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

The authors have studied relationships of renal structure and function in more than 100 patients with insulin-dependent diabetes mellitus (IDDM), aged 13-55 years (mean, 30 years) with diabetes for 1-30 years (mean, 19 years). The authors confirmed the unique nature of the diabetic lesions that, in constellation, occur in no other disease. It was found that increased fractional mesangial volume (Vv Mes) is strongly associated with decreased glomerular filtration rate (GFR), proteinuria, and hypertension and that all patients with overt diabetic nephropathy have Vv Mes in excess of 0.35 micron 3/micron 3. This relationship results from constriction of the capillary lumen and filtration surface as a consequence of increased Vv Mes. Global glomerulosclerosis (scarring) is common in IDDM patients and appears related to arteriolar hyalinosis. Focal segmental glomerulosclerosis is a rare lesion in these patients. Having a single kidney (transplanted IDDM patients) is not associated with accelerated lesion development. The presence or absence of microalbuminuria (MA), per se, does not predict underlying glomerular structure, which may vary from the normal range to a level of pathology bordering on that regularly associated with overt nephropathy. However, when MA is associated with hypertension, or reduced GFR or both, urine albumin excretion (UAE) generally exceeds 40 mg/24 hr, and glomerular pathology is always present. The authors concluded that diabetic nephropathy is a unique renal disorder that cannot be caused by hemodynamic factors alone. The authors further conclude that MA becomes a predictor only when other features of overt nephropathy are already present and that serious diabetic glomerular lesions can be present in patients with normal UAE.
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PMID:Some lessons from the studies of renal biopsies in patients with insulin-dependent diabetes mellitus. 297 62

Focal glomerulosclerosis (FGS) is commonly seen in human and in experimental models of chronic renal disease. Although considerable experimental data suggest that hypertension is important in progressive nephron damage, recent studies also have indicated that abnormal lipid metabolism may be an independent risk factor in the pathogenesis of FGS. Indeed, the synergistic impact of hypertension and hyperlipidemia in the pathogenesis of FGS may be analogous to the role of these factors in the pathogenesis of atherosclerosis. This review focuses on some of the recent and pertinent data that support a role of lipid-mediated glomerular injury in the pathogenesis of progressive renal disease.
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PMID:Hyperlipidemia and the progression of renal disease. 327 33

In summary, both the developing atherosclerotic and FSGS lesions seem to share certain postulated pathophysiologic mechanisms, including endothelial cell injury, macrophage infiltration, hyperlipoproteinemia, and hypertension. As depicted in Figure 1, any initial glomerular injury results in flux of macromolecular substances into the glomerular mesangium. As an adjunct to increased glomerular barrier dysfunction, hyperlipoproteinemia is believed to secondarily develop from the dramatic losses of albumin, stimulating increased hepatic lipoprotein synthesis and the loss of lipoprotein lipase-activating substance into the urine which would effectively produce a reduction in circulating chylomicra and triglyceride catabolism. Certain elevated circulating lipoproteins could, theoretically, pass through the damaged glomerular filter into the mesangium, thereby enhancing the flux of macromolecules. Also associated with certain experimental glomerular disorders is the development of glomerular hypertension, as manifested by an elevated glomerular capillary hydrostatic pressure (PGC), which can further augment macromolecular flux into the mesangium. Overloading of the glomerular mesangium by the above mechanisms is believed to be an injurious stimulus for MC to both proliferate and produce excess mesangial matrix substance. Both of these events are thought to be pathologic harbingers of glomerulosclerosis. Glomerular hypertension is also capable of damaging endothelial cells within the glomerular microcirculation, and this purportedly can activate platelets and result in glomerular thrombosis. At present, it is unclear how glomerular thrombosis produces increased mesangial cell injury; however, this process is believed to cause both systemic and glomerular hypertension which may serve as intermediary mechanisms producing the untoward effects of mesangial cell proliferation and matrix overproduction.
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PMID:Focal and segmental glomerulosclerosis: analogies to atherosclerosis. 329 16

The pattern of glomerulonephritis (GN) consisting of 1057 renal biopsies is presented. Primary GN accounted for 91% and secondary GN 9% of which the commonest is lupus nephritis. Asymptomatic haematuria and proteinuria was the commonest mode of presentation (41%), gross haematuria 9%, nephrotic syndrome 29% while 5.5% presented with renal impairment and 4.3% with hypertension. Mesangial proliferative GN is the commonest histopathological lesion forming 66% of all primary GN. Minimal Lesion, Focal Global Sclerosis and Focal Segmental Glomerulosclerosis accounted for 7% each. Membranous GN was uncommon (3%) while Mesangiocapillary GN, Diffuse Endocapillary GN and Crescentic GN were even rarer. If the presenting feature was asymptomatic haematuria and proteinuria the likely diagnosis was IgA nephritis, and, if nephrotic syndrome it was likely to be Idiopathic Mesangial Proliferative GN but with negative staining on immunofluorescence. The course and prognosis of the various forms of GN are next discussed. Nephrotic syndrome with Minimal Lesion has an excellent prognosis while Crescenteric GN usually carries a grim prognosis. Finally, factors affecting the progression of IgA nephritis, the commonest form of GN occurring in Singapore are examined. Patients who developed renal failure ran two different courses; one was a slowly progressive course over an average of 7.7 years before reaching end stage renal failure (ESRF), while the other was a more rapid decline to ESRF within an average of 3.3 years where severe uncontrolled hypertension seemed to be the major adverse factor. 9% had renal impairment at the end of a follow up of 50 + 1/2 - 34 months while 5% progressed to ESRF. The cumulative renal survival was 91% after 6 years with no further loss up to 14 years. Unfavourable long term prognostic indices were proteinuria of more than 2 gms, hypertension, crescents on renal biopsy, severe segmental sclerosis and medial hypertrophy of blood vessels.
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PMID:Glomerulonephritis in Singapore: an overview. 370 31

