The detection of proteins excreted in the urine has been extensively used in the assessment of renal diseases. Proteinuria identifies patients with renal damage and those at risk for worsening renal disease and increased cardiovascular morbidity. An individual with proteinuria in the setting of a normal glomerular filtration rate (GFR) is at high risk of progressive loss of renal function. The 2012 Kidney Disease: Improving Global Outcomes (KDIGO) clinical practice guideline for the evaluation and management of chronic kidney disease (CKD) includes proteinuria in the staging of CKD. It is important to note when proteinuria is present and can be reduced, as lowering proteinuria has a protective effect against further loss of kidney function.
Normal urinary protein excretion is < 150 mg/24 hours and consists mostly of secreted proteins such as Tamm-Horsfall proteins. The normal mean albumin excretion rate (AER) is 5-10 mg/day, with an AER of >30 mg/day considered abnormal. AER between 30 to 300 mg/day is called moderately increased albuminuria. Levels greater than 300 mg/day are called severely increased albuminuria. In the past, moderately and severely increased albuminuria were referred to as microalbuminuria and macroalbuminuria, respectively. Albuminuria that persists for 3 months is considered CKD. Nephrotic range proteinuria is defined as greater than 3.5 g of protein excreted in the urine over 24 hours. [1, 2]
Proteinuria can be differentiated on the basis of any of the following:
Pathophysiologically, most cases of proteinuria are classified into one or more of the following categories:
Tubular proteinuria is a result of tubulointersitial disease affecting the proximal renal tubules and interstitium. This results in decreased proximal reabsorption of proteins—in particular, low molecular weight proteins (generally below 25,000 Daltons) such as beta-2 microglobulin. Under normal conditions these proteins are completely reabsorbed in the proximal tubules. The amount of proteinuria is usually < 2 g/day and dipstick results may be negative.
Causes of tubular proteinuria include the following:
Overflow proteinuria is most commonly associated with increased production of abnormal low molecular weight proteins (eg, light chains in multiple myeloma, myoglobin in rhabdomyolysis) that exceeds the reabsorption capacity of the proximal tubule, leading to spilling of the protein into the urine. These low molecular proteins can be toxic to the tubules and can cause acute kidney injury. For example, paraprotein deposition can induce a glomerulopathy leading to the additional loss of albumin and more profound proteinuria.
Glomerular proteinuria associated with pathological damage to the glomerulus is categorized by protein quantity; the more severe the proteinuria, the more significant the glomerular disease. The primary protein lost is albumin. These patients require close follow-up and may need a kidney biopsy if they have abnormal urine microscopy results and/or impairment of kidney function.
Glomerular proteinuria can also be categorized according to whether pathological damage of the glomerulus is present. Types that do not result from pathological damage to the glomerulus include transient and orthostatic proteinuria.
Transient proteinuria occurs in persons with normal renal function, bland urine sediment, and normal blood pressure. The quantitative protein excretion is less than 1 g/day. The proteinuria is not indicative of significant underlying renal disease; it may be precipitated by high fever or heavy exercise, and it disappears upon repeat testing. Exercise-induced proteinuria usually resolved wihtin 24 hours.
Orthostatic proteinuria is diagnosed if the patient has no proteinuria in early morning samples but has low-grade proteinuria at the end of the day. It usually occurs in tall, thin adolescents or adults younger than 30 years (and may be associated with severe lordosis). Patients have normal renal function and proteinuria is usually < 1 g/day, with no hematuria. The diagnosis of orthostatic proteinuria is made by collecting the urine from the first morning void after the patient has been recumbent overnight. It is associated with good long-term prognosis. [3, 4, 5]
Accompanying findings in patients with glomerular damage may include the following (see Workup):
Isolated, post-renal, and post-transplant proteinuria also deserve mention. Isolated proteinuria is proteinuria without any abnormalities in urinary sediment, hematuria, or a reduction in GFR and in the absence of hypertenson and diabetes. Isolated proteinuria is usually found on routine urinalysis in the non-nephrotic range. It is caused by damage to tubular cells or the lower urinary tract. Post-renal proteinuria occurs with inflammation of the urniary tract. Common conditions thought to be associated with post-renal proteinuria is urinary tract infection, nephrolithiasis, and tumors of the urinary tract. Post-renal proteinuria usually resolves when the underlying condition has resolved.
