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Biomedical subjects

J Mahan

Publications and source records attributed to J Mahan.

14 recordsLinked to original sources

Multicystic dysplastic kidney.

The contemporary literature helps us to analyze and assess the various clinical risks associated with MCDK. Clearly, MCDK is not an isolated developmental anomaly, and the child born with MCDK is at increased risk, but these risks are primarily directed towards: (1) the opposite kidney and lower urinary tract, where there is a significant likelihood of coexisting obstructive disease and reflux, and (2) the patient's family (current and future). In contrast, the risks to the patient caused by the MCDK (hypertension, infection, or malignant degeneration) actually appear to be quite low. Consequently, it no longer seems advisable to routinely remove MCDK in young patients for either diagnostic or prophylactic reasons. Nor is it obvious to what degree the MCDK itself requires long-term surveillance, although associated urological abnormalities will need follow-up and the patient requires periodic blood pressure screening. Hopefully, by careful analysis of the risks to the patient and family, the results of non-operative management, and the long-term results of the Multicystic Kidney Registry, contemporary pediatric nephrologists, urologists and surgeons will be able to reassess their approach to the evaluation and clinical management of the patient with this condition.

Humans

A prospective randomized comparison of the accuracy of computer-assisted versus GUSTO nomogram--directed heparin therapy.

Failure to adequately anticoagulate the blood of patients receiving recombinant tissue plasminogen activator (TPA) leads to greater rates of rethrombosis. In a multicentered, randomized trial in 51 patients we compared the ability to achieve and maintain therapeutic anticoagulation by use of computer-assisted heparin therapy or the GUSTO (Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries) heparin nomogram guidelines in patients with myocardial infarction treated with recombinant TPA. Heparin therapy was initiated with either computer-generated starting doses or GUSTO guideline starting doses. Activated partial thromboplastin times were measured every 6 to 8 hours for the first 24 hours. The therapeutic range used in this trial was 1.5 to 2.5 times the patient's baseline activated partial thromboplastin time (APTT). Ninety-four percent of the APTT ratios in the computer group were equal to or greater than 1.5 in the first 24 hours compared with 78% in the GUSTO group (p < 0.009). No significant difference in bleeding was found (7.7% for GUSTO; 4.2% for computer). Incremental time-dependent changes in heparin dose were found (day 1, 1110 +/- 243 units/hr, APTT ratio = 2.5 +/- 1.4; day 3, 1380 +/- 374 units/hr, APTT ratio, 1.9 +/- 0.4). Computer-assisted heparin therapy TPA results in superior anticoagulation accuracy compared with the GUSTO guidelines. In addition, the pharmacodynamic response to heparin changes in the 2 to 3 days after administration of TPA, leading to greater heparin requirements.

Aged

Influence of calcium intake and growth indexes on vertebral bone mineral density in young females.

This cross-sectional study examined the relationship between current calcium intake and vertebral bone mineral density (V-BMD) in 49 healthy Caucasian adolescent females aged 8-18 y. The ability of current calcium intake to account for the variance in V-BMD in this population was compared with that seen with weight, height, maturational age (determined by the Tanner Sexual Maturity Rating), chronological age, and total energy expenditure. Calcium intake was determined from the mean of 4-d, food-intake records. Average vertebral bone mineral density from L1-L4 was measured by dual x-ray absorptiometry. A multiple-regression model revealed that 81% of the variance in V-BMD was described by maturational age, chronological age, and calcium intake, with all representing significant predictors of bone mineral density (P less than 0.0001, 0.005, 0.04, respectively). This study supports the hypothesis that better calcium nutrition during adolescence may optimize, within genetic boundaries, peak bone mass.

Adolescent

Factors in pin tract infections.

To determine the factors pertinent to the etiology of pin tract infections, 214 pins in 42 patients were examined prospectively at the time of pin removal. Eighty-nine (41.6%) pin tracts were inflamed, 49 (22.9%) pins had loose anchorages, and 160 (74.8%) pin tips cultured positive for bacteria. The predominant organism cultured was Staphylococcus epidermidis (90.6%), considered nonvirulent, followed by virulent Staphylococcus aureus (37.5%), and Escherichia coli (9.4%). There were 32 loose, inflamed pin tracts. This correlation was statistically significant (P less than .005). There were 40 loose pins whose pin tips had positive cultures. Loose pins correlated for infection with virulent species of bacteria at a highly significant level (P less than .005). Results demonstrate that most pins possess bacterial colonization. Clinically, this means that either inflamed pin tracts or pins with cultures positive for invasive organisms are probably loose and should be removed. Also, mechanical factors are the critical variable in determining the flora of external fixation pins.

Adolescent

Behavior modification in pediatric hemodialysis.

This article reports the results of a behavior modification approach for managing disruptive and noncompliant behaviors in four male hemodialysis patients ranging in age from 10 to 16 years. Each patient demonstrated some improvement in either behavior or health status during the intervention and 76.7% of available token reinforcers were earned. The intervention was inexpensive and well-accepted by the patients, families, and staff. Guidelines for the planning, implementation, and evaluation of such interventions are presented.

