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)

The published studies on histological staging and response to steroid therapy of membranous glomerulonephritis are not consistent. We analysed data from 25 adult patients with stage I (group 1, n = 7) and stage II (group 2, n = 18) disease. The interval between clinical onset and admission was similar in the two groups. At admission all patients had normal creatinine clearance; proteinuria averaged 5.4 +/- 4.0 in group 1 and 9.0 +/- 4.0 in group 2 (g/day per 100 ml GFR). All patients received 6 months steroid therapy (months 1-2, 1 mg/kg b.w. per day; month 3-5: 0.65 mg/kg b.w. e.o.d.; month 6, tapering). After this cycle of steroid therapy, proteinuria declined by 84% in group 1 (five patients being in partial remission, i.e. 0.4-2 g/day, and two patients in complete remission, i.e. less than or equal to 0.3 g/day) and by 47% in group 2 (two patients being in complete remission and six in partial remission). Only 1 patient in group 1 relapsed with nephrotic proteinuria after 36 months, and renal function was still normal in all patients at the most recent follow-up (59 +/- 32 months). In contrast, 14 patients in group 2 had nephrotic syndrome and seven renal insufficiency at the most recent follow-up. We conclude that short-term steroid therapy is effective only in patients with early membranous changes.
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PMID:Effectiveness of steroid therapy in different stages of membranous nephropathy. 251 22

We studied the efficacy of the ACE inhibitor lisinopril in treating overt proteinuria in comparison with the NSAID indomethacin, and evaluated some of the conditions that could influence this antiproteinuric effect. In 12 patients with a proteinuria varying from 3.2 to 10.5 g/24 hr, a diastolic BP ranging from 64 to 105 mm Hg, and a GFR varying from 34 to 127 ml/min, the effect of different lisinopril doses and of changing dietary sodium intake was evaluated. Proteinuria fell by 27 +/- 20% from 6.1 +/- 2.1 to 4.5 +/- 1.9 g/24 hr on a low dose (median 5 mg/day) lisinopril and by 50 +/- 17% to 3.1 +/- 1.4 g/24 hr on a higher dose (median 10 mg/day), irrespective of initial proteinuria, BP, or GFR. This antiproteinuric effect was abolished by increasing salt intake from 50 to 200 mmol/day, and was recovered again by re-instituting the sodium restricted diet. The antiproteinuric effect of 10 mg/day lisinopril was comparable to the reduction in proteinuria (by 57 +/- 21% to 2.8 +/- 2.0 g/24 hr) on 150 mg/day indomethacin, while adverse effects were less and renal hemodynamic effects were more favorable during lisinopril. In some patients it took several weeks before the effect of the ACE inhibitor on proteinuria was stabilized. Thus, the antiproteinuric effect of the ACE inhibitor lisinopril appears to be dose and time related, and is strongly dependent on dietary sodium restriction, whereas it does not depend on initial proteinuria, BP, or GFR. The effect is comparable to that of indomethacin, while adverse effects are less.
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PMID:Efficacy and variability of the antiproteinuric effect of ACE inhibition by lisinopril. 255 Jun 96

In this work 45 living related kidney donors (LRD) and 20 healthy sex and age matched controls were examined. Donors were evaluated up to 122 months after donation. Hyperfiltration was observed in the remaining kidney with a mean one-kidney GFR value of 82.9 +/- 36.8 ml/min while the control value was 71.04 +/- 31.5 ml/min. The kidney was significantly larger in the donor group than in the controls. In the LRD group, 3 were hypertensive, 7 showed microscopic haematuria and 5 had mild proteinuria. In the control group 3 were mildly hypertensive, and 2 showed microscopic haematuria. Serum creatinine of the donor group was found to be significantly higher than in the controls, yet it was stable and within the normal range (0.89 +/- 0.28 mg/dl). Examination for microalbuminuria showed that 11% of the donor group excreted higher amounts of albumin, being above the upper limit of the control group. We have concluded that kidney donation will result in minor abnormalities in kidney functions which will not affect the donor morbidity or mortality.
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PMID:Long-term follow-up of the remaining kidney in living related kidney donors. 261 85

