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Pathology - Prostate Carcinoma
Definition: A malignant epithelial tumor originating in the prostate. Epidemiology: The predominant malignant neoplasm in males. • Increasing prevalence attributed to prolonged life expectancy and enhanced detection methods. • A less significant contributor to cancer-related mortality, as numerous instances have a rather indolent progression.
Aetiology: Racial background and genetic predispositions are significant, with a 5–10-fold elevated risk in males possessing two or more affected first-degree relatives. • Dietary correlation with animal-derived items, especially red meat.
Carcinogenesis • Originates from a precursor lesion termed prostatic intraepithelial neoplasia (PIN), distinguished by the neoplastic transformation of the epithelial lining of the prostatic ducts and acini. • Contains mutations in several genes, including GST-pi, PTEN, AMACR, p27, and E-cadherin (notably, these are not conventional tumor suppressor genes or oncogenes). The majority of prostate cancers are asymptomatic and are detected when a needle biopsy is conducted due to an elevated prostate-specific antigen (PSA) level or a suspicious finding during a digital rectal examination (DRE). • LUTS may be evident. • Infrequently, patients exhibit symptoms indicative of metastatic disease.
Macroscopy • Initial instances of latent prostate cancer are improbable to be discernible macroscopically. • Larger tumors may present as firmer regions that contrast in color with the adjacent prostatic tissue.
Histopathology • Nearly all prostate carcinomas are glandular epithelial neoplasms, specifically adenocarcinomas. • A principal diagnostic characteristic of prostate cancer is the atypical architecture of the malignant glands, which exhibit crowding and a disorganized growth pattern relative to adjacent normal acini. • Malignant epithelial cells exhibit enlarged nuclei with conspicuous nucleoli and denser amphophilic cytoplasm. • Malignant glands frequently contain intraluminal crystalloids (dense crystalline structures), pink secretions, or blue-tinged mucin. • A morphological diagnosis or suspicion of prostate carcinoma can be immunohistochemically validated by the absence of basal cells encircling the malignant glands. Typical basal cell markers employed for this purpose encompass p63 and high molecular weight keratins.
Prognosis • The primary determinant is the histological grade, referred to as the Gleason score, named after the pathologist who initially developed the system. • The Gleason score varies from 2 to 10 and is derived by summing two integers between 1 and 5, reflecting the architectural growth patterns of the tumor. In actuality, patterns 1 and 2 are rarely identified, resulting in nearly all prostate tumors having a Gleason score ranging from 6 to 10. A higher score correlates with inferior tumor differentiation and adverse outcomes. Additional significant factors include the PSA level and the illness stage.
Prostate cancer screening • The utilization of serum PSA for screening is a contentious issue. • Currently, the majority of countries lack a systematic prostate screening program. Current research indicates that screening may lead to overdiagnosis and overtreatment of numerous men with prostate tumors that are unlikely to exhibit aggressive behavior.
TNM 7 pathological staging of prostatic carcinomas
Primary tumour (T)
pT1a: tumour incidental histologic fi nding in 5 % or less of TURP tissue.
pT1b: tumour incidental histological fi nding in more than 5 % of TURP
tissue.
pT1c: tumour identifi ed by needle biopsy (e.g. because of elevated PSA).
pT2a: tumour involves one half of one lobe or less.
pT2b: tumour involves more than half of one lobe, but not both lobes.
pT2c: tumour involves both lobes.
pT3a: extracapsular extension or microscopic bladder neck invasion.
pT3b: tumour invades seminal vesicle(s).
pT4: tumour invades adjacent structures other than seminal vesicles.
Regional lymph nodes (N)
pN0: no regional lymph node metastasis.
pN1: regional lymph node metastasis
Definition: A malignant epithelial tumor originating in the prostate. Epidemiology: The predominant malignant neoplasm in males. • Increasing prevalence attributed to prolonged life expectancy and enhanced detection methods. • A less significant contributor to cancer-related mortality, as numerous instances have a rather indolent progression.
