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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An elevated urinary albumin excretion (termed microalbuminuria) has been proposed as a predictor for later development of clinical diabetic nephropathy (hypertension, falling glomerular filtration rate [GFR], and urinary albumin excretion greater than 300 mg/24 h). However, review of the original reports on the predictability of microalbuminuria revealed a concomitant presence of elevated BP and a propensity to falling GFR. Thus, the predictability of microalbuminuria rests on the added evaluation of BP and GFR. Additional investigation is needed to address the possibility that microalbuminuria and either a rising BP or a falling GFR or both indicates established diabetic nephropathy rather than predicting its development.
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PMID:The predictive value of microalbuminuria. 291 61

Chronic renal failure is frequently associated with volume overload, resulting in hypertension and, in some cases, congestive heart failure. Atriopeptin III (AP III), a 24-amino acid atrial peptide, is a potent vasodilator and natriuretic/diuretic agent in normal rats. An infusion of AP III at 0.2 microgram/kg per min for 60 min produced dramatic responses in animals with chronic renal failure (5/6 nephrectomy 4 wk before study). Systemic blood pressure fell 20% by the end of infusion. A pronounced rise in glomerular filtration rate (24%) was maintained during the infusion period when urine flow rate was stable (35-60 min), even though renal blood flow was unchanged from base line. Urinary volume increased 4.4-fold and sodium excretion increased 9 to 12-fold during the infusion. Fractional excretion of sodium ranged between 9 and 15% in those animals whose initial GFR values were lower than 0.5 ml/min. We conclude that AP III is a potent natriuretic/diuretic agent in rats with reduced renal mass, presumably exerting that effect predominantly through increases in GFR. This agent may well be useful in the treatment of volume overload in patients with chronic renal failure.
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PMID:Atriopeptin III. A potent natriuretic, diuretic, and hypotensive agent in rats with chronic renal failure. 293 12

Two hundred nine hypertensive patients with high stimulated plasma renin levels were screened for renovascular hypertension using Tc-99m DTPA renal scintigraphy. Differential glomerular filtration rate (Diff-GFR) was obtained by integrating the area under the background-subtracted renogram of each kidney between 1 and 3 minutes. 50 patients who also had undergone selective renal angiography were divided into four groups according to Diff-GFR contribution by one of the kidneys. If one kidney contributed 45-50% of total GFR, this was regarded as normal. A Diff-GFR of less than 45% was very considered to be very suggestive of renovascular hypertension in the appropriate clinical setting, while a Diff-GFR of less than 20% indicated that the renal artery might not be amenable to successful balloon angioplasty. Diff-GFR following balloon angioplasty closely reflected the early clinical response of the patients--and in some cases progressive Diff-GFR improvement was observed several months later. Diff-GFR as a scintigraphic criterion for renovascular hypertension has a sensitivity of 93%, specificity of 74%, and accuracy of 85%.
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PMID:Differential glomerular filtration rate in diagnosis of renovascular hypertension and follow-up of balloon angioplasty. 293 97

Twenty-five years after the discoveries of the existence of atrial granules and of volume receptors in the heart atria the search for natriuretic hormones has led to the isolation and identification of the atrial natriuretic factors (ANF) now considered as a hormonal system. These peptides are probably synthesized and stored in the Golgi apparatus of cardiac myocytes and are released in response to atrial wall stretch following acute plasma volume expansion and increased central blood volume, e.g., during head-out water immersion, in arterial hypertension, or increased left and/or right atrial pressure in cardiac failure, but also possibly in response to increased frequency of myocardial contractions, e.g. in paroxysmal tachycardia. The mechanisms of the renal action of these potent natriuretic hormones are not yet precisely known. Increased GFR may contribute to the initial rise in urinary sodium excretion and increased renal medullary blood flow to the later phase of natriuresis. The proximal tubule, the thin descending and the ascending limb of Henle's loop and especially the medullary collecting tubule were so far incriminated as tubular sites of action of ANF. Finally, recycling of sodium in medullary tissue and secretion of sodium via back-flux from the interstitium into the medullary collecting tubule are postulated to result in the hypernatric urine observed after ANF administration. Direct suppression of the secretion of renin, aldosterone, vasopressin, and vasopressin-stimulated cAMP synthesis may also contribute to its diuretic, natriuretic, and antihypertensive effects. The renal hemodynamic and tubular as well as the adrenal and systemic vascular effects are related to enhanced cGMP synthesis in medium-sized arterial vessels, in glomeruli and specific tubular segments, and in adrenal tissue, and may be calcium dependent. Specific ANF-binding sites were detected in these target organs. Although increased ANF release was observed in response to atrial distension in various disease states, which may contribute to renal sodium elimination in human hypertension and congestive heart failure, further studies are needed to identify its precise physiological and pathophysiological significance.
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PMID:Atrial natriuretic hormones--thirty years after the discovery of atrial volume receptors. 294 41