Adolescent

Fine mapping of glycerol kinase deficiency and congenital adrenal hypoplasia within Xp21 on the short arm of the human X chromosome.

We have studied patients with Duchenne muscular dystrophy (DMD), DMD together with glycerol kinase (GK) deficiency, or DMD together with both GK deficiency and congenital adrenal hypoplasia (AHC). Analysis of deletions in these patients allows the mapping of these mutations in Xp21. The following order is proposed: Xpter - L1 - AHC - GK - DMD - Xcen. One of the boys with DMD, GK, and AHC is shown by pulsed-field-gel electrophoresis to have a deletion which has a proximal endpoint at least 500 kb distal from the pERT87 (DXS164) locus.

Acid Phosphatase

Radiological aspects of primary hyperoxaluria.

Primary hyperoxaluria is a rare metabolic disorder characterized by excessive synthesis and urinary excretion of oxalate. Nephrocalcinosis with or without calcium oxalate nephrolithiasis leads to renal failure in infancy through young adulthood. Oxalosis is the condition in which the highly insoluble calcium oxalate crystals are deposited in extrarenal tissues including bone, blood vessels, heart, and the male urogenital system. The radiographic abnormalities in 14 patients with primary hyperoxaluria are described. These abnormalities include nephrolithiasis, nephrocalcinosis, dense vascular calcifications, abnormal bone density, and characteristic metaphyseal abnormalities. Changes of renal osteodystrophy and pathologic fractures are common. Radiographic bone abnormalities are dependent on the age of the patient when renal failure occurred and the degree of success of renal transplantation. Characteristic skeletal changes are present in six of seven patients who developed renal failure when less than 7 years of age.

Adolescent

Treatment of a Down's syndrome patient for hyperthyroidism with radioactive iodine.

A Down's syndrome patient was hospitalized for evaluation of vomiting, abdominal pain, and a history of weight loss. A subsequent workup revealed that she had hyperthyroidism. The treatment of choice was radioactive iodine therapy. The patient had a history of consistent nausea and incontinence for urine and feces. Special problems posed by the patient and radiation safety are discussed.

Adult

A clinicopathologic study of forty-eight infants with nephrotic syndrome.

The clinical and histopathologic features of 48 children presenting with the nephrotic syndrome during the first year of life were analyzed. Proteinuria was discovered soon after birth to 3 months of age in 39 infants (congenital nephrotic syndrome), and nine infants had an infantile onset presenting between 4 and 12 months of age. Neither histologic parameters--microglomeruli, epithelial, or mesangial proliferation, focal segmental or global sclerosis, fibrinoid necrosis, or tubular microcysts--nor histologic classification--microcystic disease, mesangial proliferative glomerulonephritis, focal segmental glomerular sclerosis/hyalinosis-predicted the outcome. Rather, age at presentation was found to predict outcome: One of 39 infants with a congenital onset and seven of nine infants with an infantile onset underwent a complete remission (P less than 0.0001).

Child, Preschool

Effects of mannitol on the postischemic kidney. Biochemical, functional, and morphologic assessments.

UNLABELLED: To determine the effects of mannitol on the postischemic kidney rats were subjected to 25 minutes of renal artery occlusion and immediately after vascular clamp release they received a 2-ml intravenous mannitol bolus (20%). Equimolar urea-injected rats and sham-injected rats served as controls. Postischemic renal blood flow, tubular metabolic work (renal O2 consumption), adenine nucleotide pools, renal oxidant stress (tissue glutathione, malondialdehyde levels), and tubular cell/mitochondrial swelling (histomorphometry) were assessed at variable times during the early vascular reflow period (15 to 60 minutes). The severity of acute renal failure was determined by serial blood urea nitrogen and serum creatinine studies (24, 48 hours), and by renal histology (48 hours). Mannitol increased postischemic renal blood flow (2-fold), renal O2 consumptions (3-fold), and urine flow compared to urea-injected and sham-injected controls. Postischemic glutathione levels were equally depressed (reduced 33%) in all three treatment groups. Malondialdehyde did not rise. Mannitol significantly lowered total adenine nucleotide content without changing ATP at 15 minutes post renal artery occlusion. At 60 minutes post renal artery occlusion, mannitol- and urea-treated groups had comparable ATP levels, 25% higher than the noninjected controls. Mannitol and urea induced comparable decrements in proximal tubular cell swelling, returning cell volumes to normal values. However, mitochondrial swelling was unabated. Mannitol and urea caused significant and nearly identical degrees of functional and morphologic amelioration of renal injury. CONCLUSIONS: Mannitol administered after renal ischemia ameliorates both functional and morphologic aspects of acute tubular injury despite dramatically increasing tubular aerobic work. This protection appears not to be due to early postischemic improvements in adenine nucleotide content, to increased renal blood flow, to increased urine flow, or to a lessening of oxidant stress. The data are consistent with the view that protection results from acute hypertonic solute loading which either directly or indirectly decreases tubular cell but not mitochondrial swelling.

Acute Kidney Injury