[Bile salt nephropathy/cholemic nephrosis]. / Néphropathie à cristaux biliaires/néphropathie cholémique.

Bile cast nephropathy is a tubulo-interstitial nephropathy. Its diagnosis may be under-estimated. It develops in patients who have cholestatic jaundice, with high bilirubinemia. Bile salts are freely filtered through glomerulus. Under certain circumstances, it forms casts into the tubule and cause an acute tubular necrosis. The diagnosis evidence is histologic, but fulfilment of renal biopsy is often made difficult, because of the hemostatic abnormalities that patients with hepatocellular injury develop. The treatment is supportive and etiological. We report here the case of a patient who presented a drug-induced hepatic jaundice, complicated with acute kidney failure secondary to bile cast nephropathy. We present the histological diagnosis evidence.

Reduced B lymphoid kinase (Blk) expression enhances proinflammatory cytokine production and induces nephrosis in C57BL/6-lpr/lpr mice.

BLK, which encodes B lymphoid kinase, was recently identified in genome wide association studies as a susceptibility gene for systemic lupus erythematosus (SLE), and risk alleles mapping to the BLK locus result in reduced gene expression. To determine whether BLK is indeed a bona fide susceptibility gene, we developed an experimental mouse model, namely the Blk+/-.lpr/lpr (Blk+/-.lpr) mouse, in which Blk expression levels are reduced to levels comparable to those in individuals carrying a risk allele. Here, we report that Blk is expressed not only in B cells, but also in IL-17-producing γδ and DN αß T cells and in plasmacytoid dendritic cells (pDCs). Moreover, we found that solely reducing Blk expression in C57BL/6-lpr/lpr mice enhanced proinflammatory cytokine production and accelerated the onset of lymphoproliferation, proteinuria, and kidney disease. Together, these findings suggest that BLK risk alleles confer susceptibility to SLE through the dysregulation of a proinflammatory cytokine network.

A patient with nephrotic-range proteinuria and focal global glomerulosclerosis.

A young male is evaluated for nephrotic-range proteinuria, hypercalciuria, and an elevated serum creatinine. A renal biopsy is performed and shows focal global glomerulosclerosis. The absence of nephrotic syndrome suggest that glomerulosclerosis was a secondary process. Further analysis of the proteinuria showed it to be due mainly to low-molecular weight proteins. The case illustrates the crucial role of electron microscopy as well as evaluation of the identity of the proteinuria that accompanies a biopsy finding of focal and global or focal and segmental glomerulosclerosis.

Primary focal segmental glomerulosclerosis in nephrotic patients: common complications and risk factors.

BACKGROUND: Focal segmental glomerulosclerosis (FSGS) presents a range of potentially serious complications, including acute kidney injury (AKI), infection and thromboembolism. This study aimed to find out the incidence rates and risk factors for these complications in FSGS patients. METHODS: Patients with biopsy-proven primary FSGS and nephrotic-range proteinuria were included in this study. A short-term (16-week) follow-up was performed to observe the aforementioned complications. Clinical characteristics of patients were recorded upon enrollment. AKI was diagnosed as an absolute increase in serum creatinine of ≥0.3 mg/dL or a percentage increase of ≥50% within 48 hours; infection, by a combination of clinical manifestations, laboratory tests and imaging examinations; and thromboembolism, by imaging methods. Risk factors for complications were evaluated by logistic regression model. RESULTS: The study population included 90 FSGS patients (63 males, mean age 28.9 ± 12.9 years). The incidences of AKI, infection and thromboembolism were 44.4%, 25.6% and 12.2%, respectively. Patients with AKI were more likely to be male, with lower serum albumin, greater proteinuria and more severe acute tubulointerstitial damage. Patients with infection had higher proteinuria and lower serum albumin, globulin and IgG. Circulating endothelial cells (CECs) and von Willebrand factor were higher in patients with thromboembolism. Logistic regression showed that increased urine retinol-binding protein, decreased serum albumin and IgG, and increased CECs and hemoglobin were independent risk factors for AKI, infection and thromboembolism, respectively. CONCLUSIONS: AKI, infection and thromboembolism are common among FSGS patients. Awareness of risk factors and prevention of these complications are important for the prognosis of these patients.

The ACTIVE Trial: comparison of the effects on renal function of iomeprol-400 and iodixanol-320 in patients with chronic kidney disease undergoing abdominal computed tomography.

