No AccessJournal of UrologyCLINICAL UROLOGY: Case Reports1 Nov 2001BILATERAL INTRARENAL ADRENAL GLANDS IN CADAVERIC DONOR KIDNEYS RESEMBLING RENAL CELL CARCINOMA ON INTRAOPERATIVE FROZEN SECTION DEBRA L. FROMER, JOHN D. BIRKHOFF, MARK A. HARDY, ALAN I. BENVENISTY, BOYCE BENNETT, and MITCHELL C. BENSON DEBRA L. FROMERDEBRA L. FROMER More articles by this author , JOHN D. BIRKHOFFJOHN D. BIRKHOFF More articles by this author , MARK A. HARDYMARK A. HARDY More articles by this author , ALAN I. BENVENISTYALAN I. BENVENISTY More articles by this author , BOYCE BENNETTBOYCE BENNETT More articles by this author , and MITCHELL C. BENSONMITCHELL C. BENSON More articles by this author View All Author Informationhttps://doi.org/10.1016/S0022-5347(05)65683-2AboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail "BILATERAL INTRARENAL ADRENAL GLANDS IN CADAVERIC DONOR KIDNEYS RESEMBLING RENAL CELL CARCINOMA ON INTRAOPERATIVE FROZEN SECTION." The Journal of Urology, 166(5), pp. 1820–1821 References 1 : . Philadelphia: Blanchard & Lea1855: 188. Google Scholar 2 : Combined adrenorenal fusion and adreno-hepatic adhesion: a case report with review of the literature and discussion of pathogenesis. J Urol1976; 115: 323. Link, Google Scholar 3 : Unilateral adrenal heterotopia with renal-adrenal fusion. J Urol1998; 160: 116. Link, Google Scholar From the Departments of Urology, Surgery and Pathology, New York-Presbyterian Hospital, Columbia Campus, New York, New York© 2001 by American Urological Association, Inc.FiguresReferencesRelatedDetails Volume 166Issue 5November 2001Page: 1820-1821 Advertisement Copyright & Permissions© 2001 by American Urological Association, Inc.Keywordsadrenal glandskidney transplantationabnormalitiesMetricsAuthor Information DEBRA L. FROMER More articles by this author JOHN D. BIRKHOFF More articles by this author MARK A. HARDY More articles by this author ALAN I. BENVENISTY More articles by this author BOYCE BENNETT More articles by this author MITCHELL C. BENSON More articles by this author Expand All Advertisement PDF DownloadLoading ...

We report a patient who developed Henoch-Schönlein purpura (HSP) 13 years after he presented with IgA nephropathy (IgAN). In both HSP and IgAN renal biopsy most commonly reveals focal proliferative glomerulonephritis on light microscopy and immunofluorescence displays mesangial IgA deposits. In addition, patients with HSP or IgAN have elevated serum IgA levels, circulating IgA immune complexes, IgA-bearing lymphocytes, immunoglobulin-producing cells, and binding of IgG to glomerular components of similar molecular weight. The occurrence of both diseases in the same patient or the same families and the presence of immune abnormalities compatible with HSP or IgAN in relatives of patients with these diseases suggest a common pathogenesis.

We investigated the effect of captopril, an orally active angiotensin converting enzyme inhibitor, on urinary protein excretion in puromycin aminonucleoside nephrotic rats. The administration of captopril (10 mg/100 g body weight) decreased proteinuria on days 10-14 following the administration of puromycin aminonucleoside (73.0 versus 125.0 mg, p less than 0.01), without affecting glomerular filtration rate. The beneficial effect of captopril was not abolished by the continuous intravenous infusion of angiotensin II (10 micrograms/kg/h for 9 days) or subcutaneous injections of aprotinin (50,000 KIU/day for 3 days). Indomethacin, in moderate (5 mg/kg/day for 3 days) or high (10 mg/kg/day) doses, abolished the captopril attenuation in urinary protein excretion. The salutory effect of captopril was characterized by a reduction in the fractional excretion of protein without compromising the glomerular filtration rate. No difference in renal ultrastructure was noted in captopril-treated versus control animals. Captopril was ineffective in reducing urinary protein excretion in rats with adriamycin-induced glomerulopathy. We conclude that captopril acts to reduce proteinuria in renal disease states arising from depletion of the glomerular basement membrane polyanion. The mechanism of action is postulated to be an alteration in renal hemodynamics, namely increased blood flow and a decrease in the ultrafiltration coefficient, that are the consequence of increased intrarenal prostaglandin production.

