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Biomedical subjects

W B Lorentz

Publications and source records attributed to W B Lorentz.

At least 37 records · Page 2Linked to original sources
PubMed1986

Scanning electron microscopy of the acellular glomerular basement membranes in idiopathic membranous glomerulopathy.

After using a cellular digestion technique to extract cells from the basement membranes of frozen kidney tissue, we employed scanning electron microscopy to examine the acellular glomerular basement membranes (AGBM) from normal kidneys and from kidneys of patients with idiopathic membranous glomerulopathy (MGN). This method revealed, in the AGBM, previously unrecognized three-dimensional patterns of pathologic changes. These patterns correlated with increasing MGN stage as defined by Ehrenreich and Churg. On the epimembranous AGBM surface these patterns were composed of ridge-like trabeculae, irregular plaques, and reticulated crater-like deformities. The endothelial AGBM surfaces were smooth in stages I and II MGN, but in stage III MGN the endothelial surfaces were irregular and perforated. In contrast to lupus-related MGN, where some immune-complex-like material remained after cellular extraction, epimembranous immune-complex-like material in idiopathic MGN was extracted.

Adult↗
PubMed1985

Reversal of Bartter's syndrome by renal transplantation in a child with focal, segmental glomerular sclerosis.

A four-year-old girl with growth failure and clinical and laboratory evidence of Bartter's syndrome responded to indomethacin treatment with decreased urinary prostaglandin excretion, symptomatic and chemical improvement, and accelerated growth. Large doses of aspirin produced a comparable decrease in prostaglandin excretion but no improvement in any other metabolic abnormality thus suggesting that abnormalities in prostaglandins were the result rather than the cause of the electrolyte abnormalities. Progressive renal insufficiency while on indomethacin prompted a renal biopsy, which revealed morphological changes of focal, segmental glomerular sclerosis. Subsequently, the child underwent renal transplantation with complete resolution of symptoms and abnormal metabolic findings. This observation suggests that extrarenal factors were not responsible for the development of Bartter's syndrome in this child.

Alkalosis↗
PubMed1984

Intrarenal aneurysm of the renal artery in children.

Two children with hypertension had intrarenal aneurysms in the renal artery. In both children, renovascular hypertension was documented by renal vein renin assay showing elevated renin secretion from the involved kidney and suppression of renin secretion from the contralateral kidney. Transcatheter embolization of a segmental artery cured the hypertension in one case. A nephrectomy performed in the other case, because of multiple intrarenal aneurysms, was curative. Intrarenal renal artery aneurysms are an uncommon cause of renovascular hypertension in children. The aneurysms may be mycotic or congenital in origin, or secondary to diffuse vasculitis. Although spontaneous resolution of the aneurysms may occur when due to vasculitis, treatment of most aneurysms is usually necessary. Transcatheter embolization of solitary aneurysms is an attractive alternative to partial nephrectomy, since it allows maximal preservation of renal parenchyma with minimal morbidity.

Aneurysm↗
PubMed1984

Enzyme replacement therapy for infantile hypophosphatasia attempted by intravenous infusions of alkaline phosphatase-rich Paget plasma: results in three additional patients.

After biochemical and radiographic studies, enzyme replacement therapy in three patients with the infantile form of hypophosphatasia was attempted by weekly intravenous infusions of bone alkaline phosphatase-rich (BAP) plasma from patients with Paget bone disease. Subsequently, circulating BAP activity was substantially increased in each patient, and in one was maintained in the normal range for nearly 2 months. Despite partial or complete correction of the deficiency of circulating BAP activity, we observed no radiographic evidence for arrest of progressive osteopenia or improvement in rachitic defects in any of the patients. Failure of infants with hypophosphatasia to show significant healing of rickets on correction of circulating BAP activity supports the hypothesis that this isoenzyme functions in situ during normal skeletal mineralization.

Alkaline Phosphatase↗
PubMed1983

Neonatal renal failure and glomerular immaturity.

A case of acute renal failure in a neonate was observed in which there were no obvious predisposing factors. Renal biopsy showed marked glomerular immaturity with otherwise normal renal architecture. Light and ultramicroscopic abnormalities noted suggest that the glomerular immaturity caused an abnormally low glomerular ultrafiltration coefficient (Kf). An inadequate rate of glomerular filtration secondary to the low Kf could have precipitated the acute renal failure. The finding of isolated glomerular maturational arrest is a previously undescribed cause of neonatal renal failure.

Acute Kidney Injury↗
PubMed1982

Glucose transport in chronically altered rat nephrons.

Microinjection experiments were performed in anesthetized rats to study the tubular absorptive capacity for glucose (TG) in normal and chronically altered tubules, i.e., tubules that sustained anatomical repair and compensatory changes of their previously normal configuration after acute damage. TG was complete when the glucose load injected in normal or altered early or late proximal convolutions was less than or equal to 1.5 or less than or equal to 10 pmol . s-1, respectively. In normal tubules, TmG was 10 and 5 pmol . s-1 after early and late proximal microinjections, respectively. After early proximal microinjections in altered tubules, different levels of TmG were found. They related to the degree of compensatory growth. TmG was approximately 12, 24, or 35 pmol . s-1, respectively, in altered tubules with minor, moderate, or major compensatory growth. After late proximal microinjections, TmG was 15 pmol . s-1. TG variability was greater in altered than in normal tubules. Correlation between structural and functional compensatory changes was thus demonstrated. Furthermore, an important, albeit latent, absorptive capacity for glucose of the proximal straight tubule was found.

