Proteinuria and hematuria

Proteinuria

Physiologically, protein excretion is < 150 mg/day.

Proteinuria can arise from several mechanisms:

• Prerenal proteinuria is caused by an increased concentration of proteins in plasma, exceeding the reabsorption capacity of the kidney. Typical examples include intravascular hemolysis (hemoglobin) and crush syndrome (myoglobin).
• Glomerular proteinuria is usually significant, often > 2 g/day, and results from damage to the filtration barrier. This allows proteins with molecular weight > 100 kDa to pass, leading to non-selective proteinuria (albumin, immunoglobulins). In some cases, proteinuria may be selective based on size. Loss of the negative charge of the glomerular basement membrane (glycocalyx) impairs the charge barrier, leading to selective proteinuria of smaller negatively charged proteins such as albumin and transferrin.
• Tubular proteinuria (typically 0.5–1 g/day) is caused by impaired tubular reabsorption of small proteins, such as microglobulins and immunoglobulin light chains.
• 

  Nephrotic eyes
  Postrenal proteinuria results from bleeding or inflammation in the urinary tract, such as urethritis, leading to the presence of hemoglobin and various plasma proteins in urine.
• Functional proteinuria occurs transiently under conditions such as intense physical exertion, cold exposure, fever, or left-sided heart failure, due to changes in glomerular blood flow. It may also occur during pregnancy.

Nephrotic syndrome

Nephrotic syndrome

Nephrotic syndrome is a set of symptoms associated with severe proteinuria and its consequences.

It is characterized by massive proteinuria (> 3.5 g/day) leading to generalized edema. Loss of proteins stimulates compensatory protein synthesis in the liver. This includes increased synthesis of lipoproteins, causing hyperlipidemia and accelerated atherosclerosis, and increased production of coagulation factors (especially fibrinogen), leading to a hypercoagulable state and increased blood viscosity.

Hematuria

Hematuria is defined as increased erythrocytes in urine (> 10 RBC/μL).

It may be microscopic (detected only in laboratory tests) or macroscopic (brown-red urine).

Glomerular hematuria is caused by damage to the glomerular filtration barrier, resulting in deformed erythrocytes (acanthocytes). It is typically associated with increased erythrocytes and proteinuria.

microhematuria

Non-glomerular hematuria includes:

• tubulointerstitial nephritis
• renal congestion, e.g. thrombosis of the renal vein
• postrenal causes such as inflammation or tumors of the urinary tract

In non-glomerular hematuria, erythrocytes are increased, but proteinuria is usually low.

Nephritic syndrome

Nephritic syndrome is associated with acute glomerulonephritis and varying degrees of renal failure.

It is characterized by hematuria, proteinuria, and decreased renal function, leading to oliguria, hypertension, azotemia, and disturbances in mineral balance.

References

1. ZÁMEČNÍK, Josef. Patologie 1–3. 2. přepracované vydání. Praha : LD, s.r.o. – Tiskárna Prager, 2024. 950 s
2. SILBERNAGL, Stefan a Florian LANG. Atlas patofyziologie. 2. české vydání. Praha : Grada, 2012
3. MARUNA, Pavel, et al. Zkušební testy z patologické fyziologie. 1. vydání., duben 2015.