Proteinuria

WikiDoc Resources for Proteinuria
Articles
Most recent articles on Proteinuria Most cited articles on Proteinuria Review articles on Proteinuria Articles on Proteinuria in N Eng J Med, Lancet, BMJ
Media
Powerpoint slides on Proteinuria Images of Proteinuria Photos of Proteinuria Podcasts & MP3s on Proteinuria Videos on Proteinuria
Evidence Based Medicine
Cochrane Collaboration on Proteinuria Bandolier on Proteinuria TRIP on Proteinuria
Clinical Trials
Ongoing Trials on Proteinuria at Clinical Trials.gov Trial results on Proteinuria Clinical Trials on Proteinuria at Google
Guidelines / Policies / Govt
US National Guidelines Clearinghouse on Proteinuria NICE Guidance on Proteinuria NHS PRODIGY Guidance FDA on Proteinuria CDC on Proteinuria
Books
Books on Proteinuria
News
Proteinuria in the news Be alerted to news on Proteinuria News trends on Proteinuria
Commentary
Blogs on Proteinuria
Definitions
Definitions of Proteinuria
Patient Resources / Community
Patient resources on Proteinuria Discussion groups on Proteinuria Patient Handouts on Proteinuria Directions to Hospitals Treating Proteinuria Risk calculators and risk factors for Proteinuria
Healthcare Provider Resources
Symptoms of Proteinuria Causes & Risk Factors for Proteinuria Diagnostic studies for Proteinuria Treatment of Proteinuria
Continuing Medical Education (CME)
CME Programs on Proteinuria
International
Proteinuria en Espanol Proteinuria en Francais
Business
Proteinuria in the Marketplace Patents on Proteinuria
Experimental / Informatics
List of terms related to Proteinuria

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Saeedeh Kowsarnia M.D.[2]

Synonyms and keywords: Elevated urinary protein levels; Elevated urine protein

To view a comprehensive algorithm of common findings of urine composition and urine output, click here

Overview

Proteinuria (from protein and urine) means the presence of an excess of serum proteins in the urine.The protein in the urine often causes the urine to become foamy, although foamy urine may also be caused by bilirubin in the urine (bilirubinuria),retrograde ejaculation, pneumaturia (air bubbles in the urine) due to a fistula,or drugs such as pyridium.

Classification

Proteinuria is classified based upon the site and the amount of protein in the urine.

Types	Definition	Level of proteinuria
Glomerular proteinuria	Increased filtration rate of protein due to the damage to the glomerular-capillary barrier	Variable, usually > 2g/day Dipstick:Positive
Tubular proteinuria	Decreased tubular reabsorption of proteins due to tubular cell damage	< 2 g/day Dipstick:Negative
Overflow proteinuria	Increased urinary excretion of proteins due to exceeding reabsorption capacity of renal tubules	Variable up to 20g/day Dipstick:Negative
Post-renal proteinuria	Increased urinary excretion of the small amount of protein especially IgA and IgG	Variable, usually < 1g/day
Isolated proteinuria	Proteinuria with normal urinary sediment with no history of renal disease Excluding criteria: Proteinuria (≥ 3.5 g/day), edema, hypoalbuminemia, lipiduria, active urine sediment (red blood cells and/or cast), decreased GFR, hypertension	< 2 g/day

Proteinuria	Amount
Normal range	Total protein excretion in urine (proteinuria): < 150 mg/day, average 80 mg/day Albumin excretion: < 20 mg/day (15 mcg/min), 15% of urine total protein (remaining 85% constitutes Tamm-Horsfall proteins, IgA, urokinase) (The rate of proteinuria increases proportionally with age and body weight)
Albuminuria (microalbuminuria)	30-300 mg/day (20 to 200 mcg/min)
Overt proteinuria (macroalbuminuria)	Albuminuria > 300 mg/day (200 mcg/min) up to 3500 mg/day, positive dipstick
Nephrotic range	Total protein excretion: ≥ 3.5 g/day

Pathophysiology

The amount of proteins present in the urine is < 150 mg/day with an intact glomerular-capillary barrier and functioning tubules, thus increased levels of proteinuria can demonstrate kidney damage (glomerular or tubular). Overproduction of proteins which exceeds the absorption capacity of the tubules causes proteinuria in spite of relatively normal renal function (overflow). Normally filtration of all plasma proteins like albumin, globulins and other high-molecular-weight proteins through the glomerular-capillary wall is prevented by charge and size of the proteins and glomerular-capillary barrier. The type and quantity of proteins in the urine identifies the cause and site of kidney damage. As injury to the glomerular-capillary barrier causes albuminuria, tubular damage and overflow proteinuria lead to increase loads of low-molecular-weight proteins in the urine. The severity of protein loss in the urine depends on the mechanism of renal injury.

