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

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.
 ...
PMID:Blood pressure in patients with four different primary glomerulopathies. 646 43

The onset of fixed proteinuria and hypertension in insulin-dependent diabetic is generally associated with eventual renal insufficiency due to diabetic nephropathy or with a superimposed glomerulopathy. We report three adolescents with normal renal function who developed fixed proteinuria and hypertension after only 7 to 11 years of insulin-dependent diabetes mellitus. Blood pressure ranged from 130/95 to 165/104 mmHg, urinary protein excretion was 1.31 to 1.37 g/24 hours, and creatinine clearance ranged from 98-133 ml/min/1.73 m2. Renal biopsy revealed changes consistent only with diabetic glomerulosclerosis. Follow-up evaluation for 11 months to 3 1/2 years revealed blood pressure reductions to 125/78-140/85 mmHg as a result of antihypertensive medications. Creatinine clearance increased by 12-20% and urinary protein excretion remained unchanged. We conclude that these patients may represent an unusual subgroup of insulin-dependent diabetics with early development of clinical and pathological diabetic nephropathy in the face of normal renal function.
 ...
PMID:Early onset of clinical diabetic nephropathy in children--a new subgroup? 671 12

Vesicoureteral reflux is an anatomic abnormality, mostly affecting a pediatric population, which may be the second leading cause of end-stage renal failure. Most cases of reflux are due to abnormalities in the insertion of the ureters into the bladder, either congenital or acquired. Most commonly, VUR is discovered during routine evaluation of urinary tract infections, but may also be present in patients with severe hypertension or chronic renal failure. The diagnosis is confirmed radiologically, utilizing either voiding cinecystography or radioisotopic methods. VUR can result in renal failure through scarring secondary to 'chronic pyelonephritis' or through a glomerulopathy, possibly immune in origin. In most series, the glomerulopathy is felt to be the cause of the end-stage renal failure. Treatment of VUR includes conservative (medical) management with the hope that maturation of the ureterovesical junction will cure reflux. Surgical therapy is reserved for those patients in whom this maturation is not expected to occur or in those whose urinary infections cannot be controlled. In those patients who have developed the glomerulopathy secondary to VUR, surgery may not halt the progression of the renal disease. VUR in a transplanted kidney may result in a higher risk of loss of the graft due to glomerulopathy or chronic rejection.
 ...
PMID:Vesicoureteral reflux and reflux nephropathy. 676 61

A nodular glomerulopathy characterized by mesangial deposits of monoclonal kappa light chains was detected by immunofluorescence in a renal biopsy from a patient with proteinuria and hypertension. These nodules lacked the tinctorial and morphologic features of amyloid. Ultrastructurally, the nodules contained electron-dense granular deposits as well as fibrils in parallel arrangement. The fibrils measured 110-140 A in diameter. They were consistent in size with amyloid fibrils. However, they differed in lacking the randomly oriented network of typical amyloid fibrils and more closely resembled fibrils intrinsic to mesangial matrix. The patient had no bone marrow or X-ray evidence of myeloma and no evidence of free monoclonal light chains in serum or concentrated urines. Biosynthetic studies of the patient's bone marrow cells demonstrated unbalanced immunoglobulin synthesis with excess production of monoclonal kappa light chains. These observations suggest that the observed glomerulopathy results from direct deposition of monoclonal light chains. Deposits with kappa light chain determinants have been found in 7 other patients with similar nodular glomerulopathies, 4 of whom had diagnosed clinical myeloma. The lesion of nonamyloidotic nodular glomerulopathy previously described in 19 patients, nor examined by immunopathologic techniques or not shown to contain light chain determinants, may have a similar pathogenesis.
 ...
PMID:Nodular glomerulopathy associated with nonamyloidotic kappa light chain deposits and excess immunoglobulin light chain synthesis. 677 Jun 93

The relations among renal function, proteinuria, and glomerular lesions were studied in 54 patients with reflux nephropathy. The clinical course to end-stage renal disease was not appreciably altered by late surgical correction of the reflux, occurrence of urinary tract infection, or hypertension. All patients with progressive renal disease had significant proteinuria. Mesangial glomerular lesions can occur in the absence of proteinuria detectable by routine analysis, whereas lesions similar to those seen in idiopathic focal sclerosing glomerulopathy were present in the renal biopsies from proteinuric patients. Deposition of immunoproteins was limited to glomeruli undergoing sclerosis. Similarly, electron-dense deposits were confined to areas of mesangial alterations. Our results suggest that mesangial alterations occur early in the course of reflux nephropathy and may lead to the development of focal sclerosis. At later stages, counterproductive mechanisms of adaptation to the loss of viable nephrons might result in an acceleration of the clinical course to renal failure.
 ...
PMID:The progression of vesicoureteral reflux nephropathy. 699 78

