Nephrology for General Practitioners - O.I. Bakaliuk 2003

Renal Pathology in Other Diseases
Kidney Involvement in Infections and Infestations

Accurate identification of the infectious agent and prompt initiation of appropriate Treatment in the Cytology/cytology/16.html">Early stages of the disease can prevent the chronicity of Glomerulonephritis by inhibiting various mechanisms. These primarily include the direct cytotoxic effect of microorganisms on the GBM, The impact of their Antigens on cellular and humoral Immunity, and the deposition of circulating immune complexes (CICs) in the mesangium, as well as the glomerular and tubular GBM (L.A. Pyrih et al., 1999).

Renal manifestations of infectious diseases occur at various Stages of the illness. For instance, signs of nephropathy present as early symptoms in hemorrhagic fever with renal syndrome and leptospirosis, by the end of the first week in epidemic typhus, and by the second week in typhoid fever. Secondary immune-mediated nephropathies develop later—for example, on days 17–23 in scarlet fever and days 12–15 in chickenpox.

Acquired Immune Deficiency Syndrome (AIDS). The CAUSATIVE AGENT OF AIDS was isolated by Luc Montagnier (Pasteur Institute, France) in 1983 and by Robert Gallo at the National Cancer Institute in the USA in 1984. It is a matter of profound regret that the AIDS epidemic continues to spread relentlessly. In 1997, the total number of people worldwide infected with the HUMAN IMMUNODEFICIENCY VIRUS reached 18.5 million adults and 1.5 million children (D. Agati et al., 1997). According to recent estimates, these figures rose by 2001 to 40 million and 2.7 million, respectively, with annual deaths reaching 3 million. In Ukraine, as of early 2002, 45,710 HIV-infected citizens (including over 3,280 children) and nearly 300 foreigners were officially registered (unofficially, the former figure reaches 300,000); 3,100 adults and 99 children are suffering from AIDS. The leading regions in this grim statistics are Donetsk, Dnipropetrovsk, Odesa, and Mykolaiv oblasts (the newspaper Vashe Zdorovia, no. 4 (630), Feb. 1, 2002). Among the western regions, Ternopil oblast ranks fourth, trailing behind Khmelnytskyi, Volyn, and Chernivtsi oblasts. Overall, 212 HIV cases have been detected in Ternopil oblast since 1987, among which four HIV-infected women have given birth (the newspaper Medychna Akademiia, no. 10 (74), May 2002).

The number of HIV-infected individuals in our region is growing annually, with 60 such patients currently recorded (Medychna Akademiia, 2001, no. 22(62), p. 11). In 2001, 25 new cases of HIV infection were registered in the region.

The virus exhibits a pronounced tropism for helper T-lymphocytes, leading to the near-total blockade of this arm of immune reactivity or a severe reduction in its functional capacity. However, the clinical symptom complex (excluding Central Nervous system involvement) is driven by The Development of an immunodeficient state in which any opportunistic infection can become fatal. Multiplying within Cells of The Immune System, the virus periodically enters the bloodstream (the viremic phase), during which its concentration can reach 100–10,000 virions (!) per 1 mL of Blood.

Within THE SPECTRUM OF visceral pathology caused by the human immunodeficiency virus (HIV)—HTLV-III/LAV—involvement of the respiratory, digestive, and central nervous systems occupies a prominent place (V.P. Hyrin et al., 1991; H.N. Drannyk et al., 1994). The clinical picture is also characterized by fever, significant weight loss, asthenia, lymphadenopathy, and profuse sweating (M.A. Andreychyn, 1998).

Overall, the Diagnosis of AIDS should take into account:

- prolonged fever (lasting over 1 month) resistant to antipyretics, and night sweats;

- significant body weight loss (exceeding 10%) over 1–2 months without an apparent cause;

- enlargement of cervical, axillary, and inguinal Lymph Nodes;

- distinct Skin lesions, predominantly on the HEAD AND TORSO (Kaposi Sarcoma);

- drug-resistant diarrhea lasting for more than a month;

- prolonged, unexplained syndrome of unmotivated asthenia and rapid fatigue;

- characteristic stomatitis resembling focal inflammatory lesions.

According to recent data (the newspaper Vashe Zdorovia, no. 37 (515), May 31, 2000), AIDS is complicated by tuberculosis in 61% of patients, which leaves a distinct stamp on the Clinical presentation of the disease.

