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Aim: The aim of this study was to determine the effect of l-carnitine on quality of life (QOL) in chronic hemodialysis patients., Patients and Methods: This trial used a randomized, prospective, placebo-controlled, double-blind, crossover design. Inclusion criteria were patients who were older than 18 years, had been on dialysis for a minimum of one year, and had at least two of the following symptoms: intradialytic hypotension, muscle cramping, lack of energy, muscle weakness or myopathy, cardiomyopathy, or lack of responsiveness to erythropoietin (EPO). Patients were excluded if they were mentally incompetent to complete a QOL questionnaire. Sixteen patients were randomized to receive either l-carnitine (20 mg/kg) or placebo (normal saline) after each dialysis session for 12 weeks, followed by a 6-week washout, then the crossover therapy for 12 weeks. The Kidney Dialysis Questionnaire was the assessment tool used to evaluate QOL., Results: There was no significant effect of l-carnitine on QOL irrespective of treatment order. There were also no differences found in any of the secondary outcomes including incidence of muscle cramping, intradialytic hypotension, EPO requirements or hemoglobin. Adverse effects consisted of gastrointestinal symptoms, with a similar incidence between l-carnitine and placebo., Conclusion: L-carnitine did not have a benefit on QOL in our patient population.

Magnesium is an essential cation, involved in many enzymatic reactions, as a cofactor to adenosine triphosphatases. It is critical in energy-requiring metabolic processes, as well as protein synthesis and anaerobic phosphorylation. Serum Mg concentration is maintained within a narrow range by the kidney and small intestine since under conditions of Mg deprivation both organs increase their fractional absorption of Mg. If Mg depletion continues, the bone store contributes by exchanging part of its content with extracellular fluid (ECF). The serum Mg can be normal in the presence of intracellular Mg depletion, and the occurrence of a low level usually indicates significant Mg deficiency. Hypomagnesemia is frequently encountered in hospitalized patients and is seen most often in patients admitted to intensive care units. The detection of Mg deficiency can be increased by measuring Mg concentration in the urine or using the parenteral Mg load test. Hypomagnesemia may arise from various disorders of the gastrointestinal tract, conditions affecting Mg renal handling, or cellular redistribution of Mg. The gastrointestinal causes include the following: protein-calorie malnutrition, the intravenous administration of Mg-free fluids and total parenteral nutrition, chronic watery diarrhea and steatorrhea, short bowel syndrome, bowel fistula, continuous nasogastric suctioning, and, rarely, primary familial Mg malabsorption. The renal causes include Bartter's and Gitelman's syndrome, post obstructive diuresis, post acute tubular necrosis, renal transplantation, and interstitial nephropathy. Many therapeutic agents cause renal Mg wasting and subsequent deficiency. These include loop and thiazide diuretics, aminoglycosides, cisplatin, pentamidine, and foscarnet. Magnesium deficiency is seen frequently in alcoholics and diabetic patients, in whom a combination of factors contributes to its pathogenesis. Hypomagnesemia is known to produce a wide variety of clinical presentations, including neuromuscular irritability, cardiac arrhythmias, and increased sensitivity to digoxin. Refractory hypokalemia and hypocalcemia can be caused by concomitant hypomagnesemia and can be corrected with Mg therapy. The dose and route of administration of Mg in the treatment of hypomagnesemia is dictated by the clinical presentation, the degree of Mg deficiency, and the renal function.

We report the case of a 52-year-old male patient with recurrent thrombosis from 'primary antiphospholipid syndrome' who developed renal microangiopathy. Despite anticoagulant therapy with coumadin, serum creatinine progressively increased from 398 to 592 mumol/l and platelets decreased to 43,000. The patient responded to high-dose methylprednisolone and aspirin and the renal function improved. A review of the literature disclosed 4 other cases of association between primary antiphospholipid syndrome and renal microangiopathy. The clinical characteristics of these cases are discussed.

