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

When one administers a protein or amino acid load, both GFR and renal blood flow increase about 40% in normal humans as well as in dogs and rats. The protein load causes vasodilation in both the afferent and the efferent arterioles. In these prehypertensive Dahl S rats, it is likely that there is already some vasodilation of the afferent and efferent arterioles and possibly some mesangial relaxation, in order to bring the GFR to normal levels in the face of some intrinsic abnormality in glomerular filtration. Since these arterioles are already dilated, there can be little further dilation in response to the amino acid load and hence no further increase in GFR. It is possible that this limited capacity for further vasodilation could serve as a predictor of future hypertension.
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PMID:Prehypertensive Dahl S rats show no rise in glomerular filtration rate after an amino acid infusion. 326 83

Early in the course of type 1 diabetes mellitus, hypertrophy of the kidney is a consistent finding that is easily diagnosed using current noninvasive methods, especially ultrasonography. Renal functional changes occur in association with hypertrophy, most notably glomerular hyperfiltration. The structural counterpart of this functional change is an early increase in capillary filtration surface area. In most forms of nondiabetic renal hypertrophy, kidney size is closely linked to GFR. In contrast, in diabetes, persistence of hypertrophy after the clinical onset of overt kidney disease (microalbuminuria, hypertension, decreased GFR, etc.) suggests that sustained release of one or more growth factors may continue even after kidney function declines. The fact that growth factors can act in both an autocrine and paracrine fashion raises the possibility that the local effects of such substances may act as local mediators of kidney growth. Failure of renal hypertrophy to reverse following strict glycemic control for a few months may turn out to be an important prognostic indicator of future progression of the renal disease, but this remains to be established. Prospective studies of kidney size in patients with newly diagnosed type 1 diabetes, using accurate noninvasive methods, may be helpful in establishing whether irreversible ("autonomous") hypertrophy of the kidney is indeed a useful prognostic indicator. As therapies are developed that target the different microvascular complications of diabetes (retinopathy, nephropathy, neuropathy), a noninvasive estimation of kidney size may be a cost-effective method of predicting ultimate renal involvement. Since microalbuminuria occurs relatively late in the disease process, early and persistent hypertrophy of the kidney may become a useful prognostic test in the earliest stages of the disease.
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PMID:Prognostic implications of renal hypertrophy in diabetes mellitus. 328 9

We evaluated a chronic renal injury in 37 cardiac transplant recipients treated for 12 to 24 months with cyclosporine (CsA). Twenty-four cardiac transplant recipients treated with azathioprine for more than 24 months served as controls. Despite equivalent cardiac performance, GFR in those treated with CsA was depressed, 47 +/- 3 versus 94 +/- 4 ml/min/1.73 m2 (P less than 0.001). CsA therapy was also associated with significant elevation of renal vascular resistance (RVR), proteinuria, arterial hypertension, and impaired intrarenal conversion of inactive prorenin to active renin. Histopathological changes associated with CsA included an obliterative arteriolopathy with deposition of proteinaceous material in necrotic arteriolar walls, and associated tubulointerstitial damage. A minority of glomeruli exhibited either ischemic collapse or sclerosis. Area perimeter analysis revealed enlargement of the remaining glomeruli with significant expansion of the mesangium. Longitudinal examination over a 48 month period (N = 15) during which CsA was reduced in dosage or withdrawn revealed persistent hypofiltration, increasingly elevated RVR and heavier proteinuria. Further histopathological deterioration was observed when renal tissue was sampled a second time in six patients, and three members of the experimental group developed end-stage renal disease. We conclude that continuous CsA therapy for more than 12 months causes a chronic injury to renal microvessels that is rarely reversible and potentially progressive.
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PMID:The long-term course of cyclosporine-associated chronic nephropathy. 328 2