Renal Involvement in AIDS occurs in 30% of patients and is characterized by severe clinical manifestations and an unfavorable prognosis (N.A. Maksimov, 2000). Renal pathology significantly impacts the prognosis and quality of life in these patients (R.J. Glassock, 1990). Morphological findings include focal sclerosis, mesangial lesions, and membranous transformation (J. Bourgoignie et al., 1991).

Two Clinical forms of renal involvement in AIDS are distinguished: ACUTE RENAL FAILURE (ARF) and HIV-associated nephropathy proper (K.C. Siamopoulos, 1994).

The Pathogenesis of ARF in HIV infection is driven by marked hemodynamic shifts caused by dehydration (prolonged diarrhea, vomiting, restricted fluid intake leading to prerenal ARF), severe septic complications, bacterial Shock, electrolyte imbalances, hypocortisolism, and the administration of nephrotoxic drugs (azidothymidine, zidovudine, didanosine, lamivudine, crixivan). The Clinical symptoms of ARF in AIDS are identical to those arising from other prerenal causes.

HIV-associated nephropathy (J. Bourgoignie et al., 1986, 1991) is characterized by massive proteinuria, occasionally reaching Nephrotic Syndrome levels, microhematuria, cylindruria (granular casts), and aseptic leukocyturia. The etiological link between HIV nephropathy and the specific virus has not been definitively proven, nor is there a consensus on its pathogenesis due to the considerable heterogeneity of the patient cohorts studied (homosexuals, intravenous drug users, various racial backgrounds, and concurrent infections such as hepatitis B virus or cytomegalovirus). According to D'Agati et al. (1997), typical secondary glomerulonephritis with the deposition of pathogen antigen-containing immune complexes on the GBM may develop in some cases.

Features of the clinical course of HIV-associated nephropathy include a relatively low incidence of Renal Arterial Hypertension and edema despite severe nephrotic syndrome with marked hypoalbuminemia (J. Strauss et al., 1989), increased cortical echogenicity, and normal Kidney dimensions on ultrasound even in the presence of end-stage renal failure and severe cachexia (N.A. Maksimov, 1990). HIV nephropathy manifesting as glomerulonephritis with nephrotic syndrome is most frequently observed among Black individuals and drug users, and less commonly among heterosexual partners and homosexuals. There is evidence suggesting a potential genetic influence on the frequency of renal involvement, as the development of overt forms of the disease correlates with the presence of HLA antigens DR5 and B35 (J. Strauss et al., 1989).

Viral Hepatitis. Today, the traditional view of human hepatitis B virus (HBV) infection as a cause of exclusively hepatic disease has been seriously challenged. In recent years, data have emerged (A.V. Potapova et al., 1995; R. Willson, 1997) indicating the possibility of extrahepatic HBV Replication and the Integration of the HBV genome into the cellular DNA of other Tissues.

Clinical and experimental studies have identified two forms of internal organ involvement in HBV infection (Z.H. Aprosina et al., 1995): Type I—pathology driven by delayed-type hypersensitivity reactions combined with immune complex reactions, encompassing acute and chronic Disorders of the Liver, joints, skeletal Muscles, Lungs, myocarditis, pericarditis, Sjögren's syndrome, and tubulointerstitial nephritis; Type II—highly polymorphic immune complex-mediated pathology primarily caused by vasculitis resulting from the damaging action of HBV antigen-containing immune complexes. These include cutaneous vasculitis, essential cryoglobulinemia, Raynaud's disease and syndrome, polyarteritis nodosa, Takayasu's arteritis, polyneuropathy, Chronic Glomerulonephritis, and lupus nephritis.

A distinct category of HBV-induced pathology involves the hematopoietic system (immune cytopenias, autoimmune hemolytic anemia, acute and chronic leukemias), which is associated not only with HBV infection of blood-forming Organs but also with viral replication and subsequent integration into the Cells of the Bone Marrow, lymph nodes, Spleen, and mononuclear cells.

The Role of hepatitis A virus in the development of glomerulonephritis remains insufficiently studied. Histological examination of biopsy specimens has revealed moderate changes—Swelling of the glomeruli and tubular epithelium, focal hypercellularity, thickening of the glomerular capillary basement membrane, and diffuse or focal interstitial edema. Notably, inflammatory infiltration in the Kidneys was absent (M.E. Conrad et al., 1964, 1991).

