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Biomedical subjects

R E Urizar

Publications and source records attributed to R E Urizar.

At least 19 recordsLinked to original sources
PubMed1998

Wegener's granulomatosis in a patient with apparent drug-induced acute interstitial nephritis.

We describe a patient whose clinical presentation was suggestive of drug-induced acute interstitial nephritis (AIN). A renal biopsy and serologic testing led instead to the diagnosis of Wegener's granulomatosis (WG) with necrotizing crescentic glomerulonephritis. Treatment with corticosteroids and cyclophosphamide resulted initially in complete recovery of renal function, and an exacerbation of acute renal failure after doses of these agents had been tapered responded to resumption of the original regimen. We report this case to emphasize the potentially identical presentations of AIN and WG. Since the two conditions are treated differently, we suggest that the diagnosis of AIN should be accepted only after biopsy confirmation.

Acute Disease↗
PubMed1996

Nephrotic-range proteinuria in renal atheroembolic disease: report of four cases.

The protean clinical manifestations of atheroembolic disease (AED) mimic systemic disorders with kidney involvement. Acute or chronic renal failure develops spontaneously or more frequently after an inciting event in patients with AED. Significant proteinuria and nephrotic syndrome, however, constitute uncommon findings. We present four patients with AED documented histopathologically who developed nephrotic-range proteinuria. The mechanisms of proteinuria are discussed, and it is suggested that AED be considered in the differential diagnosis of nephrotic syndrome in elderly patients with serious vascular disease.

Aged↗
PubMed1989

Glomerulitis induced by cationized bovine serum albumin in the rat.

The effects of injected native and cationized bovine serum albumin (BSA- and BSA+ respectively) were evaluated in rats which subsequently received anti-BSA. Thrombocytopenia, low creatinine clearance (Ccr), increased proteinuria, capillary swelling, mild tuft necrosis and BSA+ deposits in glomeruli resulted within 24 h of BSA+ injection. Later BSA+ produced mesangial expansion glomerular capillary wall (GCW) thickening and deposits of BSA+ accompanied by rabbit anti-BSA and rat anti-BSA which correlated well with small mesangial, subendothelial and subepithelial electron-dense granular accumuli. These latter enlarged considerably after the injection of anti-BSA. BSA- controls showed minimal or no lesions. The disappearance from the blood (t1/2) of a single dose of immune complexes (IC) prepared with chromatography-purified, radioiodinated anti-BSA - BSA- and BSA+ was determined in another group of rats. The t1/2 of BSA- anti-BSA was 42.8 h (95% confidence: 39.8-46.2) while that of BSA+ anti-BSA was 52.5 h (48.1-57.8). These results suggested that serum sickness glomerulitis developed only in rats injected with BSA+, due to in situ IC which presumably grew by accretion of foreign anti-BSA. Circulating IC may have developed and colocated with the latter, with dissociation and recombination at these sites. It is postulated that the functional-immunomorphological changes and the slow removal of cationized IC reported herein could be explained by the highly positive net charge of the injected antigen.

Animals↗
PubMed1986

Disseminated intravascular coagulation (DIC) induced by liquoid (polyanetholsulfonate) in the rat. V. Effects on circulating fibronectin.

Levels of plasma fibronectin (Fn) were 63% lower than normal 15 min after the intravenous injection of liquoid (P less than 0.01); 3 h later they were still low but rebounded to 35% above normal (P less than 0.01) by 24 h. Concurrently microthrombi containing fibrinogen, Fn and Factor VIII related-antigens (VIII:Ag) were detected in the kidneys and lungs by immunohistopathological studies. Ultrastructurally, thrombi were composed of dense granular and occasional fibrillar non-striated material. In liquoid-injected rats 125I-fibrinogen mainly localized in kidneys and lungs, especially in the latter (P less than 0.01), and the lungs had a higher wet-to-dry weight ratios than did controls (P less than 0.01). It is concluded that the polyanion (liquoid)-induced intravascular coagulation-like reaction sequestered Fn concomitantly with the precipitation of fibrinogen and VII:Ag in the microclots. The reduced concentration of plasma Fn may have impaired the disposal of coagulation products thus enhancing the expression of the coagulopathy-mediated renal and pulmonary histopathology. It is suggested that the liquoid-related coagulopathy may have resulted in enzymatic lysis of Fn.