Post-transplant proteinuria occurs in about 45% of kidney transplant recipients. Typically, proteinuria from native kidneys dramatically falls after transplant. Proteinuria at levels comparable with before transplantation is a sign of damage. The common causes of post-transplant proteinuria include the following:
Plasma proteins are essential components of any living being. The kidneys play a major role in the retention of plasma proteins, using renal tubules to reabsorb them as the proteins pass through the glomerular filtration barrier. Normal urine protein excretion is up to 150 mg/day. Therefore, the detection of abnormal quantities or types of protein in the urine is considered an early sign of significant renal or systemic disease. (See Pathophysiology and Etiology.)
Complications of proteinuria include the following (see Prognosis):
See Pediatric Proteinuria for discussion of the condition in that population.
Currently, the development of proteinuria is thought to involve dysfunction of the glomerular filtration barrier, tubular dysfunction, or both.
The glomerular filration barrier seperates the kidney vasculature from the urinary space. One of the barrier’s primary purposes is to prevent the passage of plasma proteins notably albumin. The small amount of albumin and non-albumin protein that is filtered is reabsorbed in the proximal convoluted tubule (PCT).
The three components of the glomerular filtration barrier are the podocytes (epithelial cells), the fenestrated endothelial cells, and the glomerular basement membrane (GBM). Proteinuria is prevented by the negative charge and size selectivity of the glomerular filtration barrier. Crosstalk among podocytes, mesangium, and endothelium maintains the normal filtration barrier. As all three are interlinked, damage to any one of them affects the functioning of the others.
Podocytes are the terminally differentiated visceral epithelial cells of the glomerulus found outside of the glomerular capillares; they face the Bowman space and the tubular infiltrate. Podocytes cover the glomerular capillaries and have extensions called foot processes that interdigitate with neighboring podoctyes, forming slit diaphragms 25-60 nm in size. Changes or effacement of foot processes is seen in many proteinuric states. Mutations in the genes that code for the proteins comprising the structure of the slit diaphragm can result in overt proteinuria.
Glomerular capillaries are internally lined by endothelial cells that are in contact with the bloodstream. A unique feature of glomerular endothelial cells is their fenestrations—holes in the cell that permit passage of fluid across the glomerular capillary wall. Although these fenestrations are much larger than albumin, the endothelial surface has a covering coat made up of negatively charged glycocalyx, glycosaminoglycans and proteoglycans that retards the positively charged albumin and other plasma proteins. This cellular coat acts as both a size- and charge-based barrier. In addition, endothelium activation and loss of selectivity leads to prolonged exposure of podocytes to proteins. This results in the activation of renin-angiotensin in podocytes  and alteration of size selectivity. Damage to podocytes in turns leads to decrease in vascular endothelial growth factor (VEGF) required for endothelial fenestrae formation. 
The glomerular fitration barrier is also maintained by the mesangium’s mesangial cells. Mesangial cells lie close to the capillary lumen and play an important role in glomerular hemodynamics and immune complex clearance. The mesangial cells produce a matrix made up of collagen, fibronectin, and proteglycans that supports the glomerular capillaries. This is a common site of deposition of circulating immune complexes. The mesangium is disrupted by cell proliferation, as occurs in diabetic nephropathy or immunoglonin A (IgA) nephropathy. 
The GBM is made up of type IV collage, laminin, nidogen/entactin, sulfated proteoglycans, and glycoproteins. The GBM limits fluid movement. Changes in the proteins that make up the GBM, leading to proteinuria, have been described in congenital and acquired nephrotic syndrome. Proteinuria itself can cause endothelial damage: protein-mediated cytotoxicity may result in podocyte loss, leading to the production of chemokines and cytokines that initiate an inflammatory response. The end point is sclerosis and fibrosis of the glomerulus. 
High amounts of albumin are filtered in the proximal tubules, and the mechanism is thought to involve two receptors, which can process 250 g of albumin per day. Obviously, any dsyfunction in this protein retrieval pathway wouldl result in nephrotic syndrome.
