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)

It is suggested that Tamm-Horsfall protein, a specific renal glycoprotein, may be involved in the pathogenesis of some renal diseases. In cadmium nephropathy and Fanconi syndrome (primary tubular diseases of the kidney) an increased excretion rate of Tamm-Horsfall protein has been observed. Balkan endemic nephropathy is a chronic tubulointerstitial disease of unknown etiology, most probably a primary disease of the kidney tubules with secondary reaction of the interstitial tissue. Investigation of Tamm-Horsfall proteinuria in Balkan endemic nephropathy has shown that subjects living in the area where this condition is prevalent have a significantly higher Tamm-Horsfall protein /creatinine ratio than those living in the control area where the condition has not been observed. Differences in this ratio among diseased, suspect and subjects "at risk" were not observed, despite differences in their glomerular filtration rates. But excretion of Tamm-Horsfall protein per litre of glomerular filtrate was significantly different among diseased, suspect and subjects "at risk" and significantly higher compared to control subjects. a relatively significant correlation was obtained between Tamm-Horsfall protein excretion rate and glomerular filtration rate as measured by creatinine clearance in both control and subjects living in the area of Balkan endemic nephropathy. Determination of Tamm-Horsfall protein in urine together with determination of proteinuria by electrophoresis on cellulose acetate membranes as a screening procedure, and by SDS -electrophoresis in polyacrylamide gell may be useful laboratory tests in detecting this nephropathy.
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PMID:Tamm-Horsfall protein in Balkan endemic nephropathy. 400 27

Glucocorticoids and aspirin antagonize the androgenic response in mouse kidney, but not in ventral prostate or seminal vesicles. These agents impeded the testosterone-mediated increase in kidney weight, cytochrome c oxidase, and lysosomal hydrolases and urinary excretion of lysosomal hydrolases and proteins. They also attenuated the testosterone-induced decrease in enzyme latency and membrane stability of kidney lysosomes. In contrast, the antiandrogen cyproterone acetate is weakly androgenic in kidney and potentiates testosterone-induced lysosomal enzymuria and proteinuria (synandrogenic effect).
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PMID:Glucocorticoids and aspirin inhibit and cyproterone acetate enhances the androgenic response in mouse kidney. 627 Dec 47

The biopsies of 8 patients with diffuse proliferative glomerulonephritis associated with remote visceral infection (GN-RVI) were evaluated by histochemistry and electron microscopy for the presence and extent of intraglomerular monocytic infiltration. The sites of infection were cardiac valves (2 cases), ventriculoatrial shunts (2 cases), lungs (2 cases), blood (1 case) and retroperitoneal space (1 case). Seven of the patients had an elevated serum creatinine (1.5-6.5 mg/dl) and all had proteinuria, hematuria and an active urinary sediment. Histochemical investigation using the alpha-naphthyl acetate stain for nonspecific esterase (NSE) was conducted in 7 of the biopsies and showed relatively numerous intraglomerular monocytes in 5 cases. Electron microscopy demonstrated conspicuous monocytic infiltration of glomeruli in the 1 biopsy in which histochemistry was not done and in the 5 cases with high NSE indices (mean number of NSE + cells/glomerulus). The mean NSE index for the group was 4.5 (+/- 3.1) (range = 0.6-10.0). This was compared to the mean NSE indices for other types of diffuse proliferative glomerulonephritis (GN) - GN associated with mixed essential cryoglobulinemia (GN-CRY) (4 cases), membranoproliferative GN, type I (MPGN) (18 cases), post-infectious GN (PIGN) (9 cases) and diffuse lupus GN (GN-SLE) (35 cases). The NSE index for GN-RVI was less than that of GN-CRY (9.1 +/- 5.8) but greater than those of PIGN (3.5 +/- 2.5), GN-SLE (2.6 +/- 2.3) and MPGN (1.3 +/- 1.3). The differences between the GN-RVI index and those of GN-CRY, PIGN and GN-SLE were not significant but the difference between GN-RVI and MPGN was (p less than 0.01, Student's test).
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PMID:Monocytes and glomerulonephritis associated with remote visceral infection. 639 68

