Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal artery stenosis not only causes severe hypertension, but if left untreated, can progress to renal failure. A 64-year-old woman with a serum creatinine of 1.8 mg/dL and mild proteinuria developed progressively severe hypertension that was resistant to a calcium channel blocker. The patient received lisinopril, which was discontinued after 2 days because of nonspecific symptoms. One week later, an intravenous pyelogram showed a normal-sized but poorly functioning left kidney and a nonfunctional right kidney. The serum creatinine increased to 11.7 mg/dL and the patient was begun on hemodialysis. A renal arteriogram performed 6 weeks later for persistent hypertension showed bilateral renal artery occlusion; renal vein renin values from the left kidney were higher than those from the right kidney. After 11 weeks of hemodialysis, thrombolytic therapy followed by angioplasty was performed. Three weeks later, the renal function had returned to baseline (serum creatinine of 1.8 mg/dL) and hypertension was controlled with a beta-blocker. Renal artery stenosis is a potentially reversible cause of renal failure and should be considered in the evaluation of elderly patients with hypertension, even in the presence of renal failure.
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PMID:Reversible renal failure in an elderly woman with renal artery stenosis. 828 86

Diabetic nephropathy is the leading cause of uremia in Italy and other industrialized countries: once diabetic nephropathy commences, it advances slowly but inexorably to uremia. Prevention begins with strict control of blood sugar to inhibit or normalize glomerular hyperfiltration, and control of blood pressure to prevent glomerular hypertension and decrease microalbuminuria. Pharmacological measures include ACE-inhibitors and calcium channel blockers, alone or in combination, to reduce proteinuria and preserve renal function. It is believed that some classes of anti-hypertensive drugs have a direct pharmacological depressive effect on cell growth factors that lead to mesangial sclerosis: ACE-inhibitors would thus depress angiotensin II, and the calcium channel blockers would inhibit the increase in intracellular calcium of the mesangial cells which increases gene expression of early growth. Dietary sodium restriction seems to correct the expansion of the sodium pool and related volemic expansion hypertension. A protein-poor diet limits the precapillary glomerular vasodilatation resulting from protein-induced hyperaminoacidemia. The earlier dietetic and pharmacological measures are taken, the more effective they become: while they cannot arrest diabetic nephropathy once it has commenced, they are able to delay evolution of the disease to uremia.
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PMID:[The feasibility and current limits in the prevention of diabetic nephropathy]. 864 29

Previous studies have demonstrated differences in the progression to glomerulosclerosis with the use of calcium channel blockers (CCB). The results with angiotensin-converting enzyme (ACE) inhibitors are more consistent. Moreover, only two studies have examined the combined effects of these drug classes on the development of glomerulosclerosis. The aim of the study presented here was to test the hypothesis that nonhypotensive doses of the combination (VT) of a nondihydropyridine CCB, verapamil (V), and an ACE-inhibitor, trandolapril (T), will slow the development of glomerulosclerosis better than either agent alone in stroke-prone spontaneously hypertensive rats (SHRSP). SHRSP were randomized to treatment in one of three groups with nonhypotensive doses of these agents; a fourth group served as control (C). The control rats developed significant increases in proteinuria compared with the other groups (C, 190 +/- 35 mg.kg-1.d-1 versus VT, 19 +/- 12 mg.kg-1.d-1; P < 0.05). This finding correlated with the degree of glomerulosclerosis (mean severity grading for C, 3.31 +/- 0.21 versus VT, 1.6 +/- 0.51; P < 0.05). Moreover, there was no significant reduction in arterial pressure between these groups (C, 282 +/- 5 versus VT, 259 +/- 13 mm Hg; P = 0.12). Despite persisting hypertension, the rise in proteinuria was also attenuated in both the V group (57 +/- 21 mg.kg-1.d-1) and the T group (43 +/- 24 mg.kg-1.d-1). However, compared with the control rats, kidney morphology was unchanged. Lastly, creatinine clearance was better preserved in the VT group compared with the control group (C, 0.57 +/- 0.01 versus VT, 0.74 +/- 0.06 mL.min-1.100 g-1; P < 0.05). It was concluded that the combination of nonhypotensive doses of VT attenuates the rise in proteinuria and progression to glomerulosclerosis. This study supports the concept that VT may have effects on the glomerulus that are independent of blood pressure reduction.
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PMID:Individual and combined effects of verapamil or trandolapril on attenuating hypertensive glomerulopathic changes in the stroke-prone rat. 873 2

