Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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

Hypokalemia is a common electrolyte abnormality encountered in clinical practice. It can be identified in an asymptomatic patient undergoing routine electrolyte screening or can manifest itself as part of a number of functional abnormalities in a variety of organs and systems. Among the most commonly recognized complications are profound effects on the cardiovascular and neuromuscular systems, together with abnormalities in acid-base regulation. In humans, hypokalemia contributes to the development of hypertension and predisposes patients to a variety of ventricular arrhythmias, including ventricular fibrillation. Commonly recognized neuromuscular complications include weakness, cramping, and myalgia. Hypokalemia also affects systemic acid-base homeostasis by interfering with multiple components of the renal acid-base regulation and is a frequent cause of metabolic alkalosis. Less known, however, is the role of potassium deficiency in causing progressive renal failure. In animals, potassium deficiency stimulates renal enlargement because of cellular hypertrophy and hyperplasia. If potassium deficiency persists, interstitial infiltrates appear in the renal interstitial compartment, and eventually tubulointerstitial fibrosis develops. In humans, longstanding hypokalemia is associated with the development of renal cysts, chronic interstitial nephritis, and progressive loss of renal function, the so-called hypokalemic nephropathy. This review focuses on the potential mechanisms involved in the development of the hypokalemic nephropathy with emphasis on the role of ammonia and growth factors in its pathogenesis.
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PMID:The role of growth factors and ammonia in the genesis of hypokalemic nephropathy. 1210 12

Recent evidence suggests that salt-sensitive hypertension develops as a consequence of renal infiltration with immunocompetent cells. We investigated whether proteinuria, which is known to induce interstitial nephritis, causes salt-sensitive hypertension. Female Lewis rats received 2 g of BSA intraperitoneally daily for 2 wk. After protein overload (PO), 6 wk of a high-salt diet induced hypertension [systolic blood pressure (SBP) = 156 +/- 11.8 mmHg], whereas rats that remained on a normal-salt diet and control rats (without PO) on a high-salt diet were normotensive. Administration of mycophenolate mofetil (20 mg. kg(-1). day(-1)) during PO resulted in prevention of proteinuria-related interstitial nephritis, reduction of renal angiotensin II-positive cells and oxidative stress (superoxide-positive cells and renal malondialdehyde content), and resistance to the hypertensive effect of the high-salt diet (SBP = 129 +/- 12.2 mmHg). The present studies support the participation of renal inflammatory infiltrate in the pathogenesis of salt-sensitive hypertension and provide a direct link between two risk factors of progressive renal damage: proteinuria and hypertension.
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PMID:Overload proteinuria is followed by salt-sensitive hypertension caused by renal infiltration of immune cells. 1237 90

The article is concerned with the effects of specific cyclooxygenase-2 (COX-2) inhibitors and their relationship to thrombotic cardiovascular events and to renal disease. Clinical and experimental aspects of COX-2-specific inhibitors are cited. A COX-2 inhibitor, celecoxib, interferes with myocardial prostacyclin production and also produces hypertension. Data have shown that in animal experiments, celecoxib also lowers myocardial prostaglandin concentration but fails to inhibit thromboxane concentration to the same degree. In the kidney, celecoxib can result in glomerular and interstitial nephritis or papillary necrosis. As in infarcted heart muscle, the COX-2-specific inhibitor celecoxib causes a significant decline in prostaglandin in the renal medulla. It was concluded from both clinical and experimental findings that COX-2 inhibitors can cause thrombotic cardiovascular events as well as renal disease. For these reasons, care should be exercised in administering specific COX-2 inhibitors to patients with pre-existing cardiac or renal disease.
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PMID:Cyclooxygenase-2 inhibitors: is there an association with coronary or renal events? 1257 96