Glomerular-capillary barrier: It consists of endothelial cells of capillary, Glomerular basement membrane and epithelial cells. The endothelial cells of vessels organize a barrier with pores of 100 nm which impede the passing of the proteins from blood to the urinary space. Glomerular basement membrane and epithelial cells (podocytes) prevent the protein passage and trap the proteins especially with the size of > 100 kDa. The slit diaphragm acts as the most selective barrier for protein passage. The endothelial cells, podocytes, and glomerular basement membrane impede traversal of the negative-charge proteins due to the presence of negative charges in their constitution.

Tubular reabsorption: Almost all the proteins which are filtered through glomerulus are reabsorbed by proximal tubular cells by endocytosis. The tubulointerstitial diseases damage the cells cause tubular proteinuria. In circumstances which large amounts of protein is filtered, tubular proteinuria occurs due to exceeding the reabption capacity of the cells. Not all the proteins in the tubules are toxic to the cells but proximal tubule injury, light chain deposition and tubule obstruction (cast nephropathy) due to the large level of light chain may cause further proteinuria by the overwhelming capacity of tubular cells.

Proteins: The size of the protein is one of the determinants of traversal through the glomerular-capillary barrier. Immunoglobulins like IgG and other high-molecular-weight proteins have the higher molecular radius, therefore, there are not able to pass over the barrier. Low-molecular-weight proteins are the ones with < 40kDa and molecular radius < 30 Å are filtered almost completely and reabsorbed by tubular cells.

• In normal physiological condition, HMW proteins do not cross the glomerular barrier. The small percentage of albumin passes the barrier which is reabsorbed completely in the proximal tubules. LMW proteins are filtered and reabsorbed completely.

• Moderate alteration of permeability of glomerular barrier named as selective proteinuria, demonstrates with loss of negative-charged proteins like albumin, LMW proteins and small percetage of HMW proteins in the urine with exceeding the reabsorbtion capacity of tubular cells.
• Severe damage to the barrier, causes loss of the greater percentage of HMW proteins in the urine which is called nonselective proteinuria.
• Profound damage to glomerular barrier causes severe proteinuria of all classes especially LMW and HMW. Increasing loads of protein which exceed the reabsorption capability of tubular cells causes damage to tubular cells and worsens proteinuria.

(an average protein has 250 amino acids which equals molecular weight( MW) of approximately 34 kDa)

Glomerular-capillary wall, (ɔ) Image courtesy of WikiDoc.org, by "Saeedeh Kowsarnia M.D."

Causes

Classification	Etiology
Glomerular proteinuria	Diabetic nephropathy, orthostatic proteinuria, glomerulonephropathies, hypertensive nephrosclerosis, preeclampsia, collagen vascular disease, infections, cancer, lymphoma, chronic renal transplant rejection, drugs, amyloidosis, post-transplant proteinuria Transient: Exercise-induced proteinuria, fever, Infection, heart failure, joint inflammation, hyperlipidemia (LDL > 120 mg/dL), hyperglycemia (HbA1c > 8%), hypertension (BP >160/100 mmHg)
Tubular proteinuria	Tubulointerstitial diseases, cryoglobulinemia, Sjögren's syndrome, immunosuppressive agents, analgesic use
Overflow proteinuria	Light chains of immunoglobulins (multiple myeloma), lysozyme (AML), myoglobin (rhabdomyolysis), free hemoglobin not bound to haptoglobin (intravascular hemolysis), lymphoma, amyloidosis
Post-renal proteinuria	Nephrolithiasis, urinary tract tumors or infections
Isolated proteinuria	damage to tubular cells or the lower urinary tract, There is a 20% risk for renal insufficiency in the next 10 years, observation with blood pressure measurement, urinalysis and a creatinine clearance every 6 months should be considered.
Microalbuminuria	Essential hypertension, early diabetes, early stages of glomerulonephritis (especially with active sediments; RBCs, RBC casts)
Macroalbuminuria	Fever, exercise, CHF, orthostatic proteinuria, intermittent proteinuria, the kidney disease associated with myeloma, all diseases which are mentioned as the causes of microalbuminuria
Nephrotic range proteinuria	Diabetes, minimal change disease, amyloidosis, FSGS, membranous glomerulopathy, IgA nephropathy

Risk Factors

• Race and ethnicity
• Obesity
• Age
• Medications

Epidemiology and Demographics

• Prevalence of albuminuria is 6100 and 9700 per 100,000 in male and female population, respectively .
• The estimated prevalence rate of albuminuria among diabetes population is 28,800 per 100,1000.
• Approximately,16,000 per 100,000 hypertensive cases have albuminuria.
• Isolated albuminuria with normal renal function is estimated 3,300 per 100,000 adult population.