Renal involvement in hepatitis B may serve as the sole extrahepatic manifestation, with nephropathy developing many years after the acute hepatitis has resolved. Conversely, nephropathy characterized by the deposition of hepatitis B surface antigen (HBsAg) within renal structures can occur in the absence of prior liver disease. According to R.G. Filimonova et al. (1987), HBsAg is detected in 21.1% of cases and its Antibodies in 20.3%; according to M. Levy (1991), in 2–56% of patients with glomerulonephritis, and in 52–90% of those with nephrotic syndrome (I.V. Bahdasarova et al., 1991). Renal injury in these instances results from the deposition or *in situ* formation of "hepatitis" antigen-antibody complexes. HBsAg is found in large cationic complexes that deposit in the mesangium and peripheral capillary walls, reminiscent of membranoproliferative glomerulonephritis (A.B. Collins et al., 1983). It is emphasized that there is no direct parallelism between HBsAg antigenemia and the presence of HBsAg in renal structures (N.A. Shishkin et al., 1989; N.A. Shishkin, 2000). Such glomerulonephritis presents in various clinical variants (urinary syndrome, nephrotic syndrome). The data obtained by these researchers provided a rationale for incorporating antiviral agents into the therapeutic regimen for this clinical scenario with positive outcomes (S.V. Fedorchenko et al., 1996).

Due to its small molecular weight, the e-antigen (HBeAg) forms immune complexes of such size and charge that they deposit predominantly subepithelially, causing membranous GN (R.J. Johnson et al., 1990).

The core antigen (HBcAg) is rarely found in renal structures.

In patients with hepatitis C, viremia persists for life, and cryoprecipitates in many of these patients reveal viral RNA and anti-hepatitis C core antibodies (R.J. Johnson et al., 1993). These patients also frequently test positive for IgM, which exhibits rheumatoid factor properties and binds to IgG antibodies against the hepatitis C virus (R. Davda et al., 1993).

To summarize the above, we present data from S. Takeda et al. (1988), W.M. Brady (1998), A. Gonzalo et al. (1995, 1999), and D.N. Amarapurkar et al. (2001), which determine the degree of correlation between kidney damage and viral hepatitis:

- established clear correlation — membranous GN, membranoproliferative GN types I and III, glomerulosclerosis;

- doubtful correlation — IgA nephropathy, mesangial GN, focal segmental glomerulosclerosis.

Kidney involvement in HBV infection can also manifest as tubulointerstitial nephritis (TIN).

Variants of TIN in HBV infection include nephrogenic diabetes insipidus and Renal Tubular Acidosis (A.V. Potapova et al., 1995). At the same time, inflammatory and degenerative changes occur in the renal tubular epithelium—similar to those developing in hepatocytes—with the involvement of hemolymph capillaries (O.V. Lyulko et al., 1998).

The development of renal tubular acidosis can contribute to the onset or progression of Liver failure due to impaired acidification. As a result, ammonia produced in the renal tubules diffuses back from the alkaline urine along the pH gradient into the venous bloodstream, thereby exacerbating hyperammonemia.

Delayed-type hypersensitivity reactions play a leading role in the pathogenesis of TIN. These reactions are induced by the HBV antigen or immune complexes containing these antigens.

Acute intestinal infections. Renal involvement in severe forms of gram-negative Infections caused by the intestinal group of pathogens (Salmonella, Escherichia coli, Klebsiella) is quite common.

The most characteristic clinical syndromes in septic forms of these infections are ARF and hemolytic-uremic syndrome. The latter is most frequently caused by Escherichia coli O157:H7. Transient Renal Dysfunction, particularly tubular impairment, is observed quite often. Urinary sediment changes in these cases are nonspecific (PU, HU, bacteriuria).

Summarizing data on The Mechanism of renal injury in this context are as follows (O.V. Lyulko et al., 2000): systemic hemodynamic factors leading to impaired renal perfusion; the impact of non-hemodynamic factors via the action of humoral and cellular immunopathological reaction components on renal structures; renal hypofiltration and fluid retention due to systemic vasodilation; the development of disseminated intravascular coagulation; and renal ischemia.

Despite the similarity of the clinical picture, certain morphological features depend on the type of pathogen (O.V. Lyulko et al., 2000).