The effect of hypertension on the anatomy, physiology, and course of glomerulonephritis in rats was investigated by inducing deoxycorticosterone acetate-salt hypertension in animals with heterologous immune complex glomerulonephritis and vice versa. The effect of hypertension on glomerulonephritis with different degrees of intensity was also studied. Hypertension increased the proteinuria in the glomerulonephritic rat substantially (p less than 0.01), reduced the creatinine clearance (p less than 0.05), and induced an enormous thickening of the glomerular basement membrane. Furthermore, the life span was shortened (p less than 0.01) when hypertension was induced in nephritic rats, possibly due to insufficient cerebral vascular activity secondary to malnutrition. Glomerulonephritis did not influence the blood pressure in animals with severe protein loss; in rats with minor proteinuria the presence of glomerulonephritis increased the blood pressure. Hypertension lowered the antiserum dose needed to produce pathologic proteinuria (p less than 0.02). Hypertension seemed to increase the amount of glomerular immune deposits in early glomerulonephritis but lowered the amounts of glomerular rat IgG during the course of nephritis. In conclusion, hypertension increases the glomerular damage substantially in rats with heterologous immune complex glomerulonephritis, influences the glomerular deposition of immunoglobulins, and shortens the life span.
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PMID:Effect of hypertension on experimental glomerulonephritis in rats. 669 57

Experimental pathogenicity was for the first time demonstrated in a strain of C. lusitaniae of clinical origin by the use of concentrated inocula (5.10(7) Y-shaped cells) and the administration of 4 mg of methylprednisolone acetate i.m. injected 4 days before and 3 days after the inoculation. Counts on malt-agar (fig. 1) in kidney and brain showed a decrease during the first 12 hours, followed by a definite increment in cell number between the first and second day. Clinical tests showed a strong proteinuria, high levels of blood urea and creatinine, and a low GOT increase. Glycemia, GPT, and total serum protein values were normal. Histological examinations of kidney showed a delayed penetration with discrete clumps of Y-shaped cells, inflammatory focuses, and compromised tubules and glomerula (Fig. 2). After 2 weeks of study accumulations of cells followed by degenerative phenomena were seen in the various structures examined. Reparation processes were seldom observed (Fig. 3-4).
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PMID:[Experimental pathogenicity of Candida lusitaniae in mice]. 729 97

Proteinuria was analysed quantitatively and qualitatively in 156 diabetics and 63 matched controls. The study was limited to patients with a proteinuria of less than 100 ng/min in the recumbency. The urinary proteins were analysed using cellulose acetate electrophoresis, immunoelectrophoresis and sodium dodecylsulfate poly-acrylamide gel electrophoresis. Abnormal urinary protein patterns were more frequent in diabetics than in the controls (p less than 0.01). However, when the subjects were divided into 2 groups according to their age, the limit being arbitrarily chosen at 60 years, the differences were statistically not significant in the older group. By contrast, in the younger group, the proportion of perfectly normal patterns was significantly decreased in diabetics as compared to the controls (p less than 0.005). In our diabetic population, chosen on the basis of a quantitatively normal proteinuria, no clear relation could be found between the abnormalities of the urinary protein electrophoretic patterns and the patient's clinical data, with the exception of vascular and cardiac complications. Our results suggest that qualitative changes of urinary proteins might be the first signs of renal complications in diabetic patients and that diabetes might constitute an additional cause of aging for the kidneys.
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PMID:[Initial aspects of the changes in diabetic proteinuria]. 736 49

