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

As newer treatment modalities become available for patients with severe lupus nephritis, it becomes increasingly important to identify patients at risk for renal failure. In this study, the records of 90 children presenting with systemic lupus erythematosus over a 13-year period were reviewed. Nineteen were lost to follow-up prior to completion of the study. Of the 71 remaining children, 16 (22%) progressed to chronic renal failure. Persistent hypertension lasting greater than 4 months, anemia, abnormalities of the urinalysis, and elevated serum creatinine level were significantly associated with progression to renal failure. Sex, race, age, abnormalities of creatinine clearance, and 24-hour urine protein collection were not associated with progression to renal failure. Renal biopsies were obtained in 45 children. Biopsies were initially classified according to World Health Organization criteria. Diffuse proliferative glomerulonephritis was significantly associated with progression to renal failure. The 45 biopsies available were reviewed by one of the authors and categorized by activity and chronicity indices. Both the active lesions of fibrinoid necrosis, synechiae, tubular casts, and vasculitic lesions and the chronic lesion of glomerular sclerosis correlated with progression to renal failure. Of the 16 children who progressed to renal failure, 2 had cadaver kidney transplants and are well 5 years posttransplant; 4 had fulminant lupus and died within 1 month of commencing dialysis; 10 began chronic dialysis. Five of the 10 children on chronic dialysis died from sepsis. These data suggest that children with systemic lupus erythematosus who undergo dialysis do poorly.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lupus nephritis: prognostic factors in children. 140 32

The pathogenesis of hypertensive glomerular injury is complex, involving both hemodynamic and nonhemodynamic factors. One can therefore confidently predict that a wide variety of disparate therapeutic interventions, pharmacologic and nonpharmacologic, may be effective in arresting or slowing progressive glomerular injury. Based on the experimental and clinical literature available to date, it is clear that glomerular capillary hypertension is an important pathogenetic factor in this disease and that lowering of Pgc with antihypertensive drugs is associated with prevention of glomerular injury. Furthermore, the CEI may have a special renoprotective effect compared to other antihypertensive agents, most likely due to their unique renal hemodynamic actions. Pending the results of well-designed clinical trials, converting enzyme inhibitors represent the antihypertensive agents most likely to arrest the progressive decline in renal function observed in patients with hypertension and chronic renal failure. The calcium channel blockers are effective antihypertensive agents in patients with chronic renal failure, but whether they confer specific renoprotective effects remains uncertain. Since a large number of patients with chronic renal failure require more than one antihypertensive drug for adequate blood pressure control it may be of interest to evaluate the benefits of drug combinations. In this regard, it is possible that a combination of a CEI and a CCB may have complimentary effects in protecting the kidney. The development of these new classes of antihypertensive agents has had a major impact on the treatment of patients with chronic progressive renal failure. Future studies will hopefully clarify the optimal antihypertensive therapeutic regimen and allow us to move closer to the goal of eliminating end-stage renal failure.
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PMID:Antihypertensive therapy and the progression of chronic renal disease. Are there renoprotective drugs? 174 81

The deterioration rate of creatinine clearance (CCr) was studied in 40 children with chronic renal failure (CRF) on conservative treatment followed up for at least 1 year (range 1-12). The deterioration rate of CCr was significantly (p less than 0.01) higher in glomerulopathies (G) than in hypoplasias (H) and in vascular nephropathies (VN) and significantly (p less than 0.01) higher in hereditary nephropathies (HN) than in VN. The differences in the deterioration rate of CCr between H and HN and between H and VN were not explainable on the basis of the different age at diagnosis or of the different prevalence of hypertension. These data indicate that the primary renal disease is important in determining the progression of CRF.
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PMID:Progression of chronic renal failure. 175 28