Previous reviews of hematuria in children and adolescents have included patients with proteinuria and other renal functional abnormalities such as hypertension and reduced GFR. We report the clinico-pathological correlations in 76 pediatric patients, aged 3 to 19 years, who underwent a renal biopsy because of isolated hematuria during the 10-year period, 1972 to 1981. All specimens were examined by light and electron microscopy and immunofluorescence techniques. The overall prevalence of abnormal renal histology was 56%. The vast majority (41 of 43) of the abnormal biopsy specimens could be classified into four distinct histological categories: (1) Alport syndrome (N = 9); (2) IgA nephropathy (N = 8); (3) thinning of the glomerular basement membrane (N = 17); (4) vascular C3 staining (N = 7). The children were divided into three clinical subgroups (1) isolated microscopic hematuria ( IMH ), N = 42; (2) IMH plus a family history of hematuria in a first degree relative, N = 15; and (3) IMH plus at least one episode of gross hematuria, N = 19. A significant graded increase in the likelihood of obtaining an abnormal renal biopsy was demonstrated (X2 = 10, P less than 0.007) from groups one to three. Sex, age at onset, or duration of hematuria were not associated with an increased proportion of histopathologic abnormalities. These findings indicate that the yield of a renal biopsy in children with isolated hematuria can be predicted accurately from specific clinical characteristics.

Takayasu's Arteritis Renal Involvement is usually characterized by renovascular hypertension and reduction in glomerular filtration rate (GFR) has rarely been described. A twelve year old boy presented with severe hypertension (diastolic BP> 120mmHg) and oligoanuria. Aortography demonstrated irregular narrowing of the lumbar aorta and renal arteries. Chronic renal insufficiency (GFR< 2ml/min/1.73M2) necessitated maintenance hemodialysis. During this time severe hypertension persisted despite aggressive dialysis and numerous antihypertensive drugs. Plasma renin activity was persistently 15 > ng/ml/hr. Follow-up arteriograms showed no improvement in his arteritis. Renal scans demonstrated persistent poor perfusion. Renal biopsy after eight months of dialysis showed preservation of glomerular architecture with mild arteriolar intimal thickening. After 9 months on dialysis GFR improved spontaneously to 32ml/min/1.73M2 despite no improvement in his hypertension. Off dialysis, he remains severely hypertensive, with stable GFR. This report emphasises the remarkable ability of the renal parenchyma to recover function after sustained ischemia.

A 4-year-old girl, who had been in perfect health, presented with the acute onset of renal failure and abdominal mass. Investigations revealed a solitary left kidney which on histology had the typical features of xanthogranulomatous pyelonephritis. The child had no previous history suggestive of chronic renal disease and had no radiologic evidence of renal osteodystrophy. She had no improvement in renal function and has gone on to hemodialysis and transplantation. The unique mode of presentation and the unusual features of this case are discussed.

The clinical courses and biopsy findings of twenty-four children with focal segmental glomerulosclerosis (FSG) were reviewed retrospectively to determine whether the presence of significant mesangial accentuation and proliferation (MAP) has prognostic implications. At the latest assessment, 10 of 13 patients with significant mesangial involveme,t (MAP [+]) had glomerular filtration rates less than or equal to 90 ml/min/1.73 m2, with four in renal failure. In contrast, all of eleven children with no significant mesangial involvement (MAP [-]) maintain glomerular filtration rates greater than 90 ml/min/1.73 m2, (P less than 0.001). Of no prognostic importance were: age at onset of disease, type of onset, or presence or absence of hematuria. The preponderance of males in the MAP (+) group was a statistically significant difference (P less than 0.001). The two groups did not differ in regard to either the type of clinical course or the length of the period of observation, and there was no obvious effect of therapy in either group of patients. Immunofluorescence data were of no value in differentiating between the two groups. Our results imply that FSG with significant mesangial accentuation and proliferation is a unique glomerular disease of childhood, with a clinical course characterized by rapid progression to renal insufficiency. FSG without mesangial involvement, on the other hand, appears to have an excellent prognosis over long periods of time. At present, these two diseases can be differentiated only by renal biopsy.

The pattern of dissemination of prostatic carcinoma varies, but skeletal metastasis is the single most common symptomatic mode of presentation. The clinical course and treatment of the 2 cases presenting with symptomatic metastases to the retroperitoneum are described in detail and pertinent literature is reviewed.

To establish the relationship between the type of focal sclerotic lesion of glomeruli and the development of progressive renal disease, the clinical courses of 20 children with focal segmental and 7 with focal global sclerosis were analyzed. Only five patients, all of them with focal segmental sclerosis, did not have the nephrotic syndrome, although all had proteinuria. Results suggest that patients with focal global sclerosis have a course identical to that of children with the minimal lesion form of nephrotic syndrome: onset in early childhood, response to steroid therapy, and a relapsing, nonprogressive course. Focal segmental sclerosis, in constrast, is characterized by older age at onset, high incidence of nephritic symptoms, lack of response to steroid therapy, and a progressive course with histologic and functional deterioration. Since most published reports have not distinguished between these two entities, a more favorable prognosis in focal segmental sclerosis may be inferred than is actually the case.

