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)

Non invasive methods for the exploration of myocardial function permit the demonstration of preclinical diabetic cardiomyopathy. In this study, we have tried to define the relationship between the degree of diabetic retinopathy and the presence of myocardial dysfunction. We have recorded echocardiogram and phonomechanograms on thirty two insulin dependent diabetics (IDD) less than 50 years of age, without evidence of arteriosclerosis. All patients had a normal baseline electrocardiogram and a normal bicycle exercise test. These diabetics were assigned to three groups: I = no retinopathy (9 patients); II = minimum retinopathy (12 patients); III = marked retinopathy (11 patients). They were compared to ten non-diabetic control subjects of similar age (group 0). None of the parameters of systolic function was modified in the different groups of diabetics in comparison with the control group. We found, however, a very significant reduction of the maximum rate of enlargement of left ventricule and reduction of the maximum narrowing rate of the left ventricular posterior wall during the protodiastolic period in group III, v.s. group 0, I and II. Group III contained 3 patients with borderline hypertension and 5 patients with diabetic glomerulopathy. Our results indicate a diminution of myocardial compliance and relaxation in those IDD with marked retinopathy, but it raises the question of the role of borderline elevations of arterial pressure or hypertension during physical exercise, which are frequently found in diabetics with retinopathy in causing these abnormalities.
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PMID:[Exploration of left ventricular function in insulin-dependent diabetics (relation with retinopathy)]. 373 80

We present 11 patients with immunotactoid glomerulopathy, a new syndrome characterized clinically by proteinuria (11/11), microscopic hematuria (9/11) and hypertension (9/11). The patients consisted of six females and five males, aged 25 to 59 years (mean, 44.6). Proteinuria was the presenting feature and the reason for renal biopsy in all patients. The diagnosis of immunotactoid glomerulopathy was established at renal biopsy by the presence of glomerular extracellular microtubules composed of immune reactants. All the biopsies studied by immunofluorescence (10 cases) had glomerular deposits of IgG and C3. In three biopsies studied with IgG subclass specific antisera, only one patient had monoclonal immunoglobulin deposits (IgG3 kappa). In six cases the glomerular deposits were analyzed for light chains. In three the deposits contained kappa only, and three consisted of both kappa and lambda. In two cases the immune aggregates were confined to the mesangium, and in the remaining eight cases, the deposits were present in the mesangium and the glomerular basement membranes. Electron-dense deposits composed of microtubules were present in the same distribution within the glomerulus as the immune reactants. The microtubules had a uniform diameter in each biopsy, but they varied in size from case to case. They were approximately the same size in eight cases (mean, 22.3 +/- 3 [SD] nm). Three cases had much larger microtubules: 34.2 nm, 35.4 nm, and 48.9 nm in diameter. Although the 22.3-nm microtubules resembled amyloid in their appearance, glomerular distribution and random orientation in the tissue, they were more than twice the diameter of amyloid (8.9 nm), and Congo red and thioflavin T stains for amyloid were negative. Similar microtubular structures have been described in patients with cryoglobulinemia, SLE and paraproteinemia, but these diseases were excluded in our patients on clinical, serologic and in some cases histologic grounds. More important, none of our patients had clinical or histochemical evidence of amyloidosis, an entity which may be confused with immunotactoid glomerulopathy on a morphologic basis. Follow-up, from 22 to 94 months (mean, 52.6) was obtained in all 11 patients, and 2 clinical courses were noted. Six patients had progressive deterioration of renal function, with five requiring dialysis. This group had severe hypertension (4/6) and nephrotic-range proteinuria (5/6) at some point in their course. The remaining five patients with stable renal function had proteinuria of less than 2.0 g/24 hr in most cases (4/5), and none had severe hypertension. This dichotomy correlated with the distribution of immunotactoids.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Immunotactoid glomerulopathy. 401 May