With the purpose of studying the effect of exercise on renal function in hypertensive patients, renal dynamic studies were performed with the aid of 99mTc-diethylenetriamine pentaacetate (DTPA). Serial renal images were taken at rest and during bicycle ergometric stress in 14 hypertensive patients (H) and 14 normotensive controls (N). Renograms were constructed, and glomerular filtration rate was determined by the method of Gates [2]. Exercise resulted in a prolongation of peak time, an increase in radioisotope retention rate at 10 minutes (10-min counts/peak counts) on renograms, and a decrease of GFR in both H and N. Plasma renin activity, aldosterone, and catecholamines were all elevated during exercise in both H and N. Our data indicate that the exercise-induced renal dysfunction demonstrated by 99mTc-DTPA renograms is not specific to H but can also be observed in N, which may have resulted from changes common to H and N, as indicated by the change of GFR and humoral factors. These findings suggest that the renal response to exercise may be a more complex pathophysiologic process than that measured by the DTPA renogram, at least in its simplified form, and should encourage further work in this area in order to elucidate the underlying process of hypertension.
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PMID:Exercise-induced renal dysfunction studied by 99mTc-DTPA in hypertensives and normotensive controls. 333 Apr 43

Physicians may be called upon to guide patients with renal disease on the advisability of conceiving or maintaining a gestation, or to manage pregnancies permitted to continue. The prevailing view is that the degree of functional impairment and the presence or absence of hypertension prior to conception determine both pregnancy outcome and the effect of gestation on the natural history of the kidney disorder (Table 4). Normotensive women with minimal dysfunction have a 90% chance of success and there is little evidence that gestation will adversely affect the disease. Presence of hypertension increases the complications rate substantially, and prognosis is also poorer in women with moderate renal dysfunction. Most gestations in the latter group succeed, but at considerable maternal risk: over 20% of these women experience renal functional deterioration, and 30-40% of them have major problems with hypertension. Thus we tend not to recommend pregnancy in patients with moderate renal insufficiency, and definitely discourage gestation when GFR is severely impaired. There are a number of diseases in which pregnancy should not be undertaken, including scleroderma and periarteritis. Some authors believe that women with membranoproliferative glomerulonephritis also do poorly, and opinions differ on the effects of gestation on IgA nephropathy, focal glomerulosclerosis, and reflux nephropathy. Table 5 summarizes our view concerning pregnancy in a number of specific renal disorders. Finally, in addition to the controversies noted above, there are other unresolved problems requiring further study. For instance, protein restriction should be avoided until the effect of this therapeutic manoeuvre on fetal development is evaluated. Also needed are conclusive studies on whether or not the physiological hyperfiltration of human pregnancy affects adversely pre-existing renal disease.
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PMID:Gestation in women with kidney disease: prognosis and management. 333 Apr 93

In this cross-sectional study calcium and magnesium metabolism was investigated in normal pregnancies (n = 34) and pregnancies complicated by either fetal growth retardation of hypertension with or without fetal growth retardation (SGA newborns) (n = 30). Special attention has been given to the renal excretion rates of calcium and magnesium and their relationship to creatinine and sodium clearances. No differences were noted in the third trimester of pregnancy between the normal and complicated pregnancies in calcium or magnesium metabolism except for an increased serum magnesium in the SGA group. Comparing the post-partum period to normal pregnancy the following results were observed: (i) serum ionic calcium levels showed no differences; (ii) urinary calcium excretion was increased as a result of increased calcium clearance. A striking feature was the fact that the fractional calcium clearance was not increased, in contrast to the increase in relative calcium clearance. The observed results can be explained by an increased GFR and a possible dissociation between the sodium and calcium handling in the cortical thick ascending Limb of Henle's Loop.
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PMID:Urinary excretion rates of calcium and magnesium in normal and complicated pregnancies. 335 Jan 96