Idiopathic membranous nephropathy in children. Based on evidence obtained mainly from adult patients, membranous nephropathy is generally described as a progressive disease that leads to renal insufficiency. This paper presents the course of the disease in a group of 9 children ranging in age between 2 and 16 years at clinical onset. Three of these children, all older than 10 years, two of them hypertensive when first seen, deteriorated rapidly. Another group of three patients, younger than 9 years and normotensive at onset, followed a benign course characterized by prolonged remissions, preservation of normal kidney function and in one of them morphological evidence of healing. Yet another group of patients, ranging in age between 8 and 14 years and normotensive, maintained a normal function of the kidneys after 8, 3½ and 1 yr of continuous proteinuria and hematuria. No progression was detectable on the renal biopsies in two of these patients, performed after several years of observation. The relative benign course of the disease in the majority of our patients and the morphological evidence of healing in one of them suggest a better prognosis than that reported by previous investigators. This might be particularly true for patients developing the disease at a very young age. Néphropathie membraneuse idiopathique de l'enfant. En fonction d'arguments tirés essentiellement de l'étude de sujets adultes la néphropathie membraneuse est généralement décrite comme une maladie progressive qui aboutit à l'insuffisance rénale. Ce travail présente l'évolution de cette maladie dans un groupe de 9 enfants dont les âges s'échelonnaient entre 2 et 16 ans au moment du début clinique. Trois de ces enfants, âgés de plus de 10 ans, dont deux étaient atteints d'hypertension artérielle dès le premier examen, eurent rapidement une évolution défavorable. Un autre groupe de 3 malades âgés de moins de 9 ans et dont les pressions artérielles étaient normales au premier examen ont eu une évolution bénigne caractérisée par des rémissions prolongées, la conservation d'une fonction rénale normale et, chez l'un d'eux, preuve morphologique de guérison. Enfin, un autre groupe de malades, dont les âges s'échelonnaient entre 8 et 14 ans, et dont les pressions artérielles étaient normales, a conservé une fonction rénale normale après 8, 3½ et I an de protéinurie et d'hématurie persistantes. Aucune aggravation n'a été observée dans les biopsies rénales obtenues après plusieurs années d'observation chez deux de ces malades. La bénignité relative de l'évolution de la maladie chez la majorité de nos malades et la preuve morphologique de guérison chez l'un d'eux suggère nu pronostic meilleur que celui rapporté antérieurement par d'autres. Cela peut être plus particulièrement vrai pour les malades atteints à un très jeune âge.

Sensitization to soluble antigens of chemically induced tumors is demonstrable in syngeneic strain 13 (inbred) guinea pigs by specific inhibition of macrophage migration. According to their capacity to (a) inhibit the migration of peritoneal cells from sensitized strain 13 donors or (b) release migration-inhibitory factor from their lymph node cells, the soluble antigens of three different chemically induced tumors did not cross react. This is in keeping with the absence of cross-reactivity among the same three tumors in previous tests of transplantation resistance or delayed hypersensitivity in vivo. Thus, inhibition of macrophage migration may provide a feasible assay in vitro for use in defining these soluble antigens further by physicochemical methods.

Macrophages were obtained in tissue cultures with cells obtained from mouse lung, spleen, bone marrow, peripheral blood, and peritoneal cavity. In addition, macrophages from lung, spleen, bone marrow, and peritoneal cavity of guinea pigs and rats were also cultivated in vitro. Cells from the rat closely resembled those from the mouse, whereas guinea pig cells differed in several respects. In most instances, cells other than macrophages were phagocytized or died with the result that within seven days the cultures consisted entirely of macrophages. Macrophages from all these sources were actively phagocytic, were present as solitary ameboid cells, and, with the exception of certain guinea pig cells, underwent mitosis.

Peritoneal lymphocytes obtained from tuberculin sensitive guinea pigs, when cultured with purified protein derivative, elaborate into the medium a substance, presumably a protein, capable of inhibiting the migration of normal macrophages. This migration inhibitory factor appears to possess immunologic specificity, since specific antigen enhances its activity. Sensitized cells upon interaction with antigen continuously produce this factor for up to 4 days. Concomitantly, sensitized lymphocytes undergo those morphologic alterations recognized as “blast-cell” transformation.

The phagocytosis of tumor cells by peritoneal macrophages from mice was demonstrated in vitro following opsonization with isoanti-body. Phagocytosis of tumor cells occurred in the presence of isoimmune serum prepared in either H-2 compatible or H-2 incompatible strains. After ingestion, the tumor cells were destroyed by the engulfing macrophages. Normal mouse serum contained nonspecific factors that enhanced phagocytosis in the presence of specific isoimmune serum. Peritoneal macrophages from immunized animals had no inherent, specific ability to phagocytize tumor cells in vitro, apart from that due to the presence of humoral antibody in the medium. Their ability to phagocytize tumor cells was abolished by washing the peritoneal cells, but was restored by the addition of a medium containing isoantibody. Peritoneal macrophages collected from animals that had been given an i.p. injection of starch phagocytized tumor cells in greater numbers than did peritoneal macrophages from normal animals. In contrast to viable tumor cells or cells killed by prolonged storage, tumor cells killed by methanol or heat were phagocytized in the absence of isoantibody.