BACKGROUND: We performed a multicenter, double-blind, randomized, parallel-group study to compare the renal effects of iomeprol-400 and iodixanol-320 in patients with preexisting chronic kidney disease undergoing contrast-enhanced multidetector computed tomography of the liver. METHODS: One hundred forty-eight patients with moderate-to-severe chronic kidney disease, ie, serum creatinine (SCr) > or =1.5 mg/dL (132.6 micromol/L) and/or calculated creatinine clearance (CrCl) <60 mL/min, undergoing contrast-enhanced multidetector computed tomography of the liver were randomized to equi-iodine doses (40 gI) of either the low-osmolar agent iomeprol-400 (400 mgI/mL, 726 mOsm/kg, N = 76) or the isotonic agent iodixanol-320 (320 mgI/mL, 290 mOsm/kg, N = 72), injected intravenously at 4 mL/S, followed by a bolus of 20 mL normal saline solution at the same rate. SCr was obtained at screening, baseline and at 48 to 72 hours postdose. SCr measurements and CrCl calculations were performed by a central laboratory. Contrast-induced nephropathy (CIN) was defined as an absolute SCr increase of > or =0.5 mg/dL (44.2 micromol/L) from baseline to 48 to 72 hours postdose. Mean SCr changes from baseline were also assessed. A Renal Safety Review Board comprised 3 medical experts reviewed the renal safety data, demographics, medical history, CIN risk factors, concomitant medications, and hydration status of each subject in a blinded manner. RESULTS: The 2 study groups were comparable with regard to age, gender distribution, concomitant nephrotoxins, hydration status, and total iodine dose; however, the iomeprol-400 group showed a significantly higher proportion of patients with diabetes mellitus (P = 0.02). Baseline SCr was 1.7 +/- 0.6 mg/dL (150.3 +/- 53.0 micromol/L) in the iomeprol-400 group and 1.7 +/- 0.7 mg/dL (150.3 +/- 61.9 micromol/L) in the iodixanol-320 group (P = 0.87). Predose CrCl was 41.5 +/- 13.1 mL/Min in the iomeprol-400 group and 43.0 +/- 13.3 mL/Min in the iodixanol-320 group (P = 0.49). Five of 72 patient receiving iodixanol-320 (6.9%) and none of the patients receiving iomeprol-400 showed an increase of > or =0.5 mg/dL (44.2 micromol/L) from baseline [P = 0.025, 95% CI (-12.8%, -1.1%)]. The mean SCr change from baseline was significantly higher (P = 0.017 ANCOVA) after iodixanol-320 (0.06 +/- 0.27) than after iomeprol-400 (-0.04 +/- 0.19). CONCLUSIONS: The incidence of CIN was significantly higher after IV administration of iodixanol-320 than iomeprol-400. The mean rise in SCr from baseline was also higher in patients receiving iodixanol.

Validation of an autotaxin enzyme immunoassay in human serum samples and its application to hypoalbuminemia differentiation.

BACKGROUND: Autotaxin (ATX), a tumor cell motility-stimulating factor, regulates the blood concentrations of lysophosphatidic acid (LPA), an important and multi-functional bioactive lipid, through its lysophospholipase D activity (lysoPLD). The introduction of ATX measurements into clinical laboratory testing is urgently needed. METHODS: Anti-human ATX monoclonal antibodies were produced by immunization of recombinant human ATX expressed in a baculovirus system. An immunoassay for the quantitative determination of ATX was established, and human serum samples were assayed. RESULTS: The within-run and between-run precision, interference, detection limit, and linearity studies were satisfactory. The central 95 percentile reference interval for the serum ATX antigen concentration in healthy subjects was 0.468-1.134 mg/l (n=120) and was strongly correlated with the serum lysoPLD activity. The ATX concentration was significantly (p<0.001) higher in women (0.625-1.323 mg/l) than in men (0.438-0.914 mg/l). The serum ATX concentrations were increased in patients with chronic liver diseases and decreased in postoperative prostate cancer patients but were not altered in nephrosis patients. Thus, serum ATX antigen concentrations could be used to discriminate these hypoalbuminemia conditions. CONCLUSIONS: The present ATX antigen assay may be useful for clinical laboratory testing.

Serum soluble vascular cell adhesion molecule-1 (VCAM-1) concentrations in children with reflux nephropathy.

