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)

In 51 patients with type 1 and 9 patients with type 2 membranoproliferative glomerulonephritis, we found a male predominance in both types, a wide age range but with younger patients having predominantly type 2 disease, and clinical presentations that varied and included the nephrotic syndrome, an abnormal urinalysis only, acute nephritis, and recurrent hematuria. Hypertension and impaired renal function at the time of first evaluation, which were present in more than one-third of the patients, presaged a poor prognosis; in most of these patients end-stage renal failure or worsening of renal function occurred. Acute nephritis at onset was also related to a deteriorating course and was especially frequent in patients with type 2 membranoproliferative glomerulonephritis. Retrospective analysis of treatment regimens, in which patients were given an average of 1 year of therapy with prednisone alone or combined with cytotoxic agents, showed no effect in patients who had progressive forms of the glomerulopathy.
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PMID:Idiopathic membranoproliferative (mesangiocapillary) glomerulonephritis: a clinicopathologic study. 43 Nov 20

A 30 year old man developed renovascular hypertension and extreme elevation of plasma renin activity. Daily proteinuria ranged from 13 to 31 g. There were no criteria for the diagnosis of malignant hypertension. A primary glomerulopathy was excluded by a basically normal renal biopsy from the unprotected kidney. On electron microscopy the epithelial cell foot processes were not fused, thus ruling out simultaneous lipoid nephrosis. The source of renin was removed by means of a left nephrectomy. Following the procedure the patient became normotensive, the renin values normalized and the proteinuria disappeared. The results suggest that renin can cause significant proteinuria in man.
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PMID:Renin-induced massive proteinuria in man. 45 23

Rats with classic Goldblatt (two-kidney) hypertension had diabetes induced by streptozotocin. After four months of diabetes, glomeruli of the unclipped kidney of hypertensive diabetic rats had markedly increased diabetic changes, including mesangial matrix thickening and mesangial immunoglobulin (IgG and IgM) and complement (C3) localization, when compared with glomeruli of the contralateral-clipped kidneys. Further, glomeruli of the unclipped kidneys of hypertensive diabetic animals had more mesangial thickening and IgG and IgM staining than glomeruli of normotensive diabetic rats. Although glomeruli of clipped kidneys in hypertensive diabetic rats had less mesangial thickening than glomeruli of normotensive diabetic rats, this did not reach statistical significance. However, these glomeruli did have significantly less IgG, IgM, and C3 staining compared with glomeruli of normotensive diabetic animals. Mesangial thickness in glomeruli of clipped and unclipped nondiabetic hypertensive rats did not differ from that in normal animals. However, there was less mesangial IgG staining in clipped than in unclipped kidneys of nondiabetic hypertensive rats or in kidneys of normal animals. We have interpreted these results to imply that alterations in nephron hemodynamics combine with the diabetic state to influence the rate of development of diabetic glomerulopathy in rats.
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PMID:The effects of Goldblatt hypertension on development of the glomerular lesions of diabetes mellitus in the rat. 65 20

The present studies were designed to characterize the extent and pathogenesis of the glomerular lesions which occur in the viable portion of the kidney following partial renal infarction in rats. Control rats with two normal kidneys had a mean blood pressure of 112 mm Hg, minimal proteinuria and no glomerular pathology on light (LM), electron (EM) or immunofluorescence microscopy (IFM). Rats with two-thirds infarction of one kidney (stage II) became hypertensive, although less than 4% of the glomeruli from either kidney were abnormal. Rats with two-thirds infarction of one kidney and contralateral nephrectomy (stage III) developed proteinuria and hypertension whether fed a normal, low or high Na+ diet. By light microscopy 37% of glomeruli were abnormal 28 days after partial infarction and contralateral nephrectomy and thereafter the percent of abnormal glomeruli increased. Detectable amounts of immunoglobulin and complement (C3) were present in kidneys of stage II or III rats but were always accompanied by more extensive albumin and fibrin deposits. Basement membrane deposits characteristic of immune complexes were not seen on EM. Administration of antihypertensive medication to stage III rats significantly lowered blood pressure and reduced the number of abnormal glomeruli on LM; however, IFM abnormalities remained prominent. Platelet thrombi seen by EM and abundant glomerular fibrin deposits seen on IFM suggested that coagulation mechanisms may be prominent in the pathogenesis of the renal lesion. Heparin-treated stage III rats had significantly lower blood urea nitrogen concentrations, blood pressures and proportion of abnormal glomeruli although glomerular deposition of serum proteins was still present on IFM. These observations suggest that this glomerulopathy is initiated by an unknown agent(s) which increased capillary permeability. This lesion progresses via thrombotic mechanisms which are prevented by heparin administration.
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PMID:Pathogenesis of the glomerulopathy associated with renal infarction in rats. 94 Feb 76

