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

Camostat mesilate, a developed derivative of gabexate mesilate for oral use, was administered in a daily dose of 600 mg for 4 weeks to 17 patients with heavy proteinuria due to various nephropathies. Five patients had glomerulonephritis (3 patients with IgA nephropathy, one each with membranoproliferative GN and membranous nephropathy) and 3 had systemic vasculitis. These patients had been treated with glucocorticoid, cyclophosphamide, anticoagulants, and dipyridamole. Five patients had diabetic nephropathy and had been treated with conventional therapy including angiotensin converting enzyme inhibitors. Two cases with benign nephrosclerosis, one with Alport syndrome, and the rest with end-stage renal failure of undetermined cause were also included in this study. Urinary protein decreased promptly within 2 weeks (from 5.2 +/- 0.7 to 3.5 +/- 0.5, mean +/- SE, p less than 0.005), and serum total protein and albumin levels increased significantly. Serum creatinine levels did not change. Decreases in urinary protein excretion of more than 50% were observed in five out of eight patients with glomerulonephritis or systemic vasculitis, two out of five with diabetic nephropathy, and one with chronic renal failure. However, urinary protein excretion values remained at the same level in two patients with benign nephrosclerosis and a patient with Alport syndrome. We suggest that camostat mesilate caused a change in glomerular capillary permeability for macromolecules through its inhibitory effects on the kallikrein-kinin system, complement system, coagulation system, and platelet function, which contributed to the treatment of the various nephropathies.
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PMID:Effect of camostat mesilate on heavy proteinuria in various nephropathies. 279 62

Heavy proteinuria in patients with essential hypertension raises the question of underlying primary renal disease. While malignant hypertension may be associated with proteinuria in the nephrotic range, it is generally held that protein excretion in benign nephrosclerosis is almost invariably less than 0.5-1.0 g/24 h. We report 18 patients with biopsy-proven hypertensive nephropathy and heavy proteinuria, of which only 6 had malignant hypertension. In the remaining 12 patients with benign nephrosclerosis, protein excretion reached up to 6.5 g/24 h, and nephrotic range proteinuria was present in 3 patients. All patients with heavy proteinuria suffered from long-standing moderate or severe, poorly controlled hypertension and were azotemic. We suggest that hypertensive nephrosclerosis be included in the differential diagnosis of massive proteinuria accompanying azotemia in poorly controlled hypertensives.
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PMID:Marked proteinuria in hypertensive nephrosclerosis. 316 Feb 40

The progression of renal failure was analyzed in 108 patients with mild to moderate renal impairment, none of whom had received any form of dietary protein, phosphate restriction or immunosuppressive treatment. The reciprocal of plasma creatinine was plotted against time using a minimum of six plasma creatinine values taken over at least six months (mean 13 values over 41 months). Plots indicated there was linear deterioration in 70 patients, non-linear deterioration in 15 and stable renal function in 24. Progressive renal failure was common in patients with glomerulonephritis, diabetic nephropathy, chronic pyelonephritis and polycystic kidney disease. Most patients with hypertensive nephrosclerosis, analgesic nephropathy and renal impairment following acute renal failure were stable. Among those with progressive impairment the mean rates of deterioration were significantly faster for patients with glomerulonephritis and diabetic nephropathy compared to those with chronic pyelonephritis, polycystic kidney disease and undiagnosed renal disease (p less than 0.01). Hence the underlying renal pathological changes appear to be important in determining progression of renal failure and also the subsequent rate of deterioration. For those with linear progression of renal failure there was a significant correlation between 24-h urinary protein excretion and the rate of deterioration. This relationship held for glomerulonephritis and chronic pyelonephritis as separate diagnostic groups only. Proteinuria, therefore, may be a useful prognostic index for the rate of progression of established renal failure. Calcium phosphate product correlated poorly with the rate of deterioration. We were unable to demonstrate a relationship between spontaneous protein intake and deterioration of renal function. However, patients prescribed high protein diets were not included in dietary analysis and we cannot, therefore, exclude the possibility that a high dietary protein intake may accelerate renal failure. Similarly we were unable to show a significant relationship between blood pressure and progression of renal failure although there were weak correlations between mean arterial pressure and rate of deterioration for chronic pyelonephritis and glomerulonephritis.
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PMID:Renal pathology and proteinuria determine progression in untreated mild/moderate chronic renal failure. 320 6