The commonest clinical presentation of both immunoalergic interstitial nephritis (IIN) and atheroembolic renal disease (ATD) is an acute renal failure accompanied by skin lesions and eosinophilia. As a consequence, differential diagnosis between both entities is often very difficult. We have performed a comparative retrospective study of those patients diagnosed as having IIN or ATD in our Hospital in the period 1980-2000. A total of 42 patients have been diagnosed of IIN and 16 of ATD. Demographic data, as well as clinical and laboratory parameters and outcomes of every studied patient were analysed. We found a significantly higher prevalence of male sex (100% vs 57%, p < 0.01), previous history of hypertension (100% vs 55%, p < 0.01), chronic renal insufficiency (56% vs 17%, p < 0.01), ischemic heart disease (56% vs 14%, p < 0.001), peripheral ischemic disease, endovascular procedures (87% vs 7%, p < 0.001) and anticoagulant treatments (25% vs 5%, p < 0.001) among patients with ATD as compared with IIN, respectively. On the contrary, previous infections (45% vs 12%, p < 0.01) and exposure to new drugs (100% vs 40%, p < 0.001) were significantly more frequent among IIN patients in compare with ATD. ATD patients showed skin lesions consisting of livedo reticularis and digital infarcts (63% vs 31%, p < 0.05) accompanied by blood pressure increase (100% vs 24%, p < 0.001), whereas IIN patients showed fever (41% vs 19%, p < 0.05) and cutaneous rash as significant clinical manifestations, respectively. The number of ATD patients with proteinuria > 1 g/24 h was significantly higher, but no differences between both groups in the prevalence of urinary sediment abnormalities were observed. The prevalence of absolute eosinophilia was high in both groups (88% among ATD patients, 64% among IIN patients; pNS). Prognosis of both entities was clearly different: Almost all patients with ATD died (69%) or evolved to end-stage renal failure, whereas most patients with IIN showed a recovery of renal function after withdrawal of responsible drugs and steroid treatment. In summary, the analysis of clinical and laboratory data allows an initial differential diagnosis in patients suspected as having IIN or ATD.
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PMID:[Immunoallergic interstitial nephritis vs. cholesterol atheroembolism. Differentiating characteristics]. 1277 76

There are many similarities in the profile of chronic renal disease in the five North African countries, reflecting their close resemblance in ethnic background, bioecology and socioeconomic standards. The incidence of renal disease is much higher than that in the West, yet the prevalence is relatively lower, which mirrors the inadequacy of medical care facilities. The principal causes of end-stage chronic renal disease (ESRD) are interstitial nephritis (14 to 32%), often attributed to environmental pollution and inadvertent use of medications; glomerulonephritis (11 to 24%), mostly mesangioproliferative and focal segmental sclerosis; diabetes (5 to 20%) and nephrosclerosis (5 to 21%). Obstructive/reflux nephropathy, attributed to urinary schistosomiasis, is common in Egypt (7%), Libya and Southern Algeria. Primary urolithiasis is a frequent cause of obstructive nephropathy in the western (hyperoxaluria) and middle (cystinuria) regions. The incidence of tuberculosis is increasing, particularly the diffuse interstitial and hematogenous forms. It is responsible also for 10 to 40% of renal amyloidosis. The latter is also frequently associated with familial Mediterranean fever. Sickle cell anemia is an important health problem in the west, leading to a wide range of glomerular and tubulointerstitial nephropathies. Takayasu disease is increasingly recognized as a cause of ischemic nephropathy and renovascular hypertension. The management of ESRD is largely influenced by late referral, co-morbidities and lack of dialysis facilities. Hemodialysis is the most frequent modality of renal replacement therapy (RRT). CAPD is used sporadically. Renal transplantation, largely from live (often unrelated) donors, is offered to less than 5% of patients with ESRD. The reported outcome of RRT generally conforms with international standards.
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PMID:End-stage renal disease in North Africa. 1286 87

Despite advanced techniques of renal replacement therapy as well as improved medical care and control over the last decade, the overall mortality of patients with "internal" nontraumatic acute renal failure (ARF) requiring replacement therapy is still high. In a retrospective study we compared causes of nontraumatic ARF, risk factors for the development of renal failure and mortality rates in patients with nontraumatic ARF, who received hemodialysis therapy from 1981 to 1990 and from 1991 to 2000. 510 patients with nontraumatic ANV requiring hemodialysis were evaluated, 278 patients in 1981-1990 and 232 patients in 1991-2000. In both groups the chronic risk factors for ANV such as hypertension, diabetes mellitus, chronic cardiac failure, chronic hepatic failure and pre-existing renal impairment and the causes of a traumatic ARF were compared. In addition, concomitant sepsis and multi-organ failure as prognostic parameters as well as mortality rates dependent on the causes of ARF were evaluated. In the latter period, there was a significant reduction in the prevalence of acute glomerulonephritis (3.0 versus 8.3%, p < 0.05) and acute interstitial nephritis (2.6 versus 7.6%, p < 0.05) as well as acute pancreatitis (1.7 versus 7.6%, p < 0.01) as causes of ARF. On the other hand, the prevalence of drug-induced ARF increased during the latter period (10.8 versus 4.7%, p < 0.05). Other etiologies of nontraumatic ARF did not significantly differ between the two decades. Patients treated from 1991 to 2000 had chronic risk factors for the development of ARF, namely diabetes (14.6 versus 6.8%), coronary artery disease (28.0 versus 9.3%) and pre-existing renal impairment (51.7 versus 17.6%, p < 0.001), more frequently than did patients dialysed from 1981-1990. The prevalence of sepsis and multi-organ failure was approximately the same in both periods. The overall mortality (41.8 versus 44.6%, NS) and mortality secondary to causes of nontraumatic ARF were similar in both periods. In summary: the prevalence of several causes of nontraumatic ARF has changed during the last decades. Furthermore, patients treated in the 90's had chronic risk factors for renal failure, namely diabetes and pre-existing renal impairment as well as coronary artery disease, more frequently than did subjects treated in the preceding time period. The prognosis of the patients has not been significantly improved.
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PMID:[Etiology and prognosis of "internal medicine" acute renal failure in 1981-1990 and 1991-2000--an analysis of 510 cases in a single center]. 1473 67

