Microheterogeneity of urinary albumin and tubular proteinuria in juvenile diabetes mellitus

Ries, M.; Schärer, K; Wartha, R.; Schmidt, H; Gekle, D

doi:10.1007/bf00856644

Cited by 8 publications

(5 citation statements)

References 31 publications

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“…The data of the present study are in accordance with other researchers that reported a high frequency of qualitative differences in urine proteins (30) and a variety of electrophoretic patterns (15) in the urine of well controlled diabetic adolescents without microalbuminuria. These observations indicate that early stages of diabetic nephropathy may involve both glomerular and tubular dysfunction.…”

Section: Discussionsupporting

confidence: 95%

“…Increased amounts of low molecular weight proteins in the urine of diabetic patients give evidence of decreased tubular reabsorbtion as an early sign of diabetic nephropathy (5,12,13,14,30). On the other hand increased permeability of the glomerular membrane (23,24) is expected to cause increased amounts of high molecular weight proteins in the urine of diabetic children.…”

Section: Discussionmentioning

confidence: 94%

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Electrophoretic analysis of urinary proteins in diabetic adolescents

Koliakos

Papachristou

Papadopoulou

et al. 2001

Clinical Laboratory Analysis

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Pathological changes in the urine sodium dodecyl sulphate gel electrophoresis (SDS PAGE) patterns often precede the occurrence of any sign of renal involvement in diabetes. However, data concerning the most frequent SDS PAGE pattern of the urine in early stages of type I diabetes mellitus are controversial. In the present study an SDS PAGE technique has been used that provides an adequate sensitivity for the detection of the abnormal pattern. Urinary proteins have been analyzed by SDS PAGE in twenty two diabetic adolescents and twenty four age matched controls. Albumin concentration, and N acetyl-beta-D-glucosaminidase (NAG) activity were also measured in the same samples. There was no significant difference in urine albumin concentration and NAG activity between diabetic children and controls. However twelve patients showed an electrophoretic pattern characteristic for glomerulopathy, two had a pattern indicating tubular dysfunction and another two patients had a mixed pattern. Among the twenty four controls only three showed abnormal electrophoretic patterns. The results support the view that early stages of diabetic nephropathy may involve both glomerular and tubular dysfunction. However the exact clinical and prognostic significance of the information provided by SDS PAGE analysis remains to be elucidated.

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Section: Discussionsupporting

confidence: 95%

Section: Discussionmentioning

confidence: 94%

Electrophoretic analysis of urinary proteins in diabetic adolescents

Koliakos

Papachristou

Papadopoulou

et al. 2001

Clinical Laboratory Analysis

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“…Coomassie brilliant blue (Biorad) was used to measure total protein [15]. For determination of LMW and HMW proteins, we used sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) after concentration of the urine by dialysis [16,17]. We used 0.48-mm-thick slab gels with an exponential polyacrylamide gradient from 4.0% to 22.5%, according to Goerg et al [16], and the Laemmli buffer system.…”

Section: Methodsmentioning

confidence: 99%

Proteinuria and other renal functions in Wilson's disease

Sözeri

Feist

Ruder

et al. 1997

Pediatric Nephrology

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Renal lesions have repeatedly been described in Wilson's disease (WD). We investigated the excretion of total protein, albumin, low (LMW) and high molecular weight (HMW) proteins, N-acetyl-beta-D-glucosaminidase (NAG), and calcium, as well as creatinine clearance, in 24-h urine samples of 41 patients with WD aged 6-37 (mean 17) years who had been treated for a period of 0-15 (mean 4.5) years with D-penicillamine (900 mg/day). The amount of all protein excreted was significantly increased compared with controls, 39% of patients presenting with total proteinuria more than two standard deviations from the mean of controls. The changes in protein excretion depended on the duration of treatment. LMW proteinuria was elevated almost exclusively in the first 2 years after the start of treatment, indicating early tubular damage. This is supported by an initially high excretion of beta 2-microglobulin, NAG, and calcium. Increased excretion of HMW proteins, including albumin, persisted over longer periods, which suggests glomerular injury in some patients, possibly related to the use of D-penicillamine. Creatinine clearance remained roughly within normal limits. We propose that renal function should regularly be checked in patients with WD.

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“…An increase in the charge microheterogeneity of serum albumin -with an increase in the isoelectric point -has been described in adolescents with diabetes. 39 Cationization of albumin changes its spatial configuration 40 and may thus also influence its size-based exclusion by the capillary wall 39 or increase its binding to the negatively charged brush border of proximal tubule cells, thereby increasing its reabsorption. 41 Finally, albumin glycosylation cannot explain enhanced albuminuria in obese or hypertensive subjects with decreased insulin sensitivity, but no overt diabetes.…”

Section: Why Should Insulin Resistance Enhance Albuminuria?mentioning

confidence: 99%

Time to abandon microalbuminuria?

Ruggenenti

Remuzzi

2006

Kidney International

187

141

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The term microalbuminuria--a urinary albumin excretion (UAE) between 20 and 200 microg/min--has been introduced to identify subjects at increased risk of renal and cardiovascular disease. However, the relationship between albuminuria and risk is not restricted to the microalbuminuric range and extends to as low as 2-5 microg/min. On the contrary, the increase of UAE above 200 microg/min (macroalbuminuria) heralds the onset of proteinuria (urinary protein excretion above 0.5 g/24 h) and progressive renal and cardiovascular disease. Albuminuria is a component of the metabolic syndrome and may represent a marker of the increased risk of renal and cardiovascular disease associated with insulin resistance and endothelial dysfunction. Proteinuria is a sign of established kidney damage and plays a direct pathogenic role in the progression of renal and cardiovascular disease. Albuminuria reflects functional and potentially reversible abnormalities initiated by glomerular hyperfiltration, proteinuria, a size-selective dysfunction of the glomerular barrier normally associated with glomerular filtration rate (GFR) decline that may result in end-stage renal disease. Thus, the limit of 200 microg/min segregates patients with albuminuria or proteinuria who are at quite different risk. Among subjects with albuminuria, however, there is a continuous relationship between albumin excretion and risk and no lower bound between normal albuminuria and microalbuminuria can be identified that segregates subjects at different risk. Thus, the terms microalbuminuria and macroalbuminuria could be replaced by the concepts of albuminuria- and proteinuria-associated diseases. Future studies are needed to identify levels of albuminuria below which therapy is no longer beneficial.

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Microheterogeneity of urinary albumin and tubular proteinuria in juvenile diabetes mellitus

Cited by 8 publications

References 31 publications

Electrophoretic analysis of urinary proteins in diabetic adolescents

Electrophoretic analysis of urinary proteins in diabetic adolescents

Proteinuria and other renal functions in Wilson's disease

Time to abandon microalbuminuria?

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