Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sixteen children with extensive crescentic glomerulonephritis and rapid renal deterioration were selected from 476 patients with glomerulopathy for study. The patients (1-14 yr, M:F = 5:11) presented with edema, oligoanuria, hypertension, gross hematuria and uremic symptoms in 81, 62, 62, 56 and 50 per cent, respectively. The mean Scr was 804 (+/- 436) micromole/L and BUN 38 (+/- 13.4) mmole/L. Anemia was found in 100 per cent, hematuria in 100 per cent, heavy proteinuria 75 per cent, hypoalbuminemia 40 per cent, hypercholesterolemia 38 per cent and low C3 40 per cent. The underlying causes of RPGN included idiopathic 9, PSAGN 6 and LE 1. Eight patients recovered with normal or slightly elevated Scr while the diseases progressed to ESRD in 8 patients. Idiopathic RPGN and extensive (greater than 80%) crescentic glomerulonephritis correlated with a poor prognosis.
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PMID:Rapidly progressive glomerulonephritis in Thai children. 140 80

The patient was a 64-year-old female who had been treated by a local doctor for rheumatoid arthritis and hypertension for 10 years. Malaise and edema developed since July, 1990, and as proteinuria and renal dysfunction were noted, the patient was admitted to our hospital on November 2. On admission, BUN was 33mg/dl, creatinine was 2.5mg/dl, and proteinuria was about 3g/day. Renal biopsy was performed after admission. Light microscopy revealed nodular lobulation of glomeruli and occlusion of loops. Dylon staining was negative. Immunofluorescent study showed granular deposition of IgG, IgM, C3, C4, Clq in the glomerular basement membrane and mesangial area. Electron microscopy showed a large amount of electron dense deposits in the subendothelium and mesangial area and dense aggregation of tubular structure in the deposit, part of which exhibited a profile of fingerprint deposit. The tubular structures were classified into three major types, which were 120, 100, and 50nm in diameter. From these findings, a diagnosis of immunotactoid glomerulopathy was made. After renal biopsy, plasmapheresis and prednisolone were administered, and the patient has been managed conservatively to date.
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PMID:[A case of rheumatoid arthritis with immunotactoid glomerulopathy]. 148 14

To evaluate the role of glomerular hypertension, glomerular hypertrophy, glomerular lipid deposition, and plasma cholesterol levels in diabetic glomerulopathy, Munich-Wistar rats received streptozocin and daily insulin injections and were assigned to one of three groups: untreated diabetic (DMC), hydralazine-treated diabetic (DMH), and enalapril-treated diabetic (DME). Age-matched control rats were also studied. At 6-10 wk of diabetes, DMC rats showed marked elevations of glomerular pressure and glomerular filtration rate as well as slight glomerular enlargement and cholesterol elevation. DMH and DME rats exhibited arterial hypotension but no change in cholesterol or glomerular volume. Glomerular pressure was normalized by enalapril but not by hydralazine treatment. Additional rats were followed up to 12 mo of diabetes. Slight hypertension was seen in DMC rats, whereas sustained hypotension occurred in DMH and DME rats. Progressive albuminuria occurred in DMC and DMH but not in DME rats. At 12 mo, glomerular hypertension persisted in DMC and DMH rats but was still absent in DME rats. Cholesterol was elevated in DMC and slightly lower in DMH and DME rats. Glomeruli were equally enlarged in the diabetic groups. Glomerular sclerotic lesions and lipid deposits appeared in DMC and DMH but not in DME rats. These findings are consistent with the notion that glomerular hypertension may promote glomerular injury in experimental diabetes. Glomerular lipid deposition may also participate in this process, although a causal relationship was not demonstrated. Glomerular hypertrophy and cholesterol were unrelated to glomerular injury, although they may have exacerbated hemodynamically mediated damage.
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PMID:Glomerular abnormalities in long-term experimental diabetes. Role of hemodynamic and nonhemodynamic factors and effects of antihypertensive therapy. 155 88

Eight women with insulin-dependent diabetes mellitus (IDDM) with low creatinine clearance rate (CCR) and normal urinary albumin excretion (UAE) were compared with three other groups of diabetic women: 19 with normal creatinine clearance rate (CCR) and UAE, 7 with normal CCR and microalbuminuria, and 7 with low CCR and microalbuminuria. The four groups were similar in age, duration of diabetes, HbA1, incidence of urinary tract infection, prevalence of bladder neuropathy, and urinary urea nitrogen excretion rate. The prevalence of hypertension was similar among the groups, although mean arterial pressure was higher in the low CCR and microalbuminuria group. Renal area index was lower in the low CCR and normal UAE groups than in the other groups of diabetic patients, but was not different from normal. Morphometric measures of mesangial expansion and estimates of arteriolar hyalinosis and global glomerulosclerosis were increased to a similar degree in the low CCR and normal UAE, normal CCR and microalbuminuria, and low CCR and microalbuminuria groups compared with the group without abnormalities of renal function. Therefore, it is likely that diabetic glomerulopathy is, at least in part, responsible for the loss of glomerular filtration rate seen in the low CCR and normal UAE patients. Thus, the definition of incipient nephropathy may have to be expanded beyond the concept of microalbuminuria if longitudinal study of such patients reveals an increased risk of the subsequent development of overt nephropathy. Finally, screening for diabetic kidney disease among IDDM patients should include determination of glomerular filtration rate and measurement of UAE and blood pressure, especially among women.
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PMID:Glomerular structure in IDDM women with low glomerular filtration rate and normal urinary albumin excretion. 156 27