Systemic inflammatory disorders causing renal tissue damage do so by the adherence of polymorphonuclear leukocytes to endothelium, a process that is mediated by cell surface adhesion molecules. We determined the circulating levels of serum vascular cell adhesion molecule-1 (VCAM-1) in vesicoureteric reflux (VUR) patients and investigated the relationship between serum VCAM-1, grade of VUR, and secondary renal scarring. Serum levels of VCAM-1 were measured in 53 children aged between 3 months and 15 years with VUR (13 had grade III, 29 had grade IV, and 11 had grade V) and 25 controls using ELISA. Radionuclide scanning was used to assess renal scarring. Renal scarring was found in 29 of the 53 subjects. Serum VCAM-1 was significantly higher in subjects with high grades of VUR without renal scarring (grade IV: 715.9+/-121.0 ng/ml; grade V: 778.5+/-33.2ng/ml) compared with subjects with grade III VUR without renal scarring (609.8+/-64.3ng/ml, p<0.01). Serum VCAM-1 was also significantly higher in subjects with high grades of VUR with renal scarring (grade IV: 791.2+/-131.9ng/ml; grade V: 1171.8+/-235.6 ng/ml) compared with subjects with grade III VUR with renal scarring (687.3+/-163.4 ng/ml, p<0.001).

Effect of grape seed extract on puromycin-aminonucleoside-induced nephrosis in rats.

Recent studies indicate that an excessive production of oxidants plays an important role in the pathogenesis of glomerular disease. Grape seed extract (GSE) is a potent antioxidant, and the aim of this pilot study was to evaluate its effect on puromycin-aminonucleoside (PAN)-induced nephrosis in rats. Fifty Sprague-Dawley rats were divided into five groups. Groups 1 and 2 rats received water from day 0 to day 30. Rats in groups 3, 4, and 5 received GSE at 10 mg/100g of body weight (BW), which was started on day 0, 6, and 3 of the experiment, respectively. In group 5 animals the GSE dose was increased (40 mg/100g BW) on day 9. Intraperitoneal dextrose (group 1) or PAN 15 mg/100g BW (groups 2-5) was administered on day 3. Urine and blood specimens were collected at regular intervals, and the comparison between the various groups was made by analysis of variance (ANOVA). Rats in all study groups (groups 3-5) showed a decrease in urine protein and serum cholesterol and triglyceride levels, which was statistically significant in group 3 animals. No significant changes were noted in serum albumin and creatinine levels. In conclusion, GSE administration decreases urine protein excretion and serum cholesterol and triglyceride levels in rats with PAN-induced nephrosis.

Glomerular endothelial cytotoxicity and dysfunction in nephrosis with focal segmental glomerulosclerosis.

Glomerular endothelial cell dysfunction (GED) with defective release of vasodilator has been delineated in nephrosis (NS) in vivo and in vitro studies. In NS with focal segmental glomerulosclerosis (FSGS), an immunocirculatory balance may be impaired due to defective anti-inflammatory cytokine. This study aimed at simultaneous determination of both proinflammatory cytokine (tumor necrosis factor alpha) and an anti-inflammatory cytokine (interleukin-10) in NS with FSGS. An endothelial cell cytotoxicity (ECC) was also examined using nephrotic serum. It was shown that (1) the initial endothelial cell cytotoxicity was significantly different from the control, (2) ratio between tumor necrosis alpha and interleukin-10 was significantly elevated, and (3) intrarenal hemodynamics was changed significantly.

Evaluation of the pituitary-testicular function during experimental nephrosis.

