11/365. Detection of renovascular hypertension: saralasin test versus renin determinations.Angiotensin blockade was established in hypertensive patients with the competitive inhibitor saralasin and the blood pressure response was compared to prior renin determinations. Two patients with subsequently confirmed renovascular hypertension had normal peripheral renin and non-lateralizing renal vein renin ratios, yet both showed a clear-cut lowering of blood pressure after administration of the blocking agent, indicating the presence of renin-mediated hypertension. Thus, direct in vivo testing with saralasin appears to offer certain advantages over renin determinations.- - - - - - - - - - ranking = 1keywords = hypertension (Clic here for more details about this article) |
12/365. 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 = 0.33333333333333keywords = hypertension (Clic here for more details about this article) |
13/365. Coexistence of atherosclerotic renal artery stenosis with primary hyperaldosteronism.The discovery of two forms of secondary hypertension in the same patient is unusual and suggests similar pathophysiological mechanisms, a predisposition to one type in the presence of the other or a chance occurrence. We describe two patients with renal artery stenosis who after successful correction of the stenotic lesions were discovered to have primary hyperaldosteronism associated with bilateral adrenal hyperplasia. Initially prior to revascularisation of the renal artery stenosis, the diagnosis of primary hyperaldosteronism was not evident. Both patients were subjected to further diagnostic evaluation after the appearance of hypokalaemia in one patient and continued resistant hypertension in both patients. The addition of spironolactone therapy reduced blood pressure impressively in both patients. Clinicians should be aware of the possibility that these two forms of secondary hypertension may be present in the same patient and that optimal blood pressure control requires diagnostic assessment and intervention for both disorders.- - - - - - - - - - ranking = 0.5keywords = hypertension (Clic here for more details about this article) |
14/365. Gross hematuria secondary to renal vein hypertension from unilateral retroperitoneal fibrosis.We report the first case of localized, unilateral, idiopathic retroperitoneal fibrosis encasing the left renal vein, which resulted in secondary renal vein hypertension. The patient presented with sudden and dramatic gross hematuria. Surgical release and excision of the surrounding localized retroperitoneal fibrosis resulted in prompt resolution of the hematuria.- - - - - - - - - - ranking = 0.83333333333333keywords = hypertension (Clic here for more details about this article) |
15/365. Marsupialization for bilateral pararenal lymphatic cysts.A case of bilateral pararenal lymphatic cysts associated with hypertension is described. The cysts surrounded the renal parenchyma and were located underneath the renal capsule. No vascular pathology explaining the cause of hypertension was diagnosed by radiological techniques. hypertension improved following bilateral marsupialization.- - - - - - - - - - ranking = 0.33333333333333keywords = hypertension (Clic here for more details about this article) |
16/365. hypertension-hyponatremia syndrome in neonates: case report and review of literature.hypertension hyponatremia syndrome occurred in a 32-week male neonate following septicemic shock on Day 9. The systolic blood pressure rose from 60 to 85 mmHg as the serum sodium dropped from 136 to 121 mmol/L associated with natriuresis, polyuria, and dehydration. Convulsions occurred at a systolic blood pressure of 102 mmHg. Investigations for hypertension revealed hyper-reninemia without cardio/renovascular or neuroendocrine abnormalities. Salt supplementation and antihypertensive therapy with captopril led to resolution of natriuresis and hyponatremia. review of literature revealed associated renovascular pathology in all neonatal cases of the syndrome reported so far. Renal ischemia from possible renal microthrombi may have been the triggering event in our case. Decline in renin levels during follow-up favors this hypothesis.- - - - - - - - - - ranking = 0.16666666666667keywords = hypertension (Clic here for more details about this article) |
17/365. 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.- - - - - - - - - - ranking = 0.5keywords = hypertension (Clic here for more details about this article) |
18/365. 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.- - - - - - - - - - ranking = 1.3333333333333keywords = hypertension (Clic here for more details about this article) |
19/365. 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.- - - - - - - - - - ranking = 0.5keywords = hypertension (Clic here for more details about this article) |
20/365. 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.- - - - - - - - - - ranking = 0.16666666666667keywords = hypertension (Clic here for more details about this article) |
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