Proteinuria

Proteinuria is the phenomenon of protein in the urine. Proteinuria is the excretion of more protein in the urine than is considered normal. Proteinuria may occur physiologically as functional proteinuria, e.g. in conditions of increased physical exertion, stress, dehydration or fever. In this case, the daily protein excretion normally does not exceed 150 – 250 mg. Pathological proteinuria, on the other hand, means a daily protein excretion of more than 300 – 500 mg.

What causes Proteinuria?

The most common cause of proteinuria is glomerulonephritis. When glomerulonephritis occurs, damage to the filtration membrane leads to increased glomerular filtration of protein. This results in glomerular proteinuria, where proteins such as IgG, IgM, and albumin can enter the filtrate.

When albumin enters the filtrate, this phenomenon is called microalbuminuria. It is diagnosed when albumin excretion exceeds 30 mg per 24 hours.

In another type of proteinuria, known as tubular proteinuria, the glomerular barrier function is preserved. However, in the course of tubulointerstitial nephropathies, nephron insufficiency occurs. This insufficiency results in reduced reabsorption of smaller proteins such as microglobulins.

Typically, the values seen in glomerular proteinuria are higher than those seen in tubular proteinuria.

Proteinuria is the main symptom of chronic kidney disease. It can be a symptom of a number of diseases, e.g. systemic diseases such as systemic lupus erythematosus, inflammatory diseases and cancer of the urinary tract. 

It also occurs as an accompanying symptom of diabetes, sarcoidosis, Fabry Disease, Fanconi Syndrome, sickle cell anaemia, haemoglobinuria, among others. In cases of multiple myeloma and Waldenström’s macroglobulinaemia, a pathological protein called Bence-Jones protein is detected in the urine.

Signs of proteinuria

Under normal conditions, the average urinary excretion of protein is 80 +/- 24 mg/25h. Nephrotic syndrome is diagnosed with massive proteinuria over 3,5 g/24 h. It is accompanied by symptoms such as hypertension, oedema (around the eyes, around the ankles, sacral area, genital area, generalised), haematuria, reduced GFR, hyperlipidaemia, foaming of urine during urination.

Long-term proteinuria leads to hypertension, anaemia, calcium and phosphorus metabolism disorders.

How to treat proteinuria?

Progress in the treatment of the underlying disease and compensation of the aforementioned disorders correlates with the control/reduction of proteinuria.

One method with proven efficacy in the treatment of proteinuria is blockade of the renin-angiotensin-aldosterone system/axis (RAAS). The use of angiotensin-converting enzyme inhibitors, for example, may slow the progression of renal failure. 

Supportive tests for the differential diagnosis of proteinuria include ultrasound, urine sediment examination, biochemical tests (including glomerular filtration rate GFR, creatinine, calcium, phosphate, total protein, albumin, ESR, lipidogram). Proteinuria above 1 g/24h requires urgent medical consultation. Proteinuria is an independent significant cardiovascular risk factor.

The key aims of treatment of proteinuria are control of hypertension, inhibition of the RAAS system and correction of water-electrolyte disturbances.