Evidence that methylguanidine is retained in chronic renal failure

Giovannetti, S; Biagini, M; Cioni, L

doi:10.1007/bf02140809

Cited by 55 publications

(14 citation statements)

References 3 publications

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“…Method C (after Giovanetti et al, 1968a) To 10 ml of serum was added 10 ml of 20% (w/v) trichloroacetic acid and the precipitates were removed by filtration. Portions (10 ml) of the filtrates were shaken with 2 g amounts of activated charcoal in the presence of 1·5 ml of 40% (w/v) NaOH.…”

Section: Methods B (Aftermentioning

confidence: 99%

“…It has been claimed (Yatzidis, Oreopoulos, Tsaparas, Voudiclari, Stavroulaki & Zestanakis, 1966;Giovanetti, Biagini & Cioni, 1968a) that this substance is present in the serum of uraemic subjects in much higher concentrations than in normal subjects. Methylguanidine is known to have high acute toxicity (Mason, Resnik, Minot, Rainey, Pilcher & Harrison, 1937) and its chronic subcutaneous administration to normal dogs in amounts sufficient to produce methylguanidine concentrations similar to those reported in humans with severe renal failure (Yatzidis et al, 1966;Giovanetti et al, 1968a), induces a hypercatabolic state, impaired erythrocyte production and haemolysis, a decrease in platelet count, neuropathy, anorexia, vomiting, diarrhoea, gastrointestinal ulceration and haemorrhages, pulmonary oedema, tachycardia and arrhythmias (Giovanetti, Biagini, Balestri, Navalesi, Giagnoni, de Matteis, Ferro-Milone & Perfetti, 1969) (Balestri, Biagini, Rindi & Giovanetti, 1970). In such concentrations methylguanidine in vitro produces as much haemolysis as is produced by creatinine in concentrations typical of severe renal failure (Giovanetti, Cioni, Balestri & Biagini, 1968b).…”

mentioning

confidence: 95%

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A Reinvestigation of Methylguanidine Concentrations in Sera from Normal and Uraemic Subjects

Baker

Marshall

1971

Clinical Science

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1.A cation-exchange-chromatographic method for the determination of methylguanidine in serum is described.2. In ten normal subjects, the mean serum methylguanidine concentration was 0·055 (SE 0'019) mg/ 100 ml and in ten uraemic patients it was 0·175 (SE 0,038) mg/ 100 ml. This difference is significant (P<0·02).3. Recent claims that methylguanidine is present in uraemic serum in much higher concentrations are shown to be due to artifactual conversion of creatinine when methods involving charcoal chromatography are employed.4. The results of intoxication experiments, in which blood concentrations of methylguanidine similar to those found by charcoal-chromatographic methods have been reproduced, must be interpreted with caution.

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Section: Methods B (Aftermentioning

confidence: 99%

mentioning

confidence: 95%

A Reinvestigation of Methylguanidine Concentrations in Sera from Normal and Uraemic Subjects

Baker

Marshall

1971

Clinical Science

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“…These effects were observed with concentrations of methylguanidine close to the concentration found in uremic serum, according to G iovannetti [5,6].…”

Section: Lymphocyte Culturesmentioning

confidence: 96%

T-Lymphocytes and Serum Inhibitors of Cell-Mediated Immunity in Renal Insufficiency

Touraine

Révillard

et al. 1975

Nephron

115

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In acute as well as chronic renal insufficiency significant immunological abnormalities were found: diminution of delayed hypersensitivity skin reactions, lymphopenia, reduction of the absolute but not relative number of peripheral blood T-lymphocytes. Responses of lymphocytes from uremic patients to PHA, allogeneic cells, or antigens were normal when lymphocyte cultures were performed in allologous serum from a healthy individual. Sera from uremic patients had an inhibitory or toxic effect on stimulation of normal lymphocytes. Such an in vitro inhibitory activity was found not only in the whole serum but alsowhen certain substances retained in renal failure (methylguanidine, larger molecules, etc.)were added in the lymphocyte cultures.

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“…The observation that small mononuclear cells within the renal medulla are capable of normal immunoglobulin synthesis would provide data which mitigate against a primary role of urea or creatinine (19). Other investigators have demonstrated that metabolic degradation products, methylguanidine and guanidinosuccinic acid, are retained by poorly functioning kidneys (20)(21)(22)(23) …”

Section: Introductionmentioning

confidence: 99%

Defective cellular immunity in renal failure: depression of reactivity of lymphocytes to phytohemagglutinin by renal failure serum

Newberry¹,

Sanford²

1971

J. Clin. Invest.

190

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A B S T R A C T In defining host resistance factors inuremia, experiments were designed to assess the effect of renal failure serum upon the reactivity of normal human lymphocytes to phytohemagglutinin in vitro. Normal buffy coat cells were resuspended in sera obtained from normal subjects and from 14 patients with renal failure, then stimulated with phytohemagglutinin M and the cellular response measured by the increase in thymidine or uridine uptake. The mean thymidine uptake by stimulated cells in normal sera was 14,389 ± 1695 (SEM) cpm per 2 X 106 lymphocytes. Uridine uptake under the same conditions was 12,540 ±1887 cpm. Compared to these are a mean thymidine uptake of 2740 ±457 cpm and uridine uptake of 3928 ±667 cpm in renal failure sera. Both differences are significant at P < 0.01 level.For controls representing "chronic illnesses," sera from patients with pneumococcal meningitis, cirrhosis of the liver without jaundice, rheumatoid arthritis, and paraplegia with urinary tract infection did not cause suppression. No single drug had been taken by all the renal failure patients; three patients were taking no drugs.The serum from one patient with acute renal failure suppressed thymidine uptake while her serum obtained after recovery from her illness supported a normal lymphocyte response. Improvement of lymphocyte response was also noted in 9 of 10 sera obtained from patients immediately after hemodialysis. These observations plus the inhibition of stimulated cells by normal serum mixed with renal failure serum indicate the presence of a dialyzable inhibitory factor rather than the absence of a supporting factor in the renal failure sera.Lymphocytes preincubated for 24 hr in renal failure serum responded normally when transferred to normal serum and stimulated. Cells stimulated in normal serum and transferred to renal failure serum within the initial

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Evidence that methylguanidine is retained in chronic renal failure

Cited by 55 publications

References 3 publications

A Reinvestigation of Methylguanidine Concentrations in Sera from Normal and Uraemic Subjects

A Reinvestigation of Methylguanidine Concentrations in Sera from Normal and Uraemic Subjects

T-Lymphocytes and Serum Inhibitors of Cell-Mediated Immunity in Renal Insufficiency

Defective cellular immunity in renal failure: depression of reactivity of lymphocytes to phytohemagglutinin by renal failure serum

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