This study defines the nature of the renal protective effects of calcium channel blockers (Ca blockers) and the effects of the Ca blocker, amlodipine, compared to those of the angiotensin-converting enzyme inhibitor (ACEI), enalapril, on the progression of renal injury in 5/6 nephrectomized spontaneously hypertensive rats (SHR) fed a high-salt diet. Furthermore, we studied the effects of various Ca blockers on the glomerular afferent and efferent arterioles using the isolated perfused hydronephrotic kidneys of six-week-old male Sprague-Dawley rats. In the first study, forty 6-week-old male SHRs which underwent 5/6 nephrectomy were equally divided into five groups. One group received no therapy. In two groups, therapy was started at four weeks post-nephrectomy, one with amlodipine and the other with enalapril. In the remaining two groups, amlodipine or enalapril therapy was started at eight weeks postnephrectomy. Amlodipine was more effective than enalapril in reducing proteinuria and glomerulosclerosis in the group that was started on drug therapy eight weeks after surgery. In the second study, at concentrations of 10(-6) to 10(-9) M, nifedipine, nicardipine and amlodipine dilated the afferent, but not the efferent, arteriole preconstricted with angiotensin II. On the other hand, efonidipine and manidipine clearly dilated angiotensin II-induced constriction of both the afferent and efferent arterioles. These results indicated that Ca blockers are effective at reducing renal injury in 5/6 nephrectomized SHR, and that they are more effective than ACEI in advanced stages of renal injury. The observation that only certain Ca blockers can dilate the efferent arteriole suggests that the renal protective effect of Ca blockers is not necessarily dependent on the dilation of the efferent arterioles.
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PMID:Antihypertensive agents and renal protection: calcium channel blockers. 874 11

The pregnancy complication characterized by proteinuric hypertension is called preeclampsia. Preeclampsia, an important cause of maternal and perinatal death, has an onset and progression impossible to predict. Termination of pregnancy is the only cure of preeclampsia. It is indicated when the fetus can survive outside the uterus or when the maternal condition deteriorates to such a condition that continuation would bring greater harm to the mother. The etiology of preeclampsia is unknown. Preeclampsia appears to be linked to abnormal trophoblastic implantation. In normal pregnancies, implantation effects changes in the spiral arteries that supply the intervillous space and fibrin-containing trophoblast, and amorphous matrix replace the endothelium and the internal elastic lamina. These changes do not occur or are limited in pre-eclamptic women. There appears to be a familial tendency to preeclampsia. Impaired formation of blocking antibodies to antigenic sites on the placenta increases the risk of pre-eclampsia. Risk factors are primigravidity, short duration of sexual cohabitation before conception, abundance of trophoblastic tissue (e.g., multifetal and molar pregnancies), and underlying vascular disease as in diabetes. Poor placental perfusion may account for the increase in maternal blood pressure. Preeclampsia can lead to eclampsia, cerebral hemorrhage, coagulopathy, and death. Poor utero-placental circulation retards fetal growth and causes fetal distress and maybe even perinatal death. When the diastolic blood pressure is higher than 110 mmHg, pre-eclamptic women should be administered antihypertensive drugs (e.g., methyldopa, beta-blockers, calcium channel blockers, hydralazine, labetatol, or diazoxide) to prevent maternal complications, but these drugs do not improve utero-placental blood flow nor do they prevent proteinuria. Diuretics should not be administered. Proteinuria indicates that the kidneys have been affected. A large randomized trial shows that aspirin does not effectively prevent preeclampsia. Routine calcium supplementation does appear to prevent it and preterm delivery.
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PMID:Pre-eclampsia. 875 7