In an unselected series of patients with IgA glomerulonephritis, old age, high blood pressure, and high urinary protein excretion at the time of renal biopsy were found to correlate with impaired renal function, whereas sex, estimated duration of the disease, or high serum IgA levels did not. The following clinical features were favorable prognostic signs: asymptomatic proteinuria, macroscopic hematuria, and isolated microscopic hematuria. The degree of diffuse mesangial alteration and the presence of segmental glomerular lesions correlated clearly with the subsequent clinical outcome. Vascular lesions, i.e. arteriosclerosis and renal vascular deposition of C3, were most often present in patients with severe glomerulopathy. The presence of electron-dense deposits in glomerular capillary walls was also an unfavorable prognostic finding. Renal biopsy findings of interstitial infiltrates of inflammatory cells and IgA distributed along glomerular capillary walls were usually associated with extrarenal manifestations of the disease.
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PMID:Clinicopathologic correlations in a series of 143 patients with IgA glomerulonephritis. 401 21

We report a patient with documented IgA nephropathy in whom microscopic hematuria, proteinuria, and hypertension first occurred after placement of nickel alloy base dental crowns. Progressive proteinuria culminating in nephrotic-range proteinuria occurred parallel to increased nickel placement and dramatically resolved following nickel alloy removal. That immunologic alterations occur as a result of nickel exposure has already been suggested by the common occurrence of nickel contact dermatitis, often exacerbated by intraoral nickel placement, increased carcinogenesis in nickel refinery workers, and animal models of nickel-associated carcinogenesis. Our patient may represent an example of nickel-induced sensitization and associated IgA glomerulopathy. Further study of patients with immune-mediated glomerulopathy with attention to dental nickel exposure appears indicated.
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PMID:IgA nephropathy associated with dental nickel alloy sensitization. 406 6

A total of 250 renal biopsy specimens from diabetic patients and from the kidneys of 400 autopsy cases were examined histologically and compared to kidneys from 160 autopsied nondiabetics. The morphological findings were assessed in relation to hypertension. There was a high prevalence of arteriolosclerosis, glomerulosclerosis, and pyelonephritis; in addition, early diabetic glomerulopathy and glomerulonephritis, particularly of the membranous type, were noted in a remarkably high percentage of diabetic patients. Ninety-three percent of patients with hypertension had arteriolosclerosis, and a good correlation existed between the extent of this lesion and the level of blood pressure. Even in 66% of normotensive patients, however, arteriolosclerosis was found. This fact and the involvement of the vas efferens argue against the notion of arteriolosclerosis being exclusively a sequela of hypertension. More than 70% of patients with glomerulosclerosis suffered from hypertension, compared to less than 50% of patients without either that condition or early diabetic lesions. The majority of diabetic patients with pyelonephritis and glomerulonephritis were hypertensive. We conclude that hypertension in diabetic patients with renal involvement may result from different renal lesions that can be differentiated only by histological examination.
Hypertension
PMID:Renal histopathology in hypertensive diabetic patients. 407 38

Captopril (Capoten; Squibb) is a specific orally active antagonist of peptidyl-dipeptide carboxyhydrolase, the enzyme which converts angiotensin I to angiotensin II and which inactivates bradykinin. Captopril therefore reduces blood pressure in a variety of animal models of hypertension. In 96 studies on 1570 patients, captopril has been shown to be superior to placebo and equivalent to either propranolol or a diuretic in the treatment of essential hypertension. In the management of severe treatment-resistant hypertension, the response to captopril (alone or in combination with a diuretic and/or propranolol) was better than the response to standard triple therapy. Captopril, with digitalis and a diuretic, also improved the haemodynamic and clinical status of patients with refractory congestive heart failure. Side-effects include skin rashes (15%), proteinuria (1,1%, or 0,4% of patients with no prior renal disease) and the nephrotic syndrome (0,9%, or 0,3% of patients with no prior renal disease). Nearly all patients with the nephrotic syndrome in whom renal biopsies were performed were found to have membranous glomerulopathy. Neutropenia (total white cell count less than 1,000/microliter) was found in 33 of over 6,000 patients (0,4%), but in all cases there were other possible causes for this. Captopril is the first of an important group of antihypertensive and afterload-reducing drugs; its major indications are likely to be in the treatment of refractory severe hypertension or congestive heart failure.
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PMID:Captopril--an overview. 621 58