Brucellosis. Any organ in The Human Body can be infected with brucellae, and in 50% of cases, they are found in the urine. Most researchers have observed predominant involvement of the Urinary Bladder, and less frequently, the prostate, Testes, and Epididymis. Significant pyuria is noted in such cases, although microorganisms are not detected by routine staining. Cystoscopy reveals a picture of acute ulcerative cystitis resembling tuberculosis.

Renal involvement in brucellosis is observed in 4–6% of cases, more commonly during its acute phase. The morphological basis of the renal pathology is interstitial nephritis, with changes being focal or diffuse (less frequently). According to S. Signorelli (1993), the clinical forms of renal involvement include: transient benign PU, RF, GN, NS, focal nephritis, and hepatorenal syndrome. A characteristic feature of renal damage in brucellosis is rapid calcification of the renal cortex, detectable by ultrasound and urography (P.P. Kelalis et al., 1992). The prognosis is generally favorable.

Syphilis. Renal involvement in syphilis occurs in 0.48–0.70% of cases. The severity of structural renal damage depends on the clinical form of the disease.

Primary syphilis features The formation of isolated plasma Cell infiltrates and Granular degeneration of the proximal tubular epithelium, clinically manifesting as transient PU and HU. Classical NS occurs relatively rarely and is characterized by the rapid disappearance of PU within a few days after initiating specific therapy; however, complete normalization of the urinary sediment takes 1–1.5 years.

In secondary syphilis, diffuse infiltration of the renal interstitium with lymphoid and plasma cells, macrophages, and fibroblasts develops—presenting as a picture of interstitial nephritis. In some cases, Treponema pallidum can be found in the interstitium. The consequence of renal involvement in secondary syphilis is nephrosclerosis.

Gummata in the kidneys occur in tertiary syphilis (large, white-yellow nodules in both layers of the kidneys, less commonly in the renal pelvis). Clinically, symptoms include focal or diffuse GN, vascular manifestations (hypertension), and bouts of pain in the lumbar region. The process terminates in scarring, renal deformation, and the development of secondary amyloidosis. The prognosis is more favorable in focal GN.

Congenital syphilis is characterized by the development of miliary gummata in the form of small, brownish-yellow nodules; the primary clinical manifestation of renal involvement in this case is NS.

Scarlet fever. Kidney damage in scarlet fever may occur at the peak of the disease as focal or interstitial nephritis (mechanistically a direct toxic effect) and during the second or third weeks as diffuse GN (mechanistically an immune-mediated injury).

Scarlet fever interstitial nephritis typically presents with moderate PU and HU. Acute tubular necrosis with oliguria (anuria) and uremia is rare.

Diffuse scarlatinal nephritis is characterized by marked skin pallor, decreased urine output, headache, a sudden prolonged rise in body Temperature to 39–40 °C, and facial edema (rarely of the legs). Hypertension is transient, PU is moderate (up to 1 g/day), and microhematuria is a constant symptom. Overall, the course of both diffuse and interstitial scarlatinal nephritis is generally favorable, although PU and HU persist for 2–4 months after recovery.

Diphtheria. Renal involvement in diphtheria ranks third in frequency after myocarditis and polyneuritis, extending beyond the framework of the so-called "benign nephrosonephritis" reported previously (T.G. Filosofova et al., 1984; E.N. Khokhlova, 1998).

Renal complications in diphtheria are associated with the action of diphtheria toxin, leading to dystrophic and inflammatory changes primarily in the renal tubule region. This is accompanied by microcirculation disorders, impaired primary urine passage, altered reabsorption processes, hyperplasia and dilation of the lymphocirculatory bed—up to the formation of lymphatic "lacunae" and "lakes"—as well as intensive lymphocytic infiltration of the renal cortex and destruction of the capillary loops of renal glomeruli (O.V. Lyulko et al., 1999).

The clinical presentation corresponds to the symptoms of focal or diffuse interstitial nephritis; morphological changes are significantly more pronounced in children than in adults. Urinary Tract infection is detected in 8.3% of patients who have undergone the subtoxic form of diphtheria (N.I. Zryachkin et al., 1998).

Epidemic typhus. In epidemic typhus, kidney damage is quite common, usually occurring on the 2nd–3rd weeks of the disease onset. It is predominantly characterized by a vascular localization—the formation of typical inflammatory productive mural deposits in the endothelium of glomerular capillaries and arterioles (typhus nodules) followed by microthrombosis of the lumen. Depending on the predominant localization of these nodules, the clinical presentation manifests as focal or diffuse GN (when nodules are localized in glomerular capillaries) or interstitial nephritis with tubular dysfunctions (when localized in the interstitium).

