Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 64-yr-old man presented with diabetes mellitus, proteinuria, hypertension and moderate renal dysfunction. Renal biopsy revealed diabetic glomerulosclerosis (diffuse lesion), IgA nephropathy and membranous nephropathy (stage 2). Both mesangial IgA and subepithelial IgG deposits were demonstrated by immunofluorescence and immunoelectron microscopy. Electron microscopic studies by immunogold method showed localization of IgA (diameter 15nm gold particles) within mesangial dense deposits and IgG (diameter 15nm gold particles) within subepithelial dense deposits. Overlapping IgA and membranous nephropathy was revealed in the same diabetic glomeruli with functional and biochemical alternations.
 ...
PMID:[A case of superimposed renal lesions of IgA and membranous nephropathy with diabetic nephropathy]. 148 12

Ultrastructural, immunohistochemical and biochemical studies have improved our knowledge on the events occurring during the development of diabetic late complications. Immunohistochemical investigations of diabetic kidneys, using antibodies against various components of the extracellular matrix, showed increased collagen type IV (alpha 1,alpha 2-chain) deposition in the mesangial matrix, and a decrease of heparan sulphate proteoglycan in the mesangial matrix and glomerular basement membrane. Changes in matrix components seem to be the underlying cause of the alterations in renal function, as reflected by albuminuria and proteinuria. The occurrence of collagen type III in late diffuse glomerulosclerosis has been interpreted as an irreversible change in glomerular structure. The extent of alteration of the extracellular matrix correlates to a certain extent with the severity of nephropathy of the individual subject. The studies performed to date support the hypothesis that hyperglycaemia, whatever its origin, is the primary cause of diabetic late complications, although the pathobiochemical mechanisms are not yet fully understood. Increased intra- and extracellular levels of glucose and its derivatives are thought to contribute to diabetic tissue dysfunction. Three pathobiochemical theories are favoured in the current discussion: i) the polyol pathway ii) non-enzymatic glycation of proteins iii) direct influence of hyperglycaemia on the synthesis of matrix components. The evidence for the participation of the polyol pathway in the pathogenesis of diabetic nephropathy comes mainly from animal data using aldose reductase inhibitors, but only limited data are available for humans, so that the significance of this pathomechanism cannot yet be determined.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Glomerular changes in diabetes mellitus. 149 55

The pathogenesis of diabetic nephropathy relative to the changes in the glomerular extracellular matrices was investigated. Renal tissues from 10 diabetic patients were immunostained with antibodies directed against heparan sulfate proteoglycans (HS-PGs), laminin, type IV collagen and fibronectin. Seven patients were nephrotic and had advanced glomerulosclerosis with nodular lesion, while the other 3 had no renal manifestations or minor glomerular tissue alterations. Controls included kidneys removed from patients with renal tumors and specimens obtained by renal biopsy from patients with IgA nephropathy. Relationships among proteinuria, intensity of fluorescence and glomerular changes were studied. In diabetes 3 patients with minor glomerular lesions were found to have no changes in various components of extracellular matrices. A marked reduction in the intensity of staining with anti-HS-PG antibodies was observed in renal specimens from patients with nodular glomerulosclerosis and proteinuria, while a mild decrease in the intensity of fluorescence was observed in tissues stained with antilaminin antibodies. An increase compared to normal control sample findings in type IV collagen and fibronectin was observed in the mesangium of sclerosing glomeruli. No loss of HS-PG was observed in patients with IgA nephropathy. These results indicate that glomerular extracellular matrix HS-PG is lost in association with diabetic nephropathy; this loss results in alteration of the charge-selective properties of glomerular capillaries. This alteration may, in part, be the cause of the proteinuria associated with diabetic nephropathy.
 ...
PMID:Heparan sulfate proteoglycans are lost in patients with diabetic nephropathy. 150 38

We describe a 39-year-old man who developed kappa light chain nodular glomerulosclerosis with superimposed conspicuous crescent formation and extensive tubulointerstitial injury. The clinical picture was characterized by nephrotic syndrome and rapidly progressive glomerulonephritis. Incessantly progressive loss of renal function culminated in irreversible renal failure 7 weeks after initial manifestations of renal insufficiency. The patient has since been maintained on thrice weekly hemodialysis with chemotherapy for five years. At the time of pathologic diagnosis by renal biopsy, there was no evidence of multiple myeloma, and no serum M-component or Bence-Jones proteinuria was detected. An initial bone marrow aspirate revealed the presence of 0.6% atypical lymphocytes as the sole abnormality, although these were later identified as atypical plasma cells. These cells had also infiltrated the renal interstitium. Crescentic kappa light chain nodular glomerulosclerosis lacking evidence of plasma cell dyscrasia should be included in the differential diagnosis of rapidly progressive glomerulonephritis.
 ...
PMID:Kappa light chain nodular glomerulosclerosis with conspicuous crescent formation and tubulointerstitial injury. Report of a case. 150 4