Associated Conditions

Proteinuria may be a sign of renal (kidney) damage. Since serum proteins are readily reabsorbed from urine, the presence of excess protein indicates either an insufficiency of absorption or impaired filtration. Diabetics may suffer from damaged nephrons and develop proteinuria.

With severe proteinuria, general hypoproteinemia can develop which results in diminished oncotic pressure. Symptoms of diminished oncotic pressure may include ascites, edema, and hydrothorax.

Natural History, Complications, and Prognosis

Complications

• Pulmonary edema
• Renal failure
• Increased risk of infections
• Increased risk of thromboembolic events
• Increased risk of cardiovascular disease

Prognosis

• Proteinuria is associated with left ventricular abnormalities, increased atherosclerosis and cardiovascular morbidity and mortality.
• Proteinuria is an independent risk factor for developing cardiovascular disease and end stage renal disease .
• Higher amounts of albuminuria, even in normal range is associated with an increased risk of cardiovascular events.
• Microalbuminuria can be considered as a predictor of morbidity and mortality in patients with no significant renal diseases.
• The presence of proteinuria in renal transplant patients predicts graft and patients survival .
• Treatment of proteinuria in patients with chronic renal disease improves outcomes.
• Increases Urinary albumin to creatinine ratio in patients with different medical conditions increases mortality.
• Albuminuria in any measurable levels is associated with increased risk of myocardial infarction in hypertensive patients.

Diagnosis

Diagnostic Study of Choice

Qualitative measures

Urine dipstick: The standard urine dipstick is sensitive to urine albumin not to the non-albumin proteins, so the positive result indicates glomerular proteinuria. The dipstick grading is semiquantitative to the amount of protein in the urine and is dependent upon urine concentration. The sensitivity of the urinary dipstick for detection of albumin in the urine ranges from 83% to 98% with a specificity of 59% to 86% . At the lower level of albuminuria, especially microalbuminuria the urine dispstick is specific but not sensitive, therefore microalbuminuria cannot be detected easily by urine dipstick unless the urine is properly concentrated. Few data suggests using specific gravity to estimate the amount of proteinuria, especially with the dipstick result of trace or 1+. Highly concentrated urine overestimates the amount of proteinuria in the urine, similarly, highly diluted urine underestimates the degree of proteinuria detected by dipstick.

• False-positive result: Urine PH > 8, administration of radiocontrast agents (iodinated), gross hematuria
• Newer dipsticks can detect albumin-to-creatinine and total protein-to-creatinine ratios which can help to avoid errors associated with diluted or concentrated urines and non-albumin proteinuria, respectively.

Sulfosalicylic acid test (SSA): Use of SSA is indicated in patients with the possibility of myeloma in the presence of negative or trace dipstick with renal function impairment. Adding SSA to the urine precipitates all proteins, therefore positive dipstick with SSA demonstrates overflow or tubular proteinuria.

• Fals-positive result: Administration of radiocontrast agents (iodinated), gross hematuria, penicillins

Reference range for proteinuria	Standard dipstick +/- SSA
Trace	Slight turbidity (1 to 10 mg/dL)
1+	Turbidity through which print can be read (15 to 30 mg/dL)
2+	White cloud without precipitate through which print can be seen (40 to 100 mg/dL)
3+	White cloud with fine precipitate through which print cannot be seen (150 to 350 mg/dL)
4+	Fluffy precipitate (>500 mg/dL)

Quantitative measures

24-hour urine collection: It is the gold standard test to determine the amount of proteinuria in patients who presents with persistent proteinuria (normal value < 150 mg/day).As collecting urine for 24 is cumbersome and erroneous, spot urine of first and second morning samples with protein-creatinine ratio can be used as an estimate of total protein excretion in 24 hour.

24-hour protein excretion= Urine protein concentration / Urine creatinine concentration

• Urine creatinine is higher in individuals with higher body muscle mass, therefore urine-protein ratio underestimates proteinuria, similarly in cachectic patients with lower muscle mass, urine-protein ratio overestimates the degree of proteinuria.