The fawn-hooded (FH) rat develops hypertension spontaneously. Systolic blood pressure is already elevated at 5 weeks of age, increases with age, and the final range is 180-240 mmHg at the age of 1 year. Concomitantly with the rise in blood pressure proteinuria occurs and increases with age. Fawn-hooded rats reaching the accelerated phase of the hypertension are characterized by blood pressure values exceeding 220 mmHg, heavy proteinuria and increased heart, kidney, liver, adrenal and spleen weights. Those prone to malignant hypertensive disease show a period of increased water turnover for several weeks after weaning; during this period, they do not show the pronounced decrease in water intake upon fasting for 24 h as observed in FH rats of the same age prone to a milder form of hypertension, i.e. diuresis and drinking continue even when no food is consumed. The major cause of death for FH rats is malignant nephrosclerosis with the nephrotic syndrome and/or cardiac failure with chronic pulmonary congestion. Some animals die of bleeding from mesenteric vessels with periarteritis nodosa. In FH rats with malignant hypertension, heart, kidney, liver and spleen weights are significantly increased compared with FH rats of the same age with mild hypertension. Histopathology shows myocardial fibrosis and myocardial infarctions. Generalized arteriolosclerosis is common, sometimes accompanied with local fibrinoid degeneration and (peri)arteritis. Some major arteries show intimal proliferation. It is concluded that the FH rat provides an interesting model for the study of hypertension and its consequences.
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PMID:Spontaneous hypertension in the fawn-hooded rat: a cardiovascular disease model. 346 7

The fawn-hooded rat (FH rat) develops hypertension accompanied with focal and segmental glomerulosclerosis and proteinuria, resulting in premature death. In a first experiment the relationship between renal lesions and blood pressure at various ages was investigated. In a second experiment blood pressure was measured weekly from 10 to 38 weeks of age in a number of male FH rats, followed by examination of renal tissues at 40 weeks of age. Plasma renin activity (PRA) had also been determined in individual FH rats. FH rats aged 4.5 weeks had no renal morphological abnormalities. The severity of the glomerulosclerosis increased with age and showed a positive relationship with blood pressure. The scores of the proteinaceous tubular casts also increased with age and they, too, showed a positive correlation with blood pressure. The severity of glomerulosclerosis and proteinaceous casts at 40 weeks of age was related positively to the course of blood pressure throughout life. The final blood pressure level showed a positive correlation with final PRA values. Only FH rats with malignant nephrosclerosis had high PRA values. The renal glomerular and vascular lesions in the FH rat, most likely caused by the hypertension, progressively deteriorate to malignant nephrosclerosis. At that stage PRA values are increased and may be contributing to the development of renal vascular lesions and acceleration of the hypertension.
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PMID:Relationship between blood pressure level, renal histopathological lesions and plasma renin activity in fawn-hooded rats. 355 93

It had been previously thought that protein excretion in hypertensive nephrosclerosis was less than 0.5 to 1.0 g/24 h. Furthermore, it was believed that proteinuria in the nephrotic range associated with hypertension was probably due to primary renal disease, malignant hypertension, renal artery stenosis, or pheochromocytoma. We report eight patients with biopsy-proven hypertensive nephropathy and heavy proteinuria in the absence of malignant hypertension or renal artery stenosis. The 24-hour protein excretion ranged from 2.7 to 4.3 g. All patients had renal insufficiency, with serum creatinine ranging from 2.0 (176.8) to 7.8 mg/dL (689.5 mumol/L). Renal function worsened in most patients during the follow-up period despite adequate control of the hypertension, and three patients had to be started on hemodialysis. Three patients died during the follow-up period. We conclude that hypertensive nephrosclerosis must be included in the differential diagnosis of marked proteinuria in patients with essential hypertension and that heavy proteinuria, along with renal insufficiency, are poor prognostic indicators in such patients.
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PMID:Proteinuria in hypertension. 368 33

Benign nephrosclerosis seldom is associated with significant proteinuria or reduced renal function. This study demonstrated that, despite the finding of benign nephrosclerosis on a renal biopsy specimen, concomitant proteinuria is predictive of a poor prognosis. Twelve patients, ranging in age from 24 to 59 years, with hypertension, proteinuria (greater than 1 g/d), and findings of benign nephrosclerosis on renal biopsy specimens were studied retrospectively. In three of these patients, the hypertension and proteinuria were diagnosed during pregnancy. Follow-up was possible in 11 patients. Nine patients became nephrotic in the course of their disease. Two patients had endstage renal disease and required maintenance dialysis treatment. Seven patients had decreased renal function as shown by the increase in serum creatinine levels. Thus, the combination of hypertension, proteinuria (greater than 1 g/d), and benign nephrosclerosis may be indicative of a progressive condition with a high percentage of patients having renal failure.
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PMID:Proteinuria in benign nephrosclerosis. 372 31