A retrospective review of 478 renal transplant recipients receiving cyclosporin A (CsA) was conducted to determine the incidence, relative risk, and outcome of lymphoproliferative disease after transplantation. Cases of neoplasm were identified by linking the computerized databases of the British Columbia (B.C.) Transplant Society and the B.C. Cancer Agency. B.C. Cancer Statistics for 1988 were used to determine relative risk. Patients were monitored for a total of 1,054 patient years with a mean follow-up time of 26 months (range, 0.1 to 63 months). A total of 334 patients were treated with triple immunosuppression (CsA), azathioprine, and prednisone), and 144 received adjunctive antilymphocyte globulin as induction immunosuppression. Sixty-nine patients received OKT3 for the treatment of transplant rejection. Twenty-two patients developed 23 malignancies (4.8%) at a mean interval of 16 months (range, 3 to 45 months) after transplantation. Non-Hodgkins lymphoma occurred in five patients, of whom two received triple (0.6%) and three received quadruple (2.1%) therapy. All five patients, in addition, received OKT3 for the treatment of graft rejection. The relative risk of developing a neoplasm among the defined sample adjusted for age and sex was 3.08 overall, increasing to 26.9 (P less than 0.005) for lymphoma. Six of the 22 patients (27%), including all 5 patients with lymphoma, died as a result of their tumor. Renal transplant recipients receiving CsA have a significantly elevated risk of developing a de novo lymphoreticular malignancy, which is comparable to that reported for those receiving azathioprine treatment, and which appears to be increased by the use of quadruple immunosuppression and the administration of OKT3 for the treatment of acute graft rejection.

To compare the effect of type of induction immunosuppression on the quality of initial renal allograft function, we identified 35 cadaver donor kidney pairs in which one recipient of a kidney from a given pair received induction immunosuppression with Minnesota antilymphocyte globulin (MALG group) while the recipient of the contra-lateral kidney received cyclosporine from day zero (CsA group). In the absence of an existing quantitative measure to assess and compare the status of those grafts that function primarily, we defined the half-life of creatinine elimination (t1/2SCr) as such an outcome measure based on a review of creatinine elimination kinetics. All organs were procured with in-situ perfusion and en-bloc removal. Total cold storage times, rewarm times, and perioperative management were comparable for the two groups. In the MALG group, the mean t1/2SCr) was not different from that in the CsA group (1.38 +/- 0.96 days vs 1.35 +/- 1.2 days P = NS). Multiple regression analysis performed on the differences in recipient age, number of DR-B locus matches, total cold ischemia time, rewarm time, and central venous pressure at reperfusion of a given donor pair demonstrated no significant impact of any of these differences on the difference in t1/2SCr for the same pair set in this sample. The nadir of serum creatinine achieved in the first five days posttransplant was somewhat higher in the CsA group (234 +/- 131 mumol/L) as compared with the MALG group (200 +/- 132 mumol/L) but the difference was not significant. A similar nonsignificant trend was observed in the comparison of mean serum creatinine values at 30 days posttransplant (MALG group: 158 +/- 62 mumol/L vs. CsA group: 200 +/- 141 mumol/L). Only one of seventy recipients (CsA group) was dialyzed within the first 5 days posttransplant for an overall incidence of ATN of less than 2%. Fourteen of 35 (40%) recipients in both groups received treatment for acute rejection. The mean time to first treatment for acute rejection episode was shorter in the CsA group than the MALG group (10 +/- 8 days vs 23 +/- 24 days, P = 0.055). Graft survival at one year was not different for the two groups (92% vs. 87% for the MALG and CsA groups respectively, P = NS).(ABSTRACT TRUNCATED AT 400 WORDS)

Cytomegalovirus infection is an important cause of morbidity and mortality in immunocompromised individuals. The disease is usually systemic in expression although localized infection can occur, particularly in the lung, liver, retina and gastrointestinal tract. We report a case of cytomegalovirus epididymitis with limited systemic manifestations occurring 2 months after renal transplantation in a patient immunosuppressed with azathioprine, prednisone and cyclosporine. Diagnosis was confirmed by observation of typical cytopathic changes in epididymal cells. Clinical resolution occurred with epididymo-orchiectomy and 9-(1,3-dihydroxy-2-proproxymethyl)guanine therapy. To our knowledge this presentation has not been described previously in the transplant literature and it is extremely rare in other forms of inherited or acquired immune deficiency.

The effect of resin type, degree of cross-linking, bead size, and surface area on the phosphate and bile salt binding characteristics of five strongly basic Dowex anion-exchange resins in the chloride form was studied. The maximum uptake of phosphate (expressed as uptake of phosphorus) from sodium phosphate solutions was 137, 82, 86, 138, and 76 mg of phosphorus per gram of dry Dowex resins XF 43311, XY 40013, XF 43254, XY 40011, and XY 40012, respectively. The presence of simulated gastric or intestinal fluids resulted in small but insignificant alterations in phosphorus uptake by the resins. The resins all bound similar amounts of phosphorus and taurocholate (80-100% of the total phosphorus and taurocholate in solution) at physiological concentrations of phosphate and bile salt. Dowex resins XY 40013 and XF 43254, with identical physicochemical properties, but different bead sizes and surface areas, bound similar amounts of the bile salt sodium taurocholate at all taurocholate concentrations, indicating that binding was not restricted to the surface sites on the resin bead. The 2% cross-linked resins bound 3-4 times more taurocholate than the 8% cross-linked resins (at high taurocholate concentrations); the smaller pore size of the latter resins probably presents a greater mechanical exclusion barrier than the larger pore size of the 2% cross-linked resins.