The presence of abnormal amounts or types of protein in the urine may reflect any of the following:
Systemic diseases that result in an inability of the kidneys to normally reabsorb the proteins through the renal tubules
Overproduction of plasma proteins that are capable of passing through the normal glomerular basement membrane (GBM) and that consequently enter the tubular fluid in amounts that exceed the capacity of the normal proximal tubule to reabsorb them
A defective glomerular barrier that allows abnormal amounts of proteins of intermediate molecular weight to enter the Bowman space
Causes of glomerular disease can be classified as primary (no evidence of extrarenal disease) or secondary (kidney involvement in a systemic disease) and can then subdivided within these two groups on the basis of the presence or absence of nephritic/active urine sediment. In some cases, however, primary and secondary diseases can produce identical renal pathology.
Primary glomerular diseases associated with active urine sediment (proliferative glomerulonephritis) include the following
Primary glomerular diseases associated with bland urine sediment (nonproliferative glomerulonephritis) include the following:
Secondary glomerular diseases associated with active urine sediment (proliferative glomerulonephritis, including rapidly progressive glomerulonephritis) include the following:
Secondary glomerular diseases associated with bland urine sediment (nonproliferative glomerulonephritis) include the following:
Secondary focal glomerulosclerosis may result from the following:
Unlike primary focal segmental glomerulosclerosis, the secondary type usually is gradual in onset and is not usually associated with hypoalbuminemia or other manifestations of nephrotic syndrome, even in the presence of nephrotic-range proteinuria.
MPGN is usually a pattern of injury seen on light microscopy. The current immunofluorescence-based classification divides MPGN as follows  :
Other causes of proteinuria include the following:
In the third National Health and Nutrition examination Survey (NHANES III), the prevalence of albuminuria in the US population was found to be 6.1% in males and 9.7 % in females. The prevalence of albuminuria was 28.8% in persons with diabetes, 16.0% in those with hypertension, and 5.1% in those without diabetes, hypertension, cardiovascular disease, or elevated serum creatinine levels. The prevalence of proteinuria starts increasing at 40 years of age. Also, 3.3% of the US adult population was found to have persistent albuminuria with a normal estimated glomerular filtration rate (eGFR). 
According to the NHANES III survey, the prevalence of microalbuminuria is greater in non-Hispanic blacks and Mexican Americans aged 40 to 79 years compared with age-matched non-Hispanic whites. Similar results were found in the NHANES survey from 2006, where even after adjusting for covariates and medication use, racial and ethnic minorities with and without diabetes had greater odds of albuminuria compared with whites without diabetes. The results were similar when the comparison was made in patients with eGFR < 60 mL/min. [14, 15]
Many causes of proteinuria are particularly common in African Americans and certain other groups. The primary glomerular disorder, focal segmental glomerulosclerosis, has a higher incidence as well as a worse prognosis in African Americans.
In a study by Friedman et al, nondiabetic chronic kidney disease was found to occur in more than 3 million African Americans who had genetic variants in both copies of APOL1, increasing their risk for hypertension-attributable end-stage renal disease and focal segmental glomerulosclerosis. However, African Americans without the risk genotype appear to have a risk similar to that of European Americans for developing nondiabetic chronic kidney disease. 
Most primary glomerular diseases associated with proteinuria (eg, membranous glomerulonephritis) and secondary renal diseases (eg, diabetic nephropathy) are more common in males than in females. As a result, persistent proteinuria is at least twice as common in males as in females.
The incidence of hypertension and diabetes increases with age. In consequence, the incidence of persistent proteinuria (and microalbuminuria) also increases with age.
The prognosis for patients with proteinuria depends on the cause, duration, and degree of the proteinuria. Young adults with transient or orthostatic proteinuria have a benign prognosis, while patients with hypertension and microalbuminuria (or higher degrees of albuminuria) have a significantly increased risk of cardiovascular disease.
Proteinuria has been associated with progression of kidney disease,  increased atherosclerosis, and left ventricular abnormalities indirectly contributing to cardiovascular morbidity and mortality. In addition to being a predictor of outcome in patients with renal disease, microalbuminuria also is a predictor of morbidity and mortality in patients who do not have evidence of significant renal disease.
In patients with hypertension, the presence of microalbuminuria correlates with the presence of left ventricular hypertrophy. In both hypertensive and normotensive patients, the presence of microalbuminuria predicts an increased risk of cardiovascular morbidity and mortality.