Leptospirosis. Renal involvement is a frequent clinical sign of leptospirosis, caused predominantly by L. icterohemorragiae, L. pomona, L. canicula, L. sejroe, and L. bataviae, although the type and severity of renal damage are most likely determined by the host's reaction rather than the specific pathogen species.

Changes in the kidneys during leptospirosis occur primarily in the interstitial tissue and convoluted tubules (epithelial dystrophy, lymphocytic infiltration of the interstitium, hyaline casts in the tubular lumen, and occasionally serous or hemorrhagic exudate in Bowman's capsule).

Intrainfectious focal nephritis is characterized by transient urinary sediment changes (mild proteinuria, inconsistent microhematuria, leukocyturia, cylindruria) that disappear 2–3 days after body temperature normalizes. Edema is absent, and blood pressure is normal.

In the organ phase of the disease, the clinical symptoms of renal involvement are much more pronounced: reduced diuresis, hyposthenuria, and hypercreatininemia. The urinary sediment contains a large amount of renal epithelium. The prognosis is generally favorable, with recovery occurring in a relatively short time. ARF occurs in 10% of cases, more frequently in patients with oliguria or marked jaundice. The prognosis is favorable if polyuria develops during the second week of ARF; prolonged oliguria warrants hemodialysis, although even with its use, 20–30% of patients succumb.

Legionellosis. In 1976, an outbreak of infectious disease occurred in Philadelphia, affecting over 200 attendees of the American Legion convention. The infection was characterized by severe Pneumonia accompanied by simultaneous damage to other organs and systems, notably the kidneys. In 1977, a previously unknown pathogen, later named "Legionella," was isolated from the lung tissue of patients who died during this outbreak (34 individuals). In the former USSR, the first cases of legionellosis were described in 1980 by S.V. Prozorovsky.

Currently, over 30 species of this pathogen are known, half of which are pathogenic to humans. Bacteria of the genus Legionella are widespread in nature. They are natural inhabitants of freshwater bodies, and their symbiotic interactions with other bacteria and blue-green Algae, as well as intracellular parasitism in Protozoa (amoebae, flagellates), determine the ability of legionellae to multiply in Water bodies and soil. It has been proven, for example, that a single amoeba can harbor over 1,000 microbial cells. The high adaptive capabilities of legionellae enable them to successfully colonize artificial water bodies used in industry and everyday life. Human infection requires the inhalation of microdisperse aerosol particles containing legionellae or cells of protozoa infected by them into the lungs. Air conditioners, air humidifiers, shower devices, and dust generated during excavation and construction work in damp areas that is wind-borne over considerable distances serve as permanent sources of infection. Nosocomial infection cases constitute a special group. According to various authors (S.V. Prozorovsky et al., 1984, 1994; R. Gremi et al., 1998), the proportion of pneumonia caused by legionellae ranges between 6–8%.

Three forms of legionellosis are distinguished: Legionnaires' disease proper, Pontiac fever, and Fort Bragg fever. In the first case, following an incubation period (usually lasting 2–10 days), clinical symptoms of severe pneumonia appear, combined with signs of central nervous system involvement (disorientation, lethargy, delirious state, ataxia in 30–45% of cases) and gastrointestinal tract involvement (nausea, vomiting, diarrhea in 10–20% of cases).

In Pontiac fever, the clinical picture resembles Influenza—after a short incubation period (24–36 hours), hyperthermia, myalgia, fever, and headache occur, sometimes with meningism, but without the development of pneumonia. In both variants, renal involvement is characterized by symptoms of diffuse or focal GN (proteinuria, Hematuria); in a fraction of cases (2–6%), ARF develops.

Fort Bragg fever is characterized by signs of a respiratory illness with skin rashes, but without pneumonia.

The mortality rate for Legionnaires' disease proper ranges from 15–20% in uncomplicated cases to 50–80% in patients receiving glucocorticoids or immunosuppressants for other conditions; no fatalities have been reported for Pontiac and Fort Bragg fevers, although relapses are possible (14–47% of cases).

Bacterial endocarditis. Renal involvement in bacterial endocarditis occurs in 50–80% of cases and results in CRF in 10%, with the frequency of kidney damage having decreased only slightly following the Introduction of Antibiotics.