The three main causes of primary nephrotic syndrome are minimal change nephropathy, focal glomerulosclerosis and membranous nephropathy. Corticosteroids obtain remission of proteinuria in most patients with minimal change nephropathy. Many patients, however, show either frequent relapses or steroid dependency. A short course of cyclophosphamide or chlorambucil can achieve stable remission in many of these patients but alkylating agents cannot be repeated, their toxicity being cumulative. Analyses of the available studies showed that some 80% of patients can be maintained in remission with cyclosporin A (CsA) but relapse occurs when the drug is stopped. Severe side effects are rare. In particular, the mean values of creatinine clearance did not deteriorate in cyclosporin-treated patients and repeat renal biopsy showed only mild changes in some patients. There is no definite treatment for focal glomerulosclerosis. An analysis of 10 clinical trials showed that some 17% of nephrotic patients may enter complete remission of proteinuria and another 13% may attain partial remission of the nephrotic syndrome with CsA. There is concern over the use of this drug since cases of irreversible renal dysfunction have been reported. However, retrospective reviews of the available studies showed that the mean serum creatinine levels did not modify if patients had normal renal function when given CsA. A 6-month course of methylprednisolone and chlorambucil may obtain remission of the nephrotic syndrome in some 60% of patients with membranous nephropathy. Some trials have shown that CsA may improve proteinuria and there is also some suggestion that the drug might protect against renal function deterioration. Thus, when given at correct doses, CsA may exert an anti-proteinuric effect without deteriorating renal function, suggesting that the drug may represent a further tool in treating the primary nephrotic syndrome.
 ...
PMID:Treatment of the nephrotic syndrome with cyclosporin A. 150 27

The relationship between blood-lipid levels and severity of proteinuria was examined retrospectively in 30 patients (12 males, 18 females; mean age 39 [18-58] years). All patients had histologically confirmed glomerulonephritis (minimal change: n = 7, perimembranous: n = 8, focal sclerosing: n = 6, rapid progressive: n = 3, mesangio-proliferative: n = 4, membrano-proliferative: n = 1, diabetic glomerulosclerosis: n = 1). None was taking lipid-lowering drugs. Patients were classified according to the degree of proteinuria. In group 1 (proteinuria less than 5 g/d, n = 13) the LDL-HDL ratio averaged 4.4; in group 2 (proteinuria 5.0-10.0 g/d, n = 10) the average ratio was 8.8, and in group 3 (proteinuria greater than 10.0 g/d, n = 7) 13.3. Total cholesterol concentration also rose with increasing proteinuria (to 300 +/- 87 mg/dl, 375 +/- 168 mg/dl and 464 +/- 143 mg/d, respectively). The size of the LDL-HDL ratio and the level of total cholesterol did not correlate with the degree of excretory renal failure. These results point to an impressive correlation between the degree of proteinuria and the level of LDL-HDL ratio as a measure of atherogenic risk for a given patient.
 ...
PMID:[Proteinuria and atherogenic risk]. 150 44

Angiotensin-converting enzyme inhibitors (ACEI) can reduce proteinuria in diabetic and nondiabetic nephropathy. However, no studies have determined whether this antiproteinuric effect modifies the progression of renal insufficiency. We studied the evolution of 46 nondiabetic patients with nephrotic proteinuria treated with captopril for a minimum of 12 months. The follow-up period before captopril treatment was 12 to 18 months. At the end of follow-up, after captopril introduction (24.4 +/- 7.6 months), proteinuria had decreased from 6.3 +/- 2.5 to 3.9 +/- 3.1 g/24 h (P less than 0.001), with a mean decrease of 45% +/- 28%. The proteinuria decrease was higher in patients with reflux nephropathy, proteinuria associated with reduction of renal mass, inactive crescentic glomerulonephritis, nephroangiosclerosis, and IgA nephropathy, whereas patients with membranous glomerulonephritis and idiopathic focal glomerulosclerosis showed a poorer response. Patients were separated according to a proteinuria reduction greater (group A, 23 patients) or lower (group B, 23 patients) than 45% of the initial value. At the end of follow-up, renal function had not significantly changed in group A with respect to values at the start of treatment: serum creatinine (SCr) was 229 +/- 167 mumol/L (2.6 +/- 1.9 mg/dL) versus 203 +/- 97 mumol/L (2.3 +/- 1.1 mg/dL), and creatinine clearance (CrCl) was 0.80 +/- 0.52 mL/s (48 +/- 31 mL/min) versus 0.87 +/- 0.47 mL/s (52 +/- 28 mL/min). The slope of the reciprocal of Scr (1/SCr) showed a significantly beneficial change after captopril introduction.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Long-term beneficial effects of angiotensin-converting enzyme inhibition in patients with nephrotic proteinuria. 151 4