Renal biposy:

History and Symptoms

History:

• Fever
• Cardiac disease
• Renal disease
• Infections (HIV, hepatitis)
• Frothy, smoky, red urine
• Edema
• Hypertension
• Diabetes
• Family history of renal disease
• Hypercholesterolemia
• Chronic inflammatory disease
• Medications

Symptoms:

• Systemic symptoms (fever, night sweats, weight loss, bone pain)
• Heart diseases
• Edema (ankle, periorbital, labial, scrotal)
• High blood pressure
• Hematuria

Physical Examination

• Check blood pressure, orthostatic and supine, JVP
• Weight gain or weight changes
• Edema
• Signs of infectious diseases
• Signs of heart diseases
• Signs of systemic diseases
• Signs for complications (thrombosis, infections)

Laboratory Findings

Laboratory investigations to be considered in proteinuria:

The unnamed parameter 2= is no longer supported. Please see the documentation for {{columns-list}}.

2

Proteinuria is often diagnosed by a simple dipstick test although it is possible for the test to give a false negative even with nephrotic range proteinuria if the urine is dilute. False negatives may also occur if the protein in the urine is composed mainly globulins or Bence-Jones Proteins because the reagent on the test strips, Bromphenol blue, is highly specific for albumin. Traditionally dipstick protein tests would be quantified by measuring the total quantity of protein in a 24-hour urine collection test, and abnormal globulins by specific requests for Protein electrophoresis.

Alternatively the concentration of protein in the urine may be compared to the creatinine level in a spot urine sample. This is termed Protein/Creatinine Ratio (PCR). The 2005 UK Chronic Kidney Disease guidelines states that PCR is a better test than 24 hour urinary protein measurement. Proteinuria is defined as a Protein:creatinine ratio >45 mg/mmol (which is equivalent to Albumin:creatinine ratio of >30 mg/mmol) with very high levels of nephrotic syndrome being for PCR > 100 mg/mmol.

Treatment

Specific treatments of proteinuria demands proper diagnosis of the cause.

Non-specific treatments reduce the amount of proteinuaria and the rate of progression or address the complications of proteinuria.

Diuretics: The treatment of fluid overload in patients with moderate to severe proteinuria along with salt restriction is diuretics. For refractory cases two different diuretics with will be used if the increasing doses are not effective. Acute renal failure may happen due to aggressive therapy with diuretics.

ACE inhibitors and ARBs: These agents decrease the progression and the amount of proteinuria by decreasing the intraglomerular pressure. Inhibiting vasoconstriction of efferent arterioles, maintaining the glomerular-capillary wall and decreasing the sclerosis and fibrosis of glomeruls are the action of these drugs aside the anti-hypertensive effects. In normotensive individuals with proteinuria low dose of these drugs have the effect without evident hypotension. Adverse effects are cough, angioedema and hyperkalemia. Adding mineralocorticoid receptor antagonists like eplerenone, spironolactone, help reducing proteinuria further but increase the rate of hyperkalemia. Eplerenone is the new drug in this category which is not associated with hyperkalemia.

Anticoagulants: Urinary loss of proteins in the urine especially anticoagulant proteins like antithrombin III and protein S and C put the patients at the risk of thrombosis and emboli. There is no eveidence supporting the use of anticoagulants as prophylaxis.

Calcium-channel blockers: Diltiazem and verapamil decrease proteinuria by prevent vasoconstriction of both afferent and efferent arterioles. Other CCBs act on afferent arteriols only which worsen proteinuria.

T reating proteinuria mainly needs the proper diagnosis of the cause. The most common cause is diabetic nephropathy; in this case, proper glycemic control may slow the progression. Medical management consists of angiotensin converting enzyme (ACE) inhibitors, which are typically first-line therapy for proteinuria. In patients whose proteinuria is not controlled with ACE inhibitors, the addition of an aldosterone antagonist (i.e., spironolactone) or angiotensin receptor blocker (ARB) may further reduce protein loss. Caution must be used if these agents are added to ACE inhibitor therapy due to the risk of hyperkalemia. Proteinuria secondary to autoimmune disease should be treated with steroids or steroid-sparing agent plus the use of ACE inhibitors.