To investigate the pituitary-testicular function in nephrotic rats, a sequence of experiments was undertaken in adult male rats after a single dose of puromycin aminonucleoside (PAN). Endocrine modifications were evaluated chronologically throughout the experimental disease in order to determine the appearance of hormone alterations which lead to the axis dysfunction. Serum concentration of LH, FSH, androstenedione, total and free testosterone, estradiol as well as urine testosterone were measured by specific RIAs on days 3, 7 and 10 after treatment on nephrotic and control groups. Prolactin was also evaluated on day 10. Likewise, total weight of various androgen responsive tissues from both groups was recorded, and the number of androgen receptor (AR) binding sites were determined. To know the functional status of the hipophyseal-testicular unit, groups of nephrotic and control rats were stimulated with LHRH (300 ng/100 g b.w.) or with one or four doses of hCG (8 UI), respectively. Additionally, the relative in vitro biological activity of FSH from nephrotic and control rats before and after LHRH stimulus was determined. The results from the hormonal profile revealed clear endocrine disorders characterized by a progressive diminution of all serum hormones except prolactin and urine testosterone, which remained unmodified. The weight of the main androgen responsive tissues, the ventral prostate and the seminal vesicle, decreased parallelly to androgen diminution. The binding analysis of AR shows a significant elevation of the available androgen sites in all analyzed tissues except kidney and hypothalamus. The secretion of LH and FSH from nephrotic animals after LHRH administration was lower than that from intact animals at the registered times. Interestingly, the biological activity of FSH from nephrotic rats was not detectable at both, before and after LHRH administration. Testicular response to hCG stimuli, in terms of testosterone synthesis was not significantly different in the two groups analyzed with respect to the intact animals. By contrast, no response was observed in terms of estradiol production at either one or four doses of hCG. On the whole, the results presented herein allow us to conclude that experimental nephrosis has a harmful effect on the pituitary-testicular axis, and strongly suggests that the endocrine dysfunction is initiated at the hypophyseal level; even though a specific testicular damage is also present.

Influence of spontaneous platelet aggregation on progression of glomerular disease.

UNLABELLED: Platelet secretion products may play an important role in the pathogenesis and progression of the kidney disease. Amongst the parameters describing platelet hyperactivity the measurement of spontaneous platelet aggregation (SPA) seems particularly useful. In this study SPA as well as mean platelet volume (MPV), modal platelet volume (PLT Mode) and platelet count (PLT) were investigated in 60 patients with biopsy proven primary glomerulonephritis. SPA was measured using the turbidimetric method according to Born with no enhancers added. Serum creatinine concentration (Cr), reciprocal serum creatinine concentration (1/Cr) and endogenous creatinine clearance (Cl(Cr)) were used for the renal function estimation. Protein and lipid profiles as well as coagulo-fibrinolytic balance were measured in parallel. The investigated group consisted of 30 non-nephrotic patients (CGN) - in 9, SPA was found (CGN-B) while 21 had SPA <10% (CGN-A), and 30 nephrotic patients (CGN+NS) - 19 with SPA (CGN+NS-B) and 11 without (CGN+NS-A). SPA was found to be a constant platelet feature in patients with chronic glomerulopathy. The group remained under observation for 36 months. 41 patients were included in the 3-year prospective study which revealed the significant influence of the blood platelet hyperaggregability on the renal disease progression. A significantly increased serum creatinine concentration, decreased 1/Cr parameter and decreased glomerular filtration rate (Cl(Cr)) were noted in subgroups showing SPA. A significant correlation between SPA and (Delta)Cr/month (r = 0.41), (Delta)1/Cr/month (r = 0.38) as well as (Delta)Cl(Cr)/month (r = 0.52) was found. The platelet activity and thus SPA can be altered by various factors: albumin and fibrinogen plasma concentrations, thrombosis activation and possibly lipoprotein metabolism disturbances. A characteristic feature of spontaneously aggregating platelet is their increased volume (MPV). CONCLUSION: Platelet hyperaggregation in one of nonimmunological factors stimulates the progression of glomerulonephritis.

Enhanced tumor necrosis factor in the serum and renal hypoperfusion in nephrosis associated with focal segmental glomerulosclerosis.

Enhanced tumor necrosis factor alpha associated with immunocirculatory imbalance expressed as increased ratio between proinflammatory (TNFalpha) and antiinflammatory (IL-10) cytokines was observed in the serum of nephrosis associated with focal segmental glomerulosclerosis. Such altered immunocirculatory balance correlated with the reduction in renal plasma flow determined by the intrarenal hemodynamic study by which it implies that a glomerular endothelial cell injury associated with impaired renal perfusion is likely to be spontaneously induced by enhanced tumor necrosis factor in the presence of inadequate release of antiinflammatory cytokine (IL-10).

Hyperlipidaemia in cisplatin-induced nephrotic rats.

