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

Renal perfusion pressure was servo-controlled chronically in rats to quantify the relative contribution of elevated arterial pressure versus angiotensin II (Ang II) on the induction of renal injury in Ang II-induced hypertension. Sprague-Dawley rats fed a 4% salt diet were administered Ang II for 14 days (25 ng/kg per minute IV; saline only for sham rats), and the renal perfusion pressure to the left kidney was continuously servo-controlled to maintain a normal pressure in that kidney throughout the period of hypertension. An aortic occluder was implanted around the aorta between the two renal arteries and carotid and femoral arterial pressure were measured continuously throughout the experiment to determine uncontrolled and controlled renal perfusion pressure, respectively. Renal perfusion pressure of uncontrolled, controlled, and sham kidneys over the period of Ang II or saline infusion averaged 152.6+/-7.0, 117.4+/-3.5, and 110.7+/-2.2 mm Hg, respectively. The high-pressure uncontrolled kidneys exhibited tubular necrosis and interstitial fibrosis, especially prominent in the outer medullary region. Regional glomerular sclerosis and interlobular artery injury were also pronounced. Controlled kidneys were significantly protected from interlobular artery injury, juxtamedullary glomeruli injury, tubular necrosis, and interstitial fibrosis as determined by comparing the level of injury. Glomerular injury was not prevented in the outer cortex. Transforming growth factor (TGF)-beta and active NF-kappaB proteins determined by immunohistochemistry were colocalized in the uncontrolled kidney in regions of interstitial fibrosis. We conclude that the preferential juxtamedullary injury found in Ang II hypertension is largely induced by pressure and is probably mediated through the TGF-beta and NF-kappaB pathway.
Hypertension 2004 Apr
PMID:Role of pressure in angiotensin II-induced renal injury: chronic servo-control of renal perfusion pressure in rats. 1496 28

The use of herbal therapy has increased dramatically in past years and may lead to renal injury or various toxic insults, especially in renal patients. In most countries, herbal products are not regulated as medicines. Herbal poisoning may be secondary to the presence of undisclosed drugs or heavy metals, interaction with the pharmacokinetic profile of concomitantly administered drugs, or association with a misidentified herbal species. Various renal syndromes were reported after the use of medicinal plants, including tubular necrosis, acute interstitial nephritis, Fanconi's syndrome, hypokalemia or hyperkalemia, hypertension, papillary necrosis, chronic interstitial nephritis, nephrolithiasis, urinary retention, and cancer of the urinary tract. It seems critical that caregivers be aware of the potential risk of such often underreported therapy and carefully question their patients about their use of this popular branch of alternative medicine.
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PMID:Herbs and the kidney. 1521 32

Hypercalcemia can result from excessive bone resorption, renal calcium retention, excessive intestinal calcium absorption, or a combination of these conditions. Hypercalcemia may also provoke acute renal failure (ARF) or hypertension, or aggravate the tubular necrosis that is frequently found in cases of ARF. The association of ARF and hypercalcemia was studied retrospectively in eight patients based in the data in their charts. Data are expressed as median and percentile (25th; 75th). Our results show that ARF associated with hypercalcemia was related with comorbidity in all cases (cancer, multiple myeloma, hyperparathyroidism, sarcoidosis, vitamin D intoxication, and leprosy). Maximum median serum creatinine levels were 3.3 mg/dL (2.7, 3.8 mg/dL) before treatment and 1.1 mg/dL (0.9, 1.3 mg/dL) after treatment. Maximum total median serum calcium was 15.9 mg/dL (13.5, 19.8 mg/dL) before treatment and 9.1 mg/dL (8.4, 9.7 mg/dL) after treatment. Maximum median ionized serum calcium was 2.1 mmol/L (1.8, 2.2 mmol/L) before treatment and 1.1 mmol/L (1.0, 1.2 mmol/L) after treatment. Different kinds of treatment induced a rapid fall in serum calcium concentration. All patients were treated with hydration and diuretics, and three patients also received calcitonin. Serum creatinine concentration always fell simultaneously with the decrease in serum calcium in all cases. All patients progressed with nonoliguric renal failure. In conclusion, in ARF, patients are frequently hypocalcemic. Usually, the presence of hypercalcemia associated with ARF is indicative of the presence of comorbidity, as observed in all eight patients studied here. There was an improvement of renal function in all cases as serum calcium levels decreased.
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PMID:Acute renal failure and hypercalcemia. 1653 74

