Nephrology for the Family Physician - O.I. Bakaliuk 2003

Primary Semiotics of Kidney Diseases
Hematuria

AH is often the first and most formidable symptom of many genitourinary disorders, and its disappearance does not always indicate recovery or the cessation of disease progression.

A healthy human loses approximately 200,000 erythrocytes per day, with a normal range between 100,000 and 800,000. In urinalysis, this count corresponds to 1–2 erythrocytes per high-power field.

According to D. Brass (1989), the presence of 1–2 erythrocytes per field is considered normal; 3–5 erythrocytes warrant a Nechiporenko test; and the detection of 5 or more erythrocytes per field is always a sign of pathology. An erythrocyte count of up to 100–150 per field or up to 5 ∙ 10⁷/L in the Nechiporenko sample (T.D. Nykula, 2000) does not affect urine color and is referred to as microhematuria.

Urinary erythrocytes may be dysmorphic or isomorphic. Because AH can occur in numerous conditions unrelated to renal pathology (e.g., thrombocytopenia and thrombocytopathies, hemophilia, DIC syndrome, overdose of adrenocorticotropic hormone, heparin, or The Use of immunosuppressants) as well as various diseases (leukemia, hemophilia, scarlet fever, typhoid fever, infective endocarditis, etc.), topical Diagnosis is of paramount importance.

An accurate interpretation of the medical history plays a crucial role in identifying the source of AH. It is essential to determine the circumstances of AH onset, its severity, nature, and duration, its association with other symptoms (such as dysuria, lower back pain, or pain during urination), as well as the presence, shape, and size of any Blood clots in the urine. In men, visual Assessment of the character of AH is highly accurate. In women, genital bleeding must be ruled out—in such cases, a midstream sample from spontaneous urination or urine obtained via urinary catheterization should be examined. AH in women that coincides temporally with the premenstrual period should raise suspicion of Urinary Bladder Endometriosis.

To differentiate between AH originating from the lower Urinary Tract and the Kidneys, clinicians use the three-Glass test (Thompson's test) In addition to instrumental Methods.

Initial AH (occurring in the first portion of urine) indicates a lesion in the proximal Urethra; terminal AH (in the third portion) points to inflammation, tumors, or stones of the urinary bladder or prostate, or urethral stone impaction; total AH (in all portions) suggests tumors, stones, tuberculosis, renal trauma, papillary necrosis, Nephroptosis, renal venous Hypertension, Hydronephrosis, renal failure, or bladder tumors, and less commonly, prostate adenoma. Total AH in women may result from the rupture of VARICOSE Veins OF the urinary bladder, frequently observed with large uterine fibroids, ovarian tumors, and cysts.

Initial AH should be distinguished from urethrorrhagia, in which blood loss is unrelated to the act of urination. The latter is observed in urethral trauma, polyps, Papillomas, condylomas, carcinoma, and urethral mucosal prolapse.

H.L. May et al. (1994) provide the following summary data regarding the most common causes of non-traumatic AH, depending on the localization of the process and the patient's age:

- kidneys: Glomerulonephritis, Pyelonephritis, papillary necrosis, tumors;

- renal pelvis and Ureter: urolithiasis, tumors, hydronephrosis;

- urinary bladder: cystitis, tumors, calculi, post-biopsy state;

- prostate: adenoma, prostatitis, tumors, post-prostatectomy state;

- urethra: urethritis, foreign bodies, calculi, condylomas, carcinoma.

Overall, according to H.L. May et al. (1994), infection is the leading cause of AH, followed by tumors, obstruction, and lithiasis.

In children and adolescents, AH is most commonly caused by infection secondary to congenital obstruction; in young adults, infection (cystitis, prostatitis, pyelonephritis) is a more frequent cause of AH than lithiasis and tumors; in middle-aged and elderly individuals, infection still leads, although tumors, Prostatic Adenoma, and lithiasis are nearly comparable in frequency.

When AH is caused by a tumor, it is most frequently a bladder tumor, followed by prostatic and Renal Tumors.