Nine patients on long-term hemodialysis with dialysis encephalopathy were studied, with sex matched control subjects for eight of the patients. Each patient with dialysis encephalopathy and control subject were contemporaries in a similar dialysis environment. Rib and other fractures were found in excess in the patients with dialysis encephalopathy (p less than 0.005 and p less than 0.01). These patients had less radiographic hyperparathyroid bone disease, and no more osteopenia as measured by metacarpal thickness than did their control counterparts. Severe osteomalacia was documented by bone biopsy in four of te patients. In a retrospective review of clinical, biochemical and pharmacologic differences, the patients with dialysis encephalopathy were significantly older at the start of dialysis (45.6 years versus 38.6 years, p less than 0.02) and had higher mean concentrations of blood urea nitrogen (BUN) and lower serum hemoglobin in the first year of dialysis than the control subjects. Blood pressure weight, creatinine, calcium, phosphate, alkaline phosphatase and a number of transfusions did not differ significantly. There was no difference in prescribed vitamin D and elemental aluminum in phosphate binders. This study demonstrates that patients with dialysis encephalopathy had more rib fractures without more parathyroid or osteopenic bone disease than did the control subjects and suggests that the etiology of dialysis encephalopathy and osteomalacia is multifactorial.

Path analysis, a form of general linear structural equation models, is used in studies of human genetics data to discern genetic, environmental, and cultural factors contributing to familial resemblance. It postulates a set of linear and additive parametric relationships between phenotypes and genetic and cultural variables and then essentially uses the assumption of multivariate normality to estimate and perform tests of hypothesis on parameters. Such an approach has been advocated for the analysis of genetic epidemiological data by D. C. Rao, N. Morton, C. R. Cloninger, L. J. Eaves, and W. E. Nance, among others. This paper reviews and evaluates the formulations, assumptions, methodological procedures, interpretations, and applications of path analysis. To give perspective, we begin with a discussion of path analysis as it occurs in the form of general linear causal models in several disciplines of the social sciences. Several specific path analysis models applied to lipoprotein concentrations, IQ, and twin data are then reviewed to keep the presentation self-contained. The bulk of the critical discussion that follows is directed toward the following four facets of path analysis: (1) coherence of model specification and applicability to data; (2) plausibility of modeling assumptions; (3) interpretability and utility of the model; and (4) validity of statistical and computational procedures. In the concluding section, a brief discussion of the problem of appropriate model selection is presented, followed by a number of suggestions of essentially model-free alternative methods of use in the treatment of complex structured data such as occurs in genetic epidemiology.

Primary hyperoxaluria is a rare congenital disorder characterized by large quantities of urinary oxalate with resultant nephrocalcinosis and nephrolithiasis and by deposits of calcium oxalate in other organs. Renal failure occurs early in life. Reports of unsuccessful renal transplantation attempts in this disorder underscore the need for antemortem diagnosis. Percutaneous bone biopsy is a relatively new procedure that is easily done at bedside, safe, and of potentially high yield in the demonstration of tissue oxalate. Three cases presented here show the characteristic histologic picture seen in this disease. In one case, the diagnosis was established by bone biopsy.

The paper describes a patient with brown tumor of the maxilla caused by secondary hyperparathyroidism, and gives an account of pathophysiology and management.

A method for estimating intrafamilial correlations under variable family sizes involving weightings of paired data points is introduced. Classical methods of intrafamilial correlation estimation and those in current use are outlined and critically analyzed. Extensions of the proposed estimation method to more general data structures are delineated.