The use of ACE-inhibitors has increased greatly during the last years. They were first used in treating hypertension, but nowadays cardiac diseases, mainly cardiac failure, are common indications. This means that the drugs are used in the treatment of more elderly patients who often have generalised atherosclerosis. This means that the patients must be controlled more often after initiation of treatment, especially concerning kidney function, since treatment with ACE-inhibitors can cause pronounced changes in renal haemodynamics and kidney function. This review focuses on the effects of ACE-inhibitors on renal haemodynamics and kidney function, which may be positive, with preservation of kidney function in diabetic and other chronic nephropathy, or negative, for example in cases with atherosclerotic stenosis of large or small renal arteries. It is concluded, that in cases of diabetic nephropathy an ACE-inhibitor is the "drug of choice" for treatment of hypertension. Furthermore the ACE-inhibitors seem to reduce the rate of deterioration of renal function and proteinuria in other kidney diseases. It is emphasized, that during treatment with ACE-inhibitors kidney function must be controlled before and following one to two weeks of treatment, if the dose is changed and in all cases following two to three months of treatment. Special attention should be given to patients with atherosclerotic manifestations e.g. angina.
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PMID:[Renal function during treatment with angiotensin converting enzyme inhibitors]. 748 49

The follow-up of living kidney donors demands medical as well as psychological competence. In the postoperative period, attention focuses on pain management, early detection of wound complications and the prophylaxis of thromboembolism. Regular visits of the donor who may easily feel neglected should be as much part of the transplant team's post-operative routine as visits of the recipient. The later phase of recovery emphasizes strengthening abdominal wall and lumbar muscles as well as the gradual increase of physical activity. Long-term follow-up focuses on the early detection of arterial hypertension and proteinuria. Antihypertensive therapy in nephrectomized donors should include an ACE inhibitor or an angiotensin-II antagonist. In Switzerland, the long-term course after living donation is prospectively monitored by the Swiss Registry for Living Donors founded in 1993. The registry is responsible for the regular timing of follow-up examinations and assures transparency of the origin of the kidneys used for living donation in Switzerland. The registry heavily relies on the collaboration of the donor's family physicians.
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PMID:[Follow-up care of living kidney donors]. 750 64

A case is reported describing severe pre-eclampsia, treated firstly with antihypertensive drugs and Caesarean section. Contrary to expectation blood pressure did not fall and proteinuria still remained. Blood pressure reducing drugs had no effect at all. The patient was then treated with Renitec (enalapril), an ACE-inhibitor, with good result--even when given in a small dosis. No influence on lactation was documented for five weeks. Teratogenicy has been reported using ACE-inhibitors, and only a little is known about their effect on lactation. We found Renitec to have a good effect on reducing blood pressure postpartum and no effect on lactation at all.
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PMID:[Enalapril treatment of a pre-eclamptic woman]. 770 68

We evaluated the long-term effect of an intensive treatment of diabetic nephropathy (anti-hypertensive drugs, low protein diet, multiple insulin injections to achieve a good metabolic control) on glomerular filtration rate (GFR) and albumin excretion rate (AER). Fourteen type I diabetic patients (mean age 45 +/- 9.5 years, mean duration of diabetes 23.5 +/- 7.3 years, 8 males/6 females) with glomerular filtration rate < 70 ml/min-1/1.73 m2 and albumin excretion rate > 30 micrograms/min were treated intensively for 36 months. This intensive treatment consisted of multiple insulin injections, antihypertensive therapy with ACE inhibitors and a low-protein diet (0.8 g/kg body wt/day.) Renal function was evaluated as GFR and AER. HbA1c mean value decreased significantly from 8.7 +/- 0.8% to 6.5 +/- 0.5% (P < 0.0002). GFR rose from 58 +/- 12 ml/min-1/1.73 m2 to 84 +/- 11 ml/min-1/1.73 m2 (P < 0.0008). AER decreased from 208 micrograms/min (range: 73 to 500) to 63.8 micrograms/min (range 15 to 180; P < 0.05). Systolic and diastolic blood pressure decreased respectively from 144 +/- 26 mm Hg to 120 +/- 15 mm Hg and from 89 +/- 9 mm Hg to 75 +/- 8 mm Hg (P < 0.01). We obtained a rise of GFR and a reduction of proteinuria after three years of this treatment. We suggest that this intensive treatment in all patients with early stage diabetic nephropathy may be effective in slowing the progression to renal failure.
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PMID:Effect of intensive treatment on diabetic nephropathy in patients with type I diabetes. 773 Nov 51


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