Urinary System

Acid-base balance and pseudohematuria

The kidneys are directly involved in regulating blood pH. To assess their contribution to the acid-base balance (ABB), a number of parameters must be analyzed: urine pH, titratable acidity, bicarbonate excretion rate, and ammonia secretion volume.

During macroscopic urine analysis, it is important not to confuse true bleeding with false hematuria (pseudohematuria), where the red coloration is caused by pigments rather than erythrocytes. Causes may include:

• Dietary components: anthocyanins (red berries, beets).
• Artificial additives: dyes in ketchups, beverages, confectionery.
• Metabolic disorders: presence of free hemoglobin or myoglobin. Specifically, myoglobinuria imparts a specific red-brown tint to the urine.
• Pharmacological agents: phenazopyridine or phenolphthalein (the latter changes urine color in an alkaline reaction).

Evolution of the concept of "nephrotic syndrome"

The modern term "nephrotic syndrome" (NS) became generally accepted only in the late 1940s. However, as early as 1929, the prominent Russian therapist E.M. Tareev described this symptom complex in his work "Anemia of Bright's Disease Patients".

Tareev fundamentally differentiated NS from "necrotic nephrosis" (arising, for example, from mercuric chloride poisoning). The key pathomorphological difference was that in NS, degeneration affects not only the renal tubular epithelium but also the glomerular apparatus. Today, the term NS has virtually replaced the older concept of "nephrosis," although in pediatric and pathomorphological practice, the diagnosis of "lipoid nephrosis" is still retained to denote minimal change disease.

Due to the massive loss of immunoglobulins in the urine during NS, immune defense drops sharply, leading to severe infectious complications: peritonitis, herpetic lesions, and pneumonia (of viral or pneumococcal etiology).

Mechanisms of hemodynamic disorders and progression

The development of renal arterial hypertension and fluid retention is based on an imbalance of regulatory systems. There is hyperactivation of the pressor arm (RAAS) against the background of the suppression of depressor mechanisms (prostaglandin and kallikrein-kinin systems). This causes hypervolemia, sodium retention (exacerbated by a decrease in the mass of functioning nephrons), and an increase in total peripheral vascular resistance with normal or even reduced cardiac output.

The progression of renal pathology often follows a non-immune pathway, which includes three groups of factors:

1. Hemodynamic shifts: hyperfiltration, intracapillary hypertension, and glomerular hyperperfusion.
2. Massive proteinuria: toxic to renal tissue in its own right.
3. Metabolic disorders: purine metabolism disorders and dyslipidemia.

Acute renal failure (ARF)

The initial stage of ARF lacks specific manifestations of its own. Its clinical picture depends entirely on the underlying cause: these may be symptoms of shock, acute hemolysis, or severe intoxication.

Prerenal (hemodynamic) causes of ARF are divided into:

• Arterial: renal artery embolism or stenosis.
• Venous: inferior vena cava thrombosis.
• Cardiac: right ventricular failure leading to venous congestion and increased pressure in the venae cavae.

The laboratory findings of ARF show notable hematologic shifts. Anemia accompanies all periods of ARF, whereas marked leukocytosis is specific precisely to the oligoanuric phase.

Specific lesions: Goodpasture syndrome and infections

A special variant of injury is the antibody-mediated (anti-GBM) type, in which autoantibodies against the glomerular basement membrane (GBM) are produced. Histologically, this manifests as mesangial cell proliferation and severe nephron destruction, while immunofluorescence reveals characteristic linear staining along the entire membrane. A specific case is Goodpasture syndrome—a cross-reaction of antibodies against GBM and alveolar basement membranes, causing a combination of rapidly progressive glomerulonephritis and pulmonary hemorrhage.

Infectious renal injury often occurs via the ascending (urogenital) pathway, when colibacillary flora (Escherichia coli) penetrates from the lower urinary tract. Bacteria spread along the ureteral wall or through the lumen via retrograde refluxes. In women, this pathway is more common due to the anatomical features of the urethra and the presence of periurethral bacterial colonies in the vagina. Iatrogenic infection during surgical procedures or cystoscopy is also possible.

Class and exam questions

What else to study on this topic

• Mechanisms of linear staining formation in immunofluorescence
• The role of the prostaglandin and kallikrein-kinin systems in the regulation of renal blood flow
• Pathogenesis of pulmonary hemorrhage in Goodpasture syndrome
• Algorithm for the differential diagnosis between prerenal and renal ARF
• Etiology and consequences of urinary tract retrograde refluxes

Other topics in the "Urinary System" section

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