New insights into the physical chemistry and molecular epidemiology of sickle cell anemia have improved our understanding of the pathophysiology of the associated nephropathy, the predictors of this complication, and genetic and other factors that may modify it. In this article, we analyze the current clinicopathologic knowledge with reference to the predilection to nephropathy and the protection from hypertension, as well as the altered renal physiology of the sickle cell state that underlies both these phenomena. In the early stages of sickle cell anemia, the kidney is characterized by impaired function of the renal medulla, as evidenced by reduced capacity to concentrate, acidify, and excrete potassium into the urine. Meanwhile, the cortex functions supranormally, as evidenced by increased renal plasma flow and glomerular filtration rate, proximal tubular function, and urinary diluting capacity. In addition to the complications of hematuria and papillary necrosis, renal insufficiency supervenes in a subgroup of patients. The morphology of the glomerulopathy generally differs between children and adults; in the latter group there is a particularly poor prognosis and markedly shortened life expectancy. Renal replacement therapy has nonetheless been successful. Although hypertension may be found at this stage, it is extremely rare before the onset of significant renal impairment. The possible mechanism of this protection is discussed, with a focus on the compelling need for further investigation in light of the newly gained basic understanding of this hematorenal syndrome.
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PMID:The kidney in sickle cell anemia. 157 59

Glomerular hemodynamics were measured in male Sprague-Dawley rats, aged 4 to 5 months (young) or 20 to 22 months (old). Body weight (BW) and left kidney weights (KW) were higher in old rats than young (BW: 507 +/- 12 g v 342 +/- 11 g, P less than 0.001; KW: 2.0 +/- 0.1 g v 1.3 +/- 0.1 g, P less than 0.001). Arterial blood pressure (AP) was slightly higher in old rats, but within the normotensive range (106 +/- 4 mm Hg v 94 +/- 4 mm Hg, P less than 0.05). Glomerular filtration rate (GFR; factored for KW) was lower in old versus young rats (0.67 +/- 0.05 mL/min/gKW v 1.00 +/- 0.08 mL/min/gKW, P less than 0.02). The cortical surface of the kidney in old (but not young) rats showed marked heterogeneity and single-nephron (SN)GFR was measured only in filtering nephrons and was higher and more variable in old versus young rats. Glomerular blood pressure (PGC) was unchanged in old compared with young rats (53 +/- 4 mm Hg v 55 +/- 2 mm Hg). There was a significantly greater level of glomerular sclerosis (in outer cortical glomeruli) in old versus young rats, and glomerular volume was substantially greater in old rats. This study suggests that age-related glomerulopathy is not primarily mediated by glomerular capillary hypertension.
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PMID:The effect of aging on glomerular hemodynamics in the rat. 162 81

Recent studies in animal models suggest that glomerular capillary hyperperfusion and hypertension, rather than ischemia, cause renal injury. Interventions that control glomerular capillary hypertension may protect against progressive injury, even in the presence of continued systemic hypertension. In the absence of systemic hypertension, diabetes mellitus is a prominent clinical example of glomerular hypertension. Animal studies have shown that glomerular hemodynamic abnormalities, especially elevations in glomerular pressure, play an important role in the pathogenesis of diabetic glomerulopathy. A number of clinical observations suggest that angiotensin converting enzyme (ACE) inhibitors may delay the progression of diabetic nephropathy by their effects on renal hemodynamics. In experimental animals, comparisons between calcium channel blockers and ACE inhibitors have shown the latter to be more effective in protecting the kidneys. Preliminary clinical studies indicate that ACE inhibitors may have advantages in preserving renal function in hypertensive and diabetic patients with renal failure.
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PMID:Renal effects of converting enzyme inhibitors in hypertension and diabetes. 169 12

