Proteinuria: how to evaluate an important finding.

Kashif, Waqar; Siddiqi, Nauman; Dincer, Ayse P.; Dinçer, H. Erhan; Hirsch, Sheldon

doi:10.3949/ccjm.70.6.535

Cited by 54 publications

(51 citation statements)

References 57 publications

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“…Dysfunction of the glomerular capillary wall results in proteinuria, and proteins of the size of albumin (69 kD, approximately 36 Å) or larger then appear in the urine (1,2).…”

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confidence: 99%

In Vivo Degradation of Heparan Sulfates in the Glomerular Basement Membrane Does Not Result in Proteinuria

Wijnhoven¹,

Lensen²,

Wismans³

et al. 2007

Journal of the American Society of Nephrology

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Heparan sulfates (HS) are long, unbranched, negatively charged polysaccharides that are bound to core proteins. HS in the glomerular basement membrane (GBM) is reported to be important for charge-selective permeability. Aberrant GBM HS expression has been observed in several glomerular diseases, such as diabetic nephropathy and membranous glomerulopathy, and a decrease in HS generally is associated with proteinuria. This study, with the use of a controlled in vivo approach, evaluated whether degradation of HS in rat GBM resulted in acute proteinuria. Rats received two intravenous injections of either heparinase III to digest HS or neuraminidase to remove neuraminic acids (positive control). Urine samples were taken at various time points, and at the end of the experiment, kidneys were removed and analyzed. Injection with heparinase III resulted in a complete loss of glomerular HS as demonstrated by immunofluorescence staining using anti-HS antibodies and by electron microscopy using cupromeronic blue in a critical electrolyte concentration mode. In the urine, a strong increase in HS was found within 2 h after the first injection. Staining for agrin, the major HS proteoglycan core protein in the GBM, was unaltered. No urinary albumin or other proteins were detected at any time point, and no changes in glomerular morphology were noticed. Injection of rats with neuraminidase, however, resulted in a major increase of urinary albumin and was associated with an increase in urinary free neuraminic acid. An increased glomerular staining with Peanut agglutinin lectin, indicative of removal of neuraminic acid, was noted. In conclusion, removal of HS from the GBM does not result in acute albuminuria, whereas removal of neuraminic acid does.

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“…Dysfunction of the glomerular capillary wall results in proteinuria, and proteins of the size of albumin (69 kD, approximately 36 Å) or larger then appear in the urine (1,2).…”

mentioning

confidence: 99%

In Vivo Degradation of Heparan Sulfates in the Glomerular Basement Membrane Does Not Result in Proteinuria

Wijnhoven¹,

Lensen²,

Wismans³

et al. 2007

Journal of the American Society of Nephrology

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“…To monitor the progression of hypertensive nephropathy, a noninvasive biochemical marker for evaluating the activity of hypertension nephropathy is required. The most widely used method to detect proteinuria is the urine dipstick test (9). Although the dipstick test is costeffective and simple, its sensitivity is not always high enough.…”

Section: Discussionmentioning

confidence: 99%

Clinical value of urinary kidney biomarkers for estimation of renal impairment in elderly Chinese with essential hypertension

Fang

et al. 2008

Clinical Laboratory Analysis

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The purpose of this work was to observe the excretion of specific types of urinary proteins and urinary enzymes in elderly essential hypertension patients, for early detection and targeted treatment of hypertensive nephropathy in the elderly. A total of 120 elderly essential hypertensive patients and 38 healthy elderly volunteers were involved. The urinary excretion rate of retinal-binding protein (RBP), transferrin (Tf), albumin (Alb), and urinary enzyme N-acetyl-beta-D-glucosaminidase (NAG) activity were determined. Patients were divided into two groups according to their creatinine clearance (Cockroft-Gault formula). There were 88 patients in group A, whose glomerular filtration rate (GFR) was Z80 mL/min, and 32 patients in group B with a GFR o80 mL/min. Among the essential hypertensive patients, urinary excretion rates of RBP, Alb, Tf, and NAG were increased in both groups compared with the healthy controls. But the amount of urinary protein differed between group A and group B. The excretion rate of specific urinary protein and urinary enzyme had a positive relationship with the duration of course of hypertension. We believe that specific types of urinary proteins and urinary enzymes may be useful markers for early diagnosis of hypertensive nephropathy; they can also be regarded as a clinical indicator of the progression of hypertensive nephropathy, serving in the assessment of therapeutic effects.

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“…[1] The bedside detection of non-albumin proteinuria is aided by the use of a simple, inexpensive and often-overlooked investigation: addition of SSA 3% to urine. The degree of turbidity provides a semiquantitative method for proteinuria detection.…”

Section: Discussionmentioning

confidence: 99%

The utility of urine sulphosalicylic acid testing in the detection of non-albumin proteinuria

Ndamase

Freercks

2014

S Afr Med J

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A 51-year-old woman with hypertension and type 2 diabetes mellitus was referred for evaluation of her chronic kidney disease. Her creatinine was 124 µmol/L, urea 5.6 mmol/L and estimated glomerular filtration rate 40 mL/min. She had a severe normocytic anaemia, with a haemoglobin of 6.5 g/dL. On further enquiry she gave a history of unintentional weight loss of 9 kg. She was pale, with no lymphadenopathy or oedema. Urine dipstick was negative for proteinuria, but the urine protein:creatinine ratio was 0.8 g/mmol (normal range <0.02 g/mmol), indicating nephrotic range proteinuria. The addition of sulphosalicylic acid (SSA) to her urine caused immediate turbidity (Fig. 1). A diagnosis of multiple myeloma was

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Proteinuria: how to evaluate an important finding.

Abstract: Proteinuria is a common laboratory finding in outpatients and should not be discounted. When it is due to a glomerular disease, early diagnosis is important to prevent further renal damage. Proteinuria may also be a marker for progressive atherosclerosis.

Cited by 54 publications

References 57 publications

In Vivo Degradation of Heparan Sulfates in the Glomerular Basement Membrane Does Not Result in Proteinuria

In Vivo Degradation of Heparan Sulfates in the Glomerular Basement Membrane Does Not Result in Proteinuria

Clinical value of urinary kidney biomarkers for estimation of renal impairment in elderly Chinese with essential hypertension

The utility of urine sulphosalicylic acid testing in the detection of non-albumin proteinuria

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