5 patients are described who developed severe osteomalacia with spontaneous fractures after 2-4 years on dialysis. Phosphate control, vitamin D2 therapy and parathyroidectomy were ineffective. These individuals showed a hypercalcemic tendency but little histologic or radiographic evidence of osteitis fibrosa. After parathyroidectomy, the hypercalcemic tendency remained and bone biopsy revealed gross osteomalacia. A 6- to 12-month therapeutic trial with 1,25-dihydroxycholecalciferol (1,25[OH]2D3) in 3 did not arrest skeletal deterioration. 4 subsequently developed dialysis encephalopathy. These patients appear to have a unique mineralizing defect unresponsive to 1,25(OH)2D3. This "dialysis osteomalacic syndrome" may result from toxic substances associated with uremia or the hemodialysis regimen.

Progress in evaluating treatment of systemic bone disease has been hampered in the past by lack of precise in vivo quantitative techniques. Recently a method has been developed for measurement of bone mineral content (BMC), based on bone absorption of low-energy monochromatic radiation. This paper discusses a technique of photon absorptiometry using (125)l as a collimated point source. The technique is simple, with accuracy and precision within 2%.BMC and bone width (W) were measured in the distal radius of 359 normal subjects ranging in age from 5 to 82 years. A "normal" curve of BMC/W with age as the independent variable was then obtained from this population and was constructed for each sex. A positive correlation of BMC/W with height and body weight was found in a group of normal males.A series of patients with osteoporosis or malabsorption, or undergoing hemodialysis or steroid treatment, was then assessed in order to demonstrate changes in BMC/W that may occur secondary to disease or disturbances in calcium metabolism. Many of these patients were found to have a BMC/W below the normal mean value for their age and sex.

Clodronate disodium (dichloromethylene diphosphonate), a specific inhibitor of bone resorption, was given by mouth (1.0-3.2 g daily) to nine patients with primary hyperparathyroidism for two to 32 weeks so that its clinical and metabolic effects could be evaluated. Bone resorption decreased in all patients as judged by a fall in the fasting urinary calcium to creatinine and hydroxyproline to creatinine ratios. Serum calcium concentration was increased in all patients before treatment and fell in response to treatment to values near the upper end of the normal range. Hypercalcaemia and hypercalciuria recurred when treatment was stopped. In three patients treated for longer than 19 weeks clodronate failed to sustain the reduction in serum calcium concentration but the concentration remained below pretreatment values. These results suggest that clodronate may be of use in the medical management of primary hyperparathyroidism, particularly in patients in whom suppression of bone disease is desirable before surgery or in whom surgery is contraindicated.

Osteomalacia is commonly found in patients with severe renal impairment. Its aetiology is multifactional and not simply due to deficient production of active metabolites of vitamin D. Decreased availability of calcium and phosphate and the accumulation of aluminium is some dialysis-treated patients are also important aetiological factors. The treatment of osteomalacia depends, in part, upon its accurate diagnosis, and identifying and reversing the underlying cause.

Renal failure insidiously developed in three patients treated with a combination of hydrochlorothiazide and triamterene five to 10 weeks after commencing therapy. All had normal renal function prior to therapy and none had preexisting renal disease. Two of the patients had eosinophilia and two had a fever. One patient was oliguric. Renal biopsy demonstrated acute interstitial nephritis histologically. Direct immunofluorescence did not disclose evidence of either immune complex or antitubular basement membrane antibody deposition. Withdrawal of the drug led to remarkable improvement with renal function returning to normal in two patients and near normal in the third. The sequence of events and the histologic findings strongly suggest that the acute interstitial nephritis was due to a drug-induced hypersensitivity reaction. Although hydrochlorothiazide appears to be the drug responsible for the reaction, certain observations suggest a possible potentiating role for triamterene.

The two most commonly used biochemical markers of bone turnover are the serum alkaline phosphatase and the urinary excretion of peptide-bound hydroxyproline, both of which are increased in Paget's disease. Serum alkaline phosphatase is assumed to be derived from osteoblasts during the process of bone formation, whereas small peptides containing hydroxyproline are excreted in the urine following the degradation of bone collagen. The alkaline phosphatase is probably the more useful measurement for diagnosis and for following response to treatment, whereas hydroxyproline, although very sensitive, presents technical difficulties in collection and measurement. Several other biochemical changes in Paget's disease indicate abnormal bone metabolism. These include increased urinary excretion of hydroxylysine and its glycosides derived from collagen, as well as the release into the circulation and subsequent urinary excretion of fragments of pro-collagen indicative of increased collagen formation. Proteins specific to bone, such as osteocalcin, are increased in serum, bone, such as osteocalcin, are increased in serum, as are various enzymes possibly derived from bone cells, including acid phosphatase and proline imino-peptidase. Treatment of Paget's disease results in a fall in urinary hydroxyproline before alkaline phosphatase. This indicates that drug treatment, whether with diphosphonates, calcitonin or mithramycin, has a primary action to inhibit bone resorption, with a subsequent adaptive reduction in bone formation rate.