The excretion profiles of the following marker proteins of glomerular and tubular origin were studied in patients suffering from chronic renal disease (GN, N = 36, GFR: 8 to 120 ml/min/1.73 m2): angiotensinase A (ATA), a glomerular endothelial glycoprotein, tubular ala(-leu-gly)-amino-peptidase-M (APM), gamma-glutamyl transpeptidase (GGT), and the major brush border surface glycoprotein (SGP-antigen) of 240 kD. In addition, urinary excretion of proteins from kidney tissue and serum from 30 patients undergoing chronic hemodialysis (RCDT) were analyzed. Compared to the controls, ATA, APM and GGT activities were significantly higher in urine specimens of patients with GFR greater than 25 ml/min, whereas the urinary APM, GGT and SGP concentrations were decreased, and correlated with the GFR. Urinary GGT activity was negatively correlated with ATA activity but positively correlated with the decrease in GFR. Urine ATA activity of RCDT patients was higher compared to normal controls (2P = 0.001). Urinary excretion of serum proteins of RCDT patients, as assessed by SDS-polyacrylamide gel electrophoresis, disclosed heavy tubular proteinuria, indicating predominant tubular rather than glomerular alterations in handling of proteins. Histochemical evaluation of kidney sections from RCDT patients revealed clusters of hypertrophic nephrons with increased glomerular and tubular concentration of immunoreactive membrane proteins. However, there was a general decrease in renal cell-marker concentrations as observed by quantitative image analyses. These results indicate that renal injury is associated with a modulation in the synthesis of tubular and glomerular cell markers.
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PMID:Glomerular and tubular membrane antigens reflecting cellular adaptation in human renal failure. 263 72

To assess progression of renal disease and the effects of protein intake in a species phylogenically close to man, 10 young adult baboons (Papio hamadryas) were subjected to 20 to 30% infarction of the left kidney and, two months later, to right nephrectomy. They were then randomized to a synthetic diet containing either 8% or 25% protein. Hemodynamic and metabolic measurements were obtained in awake animals every four months. Baseline mean blood pressure, inulin clearance, protein and urea nitrogen excretion in intact animals on 15% protein averaged 75.5 +/- 3.5 (SE) mm Hg, 42.9 +/- 2.7 ml/min, 52 +/- 4.3 mg/24 hr, and 3.8 +/- 0.4 g/24 hr, respectively. At 12 months, values in the same baboons with a remnant kidney on 8% versus 25% protein averaged 100.6 versus 96.7 mm Hg, 29.2 versus 54.9 ml/min (P less than 0.01), 111 versus 108 mg/24 hr, and 3.4 versus 11.0 g/24 hr (P less than 0.001), respectively. Electron microscopic examination of renal biopsies obtained eight months after nephrectomy was normal but for slightly increased mesangial matrix in three animals. Thus, blood pressure increased (P less than 0.01), proteinuria doubled (P less than 0.01) and adaptations in GFR developed within four months of renal mass reduction, without significant changes occurring between four and 12 months. The adaptations in GFR were markedly attenuated by low protein intake. Further follow-up is necessary to assess progression of renal disease and the impact of different protein diets.
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PMID:Renal function of baboons (Papio hamadryas) with a remnant kidney, and impact of different protein diets. 263 78

The micromolecular proteinuria (67-11 Kd), originating from tubulo-interstitial disorders, might be determined by SDS- or gradient-PAGE or by individual marker proteins. The latter procedure in addition to PAGE is necessary in case of heavy proteinurias. The tubular resorptive capacity for microproteins, analysed by fractional beta-2-M-clearances, decreases with deteriorating GFR. Values for FrCl beta 2M above the expected level were associated with tubulo-interstitial, but also with diabetic and rapidly progressing glomerular nephropathies. In the latter group these findings might be of prognostic importance. In contrast, the U-beta-2-M-determination in long term observation of kidney transplants had no diagnostic nor prognostic value.
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PMID:[Fractional clearance of beta-2-microglobulin in the diagnostic and prognostic assessment of kidney diseases]. 266 13

This paper reviews experimental findings which support the concept that vasopressin (VP) and the process of urine concentration may be involved in the progression of chronic renal failure (CRF). The influence of dietary protein intake on the progression of CRF may also involve VP and the operation of the concentrating process. VP receptors have been identified in glomeruli and VP is able to constrict mesangial cells as does angiotensin II. Acute VP infusion increases the glomerular transcapillary hydraulic pressure difference, and chronic VP infusion increases GFR. In rats with CRF (induced by 5/6 nephrectomy), VP levels were found elevated. In rats with 5/6 nephrectomy, we increased experimentally water intake in order to decrease circulating VP levels, urine concentration, and free water reabsorption. Several indices of progression of CRF, including proteinuria, hypertension and glomerulosclerosis, were significantly reduced, thus suggesting a contribution of VP in progression. Lowering protein intake in CRF could be beneficial because proteins, but not carbohydrates or lipids, produce metabolic end products (mainly urea, ammonia, protons, etc.) that are excreted by the kidney, and concentrated in the urine. In healthy subjects (man or rat), high protein (HP) intake favors urine concentration and causes changes in kidney function and morphology very similar to those induced by chronic VP infusion or water restriction. These changes involve an increase in transport activity of the thick ascending limb (where the initial active step of the concentrating process takes place) and may affect filtration rate and/or glomerular hemodynamics secondarily, by decreasing salt concentration at the macula densa and depressing tubuloglomerular feedback.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Possible involvement of vasopressin and urine concentrating process in the progression of chronic renal failure. 270