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

Sarcoidosis is a systemic disease with multiorgan involvement. In children, renal impairment of sarcoidosis usually is caused by either hypercalcemia leading to nephrocalcinosis or interstitial nephritis with or without granulomata. We report the case of a 13-year-old boy presenting with severe arterial hypertension and acute renal failure caused by an isolated sarcoid granulomatous interstitial nephritis (GIN). Other known causes of GIN, eg, drug intake or fungal or mycobacterial infection, were excluded, and there was no evidence of extrarenal sarcoid involvement. Renal function improved initially with prednisone treatment. Blood pressure was controlled using ramipril, nifedipine, furosemide, dihydralazine, and metoprolol. Later, the patient showed signs of severe steroid toxicity and progressive renal failure. Monthly treatment with infliximab, a tumor necrosis factor-alpha antibody, was started, resulting in steady improvement in renal function and resolution of renal granulomata. In addition, antihypertensive medication could be reduced, and low-dose prednisone therapy was maintained. To our knowledge, this is the first report of successful treatment with infliximab of a patient with sarcoid GIN.
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PMID:Isolated sarcoid granulomatous interstitial nephritis responding to infliximab therapy. 1568 21

Toxic nephropathy is an important cause of reversible renal injury. This article focuses on the nephrotoxicity of several new therapeutic compounds. Selective cyclooxygenase-2 inhibitor is associated with sodium retention, hypertension, ankle edema, and acute renal failure. The incidence of renal complication is similar to conventional nonsteroidal anti-inflammatory drugs. Bisphosphonates, especially when used in high dose for prolonged duration, can cause toxic acute tubular necrosis and renal failure. Pamidronate is also associated with a specific form of collapsing focal segmental glomerulosclerosis similar to one found in patients with human immunodeficiency virus (HIV) infection. Acyclic nucleoside phosphonate, a new group of antiviral agents, can cause Fanconi-like syndrome and progressive renal impairment. On the other hand, indinavir, a potent protease inhibitor for the treatment of HIV infection, can cause crystalluria, renal stone, acute tubular obstruction and chronic interstitial nephritis. Intravenous immune globulin and hydroxyethyl starch, a new plasma expander, are associated with acute renal failure with characteristic renal histology known as osmotic nephrosis. In short, physicians should be cautious about possible renal toxicity during the use of any new therapeutic agents.
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PMID:Nephrotoxicity related to new therapeutic compounds. 1595 51

In the developing world, up to 80% of the population uses traditional medicine for primary health care. In industrialized countries, adaptations of traditional medicine, termed "complementary" or "alternative" medicine (CAM), are used by a growing number of patients for preventive or palliative care. However, alternative medicine (AM) may be an important risk for the development of acute and chronic kidney injury because of several factors: nonconventional preparations rarely meet the required essential standards of consistency in composition and biological activity; many of these products contain undisclosed over-the-counter or prescription drugs or can be adulterated with hormones and glandular extracts; herbal preparations can be contaminated by pesticides and heavy metals; and because of errors in plant identification and confusing terminology, opportunities for mistakes and deliberate substitution can occur. Furthermore, there is a lack of reports of adverse events and drug interactions because of a lack of professional surveillance, and specific data on systemic and kidney toxicity are not easily available. Kidney injury/kidney syndromes caused by AM consist of acute tubular necrosis/toxicity (eg, Fanconi's syndrome), acute interstitial nephritis, papillary necrosis, hypertension, kidney stones, urinary retention, chronic tubulointerstitial nephritis with fibrosis, urinary tract carcinoma, and acute rejection of the kidney transplant. To improve the care for patients using AM, extension of physicians' knowledge about its possible hazards and toxicity is essential. This review deals with acute and chronic kidney toxicity caused by animal-, plant-, and mineral-based, nonconventional medicine and kidney failure caused by drug interactions with AM.
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PMID:Kidney injury from alternative medicines. 1601 Jun 41


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