The following forms of renal involvement in bacterial endocarditis are distinguished: focal GN, diffuse GN, renal infarction, cortical necrosis, Renal Amyloidosis, and drug-induced renal injuries (acute tubular necrosis, acute TIN, potassium-penicillin kidney).

Focal GN develops at the onset of the disease and typically presents with an isolated urinary syndrome dominated by hematuria. Renal Functions remain fully preserved, and the prognosis is favorable (reversible resolution within 3–4 weeks).

The pathogenesis of diffuse GN (20% of cases) is associated with an immune mechanism—elevated levels of circulating immune complexes (CIC), IMMUNOGLOBULINS G and M, and the C3 Complement component in the blood. The high levels of CIC in bacterial endocarditis specifically explain the occurrence of skin vasculitis and damage to other Internal Organs and systems. In particular, a picture of mesangiocapillary or extracapillary nephritis develops in the kidneys, featuring diffuse deposition of glomerular immune complexes containing IgG, IgM, the C3 complement component, and bacterial antigens subendothelially and mesangially.

The clinical picture of diffuse GN in bacterial endocarditis develops 3–6 months after the disease onset; in 14–30% of cases, nephrotic syndrome is the presenting feature. Persistent hypertension is not typical, and a progressive decline in GFR and renal concentrating function develops relatively rapidly (within 6–10 months). Urinary syndrome is characterized by marked proteinuria, persistent microhematuria (occasionally macrohematuria), and constant cylindruria (hyaline and granular casts).

Renal infarction in bacterial endocarditis is currently relatively rare (prior to the antibiotic era, it occurred in 80% of cases). It may develop as early as the onset of the disease. Clinical symptoms are characterized by sharp pain in the right or left lumbar region, transient hypertension, followed by macrohematuria.

The development of acute cortical necrosis is associated with high blood levels of CIC, which, together with bacterial endotoxins (especially from gram-negative flora), activate platelet aggregation processes and induce intravascular coagulation, which is precisely the cause of this condition that culminates in irreversible renal failure.

Renal amyloidosis in bacterial endocarditis develops in 3–5% of cases against the Background of a prolonged course of the underlying process. Its Clinical Presentation and Selection/3.html">Stages of development do not differ from Other forms of secondary renal amyloidosis.

Iatrogenic Renal Injuries in bacterial endocarditis are caused by massive antibiotic therapy, The Use of Diuretics, and NSAIDs. The clinical picture is dominated by tubular dysfunction syndromes with symptoms of acute tubular necrosis, acute interstitial nephritis, and renal tubular acidosis.

Diagnostic challenges regarding renal involvement in bacterial endocarditis—as well as bacterial endocarditis itself, which is frequently induced by low-virulence pathogens or their associations and occurs after intercurrent infections or invasive Procedures—are currently caused by the potential absence of typical symptoms such as intermittent fever, rapid development of aortic Heart valve disease, embolisms, and thrombosis. Instead, non-specific syndromes—endogenous intoxication, vasculitis, anemia, and renal impairment—come to the forefront.

Renal candidiasis. Isolated renal candidiasis is observed in individuals who have received prolonged antibiotic therapy, especially in combination with glucocorticoids. As a rule, these are physically debilitated patients, elderly individuals with Diabetes Mellitus, malignancies, or CRF. Morphologically, this manifests as miliary candidiasis, caverns, abscesses, and interstitial nephritis.

The most pronounced clinical manifestations are observed in miliary candidiasis (severe general condition, hyperthermia, lumbar pain). Urinary sediment reveals isolated hematuria.

For the diagnosis of renal candidiasis, candiduria exceeding 100,000 colonies per 1 mL of urine is of primary importance. It should be kept in mind that asymptomatic candidiasis can be detected in 8% of subjects, particularly during Pregnancy. However, repeated detection of Fungi in the urine in the presence of clinical manifestations in a patient undergoing long-term antibiotic therapy is of decisive importance.

Serodiagnosis of candidiasis (agglutination and precipitation reactions with fungal antigen) is also given certain significance. Radiological manifestations resemble common Pyelonephritis and Renal tuberculosis.

Renal actinomycosis. Renal involvement is caused predominantly by the fungus Actinomyces israelii. Infection occurs hematogenously from a primary focus, such as carious Teeth. Typically, a single kidney is involved. Viscerally, it resembles a kidney affected by a tumor or tuberculosis.