The present study discusses the light, electron and immunofluorescence microscopy as well as some clinicopathologic correlations of rejection change in human renal allograft glomeruli. It is based on examination of 126 tissue specimens from 54 grafts obtained from 50 patients (1966-1973). The most frequent and characteristic lesion was membranous transplant glomerulopathy (MG) with irregular fibrillar thickening of capillary walls but without conspicuous hypercellularity. This thickening was caused by subendothelial depositsdifferent from classical fibrinoid lesions. During further progression, widening and peripheral extension of mesangium with degenerative changes became apparent. Advanced MG was encountered most frequently in the 2nd year after transplantation (TPL) at moderate to medium proteinuria and hypertension. It was accompanied by endarteristic rejection changes, and renal insufficiency set on usually in the course of the 3rd year. Nevertheless, the course, symptoms, and graft survival exhibited considerable variations. - The morphology and manifestations of destructive segmental transplant glomerulopathy (SG) depended on the time of its development. In the early stage (within about 3 months after TPL), the lesion was characterized by areas of fibrinoid insudation and necro(bio)sis associated with severe vascular changes, most frequently obliterative arterio(lo)pathy (OA). The ultrastructure was characterized by endothelial defects with host's polynuclear reaction and focal intravascular coagulation. The grafts thus affected failed soon, their function usually subsiding within the first trimester at a moderate, but gradually increasing proteinuria and severe persistent hypertension. The late from of destructive SG presenting as fibrohyaline obliteration of the loops with foam cells always accompanied advanced MG with severe arterial lesions. - Fluorescence microscopy revealed both linear and focal fixation of antisera, which, however had no apparent correlation with the microscopical and clinical presentations.
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PMID:Glomerulopathies in human renal allografts. 109 48

A 28 year old woman, with diabetes since age 18, had the nephrotic syndrome, hypertension and renal insufficiency. The initial renal biopsy specimen revealed diffuse glomerulosclerosis with early nodular changes. After an initial decline in renal function, her creatinine clearance progressively improved and has remained normal. Within 2 years she had a spontaneous remission of the nephrotic syndrome despite the presence of more pronounced nodular glomerular lesions. Although the renal hemodynamic functions were normal, certain tubular functions were impaired. Since we found no etiology for the nephrotic syndrome other than diabetic glomerulopathy, the complete remission of the nephrotic syndrome and improvement in renal function were very unusual events.
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PMID:Spontaneous remission of the nephrotic syndrome in diabetic nephropathy. 116 52

Systemic hypertension is an important risk factor for the progression of diabetic glomerular disease. Recognition of this detrimental aspect has prompted intensive investigation into the mechanisms by which systemic hypertension promotes diabetic glomerulopathy, as well as into potential benefits of antihypertensive therapy. Studies in diabetic rats, both normotensive and hypertensive, have established that certain antihypertensive regimens effectively slow the development of albuminuria and glomerular sclerosis. Most consistently effective have been angiotensin-converting enzyme inhibitors, which may act to protect the kidney by several different mechanisms. Other antihypertensive regimens have been less consistent.
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PMID:Antihypertensive therapy in experimental diabetes. 136 Aug 46