This prospective, double-blind, multicenter study compared enalapril plus hydrochlorothiazide with standard triple therapy (STT; hydrochlorothiazide, timolol, and hydralazine) with regard to safety, tolerability, antihypertensive efficacy, and effect on renal function in 75 patients with documented renovascular hypertension. Both groups showed a significant mean decrease in systolic and diastolic blood pressure during the double-blind study, with the enalapril group showing a mean 12 mm greater decrease in systolic blood pressure as compared to STT (less than 0.05). Effective treatment of diastolic hypertension was noted in 96% of the enalapril group as compared to 82% on STT (p less than 0.05). STT failure was seen exclusively in patients with bilateral renal artery stenosis of high grade and frequently in association with impaired renal function. cPAH, a measure of effective renal plasma flow, showed a significant increase in the enalapril group, as compared to the STT (p less than 0.05). In contrast, there was a bimodal response of CIn (GFR): 80% of patients in the enalapril group showed no significant change while 20% (10 patients) showed a mean decrease of 28% along with a 12% increase in CPAH (p less than 0.01). No acute renal failure or toxic side effects were noted in the enalapril group. Enalapril plus hydrochlorothiazide is very effective in treating renovascular hypertension and is without significant toxic side effects. The self-limited increase in serum creatinine seen in 20% of renovascular hypertensive patients receiving enalapril and hydrochlorothiazide may identify a subset of patients with unilateral or bilateral high grade renal artery stenosis who should be treated with angioplasty or operative intervention.
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PMID:A comparison of enalapril plus hydrochlorothiazide with standard triple therapy in renovascular hypertension. 301 2

It has been suggested that AII-mediated renal mechanisms limit the efficacy of moderate sodium restriction in the lowering of blood pressure (BP) in hypertension. We therefore studied renal hemodynamics and sodium handling in nine essential hypertensives in balance on 200 and on a 50 mmol sodium diet, before and during ACE-inhibition (enalapril 10 mg bid for 8 days) in a cross-over fashion. BP was similar on 50 and 200 mmol Na before enalapril, the fall in BP during enalapril was significantly more pronounced on 50 mmol Na. On 50 mmol Na, GFR and filtered Na were significantly lower, and tubular reabsorption was significantly higher than on 200 mmol Na. GFR increased during enalapril in 50 but not on 200 mmol Na. Consequently, the differences in GFR and filtered load elicited by sodium restriction were no longer present during ACE-inhibition. In contrast, the differences in tubular reabsorption between 50 and 200 mmol Na persisted during enalapril. In conclusion, moderate sodium restriction, not affecting BP, can elicit a renal hemodynamic response. As this response is blunted by ACE-inhibition it is probably mediated by AII. This blunting may contribute to the increased sodium sensitivity of BP during ACE-inhibition. The adaptation of tubular sodium reabsorption is not affected by ACE-inhibition.
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PMID:Moderate sodium restriction in hypertensive subjects: renal effects of ACE-inhibition. 303 89

Physiologic and morphologic techniques were used to study kidneys of cardiac transplant recipients treated with either low-dose (low-CsA) or high-dose (high-CsA) cyclosporine. After 12 months both low-CsA (4.6 +/- 0.4) and high-CsA (6.3 +/- 0.3 mg/Kg/24 hr, p less than 0.01) were associated with azotemia and hypertension; GFR with each regimen was depressed below values in a third group treated without CsA (no-CsA) by 40-47%, while corresponding renal vascular resistance was elevated greater than 2-fold (P less than 0.01). Morphologic changes in both CsA groups included an obliterative arteriolopathy with downstream collapse or sclerosis of glomeruli. Determination of renal arcuate vein occlusion pressure revealed an increasing renal artery-to-peritubular capillary pressure gradient between 1 and 12 months of CsA therapy. Fractional clearances of dextrans of graded size were elevated at each time compared with the no-CsA group. Analysis of dextran transport with an isoporous membrane model indicates that transglomerular hydraulic pressure difference (delta P) approximated 39 with no-CsA, but was reduced with low-CsA therapy to about 30 at 1 month, and about 34 mmHg after 12 months. We conclude that chronic CsA therapy induces constriction and eventual occlusion of afferent arterioles, causing downstream glomerular damage that is irreversible. Low versus high dosage of CsA confers only marginal protection against this serious microvascular injury.
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PMID:Chronic injury of human renal microvessels with low-dose cyclosporine therapy. 305 92

