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Biomedical subjects

E Ramos

Publications and source records attributed to E Ramos.

At least 163 records · Page 9Linked to original sources
PubMed1981

Transformation of diffuse proliferative glomerulonephritis to membranous nephritis in a patient with systemic lupus erythematosus.

Transformation of diffuse proliferative glomerulonephritis to membranous nephropathy 10 years later, in a patient with systemic lupus erythematosus, is reported. The original biopsy showed diffuse proliferative glomerulonephritis with epithelial crescent formation, 'wire loop' thickening of the capillary walls and moderately severe interstitial inflammation. Electron microscopy showed large subendothelial electron-dense deposits. Following treatment with a combination of prednisone and azathioprine for 2 years the 24-hour urine protein decreased from 8.8 g to 300 mg. In September, 1979, she again developed facial and pedal edema. With the exception of proteinuria of 6.0 g/24 h, the renal function remained normal. Repeat renal biopsy showed membranous glomerulopathy. On electron microscopy, electron-dense deposits were predominantly in a subepithelial position. The significance of the original biopsy as a predictor of eventual outcome and of sequential biopsies to the clinical management of patients with systemic lupus erythematosus is discussed.

Adult↗
PubMed1980

Surreptitious habitual vomiting simulating Bartter's syndrome.

A patient with hypokalemic alkalosis, normotensive hyperreninism, hyperaldosteronism, increased levels of urinary and plasma prostaglandin E, and vascular hyporesponsivity to angiotensin II was thought to have Bartter's syndrome. Results of a kidney biopsy showed hyperplasia of the juxtaglomerular apparatus but no renomedullary cell hyperplasia. A 24-hour urine collection showed a low chloride level and no increase in the fractional chloride clearance, thus excluding Bartter's syndrome. Subsequent disclosure of surreptitious, habitual vomiting explained the hypokalemia.

Adult↗
PubMed1980

Infectious complications in renal transplant recipients.

Infections complicated the course of 59 of 111 renal transplantations (53%) performed on 93 patients at the University of Maryland Hospital. Infections and resultant deaths were more common among the patients with cadaver transplants. The transplant wound and the urinary tract were the most common sites of infection, occurring in 33% and 24% respectively. Septicemia developed in 11 patients (10%), secondary to urinary tract infection in six and to surgical wound infection in three. Opportunistic viral, fungal, and actinomycotic infections occurred in ten patients (9%). A total of nine patients (8%) died as a result of infection. This experience with sepsis and mortality, substantially lower than previously reported, may have resulted from (1) rigorous screening and detailed histories of recipients and donors for infection at the time of transplantation, as well as bacteriologic and serologic studies; (2) discontinuation of azathioprine whenever the WBC fell to less than 5,000/cu mm; (3) aggressive surveillance and early management of infections; and (4) prompt removal of a nonviable kidney when detected by radionuclide scan and percutaneous renal biopsy.

Adolescent↗
PubMed1980

Erythrocytosis after renal allotransplantation: treatment by removal of the native kidneys.

A patient with end-stage renal disease had erythrocytosis after kidney transplantation, with a hematocrit level that ranged between 52 and 60%. Selective catheterization of venous blood from his native kidneys and the transplanted kidney revealed a threefold increase of erythropoietin activity in blood from his own kidney over systemic blood and blood from the transplanted kidney. Bilateral nephrectomy cured the condition. Postoperative hematocrit and erythropoietin levels were within normal limits.

Adult↗
PubMed1979

Episodic hypertension caused by recurrent renal artery lesions following transplantation: a case report.

A kidney transplant patient developed recurrent hypertension on two successive occasions associated with lesions of the renal artery. The first episode of hypertension was caused by renal artery stenosis and was surgically corrected; the second was caused by a sizable pseudoaneurysm at the site of arterial anastomosis which was resected, and arterial continuity was successfully re-established.

Adult↗
PubMed1979

Are the native kidneys responsible for erythrocytosis in renal allorecipients?

The development of erythrocytosis following renal transplantation has been reported to be caused by a number of factors. These include acute and chronic rejection, hydronephrosis and renal artery stenosis. In this study, seven patients were noted to have erythrocytosis with hematocrits ranging between 53.5 and 66%. Serum erythropoietin levels were elevated and ranged between 11 and 60 mU/ml with a mean of 31.9 mU/ml in six of seven patients. Selective catheterization of veins of native and transplanted kidneys in three patients revealed mean serum levels of 40.9 and 13.0 mU/ml, respectively. This suggests that excess erythropoietin is being produced from the diseased native kidneys. Bilateral nephrectomy in one patient cured erythrocytosis and dropped systemic levels of erythropoietin (EP) to 6.1 mU/ml. In four of the remaining five patients, hematocrits came down spontaneously to within normal over a 1- to 3-year period. Consequently, it appears that in a number of transplant patients the retained diseased kidneys, having lost all excretory and concentrating function, may remain capable of functioning as endocrine erythropoietin-producing organs.

Erythropoietin↗