Serum and urinary proteins, lysozyme (muramidase), and renal dysfunction in mono- and myelomonocytic leukemia

Pruzanski, W.; Platts, M. E.

doi:10.1172/jci106387

Cited by 82 publications

(37 citation statements)

References 33 publications

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“…Abnormally high urinary lysozymes occurred with serum levels as low as 18 ,ug/ml; they were presumably due to renal tubular defects since normal urinary excretion occurred with serum concentrations up to 52 ,jg/ml. Pruzanski and Platts (1970) have similarly found evidence of tubular dysfunction in leukaemia. Peterson, Evrin, and Berggard (1969).…”

Section: Normal Valuesmentioning

confidence: 82%

Lysozymuria and acute disorders of renal function

1973

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On the assumption that increased urinary lysozyme concentration (`lysozymuria') indicates tubular proteinuria and therefore impaired tubular function, urinary lysozyme has been estimated in acute disorders where transient disturbances of renal function might be expected, in cases diagnosed clinically as extrarenal uraemia, and in a few examples of acute renal disease. Reversible lysozymuria occurred with hypokalaemia, postoperative `collapse', electrolyte depletion, severe extrarenal infection, acute pyelonephritis, the nephrotic syndrome, after a few apparently uncomplicated surgical operations, and very transiently after ventricular fibrillation abolished by DC shock. There was no lysozymuria with severe uraemic heart failure, aspirin and paracetamol poisoning, or severe jaundice, nor in two cases of acute glomerulonephritis. Although lysozymuria may occasionally be useful in the clinical diagnosis of acutely disordered renal function, the results suggest that its value is limited; on the other hand, they have provided information on renal pathophysiology in acute disease.

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Section: Normal Valuesmentioning

confidence: 82%

Lysozymuria and acute disorders of renal function

1973

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“…In human cases of mononuclear cell leukemia, lysozyme is produced (45). The kidney injury seen with these neoplastic diseases has been described as similar to that produced by administration ofdecalin to male rats (46), including protein droplet accumulation in renal tubules (44,47,48). Patients with epidemic hemorrhagic fever, infused with large amounts ofconcentrated human serum albumin as a therapeutic procedure for shock, have also developed a comparable form of hyaline droplet accumulation (47).…”

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confidence: 99%

Hazard evaluation of chemicals that cause accumulation of alpha 2u-globulin, hyaline droplet nephropathy, and tubule neoplasia in the kidneys of male rats.

Hard

Rodgers

Baetcke

et al. 1993

Environ Health Perspect

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This review paper examines the relationship between chemicals inducing ewessive accumulation of a2u-globulin (ai21g) (CIGA) in hyline droplets inmale rat kidneys and the subsequent development of nephoit and rnal tubule nopaia in the male rt. This dose-responsive hyaline droplet accumulation distinguishes CIGA carcinogens fromclssical renal carcinogens. CIGA carcinogens also do not appear to react with DNA and are generally negative in short-term tests for genotoxicity. CIGA or their metabolites bind specifically, but reversibly, tomale rat a2,-g The resulting complex appears to be more resistant to hydrolytic degradation in the proximaltubule than native, unbound a2,-g Singlecell necrosis of the tubule epithelium, with associated granular cast formation and papillary mineralization, is followed by sustained regenerative tubule cell prolifertin, foci oftubulehyerl a inthe aovoited pronal bules, and renal tubule tumor Although stnrcturally similar proteins have been detected in other species, including hu_ms, renal lesios characteristic Of a2,-g nephropathy have not been observed. Epidemiologic investigation has not specifically examined the CIGA hypothesis for humans. Based on cancer bioassays, hormone manipulation studies, investigations in an ae,-g-deficient strain of rat, and other laboratory data, an increased proliferative response caused by chemically induced cytotoxicity appears to play a role in the development ofrenal tubule tumors in male rats Thus, it is reasonable to suggest that the renal effects induced in male rats by chemicals causing a2.-g accumulation are unlikely to occur in humans. IntroductionFor most hazardous chemicals, adequate human data are not available, and risk analyses must rely on information from laboratory studies of rats or mice. The inference that the results ofanimal experiments can be applied to humans is a fundamental principle of all toxicologic research. This analysis deals with a specific case, however, where the male rat seems to respond in a manner different from other laboratory species. The possibility of a unique response in the rat among laboratory animals raises questions about the applicability of the rat data to other species, including humans. Our review evaluates the matter of human 'Medical Research Council relevance and describes the types of information needed for hazard assessment of such chemicals.A variety of organic chemicals have produced specific renal lesions in male rats in the form of a protein (hyaline) droplet nephropathy accompanied by accumulation of a2%-globulin (a2.-g) [reviewed in (1,2)]. Among the chemicals tested are paraffins (3,4), decalin (decahydronaphthalene) (5,6), petroleum-based and synthetic fuels (7), military aviation propellants (8), and 2,2,4-trimethylpentane (TMP) (9). As seen in Table 1, which lists a sampling ofchemicals that have been tested, many are of considerable regulatory and commercial interest. For example, isophorone is a chemical intermediate of major industrial importance. Aviation and automotive fuels fit i...

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“…We have recently learned that rats fed TNB had testicular damage and no renal tumors. These rats were on a diet containing 5 (29,35). Immunohistochemistry demonstrated the increase in renal alpha-2u-G accumulation in treated male rats.…”

Section: Discussionmentioning

confidence: 99%

1,3,5-Trinitrobenzene-Induced Alpha-2u-Globulin Nephropathy

et al. 1997

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Male and female (F-344) and male NCI-Black-Reiter (NBR) rats were dosed with 0, 35.5, or 71 mg 1,3,5-trinitrobenzene (TNB)/kg/day for 10 days. Male F-344 rats were dosed with TNB (0 and 35.5 mg/kg) for 20 and 30 days. Hematoxylin and eosin and Mallory-Heidenhain stains and alpha-2u-globulin and proliferating cell nuclear antigen immunohistochemical stains were performed on kidney sections. All treated male F-344 rats exhibited dose-related accumulation of hyaline droplets containing alpha-2u-globulin in proximal tubules. The kidney weights were significantly increased in male and female rats treated with TNB. Significant increases in cell proliferation in proximal tubules were observed in male F-344 rats. Renal changes observed in TNB-treated rats appeared identical to those from other chemicals that induce alpha-2u-globulin nephropathy in male rats. No hyaline droplet accumulation was found in female F-344 and male NBR rats at any doses. We can conclude that TNB induces dose-related exacerbation of hyaline droplets containing alpha-2u-globulin in male rat kidney and subsequent cell proliferation.

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Serum and urinary proteins, lysozyme (muramidase), and renal dysfunction in mono- and myelomonocytic leukemia

Cited by 82 publications

References 33 publications

Lysozymuria and acute disorders of renal function

Lysozymuria and acute disorders of renal function

Hazard evaluation of chemicals that cause accumulation of alpha 2u-globulin, hyaline droplet nephropathy, and tubule neoplasia in the kidneys of male rats.

1,3,5-Trinitrobenzene-Induced Alpha-2u-Globulin Nephropathy

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