Animals↗
PubMed1984

Age-related renal, hematologic, and hemostatic abnormalities in FH/Wjd rats.

This longitudinal study compared the renal morphologic changes and hemostatic defects of FH/Wjd rats at different ages. A second aim was to determine whether the bleeding tendency becomes intensified in older animals by the concomitant renal disease. Results indicated that reduced capacity for platelet 14C-serotonin release (P less than 0.01) was found for each age group studied in comparison with Wistar controls. The nephropathy of old FH/Wjd male rats was more severe than that in either FH/Wjd females or age-matched Wistars of both sexes. The mesangial lesions showed abundant deposits of factor VIII-related antigen, fibronectin, and immunoglobulins, but not C3, along with tightly packed or loose electron-dense material. Polyethylene glycol precipitation and platelet aggregation tests detected small amounts of circulating immune complex-like material. Old FH/Wjd rats did not develop edema, and the glomerular filtration rate remained normal despite the persistent proteinuria, hematuria, and arterial hypertension characteristic of this strain. Our data indicated that the congenital platelet dysfunction does not become more severe in older animals and that the nephropathy seems unrelated, does not appear to be mediated by immune complexes, and, in contrast to the focal segmental glomerulosclerosis of persons, the lesions progress without a parallel impairment of renal function.

Aging↗
PubMed1983

Severe hypertension in newborn after pyeloplasty of hydronephrotic kidney.

A case is described, believed to be the first reported, of a newborn in whom severe hyperreninemic hypertension developed after pyeloplasty of a hydronephrotic kidney. Management of the hypertension required large doses of antihypertensive agents, including sodium nitroprusside, for six postoperative days. Propranolol had to be given for eight months after surgery. The possibility that thiocyanate level in a newborn is unreliable as indicator of sodium nitroprusside overdosage is considered.

Female↗
PubMed1983

Early renal involvement in acute lymphoblastic leukemia and nonHodgkin's lymphoma in children.

Clinical manifestations of kidney disease, particularly renal failure, caused by malignant infiltration in patients with acute lymphoblastic leukemia or nonHodgkin's lymphoma have been described rarely. We report 1 case of acute lymphoblastic leukemia and 3 cases of nonHodgkin's lymphoma in which renal disease was the only or one of the presenting manifestations of malignancy. Of these patients 2 had rapidly progressive renal failure with nephromegaly, 1 presented with bilateral abdominal masses caused by severe nephromegaly and with microscopic hematuria, and 1 had microscopic hematuria without nephromegaly. In all 4 patients kidney biopsy revealed malignant infiltration. In the 2 patients who presented with renal failure kidney function promptly returned to normal after chemotherapy and irradiation of the kidneys. Prompt and correct diagnosis of nephropathy, when it is the only or one of the presenting signs of acute lymphoblastic leukemia or nonHodgkin's lymphoma, is necessary to expedite initiation of specific antitumor therapy.

Child↗
PubMed1981

Immunologic mechanism of childhood renal diseases.

Antigen-antibody complexes and antibasement antibodies are involved in the pathogenesis of most immune-mediated renal diseases. The major feature of these two kidney tissue-damaging mechanisms, and their interrelations with amplification systems (complement, coagulation, and kinin) are outlined. A brief discussion of current immunologic concepts applicable to representative experimental models and pediatric nephropathies, and of their immunohistopathologic and ultrastructural expressions is presented.

Adolescent↗
PubMed1981

Association of infectious mononucleosis with nephrotic syndrome.

A patient had infectious mononucleosis (IM) associated with transient nephrotic syndrome (NS). A kidney biopsy sample studied by light and electron microscopy demonstrated minimal glomerular lesions. Immunofluorescent studies revealed mainly granular mesangial deposits of IgM, and to a lesser extent, deposits of IgG and of C4 and C3. No Epstein-Barr virus-related antigen could be detected in the kidney. This, and three other cases reported in the literature, suggest a causal relationship between IM and NS.

Adolescent↗