The serum and hepatic lipid concentrations were investigated in rats made nephrotic with a single intraperitoneal injection of cisplatin (6 mg kg(-1) b.wt.). The serum creatinine and urea concentrations were estimated as indices of nephrotoxicity, and the serum total bilirubin level as a liver function test. 3 The fasting serum total cholesterol, triglycerides (TG) and the cholesterol fractions associated with the various lipoproteins, as well as hepatic cholesterol and TG contents were also measured, following 5, 10 and 15 days from the cisplatin treatment. 4 The results revealed that on day 5 both serum creatinine and urea concentrations were significantly (P<0.01) increased, indicating the peak of nephrotoxicity, with no injurious effects on the liver as indicated by the unaltered serum bilirubin concentration. 5 The nephrotoxicity was accompanied by significant elevations in serum total cholesterol and TG concentrations by 49 and 42%, respectively, with significant (P < 0.05) correlations between the serum cholesterol and TG concentrations versus the serum urea (r=0.68 and r=0.60, respectively). Among the estimated lipoproteins, very low density lipoprotein (VLDL) cholesterol was severely increased to more than twofold with no severe changes in LDL- or HDL-cholesterol fractions. On day 5 the liver also showed significant accumulation of TG with no change in the cholesterol content. Animals killed 10 or 15 days post-cisplatin treatment had all the perturbed parameters returned to the normal levels. The present results indicated that rats exposed to a single cisplatin injection exhibit acute reversible nephrosis on day 5 which was accompanied by dyslipidaemia and accumulated liver TG.

Reproductive function in male rats with chronic nephrosis.

Endocrine dysfunction has been associated with renal diseases. The present study was conducted to explore reproductive function in male rats with chronic nephrosis. Experimental chronic nephrosis was induced by the administration of 7.5, 5.0 and 5.0 mg per 100 g body weight of puromycin aminonucleoside on days 0, 21 and 35, respectively. Reproductive function was evaluated on the basis of hormonal concentrations, mass of accessory sex organs and fertility during an 84 day period. Circulating LH, FSH, testosterone and oestradiol concentrations were measured by specific radioimmunoassays, while fertility was estimated by the rate of pregnancy induction. Samples were collected on days 7, 14, 28, 56 and 84. The results showed an important endocrine dysfunction characterized by low concentrations of LH and FSH during the first month, after which concentrations were similar to control values or even increased on days 56 and 84. Testosterone and oestradiol decreased significantly at all time points evaluated. The mass of the testes did not alter. However, the mass of the prostate and seminal vesicle decreased only during the first 2 weeks, and became essentially normal thereafter. The reproductive capacity of nephrotic males was eliminated on day 7, whereas on day 14, 16% of the group was able to mate successfully and subsequently most animals recovered their normal reproductive function. This study demonstrates for the first time that rats with experimental chronic nephrosis develop an important endocrine dysfunction, characterized mainly by persistent reduction in testosterone concentrations, which impairs reproductive capacity only transiently.

Cytotoxicity of sera from rats with puromycin aminonucleoside nephrosis.

Administration of puromycin aminonucleoside (PAN) to rats induces acute nephrosis with hyperlipidemia, and, in some experimental conditions, it results in chronic focal glomerulosclerosis. In this study, we examined the cytotoxicity of serum from rats with PAN-induced nephrosis, since hypercholesterolemia is considered to cause injury to vascular walls in atherosclerosis, the mechanism of which is analogous to that of glomerulosclerosis. About half of the tested sera from nephrotic rats (9 out of 17) were cytotoxic to cultured aortic endothelial cells. The toxic substance(s) was heat-stable and was extracted in the lipid fraction. Serum levels of triglyceride and cholesterol were markedly higher in the group of rats with cytotoxic serum than in the group with noncytotoxic serum. No cytotoxicity was associated with sera from control rats or the corresponding lipid fractions. Cytotoxic sera were also effective against cultured glomerular epithelial and mesangial cells. These results indicate that cytotoxic lipid is produced in rats with PAN nephrosis and the results raise the possibility that the cytotoxic lipid in nephrotic serum might contribute to lipid-mediated glomerular injury which may induce glomerulosclerosis at a subsequent stage.

Post-transplantation nephrosis in congenital nephrotic syndrome of the Finnish type.