It is well known that patients with different kidney diseases have different prevalence of hypertension, independent of renal function. To investigate whether a lesion of some portion of the glomerular tuft, without renal insufficiency, is associated more frequently with high blood pressure, we undertook a retrospective study on 189 patients analyzing by means of multiple regression analysis as independent variables : type of glomerulopathy (IgA Nephropathy, Acute Glomerulonephritis, Membranous Glomerulonephritis and Focal Glomerulosclerosis), sex, age, body weight, plasma creatinine, plasma and urinary proteins, plasma urate, time interval first symptom-renal biopsy and steroid therapy. The dependent variable was a Principal Component formed by Mean Blood Pressure and an Antihypertensive Therapy score, calculated with a computer program. Focal Glomerulosclerosis patients had a higher prevalence of hypertension and a higher Principal Component value than patients of the other 3 groups. Plasma urate was correlated and time interval first symptom-renal biopsy was inversely correlated to Principal Component. These observations suggest that sclerosis of the glomeruli is the lesion most often associated with hypertension. On the other hand, since plasma urate is correlated with blood pressure also in "essential" hypertensives, it seems likely that hyperuricemia is a phenomenon secondary to hypertension.
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PMID:Blood pressure in patients with four different primary glomerulopathies. 646 43

Renal biopsies from hypertensive pregnant women performed 8 to 10 days postpartum were processed by morphometric analysis. We allocated the 74 patients into four groups according to the respective forms of pregnancy hypertension, i.e. preeclampsia and gestational hypertension. Groups I and II included preeclamptic women, with (group I) or without (group II) de novo FSGS. Groups III and IV included biopsies of women with isolated gestational hypertension, appeared during the third trimester (group III) or earlier (group IV). The control group included 17 biopsies from age-matched nonpregnant women presenting with isolated hematuria. Glomerular lesions of typical preeclampsia were seen in all the biopsies of groups I and II, and in some of women with gestational hypertension of groups III and IV. Our morphometric analysis of these renal biopsies showed a progressive increase in glomerular size from early gestational hypertension, gestational hypertension of the 3rd trimester, isolated preeclampsia, and finally preeclamptic nephropathy associated with FSGS. The largest glomeruli were seen in preeclamptic women with severe hypertension and histologic lesions of preeclampsia with FSGS. Thus, both systemic hypertension and glomerular hypertrophy seem necessary to induce FSGS in this type of pathology.
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PMID:Preeclampsia associated focal and segmental glomerulosclerosis and glomerular hypertrophy: a morphometric analysis. 792 75

Focal segmental glomerulosclerosis (FSGS) is a common outcome of a variety of renal diseases. Among laboratory animals both puromycin aminonucleoside (PAN) and hypertension produce a similar histological pattern. Since mesangial expansion is a precursor of FGS and decreased degradation of matrix can cause expansion of mesangium we studied the glomerular matrix metalloprotease activities in the development of FSGS. Dahl salt sensitive (SS) and salt resistant (SR) rats were fed 8% salt diet for six weeks. Kidney biopsy showed features of FSGS in SS rats. Glomeruli were isolated and metalloprotease activity was measured. Sprague-Dawley rats were administered subcutaneously either saline (S) or saline containing PAN (1.67 mg/100 g B. W.) daily for 7 days. Kidney biopsy was done at day 7 and the isolation of glomeruli was performed at day 10 and at 6 weeks. Renal histology showed features of FSGS in PAN rats at 6 weeks. Glomerular metalloprotease activity was decreased in SS (SR, 148 +/- 12 vs. SS, 73 +/- 9 cpm/microgram protein, p < 0.01) as well as in PAN rats (S, 31 +/- 5 vs. PAN, 12 +/- 1 cpm/microgram protein, p < 0.01). These results suggest that decreased glomerular metalloprotease activity may play a role in the development of FSGS in SS and PAN rats.
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PMID:Glomerular metalloprotease activity modulates the development of focal segmental glomerulosclerosis. 871 46