Related Chapters

• Albuminuria
• Microalbuminuria
• List of terms associated with diabetes

Causes by Organ System

Cardiovascular	Amyloidosis, benign orthostatic proteinuria, constrictive pericarditis, dehydration, eclampsia, hypertension, Nutcracker syndrome, preeclampsia, renal artery stenosis, renal vein thrombosis, shock , subacute bacterial endocarditis, tricuspid insufficiency
Chemical/Poisoning	Nitrosourea compounds, mercury, cadmium, trichloroethlene, bromobenzene , chloroform, aristolochic acids , paraquat, diquat, ethylene glycol
Dental	No underlying causes
Dermatologic	Scleroderma
Drug Side Effect	Acetaminophen and Oxycodone, Aflibercept, anticonvulsants, Artemether and lumefantrin, bevacizumab, captopril, carmustine, caspofungin, cisplatin, deferasirox, diflunisal, febuxostat, gemcitabine, gold, heavy metal ingestion, heroin, Interferon gamma, Lenvatinib, Lincomycin Hydrochloride, lomustine, micafungin, mithramycin, NSAIDS, Olsalazine, Oxaprozin, pazopanib, penicillamine, pramipexole, rifaximin, Sodium aurothiomalate, Sorafenib, Streptozocin, sulfasalazine, sulindac, Telavancin hydrochloride, [Thalidomide]], Tolmetin , Ziv-aflibercept
Ear Nose Throat	No underlying causes
Endocrine	Diabetes mellitus, hypothyroidism
Environmental	Allergens, irradiation
Gastroenterologic	Cirrhosis of liver, Wilson's disease, hemochromatosis
Genetic	Alport syndrome, Alström syndrome, aminoaciduria, amyloidosis, Balkan nephropathy, connatal tubulopathies, cystinosis, Dent disease, diabetes mellitus, Fabry's disease, familial mediterranean fever, galactosemia, glycogen storage disease type I, hepatorenal tyrosinemia, hereditary fructose intolerance, idiopathic multicentric osteolysis, Imerslund-Grasbeck syndrome, Lecithin cholesterol acyltransferase deficiency, Nail-patella syndrome, polycystic kidney disease , recurrent hereditary polyserositis, Wilson's disease, X-linked hypophosphatemia
Hematologic	No underlying causes
Iatrogenic	No underlying causes
Infectious Disease	Epstein-barr virus, helminthic, hepatitis B, HIV, infectious mononucleosis, Legionella pneumophila, leprosy, malaria, poststreptococcal glomerulonephritis, Prostitis, acute Pyelonephritis, Subacute bacterial endocarditis, toxoplasmosis, urinary tract infection, viral illness, yellow fever, genitourinary tuberculosis
Musculoskeletal/Orthopedic	rhabdomyolysis
Neurologic	No underlying causes
Nutritional/Metabolic	extreme obesity
Obstetric/Gynecologic	Eclampsia, preeclampsia
Oncologic	Renal cell carcinoma, multiple myeloma
Ophthalmologic	No underlying causes
Overdose/Toxicity	No underlying causes
Psychiatric	stress
Pulmonary	No underlying causes
Renal/Electrolyte	Amyloidosis, Bence-jones proteinuria, crescentic glomerulonephritis, dehydration, Fanconi syndrome, fibrillary glomerulopathies, focal segmental glomerulosclerosis , hyperoxaluria, hypertension-related kidney failure, hyperuricemia, hypokalemic nephropathy, interstitial nephritis, medullary cystic kidney disease, myoglobinuria, nephritic syndrome, nephritis of pregnancy, nephrotic syndrome), Papillary necrosis, autosomal dominant polycystic kidney disease ), Poststreptococcal glomerulonephritis, Proliferative glomerulonephritis, Proximal renal tubular acidosis, acute Pyelonephritis, renal artery stenosis, renal metastases, renal neoplasm, renal tubular acidosis, renal vein thrombosis, rhabdomyolysis, toxic nephropathy, unilateral kidney, Urinary tract infection, X-linked hypophosphataemia
Rheumatology/Immunology/Allergy	Allergens, arteriolar nephrosclerosis, autoimmune conditions, Bence-jones proteinuria, Collagen vascular diseases, crescentic glomerulonephritis, Fanconi syndrome, fibrillary glomerulopathies, focal segmental glomerulosclerosis ), Henoch-schonlein syndrome, hepatitis b, IgA nephropathy (i.e., Berger's disease), IgM nephropathy, increased formation of polyclonal free light chains, interstitial nephritis, mixed cryoglobulinemia, multiple myeloma, Organ rejection- kidney transplant patients], Polyarteritis nodosa, recurrent hereditary polyserositis, rheumatoid disease, sarcoidosis, systemic lupus erythematosis, systemic sclerosis, Wegener's granulomatosis
Sexual	No underlying causes
Trauma	musculoskeletal trauma
Urologic	Retrograde ejaculation
Miscellaneous	No underlying causes