One-kidney, one-clip hypertension (1-K, 1-C HT) is initiated by increased preglomerular resistance which decreases nephron perfusion and causes several intrarenal changes that lead to increased mean arterial pressure (MAP). Elevated MAP serves to return nephron perfusion and sodium excretion to normal, so that fluid intake and output are balanced. Increased MAP usually occurs through volume homeostasis mechanisms that initially raise cardiac output and later elevate total peripheral vascular resistance via autoregulatory adjustments. However, if adequate volume is unavailable because of sodium restriction, sustained activation of the renin-angiotensin system increases blood pressure sufficiently to restore nephron perfusion. Thus, depending upon the availability of volume, renal perfusion and sodium balance can be restored either by volume retention or by increased angiotensin II (ANGII) formation and peripheral vasoconstriction. Similarities exist between 1-K, 1-C HT and low-renin essential hypertension (LRHT). In both cases, renal-pressure natriuresis is shifted to higher levels and there are marked increases in preglomerular resistance that necessitate increased MAP to maintain sodium balance. However, in 1-K, 1-C HT, there is a parallel shift of pressure natriuresis with little or no change in the slope of this curve, similar to that found in the normal-renin essential hypertension. In LRHT the slope of pressure natriuresis is decreased, indicating that blood pressure is much more salt sensitive than normal. Another difference is that PRA is low compared to normal PRA in 1-K, 1-C HT after compensatory increases in MAP. There is also no indication of glomerular membrane damage in 1-K, 1-C HT, whereas LRHT may have significant glomerulopathy, especially as hypertension progresses. These differences suggest that there may be additional factors besides preglomerular vasoconstriction involved in the etiology of LRHT. One possible factor is a reduction in nephron number in LRHT. Decreased functional nephrons would lead to glomerular hyperfiltration and increased distal tubular flow rate in the remaining nephrons, causing decreased PRA and eventually glomerular damage. Increased fractional sodium reabsorption, particularly in distal tubular segments, could also contribute to decreased PRA and cause blood pressure to be salt sensitive. These abnormalities, along with preglomerular vasoconstriction, may explain many of the characteristics of LRHT.
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PMID:Renal function in one-kidney, one-clip hypertension and low renin essential hypertension. 174 89

Focal sclerosing glomerulopathy and especially focal segmental glomerulosclerosis (FSGS) have been recognized as a distinct clinical entity, however, there still exist controversies in terms of prognostic risk factors of progression and optimal mode of treatment. A total of 32 patients (2 with focal global sclerosis; FGS, the remainder with FSGS) were followed up for a mean period of 82 months (3-240 months). Fourteen presented with nephrotic syndrome and 18 had proteinuria with or without hypertension. Thirteen patients, all of whom except 1 were nephrotic, received steroid treatment with or without other immunosuppressive agents (cyclophosphamide/cyclosporin A/azathioprine). Three of the steroid-treated remained stable in complete remission; 5 nephrotic non-responders had renal death. The mean slope of 1/creatinine versus time for steroid-treated and non-treated groups was -0.23 and -0.043, respectively (p = 0.04), suggesting that nephrotic range proteinuria might be prognostically important. However, for the population of FSGS/FGS as a whole, only the initial serum creatinine predicted renal survival (p = 0.001 by Cox's regression model). Hypertension and hypercholesterolaemia were not important variables by themselves. Nevertheless, we found that the 9 patients treated with antihyperlipidaemics (gemfibrozil/probucol/cholestyramine/maxEPA) fared better, mean slope being -0.023 versus -0.103 for non-treated, though not reaching statistical significance (p = 0.96). Controlled prospective study involving a larger number of patients might be worthwhile.
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PMID:Focal sclerosing glomerulopathy. Risk factors of progression and optimal mode of treatment. 176 95

Diabetic nephropathy, clinically defined by overt albuminuria, hypertension and declining GFR, affects 25-35% of IDDM patients. The risk of nephropathy peaks during the second decade of IDDM and declines thereafter, suggesting that only a subset of IDDM patients is at risk for nephropathy. A role for hypertension in the progression of established renal damage in IDDM is now accepted; however the role of hypertension in the genesis of diabetic nephropathy is not yet clear. Mesangial expansion is a characteristic lesion of diabetic nephropathology and correlates with renal function. Functional studies are not indicative of underlying renal pathology except relatively late, when glomerular injury is advanced. Microalbuminuria in the 'predictive' range (greater than 30 micrograms/min) and associated with hypertension and/or declining GFR is a marker of established diabetic glomerulopathy. Only carefully designed longitudinal studies of renal morphology and function with accurate blood pressure monitoring beginning early in the course of IDDM will clarify the relationships between blood pressure and renal damage in IDDM. In NIDDM the frequent presence of non-diabetic renal lesions, of hypertension at or before the onset of diabetes, and the relative paucity of clinical-pathological correlations currently make it difficult to understand the role of hypertension in the genesis and progression of nephropathy. Again, longitudinal studies of blood pressure and renal structure and function are required in NIDDM patients. Finally, animal models of hypertension and diabetes may aid progress in these areas.
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PMID:Hypertension and diabetic renal disease. 179 13


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