Cases reported "Hypertension, Renal"

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1/179. effect of kidney resection on blood pressure and plasma renin activity. Case report and clinical study.

    Acute transient hypertension following kidney trauma occurred in a 17-year-old youth due to increased activity of the renin/angiotensin system. The systemic blood pressure and plasma renin activity was also studied following elective kidney resection. In one group of patients the operation was performed with clamping of the renal vessels; in the other no clamping was performed. Only minimal changes in blood pressure and plasma renin activity was found in both groups.
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2/179. 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.
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3/179. The Ask-Upmark kidney: a form of ascending pyelonephritis?

    The case is presented of a young girl with recurrent urinary tract infection and vesico-ureteric reflux who developed a small scarred kidney and subsequently, hypertension. Pathologically, the renal changes were compatible with those of an Ask-Upmark kidney. The pathogenesis of the Ask-Upmark kidney is discussed. It is postulated that the lesion is not necessarily of congenital origin but may well be related to infection and intrarenal reflux, it is concluded that long-term follow-up of a young patient with a scarred kidney is indicated.
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4/179. Ask-Upmark kidney associated with renal and extrarenal arterial aneurysms.

    Reports of Ask-Upmark kidney, initially described as a congenital defect in renal development, are uncommon. We report a case with the features of bilateral asymmetrical segmental atrophy in a patient with childhood-onset hypertension. As an adult, she developed cerebral, celiac, and renal artery aneurysms. She underwent successful clipping of the cerebral aneurysm and renal artery repair with preservation of renal function. Novel radiologic techniques make possible the noninvasive diagnosis of segmental atrophy and its complications.
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5/179. 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.
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6/179. Nephropathy subsequent to hyperlipidemia.

    The relationship between lipid abnormalities and the pathogenesis of renal disease is still unclear. Although most patients with primary hyperlipidemia do not develop renal function impairment, experimental and clinical data indicate a possible damaging effect of a disturbed lipid metabolism on the kidney. We report the case history of a patient with hyperlipidemia and mild nephropathy in which an accidentally removed kidney showed intrarenal arteriosclerosis which occured before the development of other cardiovascular risk factors, indicating that primary dyslipidemia induced nephroangiosclerosis.
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7/179. Kawasaki disease complicated by renal artery stenosis.

    We report the case of a child who developed severe renovascular hypertension six months after acute Kawasaki disease. The hypertension was well controlled with enalapril, but there was a gradual decrease in function of the affected kidney. The lesion, an ostial stenosis of the right main renal artery, was not amenable to percutaneous balloon angioplasty, so was treated with bypass surgery. Vasculitis is an important cause of renovascular hypertension in children. This case highlights the importance of regular blood pressure monitoring in children with a history of systemic vasculitis.
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8/179. plasma brain natriuretic peptides and renal hypertension.

    Three children with renal hypertension are described. Two had histories of neuroblastoma treated by surgical resection and chemotherapy. They both presented later with unilateral atrophic kidney and marked hypertension. Only the child with severe cardiac failure demonstrated high plasma brain natriuretic peptide (BNP) concentrations. The remaining patient had a history of chronic nephritis treated with continuous ambulatory peritoneal dialysis. She also had chronic hypertension and severe cardiac failure. This child demonstrated high plasma BNP levels. The endogenous secretion of BNP is not triggered by hypertension alone, even though exogenous BNP has the pharmacological effect of reducing renin activity.
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9/179. Primary hyperaldosteronism without suppressed renin due to secondary hypertensive kidney damage.

    Primary hyperaldosteronism is characterized by high plasma and urinary aldosterone and suppressed PRA. renin suppression is due to aldosterone-dependent sodium retention and mild extracellular volume expansion. We observed three patients with primary hyperaldosteronism, severe refractory hypertension, and normal to high normal PRA levels whose aldosterone/renin ratios were still elevated because of disproportionately high aldosterone levels. All available medical data on the patients as well as publications on the aldosterone/renin relationship in primary hyperaldosteronism were reviewed to explain the unusual findings. In one patient, histologically proven renal arteriolosclerosis was the probable cause of the escape of PRA from suppression by an aldosterone-producing adenoma. In the other two patients, hypertensive kidney damage due to primary hyperaldosteronism was the most likely explanation for the inappropriately high PRA, as in patient 1. All patients had high normal or slightly elevated serum creatinine levels and responded to 200 mg spironolactone/day with increased serum creatinine and hyperkalemia. hyperkalemia was probably due to a decreased filtered load of sodium and a spironolactone-induced decrease in mineralocorticoid function. Two patients were cured of hyperaldosteronism by unilateral adrenalectomy but still need some antihypertensive therapy, whereas one patient has probable bilateral adrenal disease, with normal blood pressure on a low dose of spironolactone. In patients with severe hypertension due to primary hyperaldosteronism, PRA can escape suppression if hypertensive kidney damage supervenes. An increased aldosterone/PRA ratio is still useful in screening for primary hyperaldosteronism. These patients may respond to spironolactone therapy with a strong increase in serum creatinine and potassium. Early specific treatment of primary hyperaldosteronism is therefore indicated, and even a patient with advanced hypertension will profit from adrenalectomy or cautious spironolactone treatment.
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10/179. role of lipids in the progression of renal disease in systemic lupus erythematosus patients.

    Systemic lupus erythematosus (SLE) is an autoimmune connective tissue disease marked by immune-complex mediated lesions in small blood vessels of various organs, especially the kidneys, although other factors may also be implicated in the pathogenesis of the disease. This article focuses on the role of lipids in the progression of glomerular, vascular and tubulo-interstitial lesions in two patients with lupus nephritis associated with pronounced hyper- and dyslipidemia. The pathogenesis of progressive glomerulosclerosis in both patients appears to be multifactorial. In addition to immune complex mediated lupus glomerulonephritis, progressively active in the first patient, severe nephrotic-range persistent proteinuria, arterial hypertension associated with hyperfiltration and hyperperfusion injuries and, to a minor extent, hyper- and dyslipidemia were observed. Immunological and non-immunological factors were shown to contribute to the development of tubulo-interstitial lesions. In both patients, in addition to local immune deposits, prominent tubulo-interstitial lipid deposits were probably causally related to both hyperlipidemia and the increased permeability of the glomerular filtration barrier. Tubular lesions were highlighted by intracytoplasmic lipid droplets as well as small cleft-like spaces found to be impacted in the tubular lumina. They were seen to penetrate tubular epithelial cells and eventually lodge in the interstitium, surrounded by mononuclear cell infiltrates and foam cells. In both patients, hypertensive angiopathy and extraglomerular vascular immune deposits were demonstrated. In addition, in the second patient, arteriolar and small arterial hyaline was found at the age of 28 years to be full of lipids and calcium precipitates, suggesting a peripheral atherosclerosis-like process which never occurs as a natural age-related condition. In conclusion, all parts of the nephron may be involved in the pathogenetic process causally related or influenced by hyper- or dyslipidemia. Associated either with endothelial cell injury and consequent insudation of lipids in the vascular walls, glomerular filtration barrier injury with hyperfiltration, or tubulo-interstitial lipid deposition, the mechanism of tissue damage by lipids in all parts of the nephron shares similarities with the pathogenesis of systemic atherosclerosis.
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