Thirty-one specimens of tissue were obtained from 15 renal allografts 3-96 months after transplantation and studied by light, electron and in some cases also by immunofluorescence microscopy. All patients had a degree of renal insufficiency and almost all had proteinuria and moderate hypertension; nephrotic syndrome was present in one and hematuria in two. On histological examination one patient showed cellular proliferation suggestive of glomerulonephritis (recurrent or de novo) and another patient had numerous crescents. The most frequent glomerular lesion was widening of the lamina rara interna with subendothelial accumulation of finely granular material, formation of new subendothelial basement membrane and deposition of microfibrils and fine filaments. The mesangial changes were mainly those of mesangiolysis and mesangial sclerosis with deposition of mesangial matrix and microfibrils, but little cellular proliferation. Fragmented red blood cells were seen in nearly half of the patients. In another seven patients the lesion resembled focal segmental glomerulosclerosis. This combination of changes termed transplant glomerulopathy leads to diffuse glomerular sclerosis. Arterial intimal thickening and occasionally also thrombosis produced ischaemic changes in the kidney and in the glomeruli and contributed significantly to the process of transplant rejection.
 ...
PMID:Ultrastructure of transplant glomerulopathy. 700 Jun 58

The 1,205 renal biopsies performed at The Hospital for Sick Children, Toronto, were reviewed to identify membranous glomerulopathy. Fourteen patients had a clinicopathologic diagnosis of idiopathic membranous glomerulopathy. Typical thickening of glomerular capillary basement membranes, a spike-and-dome pattern, and subepithelial electron-dense deposits were noted. Strong deposits of IgG and weaker deposits of C3, IgM, and IgA were present in glomeruli. Stages of membranous glomerulopathy on electron microscopy were I in one biopsy, II in nine biopsies, and III in four biopsies. Two additional biopsies from one child initially showed minimal lesion-type disease; later, a third showed membranous glomerulopathy. At presentation 11 patients had nephrotic syndrome, seven had hypertension, and eight had hematuria. Now four are in remission, seven have active disease with normal renal function, and three have renal failure. Patients with hypertension tended to do worse than those without. Age at onset, presence of nephrotic syndrome or hematuria, and administration of steroids or immunosuppressive drugs did not adversely affect outcome. Furthermore, clinical outcome did not correlate with stage of disease. Hence pathologic and most clinical features do not predict long-term prognosis in children with membranous glomerulopathy.
 ...
PMID:Idiopathic membranous glomerulopathy in Canadian children: a clinicopathologic study. 713 Nov 40

Decompensated benign nephrosclerosis, a disease which was briefly described by Theodor Fahr in 1925, defended by him in 1934, and then forgotten, is reported and differentiated from compensated benign nephrosclerosis. Decompensated benign nephrosclerosis can be differentiated from compensated benign nephrosclerosis by the frequent appearance of interstitial cortical fibrosis and glomerular alterations in the sense of hypertensive glomerulopathy. Hypertensive glomerulopathy results in ascending obliteration of the glomeruli, i.e., their transformation into PAS-positive hyaline globules. In compensated benign nephrosclerosis, interstitial fibrosis, if present at all, can usually be identified only in the subcapsular areas. In decompensated benign nephrosclerosis, however, a pyramid-like structure with its base at the corticomedullary border is formed. The severity of preglomerular vascular alterations does not differ in compensated and decompensated benign nephrosclerosis. Clinically, there is no significant difference between the degree of hypertension and the development of the disease. The nephritic symptoms are more pronounced in decompensated benign nephrosclerosis, which predominantly affects middle-aged men (male:female, 5.7:1), than in compensated benign nephrosclerosis. As a result, decompensated benign nephrosclerosis is frequently diagnosed and treated as chronic glomerulonephritis.
 ...
PMID:The compensated and the decompensated form of benign nephrosclerosis. 715 80

The development of hypertension induced by DOCA/salt in rats can be reduced by epsilon-aminocaproic acid. Analogously to the clinical finding, glomerulopathy is also less marked. Recognising on the one hand the interaction between the coagulation system and the vessel wall and on the other hand the fibrinolysis-blocking properties of EACA, it can be assumed that derangements of the coagulation system are aetiologically involved i hypertension induced by salt/DOCA. As a secondary finding, it was observed that the course of an existing lung infection is deleteriously affected by fibrinolysis-blockade with EACA.
 ...
PMID:The influence of epsilon-aminocaproic acid on the mineralocorticoid hypertension of the rat. 725 Feb 99

It has recently been suggested that immunotactoid glomerulopathy be separated from much more common fibrillary glomerulonephritis by ultrastructural features of highly organized immune deposits containing tubules of more than 30 nm in diameter. We report and discuss the results of a light, immunofluorescence and electron microscopic study of a needle renal biopsy from a 75-year-old, non-insulin dependant diabetic female presented with nephrotic syndrome, hypertension and a progressive renal failure. A unique coexistence of nodular glomerulosclerosis, as traditionally ascribed to diabetes with a peculiar type of immunotactoid glomerulopathy was confirmed by the exclusion of amyloidosis, monoclonal gammopathies, systemic autoimmune diseases and cryoglobulinemia. Mesangial, scattered subepithelial and segmentally prominent subendothelial immune deposits were found highly organized in mostly parallel arrays of 40 to 91 nm thick tubules. The average thickness of 67 nm exceeds the average diameter of tubules in all other 11 published cases of immunotactoid glomerulopathy to date. By immunofluorescence, predominantly capillary wall, thick, ribbon-like glomerular deposits contained IgG, IgM, kappa and lambda light chains of equal intensity, C3, C4 and fibrin related antigens. Mild to moderate glomerular cell proliferation associated with nodular sclerosis has been assumed to be causally related to immunotactoid deposits.
 ...
PMID:Immunotactoid glomerulopathy with unusually thick extracellular microtubules and nodular glomerulosclerosis in a diabetic patient. 747 81


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>