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

Secondary hemolytic uremic syndrome (HUS) is uncommon. When it occurs, it is usually in association with pregnancy, malignancy, severe hypertension, drugs, or collagen vascular diseases. It has rarely been reported in patients with glomerular disease. Two such patients with secondary HUS are described. A 17-month-old girl with hematuria and the nephrotic syndrome, negative antistreptolycin O (ASO) titer, and low serum levels of C3 and C4 developed oliguria, progressive azotemia, thrombocytopenia, and microangiopathic hemolytic anemia. A kidney biopsy showed fibrin in glomerular capillaries and cresentic membranoproliferative glomerulonephritis. A 22-year-old man with a 16-year history of relapsing minimal change nephrotic syndrome had been in remission for 5 years when he experienced nephrotic syndrome relapse and developed thrombocytopenia, microangiopathic hemolytic anemia, and renal failure. A kidney biopsy revealed foot process fusion and obstruction of glomerular capillaries with fibrin and platelets. These cases illustrate that HUS can occur in association with other glomerular diseases and should be considered when thrombocytopenia and hemolytic anemia occur in a nephritic or nephrotic patient.
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PMID:Hemolytic uremic syndrome associated with glomerular disease. 291 69

Renal function and antihypertensive drug efficacy were determined in a prospective, double-blind, multicenter study comparing enalapril plus hydrochlorothiazide with standard triple therapy (hydrochlorothiazide, timolol, and hydralazine) in 75 patients with documented renovascular hypertension. Both groups had significant mean decreases in systolic and diastolic blood pressures. Effective control of diastolic hypertension occurred in 96 percent of patients receiving enalapril compared with 82 percent of patients receiving the triple-drug regimen. Effective renal plasma flow was significantly increased by enalapril therapy. In contrast, the glomerular filtration rate had a bimodal response. In 80 percent of enalapril-treated patients, there was no significant change in the inulin clearance, although in 20 percent of patients (10), there was a 28 percent decrease in the inulin clearance with a concomitant 12 percent increase in renal plasma flow. Seven of the 10 patients had unilateral renal artery stenosis, but in all 10, it was high-grade stenosis (more than 80 to 90 percent stenosis). Although a significant rise in the serum creatinine level occurred in one patient in association with diuretic therapy, volume repletion reversed this azotemia. No oliguric acute renal failure occurred in the enalapril-treated group. The cause of the decrease in glomerular filtration rate induced by enalapril plus hydrochlorothiazide in a minority of patients with renal artery stenosis appears to be quite complex. Although the abolishment of the autoregulation of glomerular filtration secondary to blockage of angiotensin II appears to be a primary cause, the roles of decreased arterial pressure, renal counterbalance, concurrent diuretic therapy, and other hemodynamic factors that may maintain glomerular ultrafiltration pressure must also be considered. The results of this study show that enalapril plus hydrochlorothiazide is effective in treating renovascular hypertension. Special care is needed for a small group of patients with renovascular hypertension in whom there is a decrease in the glomerular filtration rate with this therapy. This may identify a subset of patients with unilateral or bilateral high-grade renal artery stenosis in whom alternative therapy--percutaneous angioplasty or surgical intervention--may be considered.
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PMID:Comparison of effects of enalapril plus hydrochlorothiazide versus standard triple therapy on renal function in renovascular hypertension. 299 42

The effects of captopril on effective renal plasma flow and glomerular filtration rate were studied using a noninvasive radioisotopic method on individual kidneys in eight patients with renovascular hypertension and 12 patients with essential hypertension with various renin levels. Four patients with renovascular hypertension had unilateral while three had bilateral renal artery stenosis. The effective renal plasma flow and glomerular filtration rate were determined by using 131I-iodohippurate sodium and 99mTc-diethylenetriamine pentaacetic acid, respectively. Glomerular filtration rate and effective renal plasma flow were significantly reduced in the stenotic kidneys of patients with renovascular hypertension compared with values in nonstenotic kidneys (p less than 0.01). Treatment with captopril, 37.5 to 75 mg/day for 1 to 48 weeks, further reduced the glomerular filtration rate only in stenotic kidneys, and effective renal plasma flow increased in both kidney types. In two of the three renal hypertensive patients with bilateral renal artery stenosis, captopril produced a reversible azotemia that was unrelated to the fall in blood pressure, as evidenced by the lack of azotemia seen after a moderate blood pressure reduction induced by other antihypertensive medications. These results indicate that endogenous angiotensin II is essential in maintaining the glomerular filtration rate in stenotic kidneys and suggest that a reduction in glomerular filtration rate during captopril administration could indicate the presence of renal artery stenosis.
Hypertension 1986 May
PMID:Effects of converting enzyme inhibition on split renal function in renovascular hypertension. 300 26

Surgery has been used to treat renal vascular hypertension for almost 50 years. The reason for the many apparent discrepancies in the literature on effectiveness and risk have become clear only in the past decade. The results are poorest and the risk is greater, not surprisingly, in patients with advanced atherosclerosis involving many vascular beds. The results are much better in fibromuscular disease, both in terms of effectiveness and risk. Angioplasty has been available for a much shorter time, but a reasonable picture of the short-term effectiveness and the risk is emerging. The risk is substantially lower than that of surgery. The results are again best in fibromuscular disease. In atherosclerotic disease, the results are especially poor for the most common lesion, that involving the renal artery ostium. Medical therapy before the development of captopril was often difficult and often unsatisfactory. Since the development of converting-enzyme inhibition, medical therapy is an important option. In the early experience, reflecting the severity of the hypertension, the frequency with which azotemia was present, and the high dose of captopril used, the adverse reaction rate was substantial. In one study, none of 133 patients with unilateral renal arterial disease and an intact contralateral kidney developed renal failure. Among 136 patients with bilateral disease or a solitary kidney, renal failure occurred in 15 and led to discontinuation of therapy in 12. If surgery or angioplasty are contraindicated, one can modify the therapeutic goal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The treatment of renovascular hypertension: surgery, angioplasty, and medical therapy with converting-enzyme inhibitors. 303 90

