Late renal vein thrombosis associated with recurrence of membranous nephropathy in a renal allograft: a case report.

Allograft renal vein thrombosis (RVT) is an uncommon but potentially catastrophic complication. Although it usually occurs in the early posttransplant period and is associated with surgical complications or vascular rejection, it may develop later, when it is generally related with a hypercoagulable state. Typical clinical presentation is sudden oligoanuric acute renal failure, and hematuria, with a painful and swollen renal allograft. Confirmation of the diagnosis requires Doppler ultrasound and computed tomography. Herein we have reported a successfully treated case of late RVT that developed in an allograft with recurrent membranous nephropathy associated with the nephrotic syndrome. The patient fully recovered renal graft function a few days after presentation, which was related to anticoagulant therapy. We demonstrated complete recanalization of the venous thrombosis.

[Systemic fibromuscular dysplasia. Supra aortic and renal artery involvement]. / Displasia fibromuscular sistémica. Compromiso de ramas supraaórticas y renales.

We report a 39 years old male presenting with an intense hemicrania pain in the tract of the carotid artery and Claude Bernard Horner syndrome. The patient had also a high blood pressure. Magnetic resonance imaging demonstrated a left carotid artery fibrodysplastic disease. Conventional angiography of 4 cerebral vessels showed a dissection of the left carotid artery and fibromuscular dysplasia of the left vertebral artery. Renal angiography showed a stenosis and occlusion of renal artery with radiological exclusion of right kidney. On the left side there was a stenosis and occlusion of segmental branches. The diagnostic importance of Claude Bernard Horner syndrome and the need to study renal artery involvement when carotid dissection is accompanied with high blood pressure, is highlighted.

Effect of metoprolol on serial measurements of exchangeable sodium, blood pressure, renin and pulse rate in spontaneously hypertensive rats.

The cardioselective beta-blocker metoprolol was mixed with the diet (6 mg metoprolol/g food) and given to 9 spontaneously hypertensive rats (SHR) for four weeks, while 9 other SHR were given the plain diet only and served as controls. All rats were also given 0.5% drinking saline labeled with isotope 22Na (37 kBq/1) to drink. Measurements of total exchangeable sodium, blood pressure, pulse rate and weight were performed before and repeatedly during treatment. Plasma renin activity was measured at the end of the study. Before treatment exchangeable sodium, blood pressure, pulse rate and weight were no different between the groups. Metoprolol reduced the pulse rate and prevented the usual blood pressure increase in SHR. Both groups gained weight similarly. Exchangeable sodium increased similarly in both groups along with the weight increase. Plasma renin activity was not significantly different in the two groups. Thus, chronic metoprolol treatment of SHR reduced blood pressure and pulse rate in SHR but did not lower plasma renin or cause measurable sodium or fluid retention.

Effect of nitrendipine on blood pressure, plasma renin, and exchangeable sodium in DOC-salt hypertension in the rat.

Desoxycorticosterone-salt (DOC-salt) hypertension in the rat can be prevented by administration of nitrendipine. We have studied the effect of nitrendipine on exchangeable body sodium (NaE) in this model. Eighteen male Sprague-Dawley rats had a left nephrectomy and after 14 days received subcutaneous injections of deoxycorticosterone (Percorten, CIBA) 12.5 mg three times weekly for 4 weeks and were given 22Na-labeled 1% saline plus 0.2% KCl to drink. They were fed a sodium-free diet. NaE, systolic blood pressure, and body weight were measured weekly. The animals were divided into two groups of nine, one group being given subcutaneous nitrendipine 5 mg/kg twice daily, while the control group was given vehicle only. Blood samples from conscious animals were drawn at the start and at the end of the study for measurement of plasma renin concentration (PRC) and haematocrit, and at the end for atrial natriuretic peptide (ANP) measurement. Twenty-four hour urine was collected at the end of the study from eight rats of each group, and urine and blood samples were taken for biochemical analysis. In the control rats, blood pressure rose from an initial mean of 140.6 +/- 1.7 (SEM) mm Hg to 187.2 +/- 6.5 (p less than 0.001) at week 4. In the nitrendipine-treated rats, blood pressure fell from 143.9 +/- 2 at week 0 to 127.2 +/- 3.3 mm Hg at week 4 (p less than 0.001). However, body weight rose similarly in both groups and there was no difference in NaE between the groups throughout the study.(ABSTRACT TRUNCATED AT 250 WORDS)

Renin-secreting tumor. Case report.

Renin-secreting tumor, though rare, should be considered in assessing severe hyperreninemic, hypertensive patients. We studied an 18-year-old girl with hypokalemic hyperreninemic hyperaldosteronism. No angiographic lesion could be detected. The plasma renin activity (PRA) of the right/left renal vein was 7.3. With a presumptive diagnosis of renin-secreting tumor (RST), the patient was operated on, and a cortical nodule was found on the right lower pole. Partial nephrectomy was followed by a rapid fall in PRA (half-life, 33-44 min) and normalization of blood pressure (BP). At 3 1/2 months postoperatively, the patient showed normotension, normokalemia, normal aldosterone, and slightly elevated PRA unresponsive to postural changes and furosemide treatment. Tumoral PRA secretion responded to postural stimulus, spironolactone use, and nitroprusside-induced hypotension. Neither the high aldosterone excretion nor hyperreninemia decreased after 3 days of DOCA; this agrees with a previously reported case suggesting the usefulness of this test in the diagnosis of RST.