In a study of 2310 patients, Jackson et al concluded that spot urinary albumin-to-creatinine ratios (UACRs) have significant prognostic value in persons with heart failure.  These authors determined that, compared with patients with normoalbuminuria, those with an elevated UACR tended to be older, had higher rates of cardiovascular comorbidity and diabetes mellitus, and suffered from worse renal function. Even after adjustment for variables such as renal function and diabetes, an increased UACR was associated with a greater mortality risk.
In the European Prospective Investigation into Cancer in Norfolk (EPIC-Norfolk) population study, the incidence of myocardial infarction was higher in patients with microalbuminuria than in those with normal urinary albumin levels.  In a study by Rein et al, albuminuria was an important predictor of cardiovascular mortality even after adjusting for conventional risk factors.  Analysis of 1208 hypertensive, normoalbuminuric patients with type 2 diabetes from the BENEDICT trial also showed increased cardiovascular problems with any degree of measurable urinary albumin. 
Results from a study by Chiu et al of 225 proteinuric patients with type 2 diabetes mellitus indicated that vascular calcification, which can be particularly severe in nondialyzed patients with coexisting proteinuria and diabetes, is a prognostic indicator in early-stage type 2 diabetic nephropathy. 
In the study, 86% of patients were found to have coronary artery calcification, the degree of which was associated with older age, white ethnicity, and male sex. Fifty-four patients died during the follow-up period, which averaged 39 months.Univariate and multivariate analyses indicated that the degree of coronary artery calcification was, in relation to the calcification’s severity, an independent predictor of all-cause mortality in the study’s patients, with a 2.5-fold greater mortality risk found in subjects with a calcification score in the highest quartile. 
A study of 3939 subjects enrolled in the Chronic Renal Insufficiency Cohort (CRIC) study, a prospective observational cohort, found that proteinuria and albuminuria are better predictors of stroke risk in patients with chronic kidney disease than estimated glomerular filtration rate. In patients with albuminuria, treatment with renin-angiotensin blockers did not decrease stroke risk. 
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Beje Thomas, MD Assistant Professor, Department of Medicine (Nephrology), Georgetown University School of Medicine; Physician in Transplant Nephrology, Medstar Transplant Institute
Disclosure: Nothing to disclose.
Edgar V Lerma, MD, FACP, FASN, FAHA, FASH, FNLA, FNKF Clinical Professor of Medicine, Section of Nephrology, Department of Medicine, University of Illinois at Chicago College of Medicine; Research Director, Internal Medicine Training Program, Advocate Christ Medical Center; Consulting Staff, Associates in Nephrology, SC
Edgar V Lerma, MD, FACP, FASN, FAHA, FASH, FNLA, FNKF is a member of the following medical societies: American Heart Association, American Medical Association, American Society of Hypertension, American Society of Nephrology, Chicago Medical Society, Illinois State Medical Society, National Kidney Foundation, Society of General Internal Medicine
Disclosure: Author for: UpToDate, ACP Smart Medicine, Elsevier, McGraw-Hill, Wolters Kluwer.
Vecihi Batuman, MD, FASN Huberwald Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Renal Section, Southeast Louisiana Veterans Health Care System
Vecihi Batuman, MD, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, International Society of Nephrology, Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.
Tejas Desai, MD Staff Nephrologist, WG (Bill) Hefner VA Medical Center
Disclosure: Nothing to disclose.
Pankaj Jawa, MD Assistant Professor of Medicine, Division of Nephrology and Hypertension, The Brody School of Medicine at East Carolina University
Disclosure: Nothing to disclose.
George R Aronoff, MD Director, Professor, Departments of Internal Medicine and Pharmacology, Section of Nephrology, Kidney Disease Program, University of Louisville School of Medicine
George R Aronoff, MD is a member of the following medical societies: American Federation for Medical Research, American Society of Nephrology, Kentucky Medical Association, and National Kidney Foundation
Disclosure: Nothing to disclose.
Kevin McLaughlin, MBChB, PhD, MSc Associate Professor, Assistant Dean, Department of Medicine, University of Calgary Faculty of Medicine, Calgary Health Region
Kevin McLaughlin, MBChB, PhD, MSc is a member of the following medical societies: American Society of Nephrology, American Society of Transplantation, and College of Physicians and Surgeons of Alberta
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Salary Employment
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