Urinary Lysozyme, Ribonuclease, and Low-Molecular-Weight Protein in Renal Disease

Harrison, John P.; Lunt, GlenysS.; Scott, Peter; Blainey, J. D.

doi:10.1016/s0140-6736(68)91350-0

Cited by 162 publications

(74 citation statements)

References 24 publications

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“…Turnover data from these curves are shown in Tables IV and V was shown that the increased plasma lysozyme concentration found in severe uremia is due to diminished glomerular filtration whereas the high plasma levels found in certain hematological disorders with disturbed neutrophil turnover is due to increased production of plasma lysozyme probably through release of enzyme from disintegrating cells. The importance of the kidney for the degradation of plasma lysozyme has been shown in both experimental and clinical studies (4,6,(19)(20)(21)(22)(23)(24)(25) although the quantitative relationship between lysozyme turnover and kidney function has not been documented previously.…”

Section: Resultsmentioning

confidence: 99%

Lysozyme turnover in man

Hansen¹,

Karle²,

Andersen³

et al. 1972

J. Clin. Invest.

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A B S T R A C T Lysozyme turnover studies with Ilabeled human lysozyme were carried out on 22 patients, viz. nine control patients, seven nephrological patients with varying degrees of renal insufficiency, including three bilaterally nephrectomized patients, and six hematological patients with disturbed turnover of the neutrophilic granulocytes.It was found that plasma lysozyme has a rapid turnover with a fractional catabolic rate of 76%/hr of the plasma content. Lysozyme catabolism varied with the endogenous creatinine clearance; in addition however, extrarenal sites of catabolism were demonstrated since lysozyme could be broken down in the anephric patients, although only at a rate amounting to about 15% of the rate found in persons with intact kidneys.In the uremic patients the increased plasma lysozyme concentration was due to decreased rates of catabolism; in the hematological patients the increased plasma lysozyme level was due to increased rates of synthesis which supports the hypothesis that plasma lysozyme mainly stems from disintegrating neutrophilic granulocytes. Furthermore, it was shown that in the nonhematological patients examined, the rate of synthesis varied with the endogenous creatinine clearance.

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Section: Resultsmentioning

confidence: 99%

Lysozyme turnover in man

Hansen¹,

Karle²,

Andersen³

et al. 1972

J. Clin. Invest.

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“…In agreement with previous observations in uremic children and adults (46, 47), we noted increased urinary GH excretion in subjects with renal failure. This may be explained by partial saturation of tubular reabsorption/degradation (33), as reported for other microproteins such as #2-microglobulin (48) and others (49). Urinary GH excretion is increasingly used as an index of GH secretion (50, 5 1 ).…”

mentioning

confidence: 87%

Metabolic clearance of recombinant human growth hormone in health and chronic renal failure.

Haffner¹,

Schaefer²,

Girard³

et al. 1994

J. Clin. Invest.

136

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Despite the increasing therapeutic use of recombinant human growth hormone (rhGH), its metabolic clearance has not been investigated in detail. To evaluate the kinetics of rhGH as a possible function of GH plasma concentration and glomerular filtration rate (GFR), we investigated the steady state metabolic clearance rate (MCR), disappearance half-life, and apparent volume of distribution of rhGH at low and high physiological as well as supraphysiological plasma GH levels during pharmacological suppression of endogenous GH secretion in human subjects with normal and reduced renal function. GH in plasma and urine was determined by an immunoradiometric assay, and GFR by inulin clearance. In all subjects MCR decreased and plasma half-life increased with increasing plasma GH concentrations (P < 0.001 ). MCR of rhGH was approximately half in patients with chronic renal failure at each GH level and plasma half-life was increased by 25-50%. Allowing for the linear dependence of MCR on GFR and assuming single-compartment distribution, the estimated renal fraction of total MCR was 25-53 and 4-15% in controls and patients, respectively. Saturation of extrarenal disposal of GH was suggested by an inverse hyperbolic relationship between extrarenal MCR and plasma GH concentrations in all subjects. Fractional GH excretion was up to 1,000-fold higher in patients than in controls. We conclude that MCR of hGH is a function of plasma GH concentrations and GFR. Extrarenal elimination is saturable in the upper physiological range of GH concentrations, whereas renal MCR is independent of plasma GH levels. The kidney handles GH like a microprotein involving glomerular filtration, tubular reabsorption, and urinary excretion. (J. Clin. Invest. 1994.

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“…Lysozyme : Lysozyme was determined by method of Harrison et al (15).The assay is based on the lysis of Micrococcus luteus cells by lysozyme. To 1.0 ml of substrate containing Micrococcus luteus, 0.1ml of serum/standard was added and kept at 25 0 C.Readings were taken at 30 seconds and 10 minutes.…”

Section: Reduced Glutathione (Gsh)mentioning

confidence: 99%