We propose herein that there are two functionally abnormal nephron populations in essential hypertension: (1) a group of ischemic nephrons with impaired sodium excretion which chronically hypersecrete renin. Numerically, these ischemic nephrons comprise a minor subgroup since most patients with essential hypertension exhibit no overt evidence of renal insufficiency. (2) In reaction to this, a more numerous group of normal nephrons appears in adaptive hypernatriuresis. They have an increased distal sodium supply and consequently, a chronically suppressed renin secretion. One difference between patients with renovascular hypertension and those with essential hypertension is the intermingling of these two populations of nephrons. In our hypothesis, the adapting hyperfiltering normal nephrons accomplish the hypernatriuresis in response to saline infusion, that is characteristic of all essential hypertension. However, the unsuppressed secretion of renin, that arises from the ischemic nephron population attenuates this compensatory natriuresis in the following ways: (1) by inappropriately acting on the hyperfiltering nephrons to enhance proximal tubular sodium reabsorption; (2) by activating TGF-mediated afferent constriction in these nephrons, and (3) simultaneously, the reactive secretion of renin from ischemic nephrons is diluted by non-participation of the adapting hypernatriuretic nephrons so that plasma renin settles at a level which is insufficient to fully compensate GFR in the ischemic nephrons. These adaptive responses provide a basis for the observation that the inhibition of renin activity with converting enzyme inhibitors in essential hypertension increases renal blood flow and sodium excretion. They also explain why converting enzyme inhibitors can effectively reduce blood pressure, even when renin levels are not absolutely elevated, since any circulating renin imposed upon the adapting hypernatriuretic nephrons inappropriately impairs their sodium excretion. In addition, the theory explains why basal renin secretion is either not suppressed or inadequately suppressed in patients with essential hypertension. As a result, whole kidney homeostatic function is compromised because individual nephrons are responding to their individual stimuli to fulfil their individual need, rather than acting in concert with other nephrons. The net effect of this uncoordinated response is to shift total renal function so that systemic arterial hypertension is sustained by abnormal sodium retention for the inappropriately high plasma renin level, or vice versa.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:On the renal basis for essential hypertension: nephron heterogeneity with discordant renin secretion and sodium excretion causing a hypertensive vasoconstriction-volume relationship. 305 95

The activation of the renin angiotensin system is thought to be an important factor contributing to hypertension following kidney transplantation (TX). We studied 21 hypertensive renal transplant recipients, without evidence of acute graft rejection or transplant artery stenosis, 6 to 60 months post-TX. The acute responses of mean arterial pressure (MAP) and renal hemodynamics (ERPF: effective renal plasma flow, 131I-Hippuran clearance) and function (GFR: glomerular filtration rate, creatinine clearance; UNaV: urinary sodium excretion rate) to converting enzyme inhibition (CEI) by captopril were assessed. CEI induced a decrease in MAP (118 +/- 2 to 110 +/- 2 mmHg), renal resistance (RR: 0.27 +/- 0.02 to 0.21 +/- 0.01) and filtration fraction (FF: 0.31 +/- 0.02 to 0.23 +/- 0.01). ERPF (307 +/- 24 to 333 +/- 18 ml/min/1.73 m2) and GFR (88 +/- 5 to 78 +/- 5 ml/min/1.73 m2) were not significantly changed. UNaV increased by 53 +/- 24 mumol/min. Changes in MAP (r = -0.66), ERPF (r = 0.74) and FF (r = -0.88) were significantly correlated with the log of control plasma renin activity (PRA). In 10 patients with an increase of ERPF (range: + 30 to + 70%) and no change in GFR, the activated renin system could originate from the recipient's own kidneys. In the remaining 11 patients, CEI was associated with no increase in ERPF (change: + 2 to - 27%) and a fall in GFR, a response suggesting a possible intrarenal vascular damage. These results indicate that RAS participates in the regulation of systemic and renal vascular tone, with a possible predominant effect on efferent glomerular arteriole.
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PMID:[Effect of inhibition of angiotensin converting enzyme on hypertension following kidney transplantation]. 309 12

Long-term follow-up is presented of 73 patients suffering from the haemolytic-uraemic syndrome 10 years after the acute initial illness. The patients were subdivided into three groups, according to the criteria proposed by Gianantonio and based on the duration of oliguria and/or anuria. Four out of 38 patients belonging to the first group (oliguria for less than 7 days) had a slightly increased blood pressure as the only sequela. Two patients out of group two (n = 29, oliguria for 7-14 days or anuria for less than 7 days) had a diminished GFR and a reduced concentrating capacity, some proteinuria, and mild hypertension. Five other patients had slight proteinuria (less than 500 mg/24 h) and one of them a mild hypertension. All six patients belonging to the third group (oliguria for more than 14 days or anuria for more than 7 days) had late sequelae: two started haemodialysis more than 10 years after the initial phase; three have a decreased GFR and concentrating capacity. The unique remaining patient with a normal GFR without hypertension has a decreased concentrating capacity. The importance of careful treatment in children with a decreased GFR 2 years after the initial phase is stressed.
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PMID:Haemolytic-uraemic syndrome: a 10-year follow-up study of 73 patients. 314 Jan 21


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