The effects of angiotensin II (AII) blockade were compared with the effects of angiotensin converting enzyme inhibition in rats with reduced nephron number. Rats were subjected to five-sixths renal ablation and divided into four groups with similar values for blood pressure and serum creatinine after 2 wk. Group 1 then served as untreated controls, while group 2 received the AII receptor antagonist MK954 (which has previously been designated DuP753), group 3 received the converting enzyme inhibitor enalapril, and group 4 received a combination of reserpine, hydralazine, and hydrochlorothiazide. Micropuncture and morphologic studies were performed 10 wk later. Converting enzyme inhibition, AII receptor blockade, and the combination regimen were equally effective in reversing systemic hypertension (time-averaged systolic blood pressure: group 1, 185 +/- 5 mmHg; group 2, 125 +/- 2 mmHg; group 3, 127 +/- 2 mmHg; group 4, 117 +/- 4 mmHg). Micropuncture studies showed that glomerular transcapillary pressure was reduced significantly by converting enzyme inhibition and by AII blockade but not by the combination regimen (delta P: group 1, 49 +/- 1 mmHg; group 2, 42 +/- 1 mmHg; group 3, 40 +/- 2 mmHg, group 4, 47 +/- 1 mmHg). Reduction of systemic blood pressure was associated with the development of markedly less proteinuria and segmental glomerular sclerosis in rats receiving enalapril and MK954 but not in rats receiving the combination regimen (prevalence of glomerular sclerotic lesions: group 1, 41 +/- 4%; group 2, 9 +/- 1%; group 3, 9 +/- 1%; group 4, 33 +/- 6%). These results indicate that the effects of converting enzyme inhibition on remnant glomerular function and structure depend on reduction in AII activity and are not attributable simply to normalization of systemic blood pressure.
 ...
PMID:Angiotensin II receptor blockade limits glomerular injury in rats with reduced renal mass. 152 31

We report a 35-year-old man with adult polycystic kidney disease (APKD) that developed nephroptic syndrome accompanied by a rapid worsening of renal function. Histologic examination showed marked tubulointerstitial chronic abnormalities and focal glomerulosclerosis (FGS) lesions in 24% of the glomeruli. With captopril, an renal function continued to deteriorate. No other cases of nephrotic-range proteinuria were detected among 65 APKD patients with renal insufficiency. Histologic examination of an other 12 kidneys removed from patients with APKD showed striking interstitial lesions, most of the glomeruli being normal. However, those patients with higher amounts of proteinuria had more glomeruli (14-32%) with FGS lesions.
 ...
PMID:Nephrotic syndrome and focal glomerulosclerosis in adult polycystic kidney disease. 832 70

Clinicohistopathologically, we observed 109 patients with asymptomatic urinary abnormalities found via the Japanese school medical screening process. Follow-up was for a mean period of 9.3 +/- 4.0 years. More than 80% of the patients had either IgA nephropathy (IgAN, 47 cases, 43.1%), thin membrane disease (TMD; 21 cases, 19.3%) or normal glomerulus (NG; 20 cases, 18.3%). Complete remission appeared in 60.0% of the NG cases, 14.3% of the TMD cases and in 19.1% of the IgAN cases, and remission was significantly high in the NG group (p less than 0.01). No patient with TMD and NG ever progressed to the extent of pronounced proteinuria or renal failure. One patient deteriorated and required hemodialysis, and 2 patients developed renal insufficiency in IgAN. All of these cases possessed severe glomerular sclerotic change when the initial biopsies were performed. All IgAN cases that went into remission, however, had minor glomerular abnormalities. A positive family history of urinary abnormality was observed in 14.1% of both the IgAN group and the NG group, whereas we observed 71.4% in the TMD group, which was significantly high (p less than 0.01). Other cases included 4 each with non-IgA proliferative glomerulonephritis, focal segmental glomerular sclerosis, membranoproliferative glomerulonephritis and Alport's nephritis. It was concluded that the majority of patients (80.7%) with urinary abnormalities found via the school screening program had IgAN, NG or TMD. 74.5% of the IgAN group and 85.7% of the TMD group had long histories of urinary abnormalities extending into adulthood with no deterioration of the renal function.
 ...
PMID:Asymptomatic urinary abnormalities found via the Japanese school screening program: a clinical, morphological and prognostic analysis. 152 46


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