A primary role for the kidney in hypertension has long been recognized, but the pathogenetic interactions among renal hemodynamics, hormonal and hereditary factors, and dietary sodium intake remain ill defined. Reduction in the filtration surface area, whether acquired in the course of intrinsic renal disease or after surgical renal ablation, leads to systemic hypertension as well as to progressive renal insufficiency, sequellae made even more severe by dietary sodium excess. Moreover, hypertension and progressive renal disease occur in some individuals born with a solitary kidney, and occur almost invariably with more severe degrees of dysgenesis. Hypertension is also commonly observed in certain inbred rat strains in which the filtration surface area is congenitally deficient. Based on these and other lines of evidence reviewed herein, we postulate that a renal abnormality that contributes to essential hypertension in the general population is a reduced number of glomeruli and tubules, the consequences of which are limitations in the ability to excrete sodium and thus salt-sensitive hypertension. Furthermore, congenitally decreased filtration surface area may explain why only some, but not all, patients exposed to potentially injurious renal stimuli eventually manifest chronic nephropathy, and may also account for the susceptibility of subsets of type I and type II diabetics to develop overt glomerulopathy. Clinically, tests of renal reserve capacity may serve as a useful guide to identification of those patients at risk for the development of hypertension and progressive renal disease.
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PMID:The interrelationships among filtration surface area, blood pressure, and chronic renal disease. 138 55

Roughly 40% of all diabetics, whether insulin dependent or not, develop persistent albuminuria, a decline in their glomerular filtration rate, and elevated blood pressure, i.e., diabetic nephropathy. Diabetic nephropathy is the single most important cause of end-stage renal disease in the Western world, accounting for over one-quarter of all end-stage renal disease. Systemic/glomerular hypertension plays a role in the initiation and progression of diabetic glomerulopathy. Angiotensin-converting enzyme (ACE) inhibitors are superior to conventional antihypertensive drugs in preventing the development of glomerular lesions in insulin-treated streptozotocin diabetic rats. Lowering of glomerular hypertension may be the crucial factor involved. Human studies suggest that ACE inhibitors postpone the progression to clinical overt diabetic nephropathy in normotensive diabetic patients with persistent microalbuminuria. ACE inhibitors combined with a diuretic reduce albuminuria and postpone renal insufficiency in hypertensive diabetics with overt nephropathy. No treatment modality other than antihypertensive treatment has yet been proven to be effective in protecting renal function in diabetic nephropathy. All previous reports dealing with the natural history of diabetic nephropathy have demonstrated a cumulative death rate between 50 and 77% 10 years after the onset of proteinuria. Effective antihypertensive treatment has reduced the cumulative death rate to 15-20% 10 years after the onset of nephropathy.
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PMID:Renoprotective action of angiotensin-converting enzyme inhibition in diabetes mellitus. 138 60

A number of risk factors associated with the development of diabetic nephropathy has been described, such as elevated blood pressure, poor metabolic control, hyperlipidemia, and smoking. Abnormal albuminuria also is associated with progression of renal disease, but has until recently been considered principally a marker of disease activity rather than a risk factor. This article discusses the role of elevated blood pressure versus abnormal albuminuria in a genesis and prediction of renal disease in diabetes. Controversy exists regarding parental disposition to hypertension and early blood pressure elevation in the course of diabetes, but all studies agree that elevated blood pressure--in the presence of abnormal albuminuria--constitutes a risk factor. Because abnormal albuminuria is associated with progression disease, it may itself be a risk factor because increased macromolecular traffic over the glomerular membrane may produce glomerulopathy. Problems related to blood pressure measurement are important, and 24-h recordings of blood pressure may be recommended in some situations. Regarding renal structure, preliminary results suggest that structural lesions precede blood pressure elevation. The solid end point for evaluation of renal disease progression is the fall rate of GFR, with abnormal albuminuria as an intermediate end point, also in drug trials. Abnormal albuminuria may constitute a new indication for antihypertensive treatment, being, as it is, a clear indicator of organ damage, whereas elevated blood pressure with normal AER may not increase risk substantially.
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PMID:Blood pressure elevation versus abnormal albuminuria in the genesis and prediction of renal disease in diabetes. 139 16


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