The clinical picture of renal actinomycosis is nonspecific and characterized by endogenous Intoxication syndrome. Pain in the lumbar region is moderate, and dysuric disorders are mild. Changes in urine appear quite late (isolated leukocytes and erythrocytes); fungal druses in the urine are rarely found.

Important information can be provided by pyelography (pelvic deformation), vasography (pronounced disorganization of the renal vascular wall), and computed tomography (enlargement and deformation of the kidney). When There is a real threat of infection spread, a needle biopsy of the kidney for suspected actinomycosis is not performed.

Among the etiological factors of nephropathies, a certain place belongs to the causative agents of parasitic diseases, particularly helminths.

According to WHO data, there are about 2.5 billion people worldwide infected with Ascaris, and 1 billion with hookworms. Parasitic diseases caused by helminths are also quite widespread in Ukraine.

Unlike Viruses and bacteria, helminths generally do not multiply in the human body. An important feature of helminthiases is the multi-stage Development of the parasite and its ability to cause different pathological effects at various stages of this development (sensitization by metabolic products, Circulatory Disorders, mechanical factors, etc.). This impact depends on the type of pathogen, its biology, the intensity of invasion, and the state of the body's defense mechanisms.

Ascariasis. Renal involvement in ascariasis occurs in both acute and chronic periods of invasion.

The most dangerous is the larval stage, during which migration of Ascaris larvae through various organs and Tissues of the body is observed, overcoming the barriers of the intestine, liver, and lungs. Along the migration pathways, the larvae injure tissues, causing hemorrhages, nonspecific inflammatory changes, and micronecrosis. Exo- and endotoxins of the larvae trigger general and local immediate- and delayed-type allergic reactions. General allergic reactions manifest as eosinophilia, thrombocytopenia, urticaria, Bronchial Asthma, and anaphylactic shock, while local ones present as hyperergic inflammation of an alterative or infiltrative nature. Signs of delayed-type allergic reactions include hyperplastic changes in the cells of the reticuloendothelial system and the formation of a disseminated granulomatous process in various organs, including the kidneys.

Renal involvement in the migratory stage of ascariasis can manifest as acute diffuse glomerulonephritis combined with productive vasculitis of the renal Arteries. Urinary syndrome (moderate proteinuria, hematuria, cylinduria) tends to decrease under METABOLISM/18.html">The Influence of antihistamines and disappears upon completion of the migratory stage.

Trichinellosis. A helminthiasis of the nematode group, the causative agent of which is Trichinella spiralis.

There are three phases of disease development: enzymatic-toxic, immunological, and immunopathological. Involvement of internal organs, including the lungs, myocardium, kidneys, central nervous system, and vascular wall, most commonly occurs in the third phase and, in severe cases, manifests as hyperthermia, fever, diarrhea, generalized myalgia with contractures, myopathic syndrome, facial and neck edema, tachycardia, collapse, arrhythmias, hemorrhagic rashes, abdominal crises, eosinophilic pulmonary syndrome, hypereosinophilia, hypercoagulation, and hyper-alpha₂-globulinemia. Larvae surrounded by inflammatory infiltrates are detected in the kidneys and other organs. These infiltrates contain a significant number of eosinophils. Subsequently, a granulation wall forms around the larvae. Changes in the urinary sediment fully correspond to those in conventional glomerulonephritis—significant proteinuria, hematuria, leukocyturia (eosinophiluria), and cylinduria. Filtration and concentration Functions of the kidneys are generally not impaired. Acute renal failure develops rarely, but when it does, it is characterized by a severe course.

The diagnosis of trichinellosis is established based on the characteristic clinical picture (presence of the aforementioned extrarenal symptoms), epidemiological history (consumption of raw or insufficiently cooked meat), results of serological testing, and Muscle biopsy.

Echinococcosis. Renal echinococcosis (1–5% of all echinococcosis localizations) is more frequently a unilateral process.

Echinococcus embryos enter the kidneys via the hematogenous route. In the initial stages, a mononuclear reaction develops around the embryo, and after a few days, a vacuole appears as the initial stage of the internal bladder cavity. A true hydratid cyst forms within 2 to 6 months. These cysts, usually solitary, form in the renal cortex, less often in the pelvic wall, and even more rarely in the pararenal tissue.