Hypertension is associated with increased levels of oxidative stress and medullary renal injury. Previous studies have shown that elevations in renal perfusion pressure increase Na(+) delivery to the medullary thick ascending limb (mTAL), and enhancement of NaCl transport in the outer medulla has been reported in many experimental forms of hypertension. This study examined the effects of increased Na(+) and fluid delivery in mTAL perfused in vitro on the generation of superoxide. Osmolality was maintained constant between low- and high-Na(+) perfusates by adjusting with choline Cl(-). Real-time fluorescent microscopic techniques were used to determine the generation of superoxide and nitric oxide in individual mTAL cells using dihydroethidium and DAF-FM dyes, respectively. Increasing the Na(+) concentration of the perfusate from 60 to 149 mM or luminal flow rate from 5 to 20 nl/min (with fixed Na(+) concentration of 60 mM) significantly increased superoxide generation and decreased nitric oxide in mTAL. These effects were inhibited when active transport of Na(+) was inhibited by ouabain. We conclude that increases in luminal Na(+) concentration and/or flow rate can increase the generation of superoxide in mTAL and reduce nitric oxide bioavailability. This may lead to reduction in medullary blood flow and promote hypoxia and tubular necrosis within the renal medulla during in hypertension.
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PMID:Effect of sodium delivery on superoxide and nitric oxide in the medullary thick ascending limb. 1659 9

We investigated the role of angiotensin II and endothelin-1 using the angiotensin AT1 receptor antagonist losartan and the endothelin ETA receptor antagonist atrasentan, in malignant hypertension and renal failure and damage induced by nitric oxide (NO) synthase inhibition in Harlan Sprague-Dawley (SD) rats. We also evaluated whether the protective effects of losartan go beyond the blood pressure reduction. Within only 3 weeks of treatment with the NO synthase inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME), Harlan SD rats developed malignant hypertension with renal failure and injuries. The latter were comprised of fibrinoid necrosis of small arteries and glomerular and tubular necrosis. Although both losartan and atrasentan attenuated the development of hypertension and renal failure, losartan only prevented the renal damage. In contrast to antrasentan, the vasodilator hydralazine reduced blood pressure and prevented the renal injuries similar to losartan. However, when these treatments were prolonged to 5 weeks, losartan, but not hydralazine, was still effective in reducing renal failure and damage, despite a marked increase in blood pressure. Our results indicate that angiotensin II and endothelin-1 play a differential role in the pathogenesis of malignant hypertension and in vascular and renal damage induced by L-NAME in Harlan SD rats. Although the protective effects of atrasentan may depend on the reduction of blood pressure, which was shown to retard the development of renal injury using hydralazine, those of losartan go beyond the blood pressure reduction. Hence, tissue protective effects of angiotensin AT1 receptor blockade may be pivotal for long-term vascular and renal protection.
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PMID:Protective effects of angiotensin AT1 receptor blockade in malignant hypertension in the rat. 1932 69

The susceptibility to renal perfusion pressure (RPP)-induced renal injury was investigated in angiotensin II (Ang II)- versus norepinephrine (NE)-infused hypertensive rats. To determine the magnitude of RPP-induced injury, Sprague-Dawley rats fed a 4% salt diet were instrumented with a servocontrolled aortic balloon occluder positioned between the renal arteries to maintain RPP to the left kidney at baseline levels whereas the right kidney was exposed to elevated RPP during a 2-week infusion of Ang II IV (25 ng/kg per minute), NE IV (0.5, 1.0, and 2.0 microg/kg per minute on days 1, 2, and 3 to 14, respectively), or saline IV (sham rats). Over the 14 days of Ang II infusion, RPP averaged 161.5+/-8.0 mm Hg to uncontrolled kidneys and 121.9+/-2.0 mm Hg to servocontrolled kidneys. In NE-infused rats, RPP averaged 156.3+/-3.0 mm Hg to uncontrolled kidneys and 116.9+/-2.0 mm Hg to servocontrolled kidneys. RPP averaged 111.1+/-1.0 mm Hg to kidneys of sham rats. Interlobular arterial injury and juxtamedullary glomerulosclerosis were largely RPP dependent in both models of hypertension. Superficial cortical glomerulosclerosis was greater and RPP dependent in NE- versus Ang II-infused rats, which was primarily independent of RPP. Outer medullary tubular necrosis and interstitial fibrosis were also primarily RPP dependent in both models of hypertension; however, the magnitude of injury was exacerbated in Ang II-infused rats. We conclude that elevated RPP is the dominant cause of renal injury in both NE- and Ang II-induced hypertensive rats and that underlying neurohumoral factors in these models of hypertension alter the pattern and magnitude of RPP-induced renal injury.
Hypertension 2009 Dec
PMID:Pressure-induced renal injury in angiotensin II versus norepinephrine-induced hypertensive rats. 1985 6