A transplanted kidney in a patient developed focal and segmental glomerulosclerosis, associated with severe systemic hypertension, proteinuria, progressive azotemia, and allograft hypertrophy. A pediatric kidney with two main arteries was used, and occlusion of the artery supplying the upper pole resulted in infarction of this portion of the allograft. Because other known factors predisposing to focal sclerosis were absent, it is postulated that renal hemodynamic changes associated with reduction in functioning renal mass, attended by striking stimuli for renal hypertrophy, resulted in progressive damage. The implications of these concepts are discussed in relation to the progression of renal diseases.
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PMID:De novo focal glomerulosclerosis after kidney transplantation. 304 72

Acute renal failure is a most challenging clinical problem when it occurs in pregnancy. It requires an understanding of the normal physiology of the kidney in pregnancy and the natural history of different underlying renal diseases when pregnancy occurs. Because patients with chronic renal disease may present with worsening proteinuria, hypertension, and renal function, these disorders must be excluded from those conditions that cause acute deterioration of renal failure in otherwise normal women during pregnancy. As in all patients who develop acute renal failure, prerenal and obstructive causes must be excluded. Particularly important causes of prerenal azotemia in pregnancy include hyperemesis gravidarum and uterine hemorrhage, especially if it is unsuspected as in abruptio placentae. Infectious causes of acute renal failure in the pregnant woman include acute pyelonephritis and septic abortion. The clinical presentation of both these conditions should be apparent, and appropriate diagnosis and treatment can then be promptly instituted. Renal cortical necrosis is another cause of renal failure that occurs more frequently in pregnancy, and it must be differentiated from the many causes of acute tubular necrosis that may be associated with pregnancy. Those conditions that cause renal failure unique to pregnancy must always be considered when renal function deteriorates in the last trimester or the postpartum period. Severe preeclampsia, acute fatty liver of pregnancy, and idiopathic postpartum acute renal failure may all present similar complications, but the approach to each of these clinical disorders must be individualized. By understanding the causes of renal functional deterioration in pregnancy, a logical differential diagnosis can be established, allowing appropriate therapeutic decisions to preserve both maternal and fetal well-being.
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PMID:Acute renal failure in pregnancy. 305 11

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

Since their introduction in clinical practice in 1980, ACE inhibitors have been found useful in the treatment of hypertension and CHF. In hypertension, they are effective as monotherapy in 40% to 50% of the patients, and in combination with diuretics or calcium antagonists, they are effective in up to 85% of the patients. They are well tolerated, are not associated with depression, impotence, bronchospasm or metabolic derangements such as hypokalemia, hyperuricemia or hyperglycemia, and do not have adverse effects on the quality of life. As a result, they are preferred in hypertensive patients with CHF, left ventricular dysfunction, mental depression, older age, coronary artery disease, metabolic disorders, chronic destructive pulmonary disease, and peripheral vascular disease. In CHF they cause long-lasting hemodynamic and symptomatic improvement, improve exercise tolerance, and may lower mortality in certain patient subsets. Evolving new indications for ACE inhibitors include the diagnosis of renovascular hypertension, the prediction of surgical success, the treatment of scleroderma renal crisis, the reduction of proteinuria, renal protection, cardioprotection, the improvement of arterial compliance, in Bartter's syndrome and idiopathic edema, etc. ACE inhibitors are usually well tolerated but in some instances they may cause class-specific side effects such as hypotension; usually reversible azotemia or renal failure, especially in patients with renal artery stenosis or with CHF with low blood pressure; cough; angioedema; and hyperkalemia. Differences among ACE inhibitors are emerging and include chemical class (e.g., zinc ligand), biotransformation, potency, pharmacokinetics, prodrugs, tissue effects, additional pharmacologic properties, and drug interactions.
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PMID:Angiotensin converting enzyme inhibitors. II. Clinical use. 305 46

In four adults with idiopathic nephrotic syndrome and azotemia, percutaneous renal biopsy showed diabetic glomerulosclerosis, yet none had oral glucose tolerance tests diagnostic of diabetes mellitus or funduscopic evidence of diabetic retinopathy. Possible concomitant glomerular disease that may have produced proteinuria was excluded. Well documented cases of diabetic glomerulosclerosis without concurrent glucose intolerance are uncommon, and almost 30% of such patients have a past history of diabetes. Despite the absence of overt diabetes at onset of diabetic glomerulosclerosis, these patients warrant careful monitoring of plasma glucose levels and strict control of systemic hypertension.
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PMID:Diabetic glomerulosclerosis without concurrent diabetes mellitus. 305 23

Heavy proteinuria in patients with essential hypertension raises the question of underlying primary renal disease. While malignant hypertension may be associated with proteinuria in the nephrotic range, it is generally held that protein excretion in benign nephrosclerosis is almost invariably less than 0.5-1.0 g/24 h. We report 18 patients with biopsy-proven hypertensive nephropathy and heavy proteinuria, of which only 6 had malignant hypertension. In the remaining 12 patients with benign nephrosclerosis, protein excretion reached up to 6.5 g/24 h, and nephrotic range proteinuria was present in 3 patients. All patients with heavy proteinuria suffered from long-standing moderate or severe, poorly controlled hypertension and were azotemic. We suggest that hypertensive nephrosclerosis be included in the differential diagnosis of massive proteinuria accompanying azotemia in poorly controlled hypertensives.
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PMID:Marked proteinuria in hypertensive nephrosclerosis. 316 Feb 40


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