Three cases of the Crow-Fukase syndrome without radiographic changes of multiple myeloma are reported, with special reference to the glomerular changes seen. Proteinuria was detected in one case, although decreased renal function was observed in all (GFR: 41.0, 62.0, 74.1 ml/min respectively) at the time of renal biopsy. Glomerular changes were similar in all three cases. The main characteristic changes were mesangial proliferation and thickening of the glomerular capillary walls. Pictures by light microscopy were therefore similar to that of MPGN. On electron microscopy, the thickened capillary walls showed circumferential mesangial interposition and the subendothelial zone was electron-lucent and contained small dense granules or flocculent deposits. By immunofluorescent microscopy, no immunoglobulins, complement components or light chain were detected in the glomeruli except in one case.
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PMID:Glomerular lesions associated with the Crow-Fukase syndrome. 308 38

Long-term follow-up is presented of 73 patients suffering from the haemolytic-uraemic syndrome 10 years after the acute initial illness. The patients were subdivided into three groups, according to the criteria proposed by Gianantonio and based on the duration of oliguria and/or anuria. Four out of 38 patients belonging to the first group (oliguria for less than 7 days) had a slightly increased blood pressure as the only sequela. Two patients out of group two (n = 29, oliguria for 7-14 days or anuria for less than 7 days) had a diminished GFR and a reduced concentrating capacity, some proteinuria, and mild hypertension. Five other patients had slight proteinuria (less than 500 mg/24 h) and one of them a mild hypertension. All six patients belonging to the third group (oliguria for more than 14 days or anuria for more than 7 days) had late sequelae: two started haemodialysis more than 10 years after the initial phase; three have a decreased GFR and concentrating capacity. The unique remaining patient with a normal GFR without hypertension has a decreased concentrating capacity. The importance of careful treatment in children with a decreased GFR 2 years after the initial phase is stressed.
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PMID:Haemolytic-uraemic syndrome: a 10-year follow-up study of 73 patients. 314 Jan 21

Although most patients respond well to loop diuretics, poor response is sometimes a problem and some underlying mechanisms were addressed in this study. The renal response to continuous infusion of furosemide was investigated in eight healthy volunteers during controlled isotonic dehydration and after full restoration of volume losses. A rapidly reversible acute tolerance developed in parallel with dehydration and activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS). Dehydration also reduced the renal clearance of furosemide substantially, but only decreased the urinary delivery rate of the drug (the principal determinant of the diuretic effect) to a minimal extent. Delayed tolerance to an i.v. bolus dose of furosemide was found in 12 healthy volunteers after 1 week of oral furosemide treatment with and without angiotensin converting enzyme inhibition. No pharmacokinetic changes were seen. This type of tolerance was not related to dehydration or activation of RAAS. Thus, the induced decrease in renal sensitivity to furosemide was probably due to an intrarenal (structural?) adaptation. The pharmacokinetics and pharmacodynamics of piretanide were studied in six healthy volunteers and 22 patients with chronic renal failure (glomerular filtration rate 1-28 ml/min). Poor response to the diuretic action of the drug was found in the patients. This was entirely due to a decrease in the fraction of piretanide excreted unchanged in the urine, and the renal sensitivity to the drug was normal. Multiple daily doses of piretanide of maximally 24 mg are recommended for optimal efficiency in renal failure. Substantial changes in pharmacokinetics of furosemide were found after manipulation of plasma albumin in five patients with nephrosis, while the urinary delivery of the drug scarcely changed. Neither the induced alterations in proteinuria nor those in plasma volume influenced the renal sensitivity to furosemide significantly. Some methodological observations proved to be of significance. Creatinine was found to be an unreliable marker of GFR because of its substantial tubular secretion and reabsorption, both of which were related to the degree of hydration. Likewise, lithium was considered an unreliable marker of proximal tubular reabsorption, since there were reasons to suspect furosemide-sensitive distal lithium reabsorption.
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PMID:Mechanisms of reduced effects of loop diuretics in healthy volunteers and in patients with renal disease. 320 Nov 62


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