Animals↗
PubMed1981

Home peritoneal dialysis during infancy.

We have recently trained two sets of parents to perform home peritoneal dialysis on their infants with chronic renal failure. Chronic dialysis was initiated before the age of one year with a body weight of less than 10 kg. The infants were maintained on dialysis for 10 and 13 months respectively awaiting cadaveric transplantation. Both infants had marked growth failure while on chronic home dialysis. Although one infant had three episodes of peritonitis, the other had none during 10 months of dialysis. Chronic home peritoneal dialysis was well tolerated in both infants.

Body Weight↗
PubMed1979

Association of crossed fused renal ectopia and multicystic kidney.

A male newborn presented with mild azotemia, an abdominal mass and non-visualized right kidney on excretory urography. Evaluation, including ultrasound and surgical exploration, revealed the simultaneous occurence of crossed fused renal ectopia and multicystic kidney.

Humans↗
PubMed1979

Ketotic hypoglycemia and hypopituitarism.

A 5-year-old girl had hypoglycemia and was of short stature. Studies of pituitary function demonstrated combined growth hormone and adrenocorticotropic hormone (ACTH) deficiency. She was shown to have ketotic hypoglycemia. In contrast to patients previously reported with hypopituitarism and ketotic hypoglycemia, she had no deficiency of gluconeogenic substrate. Serum levels of alanine and other gluconeogenic amino acids were normal during fasting and hypoglycemia. These studies suggest that inadequate gluconeogenic precursors are not the cause of her ketotic hypoglycemia. Ketotic hypoglycemia in association with hypopituitarism may be secondary to multiple biochemical defects.

Acidosis↗
PubMed1979

Comparison of urinary lactic dehydrogenase with antibody-coated bacteria in the urine sediment as means of localizing the site of urinary tract infection.

Two noninvasive methods of localizing the site of urinary tract infection, urinary lactic dehydrogenase (LDH) isoenzymes and antibody coating of bacteria in the urinary sediment, have been prospectively compared with the bladder washout technique in a series of children with urinary tract infection. Fifteen children had infection localized in the upper tract. Urinary LDH isoenzymes correctly localized the infection in 14 children; however, the infection was correctly localized by the antibody coating of bacteria in only eight patients (P less than .02). Fourteen children had lower tract infection by the bladder washout technique. Urinary LDH isoenzymes localized the infection in all 14 children, whereas the antibody coating correctly localized the infection in ten children (P less than .05). This study shows the urinary LDH isoenzyme pattern to be a more accurate technique than the detection of antibody-coated bacteria for localizing the site of urinary tract infection.

Adolescent↗
PubMed1979

Localization of urinary tract infection.

Both the antibody-coating and LDH isoenzyme techniques theoretically fulfill the criteria for an ideal localization test. Both are noninvasive. They are relatively easy to perform and well within the capability of most clinical laboratories. Both can be done rapidly and the results can be in the clinician's hands in a matter of a few hours. The results of the antibody-coating technique do not appear to be valid for children. Since only one controlled study with comparison with other localization techniques has been done in adults, further evaluation needs to be done. The LDH isoenzyme pattern has not been studied in adults but appears to be accurate in children. A prospective comparison of both procedures in adults using either the Fairly bladder washout technique or the Stamey ureteral catheterization method to localize definitively the site of infection would be most helpful. Definitive noninvasive localization techniques could lead to therapy being initiated with the site of infection defined. This would facilitate earlier and more intensive antibiotic therapy in those patients at risk for renal parenchymal damage from upper tract infections.

Antibody-Coated Bacteria Test, Urinary↗
PubMed1977

Malakoplakia of kidney simulating renal neoplasm.

In a nine-year-old girl with renal hypertension and a urinary infection, angiographic studies of the left kidney suggested an intrarenal pheochromocytoma. After nephrectomy, the kidney was found to contain only a cystic lesion characterized by multiple small, friable excrescences. Under the light microscope these appeared to be formed by granulovacuolated macrophages. Electron microscopy showed intracytoplasmic inclusion identified as Michaelis-Gutmann bodies in various stages of formation. Images suggestive of degraded bacteria were also observed within phagolysosomes.

Child↗
PubMed1977

Nephronophthisis. Renal function and histologic studies in a family.

Nephronophthisis (previously described as familial juvenile nephronophthisis and medullary cystic disease) is characterized by insidious renal failure, its main features being increased urinary sodium loss, pitressin-resistant hypotomic polyuria, polydipsia, normal urine sediment and absence of hypertension. Renal function and histologic studies were performed in a family in which two siblings had this disorder, while the parents and two other siblings appeared clinically normal. Both parents demonstrated a moderate impairment of maximum urinary concentration. The values for tubular free water reabsorption (TcH2O) were relativley normal in the parents and the healthy siblings. One of the index patients showed only minimal sodium wasting even though he had hyposthenuria, thus suggesting an involvement of the collecting ducts in the early stage of neophronophthisis. No evidence of proximal tubular dysfunction was found. Although the light-microscopic examination of renal biopsies from the parents and the healthy siblings was unremarkable, electron microscopy revealed probable abnormalities in all four. An autosomal recessive mode of inheritance is, therefore, suggested in this family. The etiology of nephronophthisis is obscure but a likely possibility is that the renal damage results from an inborn metabolic error.

Adolescent↗