Reproducibility of estimates of cortical bone quantity in the appendicular skeleton by two methods was studied in healthy individuals and patients undergoing long-term hemodialysis. Repeated measurements of cortical thickness (CT) at the midpoint of the second metacarpal were taken from single radiographs of both hands by two independent observers. Repeated measurements by the same observer were more reproducible and the degree of reproducibility was far greater in healthy subjects than in dialysis patients. Repeated measurements were made of bone mineral content (BMC) and bone width (W) of the distal radius by photon absorptiometry. Repeated BMC/W determinations were highly reproducible in both healthy subjects and dialysis patients. High correlation was found between BMC and cross-sectional cortical area and between both simple cortical thickness and cortical area/width. Thus the photon absorptiometric technique is superior for the serial monitoring of bone quantity, particularly in patients with uremic osteodystrophy, but results obtained by the two methods in group studies should be comparable.

We have assessed the effects of the diphosphonate, dichloromethylene diphosphonate (Cl2MDP), in 19 patients with hypercalcaemia and increased bone resorption due to myeloma. Cl2MDP (800-3200 mg daily by mouth or 300 mg daily by intravenous infusion) decreased plasma calcium and biochemical indices of increased bone resorption in 16 of 19 patients. This effect persisted for the duration of treatment (up to 14 weeks). Prolonged treatment was associated with a progressive rise in serum alkaline phosphatase and only a transient fall in hydroxyproline suggesting the stimulation of bone repair. Since myeloma is associated with significant morbidity and mortality due to progressive bone loss, these results suggest that long-term treatment of myeloma with Cl2MDP is worthy of further study.

The uptake of phosphate [expressed as phosphorus (P)] by the anion exchange resins, Dowex 1-X8, Dowex SBR, and Bio-Rex 5, aluminum hydroxide, and sucralfate tablets was evaluated. The maximum uptake capacities (in mg P per gram of "wet" resin or solid) were 56, 49, and 84 mg for Dowex SBR, Dowex 1-X8, and Bio-Rex 5 resins, respectively, and 164-168 mg for aluminum hydroxide and sucralfate. At a concentration of P considered to approximate that encountered in the stomach (0.3 mg/ml), Bio-Rex 5 resin, aluminum hydroxide, and sucralfate bound similar amounts of P. Physiologic concentrations of bicarbonate or chloride and simulated gastric or intestinal fluids caused small changes in P uptake by Bio-Rex 5 resin. The resins bound large quantities of taurocholic (TA) and glycocholic (GA) acids. However, when Bio-Rex 5 was converted to the taurocholate form, it bound the same amount of P as the original chloride-form resin, and the binding of TA was prevented.

This study was undertaken to investigate the effect of various forms of hormone replacement therapy (HRT) upon postmenopausal women while controlling as many variables as possible. It was felt that the age, duration of amenorrhoea and the general health of the patients should be as comparable as possible and that each patient should provide her own pretherapy and post-therapy control data. In addition, it was felt that any placebo effect should be investigated and the patients were therefore randomly allocated to placebo tablets or one of six available forms of HRT. The age/sex registers of two large general practices were scrutinized and all women between 49 and 54 years of age were asked to cooperate; for a variety of reasons only 56 women were suitable and willing to take part in the project, yielding 8 women for each of the seven possible therapy groups. Blood samples were taken at 7-day intervals three times before therapy was given and the mean of the three values was used as the control value. The women returned on day 21 of each subsequent therapy cycle for six consecutive months and finally three months after discontinuing therapy. From the data the following broad conclusions can be drawn: (i) some women have classic symptoms of hot flushes and sweating despite high endogenous oestrogen concentrations; (ii) vaginal cytology is a relatively poor indicator of endogenous oestrogen status; (iii) while follicle stimulating hormone (FSH) and luteinizing hormone (LH) concentrations are reduced on HRT neither is decreased to anywhere near premenopausal values while prolactin is unaffected; (iv) plasma cholesterol levels are reduced on HRT, the pulse rate is slower and both systolic and diastolic blood pressure are reduced to a small but significant extent; (v) there is no adverse effect upon blood clotting; and (vi) most women experience significant or complete relief of symptoms on all forms of HRT as do some women taking a placebo. The combined preparations containing an oestrogen and progestogen produced vaginal bleeding in only 80 per cent of the women. Thus protection by regular endometrical shedding may not be afforded to all women. As vaginal bleeding is unacceptable to most women if they can achieve the same symptomatic relief without inducing menstruation, it is suggested that women have a low dose oestrogen preparation prescribed cyclically for 6 to 12 months. If therapy is to be maintained for a longer time, uterine curretage should be undertaken at regular intervals to exclude the possibility of endometrial carcinoma developing.