Arterial contractile responses were studied in experimentally uremic rats. The ligation of 75% of the terminal branches of the left renal artery, followed by contralateral nephrectomy induced a chronic renal failure, as evidenced by significantly higher BUN concentrations and an elevation in blood pressure. Uremic rats exhibited elevations in total and HDL cholesterol, increased triglyceride levels, and significantly lowered HDL/total cholesterol ratios compared to control groups: 1) untreated control, 2) experimental control receiving renal infarction without contralateral nephrectomy, and 3) two kidney, one clip (2K1C) model of hypertension. Plasma total cholesterol levels in uremic rats increased by 50% in the first week following final surgery and plateaued at approximately 100% above control levels during postoperative weeks 3 through 10. Plasma transaminase levels were similar among all of the groups of rats studied indicating no effects of surgery on hepatic function. The contractile responses of aortic rings from uremic rats to submaximal concentrations of serotonin and clonidine were significantly increased and decreased, respectively, whereas the contractile response to norepinephrine was not altered. The enhanced sensitivity to serotonin of aortic rings from uremic rats was abolished following disruption of the endothelium. Neither the alteration of aortic contractile properties nor changes in plasma BUN and cholesterol concentrations were observed in hypertensive 2K1C rats. However, there was a tendency for decreased acetylcholine-induced relaxation in aortic rings of uremic and 2K1C rats. No significant histological evidence of atherosclerosis was found in aortic tissues of uremic rats during the interval of study. These results indicate that hypercholesterolemia, hypertriglyceridemia, and altered vascular sensitivity to serotonin and clonidine are likely to be primary changes in the uremic rat and are not secondary to the development of blood pressure elevation or overt evidence of structural change in the vessels of this model.
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PMID:Hypercholesterolemia and changes of vascular contractile responses in experimentally uremic rats. 176 Aug 90

In 33 patients with autosomal dominant renal polycystosis the urine excretion of the electrolytes sodium and potassium was examined and analyzed in relation to the renal function and the arterial pressure. The clearances, the urine ratio and the excreted fractions of both electrolytes were calculated. It was established that by normal renal function and without arterial hypertension there were no significant differences in the parameters studied between the patients and the healthy controls. In the patients with arterial hypertension and preserved renal function the sodium clearance and urine excretion were lower, but the differences with the normotensive patients were not statistically significant. In the patients with chronic renal failure (when diuretic was applied) higher mean values of the excreted fractions of sodium and potassium were established. The results support the thesis that hypertension in renal polycystosis is of volumetric character.
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PMID:[Urinary electrolyte excretion in autosomal dominant polycystic kidney]. 177 65

The anionic component of sodium salt has been reported to contribute to hypertension in some animal models and hypertensive patients. In the present study, the anionic effects on exacerbation of hypertension in spontaneously hypertensive rat (SHR) were investigated by chronic loading tests with two sources of sodium, viz. sodium chloride (NaCl; 0.9% solution) and sodium bicarbonate (NaHCO3; 1.28% solution), using SHRs with normal renal function (NRF) and with chronic renal failure (CRF; produced by cryosurgery). In addition, extracellular fluid volume (ECFV: inulin space) was measured in SHRs with NRF and CRF. In the NRF groups, systolic blood pressure (SBP) reached 230 mmHg at Week 13, and there was no significant difference in SBP between the NaCl and NaHCO3 groups. In the CRF groups, SBP of the NaCl group was significantly higher (p less than 0.01) than that of the NaHCO3 group (280 mmHg vs. 230 mmHg at Week 15). ECFV was also greater in the NaCl group than in the NaHCO3 group (ECFV: NaCl vs. NaHCO3, 15.9 +/- 1.7 vs. 14.0 +/- 0.9 at Week 13; and 16.2 +/- 1.1 vs. 14.2 +/- 1.2 at Week 15, respectively). These results indicate that chloride ion plays an important role in the pathogenesis of hypertension in SHR with CRF. Expansion of ECFV is considered to be one of the mechanisms whereby the hypertension is exacerbated.
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PMID:Effect of dietary chloride on spontaneously hypertensive rat. 177 41

