1/27. Possible induction of renal dysfunction in patients with lecithin:cholesterol acyltransferase deficiency by oxidized phosphatidylcholine in glomeruli.To clarify the causes of renal dysfunction in familial lecithin:cholesterol acyltransferase (LCAT) deficiency, kidney samples from 4 patients with LCAT deficiency (3 homozygotes and 1 heterozygote) were examined immunohistochemically. All of the patients exhibited corneal opacities, anemia, renal dysfunction, deficiencies in plasma high density lipoprotein and LCAT activity and mass, and an increase in the ratio of plasma unesterified cholesterol to esterified cholesterol. Renal lesions began with the deposition of lipidlike structures in the glomerular basement membrane, and these structures accumulated in the mesangium and capillary subendothelium. By electron microscopy, 2 types of distinctive structure were found in glomerular lesions: vacuole structures and cross-striated, membranelike structures. The plasma oxidized phosphatidylcholine (oxPC) -modified low density lipoprotein (LDL) levels in LCAT-deficient subjects were significantly (P<0.01) higher than those in controls (1.30 /-0.82 versus 0.42 /-0.32 ng/5 microg LDL, respectively), and a significant (P<0.01) difference was observed even after adjustment for confounding factors by an analysis of covariance. The patient with the highest plasma oxPC-modified LDL had the most membranelike structures in the glomeruli and showed the greatest renal deterioration from a young age. In glomerular lesions, although there was an abundance of apoB and apoE, oil red O-positive lipids, macrophages, apoA1, and malondialdehyde were scarce. OxPC was found extracellularly in glomerular lesions, and although its distribution differed from that of apolipoproteins, it was quite similar to that of phospholipids. In conclusion, these results indicate that oxPC in plasma and glomeruli is distinctive for patients with LCAT deficiency. Therefore, oxPC may be a factor in the deterioration of kidneys in patients with familial LCAT deficiency.- - - - - - - - - - ranking = 1keywords = sample (Clic here for more details about this article) |
2/27. Hypertension due to renal tuberculosis: assessment by renal vein renin sampling.A 36-year-old man with asymptomatic hypertension was shown to have destruction of the right kidney due to renal tuberculosis. The peripheral renin level was normal, but renal vein renin sampling showed predominant renin secretion from the right kidney both in basal samples and after acute stimulation of renin release with intravenous diazoxide. nephrectomy has resulted in marked reduction of blood pressure without treatment one year after operation. The findings support the predictive value of renal vein renin sampling when hypertension is associated with renal parenchymal disease, even when peripheral renin is normal.- - - - - - - - - - ranking = 1keywords = sample (Clic here for more details about this article) |
3/27. Perinatal renal ischemia resulting in hypertensive cardiomyopathy.Three neonates presented with malignant hypertension during the first week of life; 2 of them had congestive heart failure. Although none had indwelling umbilical artery catheters, unilateral renovascular lesions were diagnosed by nuclear perfusion scans. Angiotensin-converting enzyme inhibitor therapy produced rapid recovery. Hypertension must be included in the differential diagnosis of infants presenting with congestive heart failure and acidosis. ultrasonography is not sensitive enough to exclude renovascular lesions. We emphasize the importance of early diagnosis and treatment.- - - - - - - - - - ranking = 0.40124063758516keywords = size (Clic here for more details about this article) |
4/27. Small atrophic kidney secondary to renal vein thrombosis: report of a case diagnosed arteriographically.Although rena vein thrombosis usually presents with a large or normal-sized kidney radiographically, a small atrophic kidney may be the end stage result of complete renal vein thrombosis with subsequent hemorrhagic infarction. A small atrophic kidney secondary to renal vein thrombosis (probably of neonatal origin) was diagnosed by selective renal arteriography in a 31-year-old woman being studied for hypertension of unknown etiology.- - - - - - - - - - ranking = 0.40124063758516keywords = size (Clic here for more details about this article) |
5/27. Massive spontaneous perirenal hematoma and accelerated hypertension in a patient with polyarteritis nodosa.A 43-year-old Albanian man is presented who underwent nephrectomy for a huge right spontaneous perirenal hematoma. The diagnosis of polyarteritis nodosa as the etiology of the hematoma has been made only by histological examination, because of the quick and unforeseeable onset of this complication and the nonspecificity of symptoms. We hypothesize a relationship between reactivation of polyarteritis nodosa and treatment with rifampicin and isoniazid.- - - - - - - - - - ranking = 0.40124063758516keywords = size (Clic here for more details about this article) |
