The most common cause of proteinuria is diabetes, and in any person with proteinuria and diabetes, the cause of the underlying proteinuria should be separated into two categories: diabetic proteinuria versus the field. With severe proteinuria, general hypoproteinemia can develop which results in
diminished oncotic pressure. Symptoms of diminished oncotic pressure may include ascites, edema and hydrothorax. Conditions with proteinuria
Proteinuria may be a feature of the following conditions:
Nephrotic syndromes (i.e. intrinsic kidney failure)
Pre-eclampsia
Eclampsia
Toxic lesions of kidneys
Amyloidosis
Collagen vascular diseases (e.g. systemic lupus erythematosus)
Dehydration
Glomerular diseases, such as membranous glomerulonephritis, focal segmental glomerulonephritis, minimal change disease (lipoid nephrosis)
Strenuous exercise
Stress
Benign orthostatic (postural) proteinuria
Focal segmental glomerulosclerosis (FSGS)
IgA nephropathy (i.e. Bergers disease)
IgM nephropathy
Membranoproliferative glomerulonephritis
Membranous nephropathy
Minimal change disease
Sarcoidosis
Alport syndrome
Diabetes mellitus (diabetic nephropathy)
Drugs (e.g. NSAIDs, nicotine, penicillamine, lithium carbonate, gold and other heavy metals, ACE inhibitors, antibiotics, or opiates (especially heroin)
Fabry disease
Infections (e.g. HIV, syphilis, hepatitis, poststreptococcal infection, urinary schistosomiasis)
Aminoaciduria
Fanconi syndrome in association with Wilson disease
Hypertensive nephrosclerosis
Interstitial nephritis
Sickle cell disease
Hemoglobinuria
Multiple myeloma
Myoglobinuria
Organ rejection:
Ebola virus disease
Nail–patella syndrome
Familial Mediterranean fever
HELLP syndrome
Systemic lupus erythematosus
Granulomatosis with polyangiitis
Rheumatoid arthritis
Glycogen storage disease type 1
Goodpasture syndrome
Henoch–Schönlein purpura
A urinary tract infection which has spread to the kidney(s)
Sjögren syndrome
Post-infectious glomerulonephritis
Living kidney donor
Polycystic kidney disease

Bence–Jones proteinuria
Amyloidosis
Pre-malignant plasma cell dyscrasias:
Monoclonal gammopathy of undetermined significance
Smoldering multiple myeloma
Malignant plasma cell dyscrasias
Multiple myeloma
Waldenströms macroglobulinemia
Other malignancies
Chronic lymphocytic leukemia
Rare cases of other Lymphoid leukemias
Rare cases of Lymphomas

Pathophysiology
Protein is the building block of all living organisms. When kidneys are functioning properly by filtering the blood, they distinguish the proteins from the wastes which were previously present together in the blood.
The 2005 UK Chronic Kidney Disease guidelines state that protein/creatinine ratio is a better test than 24-hour urinary protein measurement. Proteinuria is defined as a protein/creatinine ratio greater than 45 mg/mmol (which is equivalent to albumin/creatinine ratio of greater than 30 mg/mmol or approximately 300 mg/g) with very high levels of proteinuria having a ratio greater than 100 mg/mmol.Protein dipstick measurements should not be confused with the amount of protein detected on a test for microalbuminuria which denotes values for protein for urine in mg/day versus urine protein dipstick values which denote values for protein in mg/dL. That is, there is a basal level of proteinuria that can occur below 30 mg/day which is considered non-pathology. Values between 30 and 300 mg/day are termed microalbuminuria which is considered pathologic. Urine protein lab values for microalbumin of >30 mg/day correspond to a detection level within the "trace" to "1+" range of a urine dipstick protein assay. Therefore, positive indication of any protein detected on a urine dipstick assay obviates any need to perform a urine microalbumin test as the upper limit for microalbuminuria has already been exceeded. Analysis
It is possible to analyze urine samples in determining albumin, hemoglobin and myoglobin with an optimized MEKC method. Treatment
Treating proteinuria mainly needs 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.