB/c mice were inoculated with 1×107 P. berghei NK65-infected red blood cells, the rodents died an average of 7.4 days after inoculation. Anemia developed on day 5 after inoculation and progressed markedly on days 6 and 7. Plasma urea nitrogen increased rapidly on day 6 or 7, after which death occurred within 24 h. In contrast, urinary urea nitrogen excretion decreased on the same day. Urinary β-N-acetyl-d-glucosaminidase (NAG) activity increased from day 3 to day 5, then decreased to normal levels on day 7. Renal ATP concentration and energy charge decreased markedly on day 7. These data indicate that the blood oxygen supply to the tissues began to decrease on day 6 and that renal insufficiency developed in the terminal stage of infection. We concluded that even a moderate increase in the level of plasma urea nitrogen could be a useful index of renal insufficiency in this infection system.
Similar content being viewed by others
References
Aikawa M, Jacobs G, Whiteley HE, Igarashi I, Ristic M (1988) Glomerulopathy in squirrel monkeys with acutePlasmodium falciparum infection. Am J Trop Med Hyg 38:7–14
Atkinson DE (1968) The energy charge of the adenylate pool as a regulatory parameter. Interaction with feedback modifiers. Biochemistry 7:4030–4034
Boonpucknavig V, Srichaikul T, Punyagupta S (1984) Clinical parasitology. In: Peters W, Richards WHG (eds) Antimalarial drugs I. Springer, Berlin Heidelberg New York, pp 127–176
Chapman AG, Fall L, Atkinson DE (1971) Adenylate energy charge inEscherichia coli during growth and starvation. J Bacteriol 108:1072–1086
Ellis BG, Tucker SM, Thompson AE, Price RG (1975) Presence of serum and tissue forms ofN-acetyl-β-glucosaminidase in urine from patients with renal disease. Clin Chim Acta 64:195–202
Hioki A, Yoshino M, Kano S, Ohtomo H (1987) Pathophysiology of hypoxia in mice infected withPlasmodium berghei. Parasitol Res 73:298–302
Johnson WJ, Stavric B, Chartrand A (1969) Uricase inhibition in the rat bys-triazines: an animal model for hyperuricemia and hyperuricosuria (33791). Proc Soc Exp Biol Med 131:8–12
Kunin CM, Chesney RW, Craig WA, England AC, DeAngelis C (1978) Enzymuria as a marker of renal injury and disease: studies ofN-acetyl-β-glucosaminidase in the general population and in patients with renal disease. Pediatrics 62:751–760
Miller LH, Pavanand K, Buchanan RD, Desowitz RS, Athikulwongse E (1968)Plasmodium berghei: renal function and pathology in mice. Exp Parasitol 23:134–142
Miller TR, Anderson RJ, Linas SL, Henrich WL, Berns AS, Gabow PA, Schrier RW (1978) Urinary diagnostic indices in acute renal failure. A prospective study. Ann Intern Med 89:47–50
Phillips RE, Warrell DA (1986) The pathophysiology of severe falciparum malaria. Parasitol Today 2:271–282
Sitprija V, Vongsthongsri M, Poshyachinda V, Arthachinta S (1977) Renal failure in malaria: a pathophysiologic study. Nephron 18:277–287
Stein JH, Meyer DL, Larry DB (1978) Current concepts on pathophysiology of acute renal failure. Am J Physiol 234:F171-F181
WHO Malaria Action Programme (1986) Severe and complicated malaria. Trans R Soc Trop Med Hyg 80 [Suppl]:3–50
WHO Scientific Group (1984) Advances in malaria themotherapy. WHO Technical Report Series, 711. WHO, Geneva
Wooliscroft JO, Colfer H, Fox IH (1982) Hyperuricemia in acute illness: a poor prognostic sign. Am J Med 72:58–62
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Hioki, A., Ohtomo, H. Significance of blood urea nitrogen as an index of renal function in mice infected withPlasmodium berghei . Parasitol Res 76, 127–130 (1989). https://doi.org/10.1007/BF00930833
Accepted:
Issue Date:
DOI: https://doi.org/10.1007/BF00930833