We have recently developed a micropuncture technique to assess repeatedly function of the same nephrons in chronic renal disease and subsequently examine the morphology of their glomeruli by serial thin-section histological analysis. Using this approach, a potential causal linkage between early functional patterns and late structural abnormalities was examined in glomeruli of two established rat models of glomerular sclerosis. The models are (a) puromycin aminonucleoside (PAN) administration in unilaterally nephrectomized Munich-Wistar rats and (b) adriamycin (ADM) treatment in nonnephrectomized Munich-Wistar rats. Single nephron GFR (SNGFR) and glomerular capillary hydraulic pressure (PGC) were measured repeatedly for 8 (PAN rats) or 31 wk (ADM rats). In all animals studied, values for PGC remained at, or slightly below, levels measured before PAN or ADM administration. SNGFR values declined progressively in all glomeruli in PAN rats. Although some glomeruli in ADM rats had an increase in SNGFR above levels observed in nonnephrectomized control rats, these hyperfiltering glomeruli did not have abnormally high PGC nor did they exhibit glomerular sclerosis at the completion of the study. Histological analysis revealed the existence of a significant inverse correlation between the degree of sclerosis and SNGFR assessed at the time of sacrifice in both PAN and ADM groups. Chronic administration of captopril, an angiotensin I converting enzyme inhibitor, in PAN rats substantially attenuated development of glomerular sclerosis without affecting PGC in earlier stages. The observations in these models indicate that glomerular hyperfiltration and hypertension are not required for the development of glomerular sclerosis in renal diseases, and angiotensin I converting enzyme inhibitor can exert its protective effect independently of its effect on glomerular capillary pressure.
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PMID:Serial micropuncture analysis of glomerular function in two rat models of glomerular sclerosis. 339 11

The clinical presentation, initial laboratory and renal biopsy findings, and subsequent clinical course in 205 children with IgA nephropathy were studied retrospectively. The findings in the 119 patients with macroscopic hematuria and those in the 86 without macroscopic hematuria were compared. There were no differences with regard to sex distribution, age at onset, initial renal function, incidence of hypertension, degree of proteinuria and degree of mesangial proliferation. At the latest follow-up, 3% of the patients with macroscopic hematuria and 8% without macroscopic hematuria had developed chronic renal failure; 8% of the patients with macroscopic hematuria and 20% without had heavy proteinuria with or without hypertension (p less than 0.01); 41% of the patients with macroscopic hematuria and 24% without macroscopic hematuria had normal urine, blood pressure and GFR (p less than 0.05). The disease appears to follow a significantly more benign course in children with macroscopic hematuria than in those without macroscopic hematuria. These observations suggest some macroscopic hematuria-related differences in the natural history of childhood IgA nephropathy.
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PMID:Macroscopic hematuria in childhood IgA nephropathy. 342 31

Spontaneously hypertensive rats (SHR) were mated with Munich-Wistar rats (MW), and the F1 hybrids were called Escola Paulista de Medicina (EPM) rats. The EPM rats present spontaneous hypertension and superficial glomeruli, allowing a study of glomerular haemodynamics. Mean whole kidney (GFR) and single nephron glomerular filtration rate (SNGFR), and mean total and glomerular plasma flow, were similar in EPM and MW rats. However, a higher glomerular capillary hydraulic pressure and a reduced ultrafiltration coefficient (Kf) of EPM rats were observed. The glomerular hypertension may be the cause of low Kf, a possible initial lesion of glomerular sclerosis. When mean arterial pressure levels were reduced to about 90 mmHg, a maintenance of SNGFR, with a 40% reduction in GFR, in EPM rats were achieved, suggesting an autoregulatory mechanism in the superficial but not in the juxtamedullary nephrons. The decrease on urinary sodium excretion (UNaV) in this condition, which was also lower than in MW rats, showed an impaired sodium handling by EPM kidneys, a possible role in the hypertension genesis. Thus, the data suggest that EPM rats can be a useful model for glomerular haemodynamics and microcirculatory studies in the spontaneously hypertensive state.
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PMID:Renal haemodynamics in spontaneously hypertensive rats with superficial glomeruli. 346 5

Based on 28 reported patients, constant features of the syndrome of hypertension and hyperkalaemia are hyperkalaemia, hyperchloraemia, normal renal glomerular function and, in all adult patients, hypertension. Inconstant features include short stature, intellectual impairment and muscle weakness. Levels of renin and aldosterone are low, but respond to dietary salt restriction and diuretic therapy, both of which reverse the hypertension and hyperkalaemia. The basic abnormality is excessive renal sodium retention, leading to chronic suppression of renin and aldosterone; the latter is then hyporesponsive to the hyperkalaemic stimulus. Dietary salt loading or impaired production of any natriuretic or chloriuretic factor (for example atrial natriuretic peptide or renal natriuretic prostaglandins) would predispose to development of the syndrome. With normal GFR, this appears to be a unique mechanism for hypertension and hyperkalaemia.
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PMID:The syndrome of hypertension and hyperkalaemia with normal GFR. A unique pathophysiological mechanism for hypertension? 352 20


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