Continuous sensitization of the body by the parasite's metabolic products leads to the development of predominantly tubulointerstitial changes, while the mechanical pressure of the cyst and the formation of a fibrous capsule result in significant Atrophy of the renal parenchyma. The outer layer of the fibrous capsule contains many Blood Vessels, A large number of epithelioid, plasma, and giant cells, as well as eosinophils.

In the early stages of development, the Echinococcus's ability to counteract the host's defense mechanisms is realized through the release of metabolic products that possess immunosuppressive properties, suppressing or altering the cellular and humoral Branches of the host's immunity.

After the formation of a dense fibrous capsule, The production of immunosuppressants by the Echinococcus decreases, and mechanical symptoms come to the forefront—Displacement of the kidney, its deformation, and atrophy of the renal parenchyma. As it grows, the cyst may fuse with adjacent organs, such as the liver, spleen, or intestine, which somewhat alters the clinical symptoms.

Clinical manifestations of renal echinococcosis are determined by the localization, size of the cyst, complications, and the degree of compression of adjacent organs. Echinococcus is characterized by very slow growth, so symptoms of renal damage may be absent for a long time. In rare cases, the Echinococcus may die, and the cyst may calcify, leading to spontaneous recovery.

With disease progression, a nonspecific endogenous intoxication syndrome and general allergic reactions arise, joined by pain in the lumbar region radiating to the scapula and legs, dysuria, and attacks resembling Renal Colic. In some cases, the cyst may rupture into the renal pelvis, accompanied by renal colic and the appearance of daughter vesicles in the urine. Closure of the ureteral lumen by daughter vesicles causes urinary retention and the development of acute pyelonephritis. After cyst rupture, the patient's general condition improves only for a certain period; as hydatid fluid reaccumulates, deterioration sets in again.

Urinary sediment is characterized by pyuria, hematuria, and moderate proteinuria; the urine is turbid and visually contains sediment in the form of plaque-like masses and pieces of necrotic tissue.

A severe complication of renal echinococcosis is suppuration of the cyst. This is manifested by a substantial increase in pain, hyperthermia, leukocytosis with a left shift, and the onset of acute renal failure symptoms.

Parasitological confirmation of the disease is possible only upon detecting daughter vesicles or remnants of the parasite itself in the urine via Microscopy (scoleces, hooks). In all other cases, clinical Methods (enlarged kidney size, presence of an elastic mass) and instrumental methods (plain urography, ultrasound, excretory urography, computed tomography, angiography) are used for the diagnosis of renal echinococcosis. Important diagnostic significance is attached to positive serological reactions with echinococcal antigen: latex agglutination, indirect hemagglutination, and enzyme-linked immunosorbent assay (ELISA).

Plain urography determines changes in the contours of the affected kidney; excretory urography reveals renal deformation and provides an approximate characterization of the mass; ultrasound, angiography, and computed tomography determine the localization and size of the cyst, its internal Structure, and contents. With a prolonged course of echinococcosis, renal amyloidosis with nephrotic syndrome may develop.

Alveococcosis. Primary alveolar echinococcosis of the kidney is rare; however, the kidneys are consistently involved in the pathological process in other localizations of alveococcosis, most frequently hepatic alveococcosis.

The disease is caused by the larval stage of Alveococcus multilocularis. Unlike echinococcosis, the primary focus in alveococcosis develops exclusively in the liver, where hematogenous dissemination leads to the formation not of a parasitic cyst, but of a parasitic tumor characterized by slow infiltrative growth, The ability to invade adjacent organs, and metastasis to the lungs, Brain, and kidneys.

Macroscopically, alveolar echinococcosis Metastases in the kidneys resemble neoplasms; they are grayish-white in color and have a nearly cartilaginous consistency. Microscopically, the metastasis consists of small necrotic foci containing tiny, interconnected vesicles undergoing exogenous budding. These foci are surrounded by a granulation tissue wall, while the renal parenchyma adjacent to the node exhibits atrophic changes and sclerosis.

Diagnosing alveococcosis is challenging. Clinical and laboratory findings closely resemble those of echinococcosis, whereas instrumental findings mimic renal neoplasms.

A correct diagnosis can be facilitated by a detailed Analysis of the medical history (long-term progression), identification of the primary hepatic lesion, and positive serological tests. The overall prognosis is unfavorable.