We retrospectively analysed the effects of a 12-month treatment with captopril (Tensiomin) in 46 patients. All of the patients had hypertension lasting for years (9 essential, 37 with chronic renal failure), 32 of them had proteinuria. Captopril was given in addition to, or in exchange for, other antihypertensive drugs. Under treatment with ACE-inhibitors, a small but significant decrease in diastolic blood pressure (0.4 torr/month) and in proteinuria (0.19 g/month) was seen (regression analysis). Discriminant analysis showed proteinuria and diastolic blood pressure to be the more modifiable, the younger the patients, the higher the proteinuria at the beginning and the longer the history of hypertension. Serum creatinine, blood urea nitrogen, serum protein and serum potassium did not change.
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PMID:[Effect of the ACE-inhibitor captopril on the blood pressure and kidney function of patients with essential and renal hypertension]. 177 7

Duplex Doppler ultrasonography may explore renal perfusion in frequent diseases such as renal obstruction, reno-vascular hypertension, acute or chronic renal failure or diabetic renal complications by measuring Pourcelot's resistive index (RI) of renal parenchyma arteries for each kidney. A statistical and prospective study was performed on 574 patients. In healthy patients, the RI values, equal for each kidney were included in 0.45 and 0.7 (mean RI = 0.59). For other values, there was a renal pathology. Patients with idiopathic hypertension (mean RI = 0.59) or non obstructive dilatation (mean RI = 0.61) did not have an RI significantly different from healthy patients. In cases of renal obstruction, there was a significant increase in the RI for the pathological kidney (mean RI of 0.73). The sensitivity and the specificity was 100% for acute obstructions examined during the first 48 hours. In contrast, in case of renal artery stenosis greater than 70% there was a significant decrease in the RI for pathological kidney. So the RI increased significantly in both kidneys: when there was renal failure with active disease within the tubulo-interstitial compartment (mean RI of 0.77); in all cases of diabetic nephropathy (mean RI of 0.74) where the RI increased early before laboratory signs. Duplex Doppler ultrasonography may be an original method for renal explorations by providing not only morphological data but also physiological data with the perfusion study.
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PMID:[Duplex Doppler ultrasonography of intra-renal arteries. Normal and pathological aspects]. 177 87

Examination of the effects of dietary manipulation on progression of chronic renal failure (CRF) has been of interest for two reasons: dietary protein restriction is an effective method of ameliorating uremic symptoms and studies of changes in serum creatinine (and later, creatinine clearance or glomerular filtration rate, showed that the course of renal insufficiency is predictable. Results from studies of patients and animals with CRF suggested that a low-protein, phosphorus-restricted diet could slow the rate of loss of renal function. Animal studies have identified several mechanisms for progressive renal damage. These include glomerular hypertension causing capillary damage, glomerular damage from hypertrophic stimuli or hypermetabolism, calcium-phosphorus deposition and nephrotoxicity of the diet. The scientific basis for these different mechanisms will be discussed and each mechanism will be analyzed in terms of experimental studies in patients with CRF.
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PMID:Dietary manipulation and progression of chronic renal failure. 177 91

The incidence of hypertension (HT) in renal parenchymal disease of the young is very high, varying from 38 to 78%. This points to the central role of the kidneys in normal blood pressure control. HT in chronic renal failure (CRF) and end-stage renal disease (ESRD) depends on the nature of the underlying disease. The degree of renal failure has a highly variable effect. The clinical signs and symptoms of this form of HT are often superimposed on those of the basic (renal) disorder. The pathogenesis of HT in CRF is dominated by volume- and renin-mediated mechanisms. In addition, a wide variety of humoral and neural factors play a role. The HT seen in patients on renal replacement therapy (RRT) and after renal transplantation (Tx) poses special problems. In this paper these various aspects of HT in CRF are discussed and the principles of treatment are reviewed. It has been shown beyond any doubt that control of HT in young patients with CRF and ESRD, treated conservatively or on RRT and after renal Tx is of utmost importance for their long-term outcome. This is an important challenge for all pediatricians looking after young patients with CRF and ESRD.
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PMID:Hypertension in children and adolescents with chronic renal failure and end-stage renal disease. 177 94


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