This review compares the biopsy patterns, complications, responses to therapy, and long-term outcomes of idiopathic NS in children and adults. On first examination, distinctions between the pediatric and adult diseases seem more quantitative than absolute. However, underlying determinants of outcome, including immunocompetence, growth, maturity, and senescence, can present very different challenges for pediatricians and internists. The major biopsy patterns in pediatric NS include MCD, FSGS, and DMP. MCD is overwhelmingly the most frequent and most steroid-responsive of the three but commonly presents problems of massive edema, serious bacterial infections, and multiple relapses. Because of the prompt response of pediatric MCD to corticosteroids, steroid resistance in children has generally been defined as persistence of proteinuria after 1 month of daily followed by 1 month of intermittent prednisone administration. By this criterion, nephrotic FSGS is usually steroid-resistant and, if not controlled by more aggressive therapy, typically progresses to ESRD. DMP is commonly steroid-resistant but may slowly resolve. It is not clear to what extent remissions of DMP represent a delayed response to steroids or would have occurred without treatment. Biopsies showing a few globally obsolescent glomeruli or mild mesangial hypercellularity may be associated with greater difficulty in management but have been included in the broad category of MCD. Moreover, evolution of patterns in serial biopsies, variable steroid-responsiveness of FSGS and DMP, and progression of some cases of MCD to ESRD suggest common features in the three major categories. Among adults with idiopathic NS, FSGS is the most frequent biopsy pattern, followed by MN (which is rare in children) and then by MCD. In contrast to its pediatric counterpart, MCD in adults is less regularly and more slowly responsive to corticosteroids and in the elderly is more commonly associated with hypertension and renal failure. MCD in adults is less likely to relapse once remission is achieved. Adults with FSGS present less commonly with severe edema than do children with this lesion. Although children and adults with FSGS present similar challenges of resistance to therapy and loss of renal function, the more aggressive oral steroid regimens used by internists preclude strict comparisons between pediatric and adult series. There is insufficient information to support a systematic analysis of DMP in adults. Cytotoxic agents and cyclosporine have been used with varying success in children and adults with difficult cases of NS. In MCD, an alkylating agent can increase the likelihood and duration of remission. Cyclosporine can also improve control in MCD, but continued treatment is often needed to maintain remission. Significant control of steroid-resistant FSGS has not been achieved with limited courses of an alkylating agent or cyclosporine. Longer courses of either of these immunosuppressants, especially when combined with intermittent steroid administration, can produce more complete and/or more sustained remissions. However, cyclosporine nephrotoxicity is more severe in FSGS than in MCD and in steroid-resistant than in steroid-dependent NS, regardless of biopsy pattern. A protocol combining iv M-P pulses, alternate-day prednisone, and an alkylating agent in steroid-resistant pediatric FSGS has produced the highest percentage of sustained remissions with normal renal function, of all reported regimens. Controlled trials of this and other combined drug protocols are needed in children and adults.
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PMID:Treatment of the idiopathic nephrotic syndrome: regimens and outcomes in children and adults. 917 55

Focal segmental glomerulosclerosis (FSGS) is thought to have several causes, including hypertension, reduction of nephron mass, or immunologic processes. Experimental studies have underlined the role of glomerular adaptation to capillary pressure in the growing kidney after partial nephrectomy. We report here the occurrence of FSGS in one of two "en bloc" pediatric kidneys transplanted in an adult recipient. One of the kidneys sustained early ureteral obstruction requiring reoperation and subsequently developed pathological changes on biopsy consistent with FSGS, whereas the mate kidney did not, although both kidneys grew at equal rates and to equivalent sizes.
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PMID:Focal segmental glomerulosclerosis in one of two "en bloc" pediatric transplanted kidneys. 926 Oct 40

Little attention has been paid to nephropathies and proteinuria in renovascular hypertension (RVH). Recently there has been a growing interest in the conditions induced by RVH. 10 cases of RVH were diagnosed by angiography and renin sampling from renal veins in the last 6 years in our hospital. The patients were all male and mean age was 64 +/- 8 (SD) years. Data were as follow: protein excretion was 3.8 +/- 2.2 g/day (> or = 3.5 g/day in 8 patients), sBP 202 +/- 24 mmHg, dBP 113 +/- 17 mmHg, serum renin concentration 64 +/- 45 pg/ml, and ipsilateral/contralateral renal vein renin ratio 3.3 +/- 1.0. RVH was treated by nephrectomy in 3 patients, percutaneous transluminal renal angioplasty (PTA) in 2, and angiotensin converting enzyme inhibitors (ACE-I) administration in 8. Biopsies were performed on contralateral kidney in 4 patients. Focal segmental glomerulosclerosis (FGS) was found in 3 patients, and nephrosclerosis in 1, whereas only nephrosclerosis was found in nephrectomized kidneys in all 3 patients. After nephrectomy, PTA and the treatment by ACE-I, not only blood pressure but also proteinuria was markedly reduced. These findings suggest that severe stenosis of the renal artery led to renal ischemia, which activated renin excretion, to cause glomerular hyperfiltration through vasoconstriction of the efferent arterioles in the contralateral kidney. FGS-like lesion thus induced appeared to have caused massive proteinuria.
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PMID:Renovascular hypertension may cause nephrotic range proteinuria and focal glomerulosclerosis in contralateral kidney. 935 55


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