Histological studies were performed on 3 patients with gout and proteinuria measured at 1.0 g a day or more. Light microscopy revealed diffuse thickening of the glomerular capillary walls accompanied by spike formation and bubble-like appearance as well as tophaceous granuloma in the interstitium, tubular atrophy and benign nephrosclerosis. Immunofluorescence technique showed fine granular deposits of IgG and C3 along the glomerular capillary walls together with the renal tubular epithelial antigen (RTE) in 1 patient. Subepithelial dense deposits were also observed by electron microscopy. These findings suggest that the association of membranous nephropathy should be considered in patients with gout having moderate to severe proteinuria and that RTE may be involved in the pathogenesis of subepithelial deposits in gouty membranous nephropathy.
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PMID:Gouty kidney associated with membranous nephropathy: participation of renal tubular epithelial antigen. 379 76

The role of the pathologic features and dysfunction of glomerular epithelial cells (GECs) in the pathogenesis of glomerular scarring was studied in the remnant kidney model (RK) (1 and 5/6 nephrectomy) in rats. Three weeks after surgery serum creatinine was greater in the RK than either sham-operation controls (SHAM) or spontaneously hypertensive rats (SHRs). Blood pressure was higher in the RK (181 +/- 26 mm Hg) than in SHAM (129 +/- 17, P less than 0.05) but not SHR (195 +/- 15, P less than 0.05). GEC endocytosis, assessed by protamine heparin aggregate (PHA) disappearance (10), was not different from that in SHAM. Glomerular damage was greater in RK (glomerular damage index, 30 +/- 18) than in SHAM animals (4 +/- 3, P less than 0.05) and SHR (0, P less than 0.05), and 2 of 11 RK animals had fibrinoid necrosis and thrombosis of arterioles and glomeruli. Segmental sclerosis occurred in only 1 RK animal (0.6% of glomeruli). Six weeks after surgery serum creatinine and urinary protein excretion remained higher in the RK than in the SHAM animals. Blood pressure was higher in RK (158 +/- 34 mm Hg) than in SHAM animals (144 +/- 24), but the difference was not significant. PHA disappeared from the glomerulus at a slower rate in RK than in SHAM animals (outside the 95% confidence limits of SHAM). Glomerular pathology was more widespread in RK than in SHAM animals (glomerular damage index, 73 +/- 62 versus 3 +/- 8, P less than 0.05), and 4 of 11 animals had acute hypertensive injury in arterioles and glomeruli. Segmental glomerular sclerosis was only seen in the animals with necrotic glomeruli. GEC dysfunction is not demonstrable until long after proteinuria and hypertension are established, and it only occurs in the context of severe, acute glomerular injury when the epithelial cells separate from the capillary wall and undergo severe degenerative changes and necrosis. The acute glomerular and vascular lesions in the RK model are morphologically similar to malignant nephrosclerosis in humans. Segmental glomerular sclerosis occurs only after proteinuria is well established in the context of severe glomerular injury, and it appears to represent, at least partially, progression of more proximate glomerular capillary injury.
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PMID:Glomerular epithelial cell function and pathology following extreme ablation of renal mass. 382 97

A review of 693 renal transplant recipients revealed 77 (11%) in whom persistent, heavy proteinuria (greater than 2 g/24 hr) developed. Renal histology was available in all 77 patients. Twenty-one patients had received kidneys from living-related donors, the remaining 56 from cadaveric donors. The cause of proteinuria in these 77 patients was as follows: transplant glomerulopathy (30), allograft glomerulonephritis (22), chronic rejection (21), renal vein thrombosis (2), diabetic glomerulosclerosis (1), and hypertensive nephrosclerosis (1). Of the 22 patients who developed glomerulonephritis in the transplanted kidney, 6 had recurrent disease (3--membranous glomerulopathy, 2--focal sclerosis and hyalinosis, 1--membranoproliferative glomerulonephritis); 6 developed de novo glomerulonephritis; and in 10 the type of glomerulonephritis could not be classified as recurrent or as de novo because of lack of characterization of the original kidney disease. Renal vein thrombosis occurred in association with other lesions in an additional 5 cases (3--chronic rejection; 2--membranous glomerulopathy). In follow-up only 23.4% (18 of 77) of the patients maintained prolonged graft function; the majority of grafts being lost within one year of the development of persistent, heavy proteinuria. Of the 18 patients who retained their grafts, 8 had glomerulonephritis, 5 transplant glomerulopathy, and 5 chronic rejection. This study confirms the poor prognosis that has been reported with the development of nephrotic-range proteinuria in renal allograft recipients.
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PMID:Proteinuria following transplantation. Correlation with histopathology and outcome. 639 Aug 21


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