Hematuria syndrome

Clinical forms and place in classification

Based on clinical and laboratory data, several typical nephropathological conditions are distinguished where hematuria plays a leading role:

• Urinary syndrome. Characterized by an asymptomatic course where red blood cells (sometimes along with protein) are detected only laboratory-wise. The patient has no complaints, but the condition requires active screening.
• Acute nephritic syndrome. Hematuria acts as an obligate sign occurring against the background of acute glomerular injury (e.g., in acute diffuse glomerulonephritis).
• Mixed variants. In membranoproliferative glomerulonephritis, hematuria is combined with massive proteinuria and hypoproteinemia, characteristic of nephrotic syndrome, as well as a rapid decrease in the glomerular filtration rate (GFR).

Characteristics of hematuria in nephritic syndrome

Within the classical cyclic course of acute nephritic syndrome, hematuria is part of the triad along with arterial hypertension and edema (morning facial edema — facies nephritica is typical).

1. Gross hematuria. Observed in approximately half of patients. The color of the discharge is determined by the acidity of the environment: in acidic urine, hemoglobin transforms, making it dark brown. In an alkaline environment, the urine acquires a reddish hue ("meat slops").
2. Microscopic hematuria. If gross hematuria is absent, red blood cells and erythrocyte casts are consistently detected upon sediment microscopy.

The process is frequently accompanied by oliguria (up to anuria) and azotemia due to the narrowing of the glomerular capillary lumen and a drop in GFR.

Differential diagnosis

The algorithm for searching for pathology is based on evaluating concomitant changes:

• Isolated hematuria. The absence of proteinuria, edema, and hypertension is typical for IgA nephropathy, thin basement membrane disease, and urological problems (nephrolithiasis, trauma, tumor).
• Hematuria + proteinuria + hypertension + edema. The classical picture of acute glomerulonephritis with the risk of acute kidney injury (AKI).
• Transient reactive hematuria. Occurs cyclically during infections. For example, in hemorrhagic fever with renal syndrome (HFRS), micro- and macrohematuria with massive proteinuria and Dunaevsky cells are noted during the oliguric period. During the polyuric period, sediment changes are replaced by hyposthenuria.

Concomitant pathogenetic mechanisms

Renal involvement in hematuria syndrome is accompanied by systemic disorders:

• Pathogenesis of edema. Unlike the hypooncotic mechanism (as in protein loss), sodium and water retention due to decreased filtration plays the main role here. Additionally, vascular wall permeability increases against the background of immune inflammation.
• Arterial hypertension. Fluid retention leads to an increase in circulating blood volume and cardiac output (hypervolemic, volume-dependent mechanism).
• Pain syndrome. Lower back pain is associated with inflammatory edema of the parenchyma, organ enlargement, and stretching of the fibrous capsule, which is rich in pain receptors.

Class and exam questions

What else to study on this topic

• Pathogenesis of nephritic and nephrotic edema: what is the difference?
• Volume-dependent mechanism of arterial hypertension in nephropathies
• Dynamics of urinary syndrome in infectious processes (HFRS, ARVI)
• "Masks" of renal diseases: ophthalmological, neurological, and cardiological
• Acute kidney injury and criteria for acute renal failure

Other topics in the "Additional Topics" section

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.