Hypertension is a common finding in patients with renal parenchymatous diseases. Development of hypertension causes increased proteinuria, decline in glomerular filtration rate and reduced life span in experimental models of glomerulonephritis. Hypertension has been shown to reduce glomerular filtration rate in man. It is therefore important to treat hypertension. The blood pressure should be reduced to about 140/80 mm Hg. Reduction of glomerular capillary pressure, inhibition of glomerular permeability, renal hypertrophy and inhibition of mesangial metabolism are the main mechanisms of renal protection during antihypertensive therapy. Autoregulation of the renal blood flow probably has an impact on these mechanisms. Impaired autoregulation is found in kidneys with low glomerular filtration rate and during treatment with calcium channel blockers. Alpha receptor blockers, angiotensin converting enzyme inhibitors (ACE-) and angiotensin II receptor blockers do not interfere with autoregulation. All types of antihypertensive drugs provide similar renal protection when the glomerular filtration rate is reduced. When calcium channel blockers are used in kidneys with normal or slightly reduced function, either blood pressure should be kept strictly at normal levels or these type of drugs should be combined with ACE inhibitors or angiotensin II receptor blockers.
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PMID:[Treatment of hypertension in renal parenchymal diseases]. 876 45

Elevated systemic blood pressure is associated with more rapid progression of renal failure, as recently documented by prospective observations. Intervention studies with antihypertensive medication have clearly documented that progression can be attenuated by antihypertensive medication. Experimental studies and, more recently, controlled prospective trials in humans, have provided evidence that in this respect angiotensin converting enzyme (ACE) inhibitors are superior to equipotent doses of alternative antihypertensive agents, suggesting a specific nephroprotective action. Experimental studies suggest that this is not only due to hemodynamic, but also to nonhemodynamic, mechanisms. The effect of calcium channel blockers on this progression is less uniform and may depend on the model used, the percentage of blood pressure lowering, and possibly also the type of calcium channel blocker. Despite some discrepancies in experimental studies, recent controlled clinical trials show a similar slowing of progression with either ACE inhibitors or calcium channel blockers. Since combination therapy is required in most patients with advanced renal failure, recent experimental studies on development and glomerular sclerosis and clinical studies showing at least additive effects on reduction of proteinuria independent of blood pressure argue for combining ACE inhibitors and calcium antagonists.
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PMID:Are antihypertensive drugs similar in protecting the kidney? 884 84

In the present study we investigated the effect of a selective alpha 1-adrenergic blocker (doxazosin), an angiotensin-converting enzyme (ACE) inhibitor (captopril), and a calcium channel antagonist (nifedipine) on renal function in hypertensive non-insulin-dependent diabetic patients. 30 NIDD hypertensive patients (age = 50 +/- 3 years; BMI = 30 +/- 1 kg/m2) (mean +/- SEM) were studied before and after a 12-week period of antihypertensive treatment. Ten patients were treated with doxazosin (Cardura) (2-8 mg once daily or 8 mg b.i.d.), 9 with captopril (Capoten) (25-50 mg b.i.d.), and 11 with nifedipine (Procardia-XL) (30-60 mg once daily). Blood pressure, creatinine clearance, 24-hour urinary protein excretion, fasting plasma glucose concentration and glycosylated hemoglobin were measured before and after drug treatment. Fasting plasma glucose and glycosylated hemoglobin (HbA1c) were similar in all three groups prior to the start of antihypertensive therapy and did not change significantly from baseline in any treatment groups. In the doxazosin group creatinine clearance rose from 99 +/- 8 to 122 +/- 8 ml/1.73 m2.min (p < 0.01), while 24-hour urinary protein excretion declined from 2.66 +/- 0.05 to 1.76 +/- 0.02 mg/day/ml/1.73 m2.min (p < 0.01). In diabetics treated with captopril creatinine clearance rose from 93 +/- 6 to 109 +/- 9 ml/1.73 m2.min (p < 0.05), while the 24-hour urinary protein excretion fell from 2.70 +/- 0.05 to 2.03 +/- 0.04 mg/day/ml/1.73 m2.min (p < 0.05). In patients treated with nifedipine creatinine clearance did not change (97 +/- 6 vs. 94 +/- 7 ml/1.73 m2.min), while 24-hour urinary protein excretion decreased from 2.84 +/- 0.04 to 1.95 +/- 0.03 mg/day/ml/1.73 m2.min. Systolic and diastolic blood pressure were similar in doxazosin (150 +/- 3/95 +/- 2 mm Hg), captopril (153 +/- 3/93 +/- 1), and nifedipine (155 +/- 4/93 +/- 1) groups prior to the start of antihypertensive therapy and declined to 143 +/- 3/84 +/- 3 (doxazosin), 139 +/- 3/82 +/- 3 (captopril), and 141 +/- 3/84 +/- 1 (nifedipine) mm Hg (all p < 0.01 vs. pretreatment). In summary, both doxazosin and captopril treatment were associated with significant rises in GFR, while all three antihypertensive agents caused a significant decline in proteinuria. These results indicate that alpha-adrenergic blockers, ACE inhibitors, and calcium channel antagonists can safely and effectively be used in the clinical management of non-insulin-dependent diabetic patients with hypertension.
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PMID:Effect of alpha-adrenergic blockers, ACE inhibitors, and calcium channel antagonists on renal function in hypertensive non-insulin-dependent diabetic patients. 885 95