Aetiology: Racial background and genetic predispositions are significant, with a 5–10-fold elevated risk in males possessing two or more affected first-degree relatives. • Dietary correlation with animal-derived items, especially red meat.
Carcinogenesis • Originates from a precursor lesion termed prostatic intraepithelial neoplasia (PIN), distinguished by the neoplastic transformation of the epithelial lining of the prostatic ducts and acini. • Contains mutations in several genes, including GST-pi, PTEN, AMACR, p27, and E-cadherin (notably, these are not conventional tumor suppressor genes or oncogenes). The majority of prostate cancers are asymptomatic and are detected when a needle biopsy is conducted due to an elevated prostate-specific antigen (PSA) level or a suspicious finding during a digital rectal examination (DRE). • LUTS may be evident. • Infrequently, patients exhibit symptoms indicative of metastatic disease.
Macroscopy • Initial instances of latent prostate cancer are improbable to be discernible macroscopically. • Larger tumors may present as firmer regions that contrast in color with the adjacent prostatic tissue.
Histopathology • Nearly all prostate carcinomas are glandular epithelial neoplasms, specifically adenocarcinomas. • A principal diagnostic characteristic of prostate cancer is the atypical architecture of the malignant glands, which exhibit crowding and a disorganized growth pattern relative to adjacent normal acini. • Malignant epithelial cells exhibit enlarged nuclei with conspicuous nucleoli and denser amphophilic cytoplasm. • Malignant glands frequently contain intraluminal crystalloids (dense crystalline structures), pink secretions, or blue-tinged mucin. • A morphological diagnosis or suspicion of prostate carcinoma can be immunohistochemically validated by the absence of basal cells encircling the malignant glands. Typical basal cell markers employed for this purpose encompass p63 and high molecular weight keratins.
Prognosis • The primary determinant is the histological grade, referred to as the Gleason score, named after the pathologist who initially developed the system. • The Gleason score varies from 2 to 10 and is derived by summing two integers between 1 and 5, reflecting the architectural growth patterns of the tumor. In actuality, patterns 1 and 2 are rarely identified, resulting in nearly all prostate tumors having a Gleason score ranging from 6 to 10. A higher score correlates with inferior tumor differentiation and adverse outcomes. Additional significant factors include the PSA level and the illness stage.
Prostate cancer screening • The utilization of serum PSA for screening is a contentious issue. • Currently, the majority of countries lack a systematic prostate screening program. Current research indicates that screening may lead to overdiagnosis and overtreatment of numerous men with prostate tumors that are unlikely to exhibit aggressive behavior.
TNM 7 pathological staging of prostatic carcinomas
Primary tumour (T)
pT1a: tumour incidental histologic fi nding in 5 % or less of TURP tissue.
pT1b: tumour incidental histological fi nding in more than 5 % of TURP
tissue.
pT1c: tumour identifi ed by needle biopsy (e.g. because of elevated PSA).
pT2a: tumour involves one half of one lobe or less.
pT2b: tumour involves more than half of one lobe, but not both lobes.
pT2c: tumour involves both lobes.
pT3a: extracapsular extension or microscopic bladder neck invasion.
pT3b: tumour invades seminal vesicle(s).
pT4: tumour invades adjacent structures other than seminal vesicles.
Regional lymph nodes (N)
pN0: no regional lymph node metastasis.
pN1: regional lymph node metastasis
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Pathology – Testicular Germ Cell Tumors
Testicular germ cell neoplasms: A group of malignant tumors of the testis derived from germ cells. Epidemiology More than 90% of testicular cancers are categorized as germ cell tumors, predominantly affecting young men between the ages of 20 and 45.
Aetiology The principal risk factor is cryptorchidism, which increases the risk by three to fivefold. Additional prenatal risk factors include low birth weight and being tiny for gestational age. No reliable risk factors for adulthood have been discerned.