Congenital nephrotic syndrome of the Finnish type (CNF) is an autosomal recessively inherited disease manifesting as massive proteinuria, edema and ascites in the neonatal period. The disease is believed to be limited to the kidneys and recurrences after renal transplantation have not been reported. At our center 29 transplantations have been performed on 28 CNF patients. One to 33 months after transplantation, seven grafts (24%) of six patients have developed a steroid-resistant nephrotic syndrome. The clinical data and renal histology of these patients were analyzed in order to elucidate the cause of the proteinuria. At the onset of six of the seven episodes of nephrosis, the patient had evidence of a preceding CMV- or EBV-infection and the remaining patient had sinusitis. Upon light and electron microscopy examination, endothelial swelling of the glomerular capillaries resembling transplant glomerulopathy (TG) was seen, but unlike TG, the glomerular basement membranes were normal. The response of proteinuria to steroid or cyclophosphamide therapy was poor, with total remission in only two patients and partial remission in one patient, all treated with methylprednisolone and cyclophosphamide immediately after the diagnosis. Four grafts have been lost. Our data show that CNF patients have an increased tendency for post-transplantation nephrosis.

Arginine augments neither albuminuria nor albumin synthesis caused by high-protein diets in nephrosis.

Dietary protein independently modulates albuminuria (U(Alb)V) and albumin synthesis (AlbSyn) in nephrotic rats. While some amino acids are without effect on renal hemodynamics, arginine (Arg) augments renal blood flow and glomerular filtration rate, increases AlbSyn in tissue culture and isolated perfused livers, and could be one specific amino acid causing both decreased glomerular permselectivity and increased AlbSyn. Nephrotic rats were fed 10% casein (LP); 30% casein (HP); 30% casein with the inhibitor of nitric oxide (NO) synthesis N omega-nitro-L-arginine methyl ester (HP + L-NAME); 10% casein supplemented with Arg and amino acids that are Arg precursors of or are derived from Arg (proline, glutamate, and aspartate) in an amount in the increment between 10 and 30% casein (ArgAA); ArgAA supplemented with NH4 acetate to provide a diet isonitrogenous to 30% casein (ArgAA + NH4); or 10% casein plus an incomplete mixture of amino acids (Inc) containing the increment in histidine, phenylalanine, tryptophan, tyrosine, lysine, glycine, alanine, serine, threonine, cysteine, and methionine provided when the diet was changed from 10 to 30% casein. U(Alb)V increased significantly in HP and by a significantly greater amount in HP + L-NAME, but did not change in LP, ArgAA, or ArgAA + NH4. U(Alb)V tended to increase in Inc, was significantly greater than in LP or in ArgAA + NH4, but less than in HP. AlbSyn ([3H]phenylalanine incorporation) was no different in Inc than in HP, and was significantly greater than in either ArgAA + NH4 or LP. Increased AlbSyn results from increased ingestion of one or more of amino acids in Inc, but not from Arg or its precursors or products or from total dietary nitrogen.(ABSTRACT TRUNCATED AT 250 WORDS)

Rare causes of elevated maternal serum alpha-fetoprotein. A report of three cases.

Three rare conditions--amniotic band disruption sequence, placental chorioangioma and congenital nephrosis--were diagnosed in midtrimester because of elevated maternal serum alpha-fetoprotein. The diagnosis is important for genetic counseling and obstetric follow-up.

Detection of lysozyme and alpha 2-macroglobulin--lysozyme complexes by immunoblotting.

An immunoblotting technique was developed to detect human lysozyme and lysozyme complexes in body fluids. The unoccupied binding capacity of proteins was demonstrated by addition of surplus lysozyme. The sensitivity of immunoblotting to the free enzyme in human albumin solution was less than 5 ng. In serum and pleural fluid, part of exogenous lysozyme was bound to alpha 2-macroglobulin (alpha 2-M). At high concentrations of lysozyme in leukemic sera, part of the enzyme formed an endogenous alpha 2-M complex. On the other hand, the formation of alpha 2-M complexes with exogenous lysozyme was especially striking in sera from nephrotic patients with elevated alpha 2-M. The findings corroborate with previous reports on lysozyme binding to purified alpha 2-M in vitro and suggest that the binding is concentration-dependent with respect to both reaction partners. In vivo the mechanism may provide a pathway for extrarenal lysozyme catabolism medicated by reticuloendothelial cells. No other binding proteins were seen in the present study: lysozyme did not bind to serum immunoglobulins in 35 samples with an immunoglobulin paraprotein, three samples with polyclonally elevated gamma-globulins, 20 other patient sera and 10 normal sera. Neither did lysozyme bind to urinary proteins in five samples from patients with myeloic leukemias nor in 10 samples from myeloma patients with urinary excretion of a monoclonal immunoglobulin light chain.