Cyclosporine (CsA) (37.4 mumol/kg per day for 7 days) treated female Wistar rats exhibited significantly decreased creatinine clearance (Ccr) and body weight loss (BWL), but had neither proteinuria (PU) nor alteration in their urine volume (V). Light microscopic (LM) sections of rat kidneys showed that all kidneys were affected by lesions, mainly diffuse vacuolization. These changes were associated with decreased urinary excretion ratios of 6-ketoprostaglandin F1 alpha to thromboxane B2 (6kPGF1 alpha/TXB2) and prostaglandin E2 to TXB2 (PGE2/TXB2). When OKY-046, a TXA2-synthetase inhibitor or nifedipine (NFD), a calcium channel blocker and an antagonist of endotheline (ET), were administered in addition to CsA, they restored Ccr and increased urine V but they did not prevent BWL. LM sections showed that only 5 or 7 out of 9 kidneys of animals were affected, respectively. These changes were associated with prevention of the diminished ratios of urinary PGE2/TXB2 and 6kPGF1 alpha/TXB2 mainly in the OKY-046 treated animals. In conclusion, our results suggest that inhibitors of TXA2 or antagonists and/or inhibitors of endothelin play a protective role in the development of the dysfunction induced by CsA. However, the protection observed using OKY-046 and NFD did not reach that obtained by evening primrose oil (EPO) or Ketanserine (KTS), substances which prevented the fall of Ccr and BWL. Furthermore, with these protective agents only 5 out of 9 kidneys were affected and the lesions were of minor importance.
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PMID:Effects of OKY-046 and nifedipine in cyclosporine-induced renal dysfunction in rats. 895 93

The preponderance of the medical literature supports the concept that modest or moderate dietary salt restriction enhances the blood pressure lowering responses to most antihypertensive medications and may permit either dose reduction or, in a few cases, complete drug withdrawal. Moreover, reduction in salt intake has a permissive action on the antiproteinuric responses of angiotensin converting enzyme inhibitors and nondihydropyridine calcium channel blockers. It does not, however, affect proteinuria in those receiving dihydropyridine calcium channel blockers. The importance of selecting out those individuals who can most benefit from dietary salt modification (the "salt sensitive" groups of hypertensive patients) is important. Prospective randomized clinical studies are needed to assess the correlation between dietary salt intake and renal endpoints, such as time dialysis. This will be particularly important in different demographic groups that may have a greater predisposition to salt sensitivity, such as elderly or obese hypertensives, hypertensives of black or Hispanic descent, and those with non-insulin-dependent diabetes mellitus.
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PMID:Salt intake and reductions in arterial pressure and proteinuria. Is there a direct link? 896 35


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