Causes in Alphabetical Order

• Acute pyelonephritis

• Aflibercept

• Allergens

• Alport syndrome

• Alström syndrome

• Aminoaciduria

• Amyloidosis

• Anticonvulsants

• Arteriolar nephrosclerosis

• aristolochic acids

• Artemether and lumefantrin

• Autoimmune conditions

• Autosomal dominant conditions

• Autosomal dominant polycystic kidney disease

• Autosomal recessive conditions

• Bacteria and bacterial conditions

• Balkan endemic nephropathy

• Bence-jones proteinuria

• Benign orthostatic (postural) proteinuria

• Bevacizumab

• Bromobenzene

• cadmium
• Captopril

• Carmustine

• Caspofungin

• Chronic lymphocytic leukemia

• Chronic pyelonephritis

• Choloroform

• Circulatory failure

• Cirrhosis of liver

• Cisplatin

• Collagen vascular disease

• Congenital conditions

• Connatal tulbulopathies

• Constrictive pericarditis

• Crescentic glomerulonephritis

• Cystinosis

• Cystitis

• Cytomegalovirus

• Deferasirox

• Dehydration

• Dent disease

• Diabetes mellitus

• Diquat

• Ebola hemorrhagic fever

• Eclampsia

• Epstein-Barr virus

• Ethylene glycol

• Exercise-induced

• Fabry's disease

• Familial mediterranean fever

• Fanconi syndrome

• Fibrillary glomerulopathies

• Focal segmental glomerulosclerosis

• Galactosemia

• Gemcitabine

• Genitourinary tuberculosis

• Glycogen storage disease type I

• Gold

• Heavy metal ingestion

• Helminthic

• Hemoglobinuria

• Henoch-Schonlein syndrome

• Hepatitis B

• Hepatorenal tyrosinemia

• Hereditary fructose intolerance

• Heroin

• High blood pressure

• High fever

• HIV

• Hyperoxaluria

• Hypertension-related kidney failure

• Hyperuricaemia

• Hypokalemic nephropathy

• Hypothyroidism

• Idiopathic multicentric osteolysis

• IgA nephropathy (i.e., Berger's disease)

• IgM nephropathy

• Imerslund-Gräsbeck syndrome

• Increased formation of polyclonal free light chains

• Infectious Mononucleosis

• Interferon gamma

• Interstitial nephritis

• Irradiation

• Lecithin cholesterol acyltransferase deficiency

• Legionella Pneumophila

• Leprosy

• Lomustine

• Malaria

• Malignancies (e.g., lymphoma, other cancers)

• Massive obesity

• Medullary cystic kidney disease

• Mercury
• Micafungin

• Mithramycin

• Mixed cryoglobulinemia

• Multiple myeloma

• Myoglobinuria

• Nail patella syndrome

• Nephritic syndrome

• Nephritis of pregnancy

• Nephrolithiasis

• Nephrotic syndromes

• Nitrosourea compounds

• NSAIDS

• Nutcracker syndrome of left renal vein

• Obstetric conditions

• Orthostatic proteinuria

• Oxaprozin

• Papillary necrosis

• paraquat

• Pazopanib

• Penicillamine

• Polyarteritis nodosa

• Poststreptococcal glomerulonephritis

• Preeclampsia

• Proliferative glomerulonephritis

• Prostatitis

• Proximal renal tubular acidosis

• Recurrent hereditary polyserositis

• Renal artery stenosis

• Renal metastases

• Renal neoplasm

• Renal tubular acidosis

• Renal vein thrombosis

• Retrograde ejaculation

• Rhabdomyolysis

• Rheumatoid disease

• Sarcoidosis

• Shock

• Sickle cell disease

• Sorafenib

• Streptozocin

• Stress

• Subacute bacterial endocarditis

• Sulphasalazine

• Systemic lupus erythematosis

• Systemic sclerosis

• Telavancin hydrochloride

• Toxic nephropathy

• Toxoplasmosis

• Transplant rejection

• Tricuspid insufficiency

• Tricholoroethelene

• Unilateral kidney

• Urinary tract infection

• Vasculitis

• Viral

• Waldenstrom's macroglobulinemia

• Wegener's granulomatosis

• Wilson's disease

• X-linked hypophosphatemia

• Yellow fever