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Biomedical subjects

J E Springate

Publications and source records attributed to J E Springate.

52 records · Page 3Linked to original sources
PubMed1986

The nevoid basal cell carcinoma syndrome.

The nevoid basal cell carcinoma syndrome is a rare and complex disease with multiple manifestations. As an example, we present the case of an eight-year-old girl with this syndrome whose initial complaint was acute abdominal pain secondary to torsion of an ovarian fibroma. Because of its multisystem effects, patients with this syndrome can present to any of a number of medical or surgical specialists. Close attention to the family and past medical history and physical examination will alert the clinician to its presence, allowing for appropriate genetic counseling and serial screening for the development of malignancies and other complications.

Basal Cell Nevus Syndrome↗
PubMed1986

Acute renal failure. II. Management of suspected and established disease.

Because the pathogenesis of acute renal failure is multifactorial, clinical evaluation and ancillary studies must be performed systematically to reliably differentiate the various disorders. This assessment includes measurement of the serum creatinine and urea concentrations, urine composition and flow rate, and fractional excretion of sodium. Radiodiagnostic techniques such as ultrasound, radionuclide renal scans, and nuclear magnetic resonance may provide useful anatomic and functional information. With this data base, the physician can prescribe an individualized management plan that addresses the fluid, metabolic, and nutritional necessities of the child.

Acute Kidney Injury↗
PubMedDate not supplied

Ifosfamide metabolite chloroacetaldehyde causes renal dysfunction in vivo.

Renal injury is a common side-effect of the chemotherapeutic agent ifosfamide. Current evidence suggests that the ifosfamide metabolite chloroacetaldehyde may be responsible for this nephrotoxicity. The present study examined the effect of increasing amounts of intrarenally infused chloroacetaldehyde on kidney function, glutathione content and malondialdehyde formation. The ability of the uroprotectant medication sodium 2-mercaptoethanesulfonate (mesna) to prevent chloroacetaldehyde-induced renal injury was also assessed. Intrarenal chloroacetaldehyde infusion caused dose-dependent declines in glomerular filtration rate and p-aminohippuric acid clearance and increases in urine flow rate, sodium, glucose and protein excretion. These abnormalities were associated with progressive kidney glutathione depletion and malondialdehyde accumulation. Mesna infusion did not affect renal function but did cause a significant fall in kidney glutathione content. Simultaneous administration of chloroacetaldehyde and mesna only partially corrected renal functional abnormalities and prevented malondialdehyde accumulation but not glutathione depletion. These results show that the ifosfamide metabolite chloroacetaldehyde causes kidney dysfunction, glutathione depletion and lipid peroxidation in vivo. Mesna provides limited protection against chloroacetaldehyde nephrotoxicity, potentially explaining its inability to completely prevent ifosfamide-related renal injury in clinical practice.

Acetaldehyde↗
PubMedDate not supplied

Nephrotoxicity of ifosfamide in rats.

Renal proximal tubule cell injury is an important side effect of the chemotherapeutic agent ifosfamide in humans. We investigated the effect of this medication on kidney function in rats. Animals received either 40 or 80 mg kg(-1) ifosfamide intraperitoneally daily for 3 days every 3 weeks for a total of four treatment courses. Ifosfamide-treated rats had significantly lower body weight and hematocrit than sterile water-treated control rats. Animals receiving 40 mg kg(-1) ifosfamide developed isolated phosphaturia after their fourth and final treatment course. Rats receiving 80 mg kg(-1) ifosfamide had low-grade glucosuria, phosphaturia and proteinuria throughout the study. Urine flow rate, creatinine clearance, urinary sodium and potassium excretion and kidney glutathione and malondialdehyde content were not affected by ifosfamide at either dose. These findings indicate that ifosfamide produces abnormalities in rat renal function resembling subclinical Fanconi syndrome.

Analysis of Variance↗
PubMedDate not supplied

Spectrum of glomerulocystic kidneys: a case report and review of the literature.

An 8-year-old boy developed end-stage renal disease 7 years after the in utero diagnosis of bilateral cystic kidneys. There was no history of cystic renal disease in the family. Initial ultrasonographic screening of the parents failed to reveal cysts in the kidneys. Pathological evaluation of the kidney biopsy findings was consistent with the glomerulocystic kidney disease. He had bilateral nephrectomies in preparation for a living related renal transplant at 7 years of age. At that time, a repeated renal ultrasound examination of the mother showed bilateral cystic kidneys. Pathological evaluation of the nephrectomy specimens confirmed the diagnosis of autosomal dominant polycystic kidney disease. In this report, a discussion of the differential diagnosis of glomerular cysts and the relationship of glomerulocystic kidney disease and autosomal dominant polycystic kidney disease is provided.

Child↗
PubMedDate not supplied

Glomerulonephritis and chronic myelogenous leukemia.

An adolescent with chronic myelogenous leukemia (CML) developed gross hematuria. Evaluation included renal biopsy revealing a proliferative glomerulonephritis with mesangial deposits of immunoglobulins A and G. An association between CML and immune-complex glomerulonephritis has not been previously reported and may represent a paraneoplastic phenomenon.

Adolescent↗