Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.15.1 (ACE)
 18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal artery stenosis (RAS) may cause hypertension, azotemia, episodes of flash pulmonary edema and congestive heart failure. Renal artery angioplasty and stenting was performed in 207 patients from 1991 to 1997. Thirty-nine of these patients (19%) underwent renal artery stenting for the control of recurrent episodes of congestive heart failure and flash pulmonary edema. All patients had angiographic evidence of severe (>70%) bilateral RAS (n = 18) or severe RAS to a solitary functioning kidney (n = 21). Sixteen patients (41%) were male and 23 (59%) were female, mean age 69.9 years (range 50-85 years). Of the 18 patients with bilateral RAS, 12 (66.6%) underwent bilateral stenting. Mean blood pressure decreased from 174/85 +/- 32/23 mmHg to 148/72 +/- 24/14 mmHg (p < 0.001). Mean number of blood pressure medications decreased from 3 +/- 1 to 2.5 +/- 1 (p = 0.006). Twenty-eight patients (71.8%) had improvement in blood pressure control. The mean serum creatinine decreased from 3.16 +/- 1.61 to 2.65 +/- 1.87 (p = 0.06). Six of 39 patients (15.4%) used angiotensin converting enzyme (ACE) inhibitors prior to stenting whereas 19 of 39 patients (48.7%) used ACE inhibitors poststenting (p = 0.004). Twenty of 39 patients (51.4%) demonstrated improvement in serum creatinine, 10 of 39 patients (25.6%) had stabilization of serum creatinine and nine of 39 patients (23%) demonstrated worsening. The number of hospitalizations due to congestive heart failure in the year preceding renal artery stenting was 2.4 +/- 1.4 and poststenting was 0.3 +/- 0.7 (p < 0.001). The New York Heart Association Functional Class decreased from 2.9 +/- 0.9 prestenting to 1.6 +/- 0.9 poststenting (p < 0.001). Thirty of 39 patients (77%) had no hospitalizations for congestive heart failure during a mean follow-up period of 21.3 months. Nine patients expired during the course of follow up; eight of the nine patients died within the first year after renal artery stenting. Renal artery stenting decreased the frequency of congestive heart failure, flash pulmonary edema, and the need for hospitalization in most patients. Blood pressure was markedly improved in the majority of patients with improved or stabilized renal function. Evaluation for RAS is important in hypertensive patients who present with recurrent congestive heart failure or flash pulmonary edema.
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PMID:Clinical benefit of renal artery angioplasty with stenting for the control of recurrent and refractory congestive heart failure. 1271 Aug 43

Renal crisis occurs in patients who have systemic sclerosis with rapidly progressive diffuse cutaneous thickening early in their disease. SRC is characterized by malignant hypertension, hyperreninemia, azotemia, microangiopathic hemolytic anemia, and renal failure. SRC was almost uniformly fatal, but in most cases it can now be successfully treated with ACE inhibitors. This therapy has improved survival, reduced the requirement for dialysis, and often allowed for the discontinuation of dialysis 6 to 18 months later. Prompt diagnosis and early, aggressive initiation of therapy with ACE inhibitors will result in the most optimal outcome.
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PMID:Scleroderma renal crisis. 1284 Dec 97

There is evidence to suggest that antiplatelet aggregation and inhibition of angiotensin converting enzyme will attenuate the progression of renal disease. In the present study, dipyridamole (DPM; 30 mg/kg per day, p.o.) or fosinopril (FOS; 20 mg/kg per day, p.o.) was given to rats for 5 weeks starting immediately after renal mass reduction (right uninephrectomy and ligation of approximately two-thirds of the blood supply to the left kidney). Renal mass reduction caused increased mean arterial blood pressure, reduced effective renal plasma flow (ERPF) and glomerular filtration rate (GFR), azotemia and proteinuria. Neither proteinuria nor hypertension was affected by DPM, although renal function improved markedly. Rats receiving FOS showed normalization of blood pressure with a significant increase in both ERPF and GFR, along with a lower degree of proteinuria. A histological examination of the remnant kidney detected the presence of vasodilation with a lower degree of podocyte swelling in both treatment groups, with a remarkable effect in the FOS group. These data indicate that both FOS and DPM attenuate the progression of glomerular disease associated with renal mass reduction in rats. However, FOS was more beneficial than DPM because it reduced proteinuria and lowered blood pressure.
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PMID:Comparison of dipyridamole and fosinopril on renal progression in nephrectomized rats. 1501 38

Angiotensin-converting enzyme inhibitors (ACEIs) are contraindicated in patients with bilateral renal artery stenosis due to risk of azotemia resulting from preferential efferent arteriolar vasodilation in the renal glomerulus due to inhibition of angiotensin II. Patients with renal artery stenosis who can derive survival benefit from ACE inhibition, therefore, may not receive ACEI therapy. We evaluated the safety of ACEI therapy in patients with bilateral renal artery stenosis following successful revascularization using renal artery stenting. This study is a retrospective analysis of 25 patients who underwent bilateral renal artery stenting for refractory hypertension and had a strong clinical indication for long-term ACEI use (left ventricular dysfunction or diabetes). Eighteen of the 25 patients (72%) have been safely maintained on a target dose of ACEIs, 2 of the 25 have been treated with angiotensin receptor blockers due to cough, and 5 of the 25 are being treated with a hydralazine/nitrate combination due to cough (2 patients) or baseline renal insufficiency (3 patients). We conclude that patients with bilateral renal artery stenoses that have been successfully revascularized using renal stenting may be safely treated with long-term ACEI therapy.
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PMID:Safety of angiotensin-converting enzyme inhibitors in patients with bilateral renal artery stenosis following successful renal artery stent revascularization. 1685 64

Nephrotoxicity is the most common and clinically significant adverse effect of calcineurin inhibitors. Cyclosporine and tacrolimus nephrotoxicity is manifested by both acute azotemia and chronic progressive renal disease and tubular zdysfunction. An elevation in the plasma potassium concentration due to reduced efficiency of urinary potassium excretion is common in cyclosporine-treated patients; it may be severe and potentially life-threatening with concurrent administration of an angiotensin converting enzyme inhibitor, which diminishes aldosterone release. Tubular injury induced by cyclosporine can also impair acid excretion. This may be presented as a hyperchloremic metabolic acidosis associated with decreased aldosterone activity and suppression of ammonium excretion by hyperkalemia. Some patients treated with cyclosporine develop hypophosphatemia due to urinary phosphate wasting. Renal magnesium wasting is also common presumably due to drug effects on magnesium reabsorption. Hypomagnesemia has also been implicated as a contributor to the nephrotoxicity associated with cyclosporine. Both cyclosporine and tacrolimus are associated with hypercalciuria. Attention must be paid to drug dose, side effects, and drug interactions to minimize toxicity and maximize efficacy.
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PMID:Electrolyte and Acid-base disturbances induced by clacineurin inhibitors. 2445 11


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