Postischemic acute renal failure is worsened when occurs in a various conditions with impaired nitric oxide (NO) synthesis, such as arterial hypertension. Reoxygenation itself increases ischemic injury through the massive production of oxygen-free radicals. Therefore, we have directed our investigations to effects of both NO donor and antioxidant treatment on course of acute renal failure in experimental hypertension. Experiments were performed in anesthetized, adult male spontaneously hypertensive rats. In ARF groups the right kidney was removed, and rats were subjected to renal ischemia by clamping the left renal artery for 40 min. Experimental group received NO donor L-arginine (2 g/kg b.m.) (LArg group), or oxidant scavenger vitamin C (100 mg/kg b.m.) (Vit C group) during 3 days before the period of ischaemia. All parameters were measured 24 h after reperfusion. The mean arterial pressure was markedly reduced and renal vascular resistance significantly dropped in the ARF+L-Arg group vs. ARF group. Tubular injuries were similar between the ARF+L-Arg and ARF groups. Intensity of tubular necrosis and dilatation was markedly reduced in ARF+Vit C group in comparison to ARF. L-arginine failed to reduce tubular injury, despite its evident improvement of systemic and renal haemodynamic, thus NO seems to act as a double-egged sword, but reduction of tubular injury promotes vitamin C as an effective chemoprotectant against ishemia-reperfusion tubular injury in hypertension.
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PMID:Comparative effects of L-arginine and vitamin C pretreatment in SHR with induced postischemic acute renal failure. 1989 87

Objective. Uncertainty has arisen as to whether renal function can be recovered from after long-term regular dialysis treatment. We therefore conducted an analysis and scrutinized one patient report. Material and Methods. Swedish registry of patients with kidney disease and one patient case. Results. 39 patients (0.2%) from the Swedish registry comprising 17590 patients who commenced RRT (renal replacement therapy) between 1991 and 2008 had recovered from renal function after more than 365 days of regular dialysis treatment. The most common diagnosis was renovascular disease with hypertension but a large group had uremia of unknown cause. HUS, cortical/tubular necrosis, and autoimmune diseases were also found. The mean treatment time before withdrawal was 2 years. Conclusions. A small number of patients recover after a long period of regular dialysis treatment. One could discuss whether it is difficult to identify patients who have recovered while undergoing regular dialysis treatment. Regular monitoring of renal function may be important.
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PMID:Recovery of renal function after one-year of dialysis treatment: case report and registry data. 2118 40

All types of acute kidney injury (AKI) (functional /pre-renal, parenchymal/intra-renal, obstructive/post-renal) result in a sharp drop of the glomerular filtration rate, with variable reversibility according to the initial cause. In one case out of five, drug intake can be related to the onset of AKI. Antibiotics, analgesics and nonsteroidal anti-inflammatory drugs, angiotensin converting enzyme inhibitors and angiotensin II receptor antagonists are the agents mostly involved, as well as iodinated radio-contrast agents. Mechanisms are often complex: toxic cellular effect directed on a nephron segment (tubular necrosis) associated or not with intraglomerular hemodynamic changes, or immune process leading to acute tubule-interstitial nephritis. Each underlying risk factor (age > 60 year, cardiac or hepatic failure, hypertension, diabetes, intra-vascular volume depletion, preexisting or unknown chronic kidney disease) must be taken into consideration by the prescribing physician because it reduces the chance of functional recovery and worsens the renal and the overall prognosis. A pre-renal additional component is often present and avoidable thanks to a strict hemodynamic monitoring. The present article summarizes some recent physiopathological aspects of AKI and makes the link between clinical situations and currently prescribed drugs. Lessons from the radio-contrast induced nephropathy are examined by taking into account prevention aspects and risk factors screening. An effective collaboration between the general practitioner and the nephrologist would benefit in optimizing the treatment of difficult cases.
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PMID:[Acute kidney injury and drug-induced nephropathies]. 2203 61

The reactive oxygen species take role in pathogenesis of many diseases including hypoxia, hypercholesterolemia, atherosclerosis, nephropathy, hypertension, ischemia-reperfusion damage, and heart defects. The aim of this study was to evaluate whether crocin administration could protect kidney injury from oxidative stress in streptozotocin-induced diabetic rats. The rats were randomly divided into 3 groups each containing 10 animals as follows: group 1, control group; group 2, diabetes mellitus (DM) group; and group 3, DM + crocin group. At the end of the study, trunk blood was collected to determine the plasma levels of blood urea nitrogen (BUN) and creatinine (Cr). The kidney tissue was removed, and biochemical and histological changes were examined. Diabetes caused a significant increase in malondialdehyde (MDA) and xanthine oxidase (XO) activities and a decrease in glutathione (GSH) contents (p < 0.01) when compared with control group in the rat kidneys. Crocin given to DM rats significantly decreased MDA (p < 0.01) and XO (p < 0.05) activities and elevated GSH (p < 0.05) contents when compared with DM group. Plasma levels of BUN and Cr were significantly higher in the DM group when compared with the control group (p < 0.01). Pretreatment of the DM animals with crocin decreased the high level of serum Cr and BUN. Control group was normal in histological appearance, but congestion, severe inflammation, tubular desquamation, tubular necrosis, and hydropic degeneration in tubular cells were observed in the DM group. Histopathological changes markedly reduced, and appearance of kidney was nearly similar to control group in DM + crocin group. Our results show that crocin could be beneficial in reducing diabetes-induced renal injury.
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PMID:Protective effects of saffron (its active constituent, crocin) on nephropathy in streptozotocin-induced diabetic rats. 2492 68


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