Patients on long-term hemodialysis via arteriovenous fistula received heparin when the fistula needle was inserted, before a sample of blood was obtained for chemical analysis. The resultant release of lipoprotein lipase activity in vivo and continued lipolytic activity in vitro sometimes produced sufficient free fatty acid to precipitate calcium soaps. The consequent spurious hypocalcemia was most frequently observed when the patients had chylomicronemia. This cause of apparent hypocalcemia was eliminated either by immediate analyses of the blood samples or by obtaining samples before systemic heparinization.

Six long-term hemodialysis patients with progressive skeletal deterioration during long-term pharmacologic vitamin D2 therapy were treated for six to 12 months with oral 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) to determine its therapeutic effectiveness in vitamin D2-unresponsive osteodystrophy. On bone biopsy, three of the patients had severe osteomalacia and three showed predominant osteitis fibrosa. Previous therapies, including phosphate binders and dialysis schedules, were maintained. The three patients with osteomalacia and the two with osteitis fibrosa showed clinical deterioration. There was no significant change in serum calcium, phosphate, alkaline phosphatase, bone densitometry, immunoreactive parathyroid hormone levels or bone histology. Roentgenograms showed multiple new fractures of ribs and femoral necks in the patients with osteomalacia and increased bone resorption in two of three patients with osteitis fibrosa. 1,25-(OH)2D3 dosage had to be decreased in all patients because of hypercalcemia with a mean tolerated dose of 0.22 microgram/day. In these patients, 1,25-(OH)2D3 was not effective therapy for progressive osteodystrophy unresponsive to pharmacologic vitamin D2.

The ADPglucose pyrophosphorylases of 7 plant-leaf tissues were partially purified and characterized. In all cases the enzymes showed stability to heat treatment at 65 degrees for 5 minutes in the presence of 0.02 m phosphate buffer, pH 7.0. The leaf ADPglucose pyrophosphorylases were activated 5 to 15-fold by 3-phosphoglycerate. Fructose-6-phosphate and fructose 1, 6-diphosphate stimulated ADPglucose pyrophosphorylase to lesser extents. The A(0.5) (conc of activator required to give 50% of the observed maximal activation) of 3-phosphoglycerate for the barley enzyme was 7 x 10(-6)m while for the sorghum enzyme it was 3.7 x 10(-4)m. Inorganic phosphate proved to be an effective inhibitor of ADPglucose synthesis. The I(0.5) (conc of inhibitor that gave 50% inhibition of activity for the various leaf enzymes varied from 2 x 10(-5)m (barley) to 1.9 x 10(-4)m (sorghum). This inhibition was reversed or antagonized by the activator 3-phosphoglycerate. These results form the basis for an hypothesis of the regulation of leaf starch biosynthesis.

By the use of the proteolytic substrates benzoyl-dl-arginine-p-nitroanilide and benzoyl-l-arginine ethyl ester the enzyme arachain has been purified 325-fold from acetone powders of ungerminated peanuts. The pH optimum for the hydrolysis of benzoyl-dl-arginine-p-nitroanilide was 8.1 in tris buffer, and for benzoyl-l-arginine ethyl ester was 7.5 using N - 2 - hydroxyethylpiperazine - N' - 2 - ethanesulfonic acid buffer. The purest fraction showed one main band with one to three minor bands on disc gel electrophoresis. The major protein component had an S(20,w) of 6.20. The energy of activation for the hydrolysis of benzoyl-dl-arginine-p-nitroanilide was calculated to be 16 kilocalories. The Michaelis constant for benzoyl-dl-arginine-p-nitroanilide was 10 micromolar and for benzoyl-l-arginine ethyl ester was 110 micromolar. The enzyme showed essentially no activity with casein, dimethyl casein, or bovine serum albumin as substrates. A large number of peptides were hydrolyzed by the enzyme, only l-leucyl-l-tyrosine being resistant of the peptides tested. The results suggest that arachain is not a "trypsin-like" protease but is a peptide hydrolase.