The Mechanism of purely renal AH is associated with multiple factors: mechanical damage and destructive processes within the renal parenchyma, renal venous hypertension, necrotizing renal angiitis, acquired or hereditary abnormalities of glomerular basement membrane permeability, intrarenal intravascular hypercoagulation, and toxic or inflammatory interstitial injury.

Transmembrane passage of erythrocytes from blood into urine is facilitated by the loss of their normal surface charge. Immune mechanisms associated with the IgA antibody response play a specific role in erythrocyte damage (E.C. Larkin et al., 1995).

Depending on the intensity of AH, blood clots may be observed: large, amorphous clots (formed in the urinary bladder), worm-like clots (formed in the Ureters), and long (7–10 cm), cylindrical clots (formed in the kidneys). However, worm-like clots can also form in the urethral lumen (e.g., following traumatic catheterization in patients with prostate adenoma), and amorphous blood clots may likewise indicate renal AH.

It should also be noted that urological diseases (trauma, tumors, calculi, vascular malformations, renal vessel thrombosis) are more frequently accompanied by unilateral, isolated, painful macrohematuria. This is less typical for nephropathies of other origins, although such a clear distinction remains relative.

To clarify the genesis of AH, clinicians also take into account the so-called protein-to-erythrocyte dissociation (V.H. Vasylylenko, 1974): glomerular AH is typically characterized by its combination with significant proteinuria, whereas AH combined with minimal proteinuria indicates an extrarenal origin (from the renal pelvis, ureter, or bladder).

However, this hypothesis is not shared by all researchers. Specifically, it is difficult to attribute the clinical discrepancy between pronounced AH and moderate proteinuria solely to extrarenal mechanisms; in such cases, Electron Cell/15.html">Microscopy has revealed direct diapedesis of erythrocytes across the glomerular capillary basement membrane (M. Miura et al., 1997).

To differentiate between so-called glomerular and non-glomerular AH, clinicians also analyze erythrocyte Morphology using light or Phase-contrast microscopy.

According to Australian researchers (R. Fassett et al., 1982), who developed diagnostic criteria for these types of AH, the detection in urine of over 75–80% structurally altered erythrocytes (dysmorphic, with disrupted undulating membranes, and of varying sizes) indicates a glomerular origin of AH. Conversely, the presence of over 80% isomorphic (regularly shaped and sized) erythrocytes suggests a non-glomerular origin (J.A. Schrier / J.A. Sheiman, 1999). If neither type of erythrocyte clearly predominates, the AH is classified as mixed.

Finally, the term «essential renal hematuria» can be considered justified. It encompasses a range of conditions in which the underlying cause of renal Hemorrhage cannot be identified. The advent of modern diagnostic techniques (renal angiography, selective venography, needle biopsy, urocinematography, computed tomography, etc.) has minimized the number of cases formerly classified as «essential renal hematuria.» However, even after ruling out renal tumors, necrotizing papillitis, pyelovenous reflux, varices, papillary cystic changes, Alport syndrome, sponge Kidney, nephroptosis, and renal vascular pathology as the most frequent causes of «essential renal hematuria» (A.Ya. Pytel et al., 1973), this diagnosis remains valid for a certain period, provided the patient is placed under comprehensive follow-up care.

Occasionally, microscopy of the urinary sediment reveals no erythrocytes despite specific discoloration of the urine. This phenomenon is known as hemoglobinuria, where the abnormal urine color results from The breakdown of red Blood Cells in the bloodstream and The excretion of Hemoglobin in the urine.

Hemoglobinuria is observed following incompatible blood transfusions, in cases of hemolysis, hemolytic jaundice, poisoning (by aniline or death cap mushrooms), prolonged exposure to cold, massive Burns, septic abortion, malaria, and typhus. Notably, the color of urine in hemoglobinuria does not change even upon prolonged standing, whereas in macroscopic hematuria, erythrocytes rapidly settle to the bottom of the container, leaving the upper layers of urine with a normal yellowish appearance.

Urine coloration resembling macroscopic hematuria may also occur in urosuria (reddish), Crush syndrome (red-brown due to Myoglobin), or following the consumption of table beets (red) or common madder (brown-red).