6/27. Segmental renal vein renin assay and segmental nephrectomy for correction of renal hypertension.Selective segmental renal vein catheterization was used to obtain venous blood samples for renin assay. With this technique a localized source of hypersecretion of renin was identified in 2 patients. Using samples from the main renal veins we found no significant difference in renin activity and, therefore, the etiology of the hypertension in these 2 patients would have been missed. Segmental nephrectomy resulted in a cure of the hypertension in both patients who were followed for a minimum of 14 months.- - - - - - - - - - ranking = 2keywords = sample (Clic here for more details about this article) |
7/27. High renin hypertension associated with renal cortical cyst.A fifty-seven-year-old patient with a five to one elevation of right renal vein plasma renin activity associated with a large, simple cortical cyst of the right lower pole is presented. Marsupialization of the cyst was associated with improvement in the patient's hypertension and the finding of bilaterally equal renal vein renin activity three months postoperatively. Possible mechanisms for hypertension are discussed in context of the experimental models of Goldblatt and Page in such lesions as cortical cysts of large size causing hydronephrosis, vascular stretching, or renal parenchymal compression.- - - - - - - - - - ranking = 0.40124063758516keywords = size (Clic here for more details about this article) |
8/27. Erosion of embolization coils and guidewires from the kidney to the colon: delayed complication from coil and guidewire occlusion of renal arteriovenous malformation.Percutaneous transarterial embolization is a useful, nondrastic, valuable, and commonly used therapeutic option for the treatment of renal arteriovenous malformation (AVM). Compared with partial or total nephrectomy, transarterial embolization is more conservative and preserves renal function. However, it has some limitations and complications that could cause renal infarction and progression of hypertension, renal insufficiency, and pulmonary embolism. Large-sized AVM and multiplicity of abnormal vessels also limit the use of the embolization technique. The authors experienced erosion of the coils and guidewires that were used for embolization of renal AVM from kidney to descending colon. Coil embolization is practiced extensively, but a complication such as this does not appear to have been described.- - - - - - - - - - ranking = 0.40124063758516keywords = size (Clic here for more details about this article) |
9/27. Neonatal renovascular hypertension due to prenatal traumatic retroperitoneal hematoma.This report describes severe hypertension in a 7-week-old male infant found to have renovascular disease from an organized hematoma due to prenatal trauma. As such, this case illustrates a novel acquired, congenital mechanism of renovascular hypertension. The importance of considering prenatal as well as postnatal etiologies of acquired renovascular hypertension in neonates is emphasized. Likewise, attention must be drawn to the classic presentation of congestive heart failure in a child with severe hypertension.- - - - - - - - - - ranking = 0.40124063758516keywords = size (Clic here for more details about this article) |
10/27. Hypertension due to a renin-secreting tumour localised by segmental renal vein sampling.An 18-year-old female was found to be hypertensive on routine medical examination. Further investigation disclosed persistent hypokalaemia and elevated plasma renin activity in peripheral venous blood. Segmental renal vein sampling with assay of blood samples located the source of excess renin secretion in the lower mid-zone of the left kidney. This localization was not confirmed by either angiography or by palpation of the exposed kidney before nephrectomy but macroscopic examination of the freshly sectioned kidney revealed a small tumour in the region suggested by renal vein sampling. The tumour had the morphologic pattern fo an haemangiopericytoma with abundant ultrastructural specific granules and very high renin activity by tissue assay. plasma renin activity fell precipitously after nephrectomy and remained very low for the first week. Although the immediate post-operative blood pressure fell to normal, hypertension recurred temporarily and was associated with elevated plasma aldosteron, producing a syndrome similar to primary aldosteronism. All variables returned to normal without specific therapy and hypertension has not subsequently recurred.- - - - - - - - - - ranking = 1keywords = sample (Clic here for more details about this article) |
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