A rarely diagnosed nodular glomerulopathy is presented arising secondary to kappa light chain deposition and clinically characterized by hypertension, congestive heart failure, massive proteinuria and slowly progressive azotemia. Kappa light chains were detected in the urine, the glomerular nodules, and the basement membranes of both glomeruli and tubules. A malignant proliferation of plasma cells could not be detected. Two morphologic features were unusual: the presence of microaneurysms, and the deposition of immunoglobulin and complement in a similar pattern to the kappa light chains. Noteworthy clinical aspects included the elusiveness of the proper diagnosis, the massive proteinuria in the absence of amyloid deposits, and the remarkable improvement in renal function following intermittent chemotherapy.
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PMID:Kappa light chain nephropathy without evidence of myeloma cells. Response to chemotherapy with cessation of maintenance hemodialysis. 622 48

Membranous glomerulopathy and proteinuria have occurred in patients receiving captopril for hypertension. In this case of captopril-associated nephrotic syndrome, a pretreatment biopsy specimen showed normal histologic appearance and glomerular ultrastructure. A posttreatment biopsy specimen showed membranous glomerulopathy. It seems likely that captopril caused the membraneous glomerulopathy.
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PMID:Membranous glomerulopathy and nephrotic syndrome after captopril therapy. 635 23

The earliest manifestations of clinical diabetic nephropathy, including proteinuria, hypertension, and declining GFR, represent very advanced diabetic glomerulopathy with especially prominent mesangial expansion. Mesangial expansion, by restricting glomerular capillary filtration surface and lumenal volume, stimulates compensatory mechanisms analogous to those resulting from a marked reduction in nephron number. These compensatory mechanisms involve alterations in glomerular hemodynamics designed to maintain glomerular filtration but which ultimately injure the kidney. These hemodynamic perturbations are not specific to diabetes but represent a final common pathway toward endstage renal failure that also characterizes the remnant kidney. This thesis concludes that the onset of clinical diabetic nephropathy augurs inevitable decline in kidney function, and that only studies and interventions exercised before clinical nephropathy develops can influence understanding and outcome of diabetic nephropathy.
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PMID:Diabetic nephropathy. A perspective. 640 Jun 68

Sixty-seven children with hemolytic-uremic syndrome (HUS) were admitted between 1974 and 1981. Of these, 52 (78%) were aged less than 3 years. All children had acute renal failure and 48 (72%) required peritoneal dialysis. The etiology in twenty cases varied from bacterial and viral infections (7 and 5 cases, respectively) to renal irradiation with chemotherapy (2) and preexisting glomerulopathy (1). 5 (7%) children died during the acute phase of the illness. Long-term follow-up (mean 3 years 3 months) of 56 cases showed that 37 children (60%) had so far experienced no functional sequelae and 8 (13%) only mild sequelae while 3 (5%) were on iterative hemodialysis, 3 had severe chronic renal failure and high blood pressure (HBP) and 5 (8%) had HBP and normal kidney function. While the recovery rate was approximately 60% in all age groups, the mortality rate and serious after-effects were twice as frequent (42%) in children over 3 years of age as in those less than 3. Renal histology (total of 37) showed 12 cases of cortical necrosis, 22 of glomerular thrombotic microangiopathy (TMA) and 3 arterial TMA. Prognosis was poor for all cases of arterial TMA and 58% of those exhibiting cortical necrosis.
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PMID:Hemolytic-uremic syndrome: an analysis of the natural history and prognostic features. 646 38


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