Carcinogenesis: Most germ cell malignancies arise from a precursor condition known as intratubular germ cell neoplasia (ITGCN), characterized by neoplastic germ cells localized within the seminiferous tubules. The disease process likely begins in fetal development, with ITGCN observable in childhood and young adulthood, during which further genetic abnormalities lead to malignant transformation. A commonly identified structural chromosomal aberration is the gain of 12p sequences.
Presentation • Most individuals present with a non-painful testicular tumor. Approximately 10% have symptoms indicative of metastatic disease, primarily back pain attributed to retroperitoneal lymph node metastases or cough/dyspnea stemming from pulmonary metastases. Serum neoplastic biomarkers Alpha-fetoprotein (AFP) is frequently associated with the presence of yolk sac elements. Beta human chorionic gonadotrophin (B HCG) is associated with the presence of syncytiotrophoblastic cells, which may appear individually in a pure seminoma or as a key component of choriocarcinoma. Macroscopy: Pure seminomas generally exhibit lobulated tan lesions. Teratomas often have both cystic and solid components. Mixed cancers generally have diverse morphological characteristics. Histopathology
Seminoma comprises sheets or clusters of polygonal cells distinguished by translucent or eosinophilic cytoplasm and spherical nuclei containing one or two nucleoli. A lymphocytic infiltration is commonly detected within the tumor.
Teratoma comprises tissues that mimic either undeveloped fetal tissues or mature adult tissues.
Embryonal carcinoma comprises anaplastic cells distinguished by large vesicular nuclei featuring prominent nucleoli. The tumors may manifest in solid sheets or form glandular structures.
The yolk sac tumor comprises small, somewhat pleomorphic cells that display various architectural configurations, primarily reticular and microcystic.
Choriocarcinoma has a mixture of syncytiotrophoblastic and cytotrophoblastic cells. Profuse bleeding and necrosis often transpire. Germ cell cancers may comprise entirely one subtype or a mixture of multiple kinds.
Prognosis: Excellent, with 5-year survival rates of 98% in the majority of countries. This indicates the high sensitivity of germ cell cancers to modern platinum-based chemotherapy protocols.
TNM 7 pathological staging of testicular germ cell
tumours
Primary tumour (T)
pT1: tumour limited to the testis without lymphovascular invasion.
pT2: tumour limited to the testis with lymphovascular invasion or
tumour extending through the tunica albuginea with involvement of the
tunica vaginalis.
pT3: tumour invades the spermatic cord with or without lymphovascular
invasion.
pT4: tumour invades the scrotum with or without lymphovascular
invasio
Testicular germ cell neoplasms: A group of malignant tumors of the testis derived from germ cells. Epidemiology More than 90% of testicular cancers are categorized as germ cell tumors, predominantly affecting young men between the ages of 20 and 45.
Aetiology The principal risk factor is cryptorchidism, which increases the risk by three to fivefold. Additional prenatal risk factors include low birth weight and being tiny for gestational age. No reliable risk factors for adulthood have been discerned.
Carcinogenesis: Most germ cell malignancies arise from a precursor condition known as intratubular germ cell neoplasia (ITGCN), characterized by neoplastic germ cells localized within the seminiferous tubules. The disease process likely begins in fetal development, with ITGCN observable in childhood and young adulthood, during which further genetic abnormalities lead to malignant transformation. A commonly identified structural chromosomal aberration is the gain of 12p sequences.
Presentation • Most individuals present with a non-painful testicular tumor. Approximately 10% have symptoms indicative of metastatic disease, primarily back pain attributed to retroperitoneal lymph node metastases or cough/dyspnea stemming from pulmonary metastases. Serum neoplastic biomarkers Alpha-fetoprotein (AFP) is frequently associated with the presence of yolk sac elements. Beta human chorionic gonadotrophin (B HCG) is associated with the presence of syncytiotrophoblastic cells, which may appear individually in a pure seminoma or as a key component of choriocarcinoma. Macroscopy: Pure seminomas generally exhibit lobulated tan lesions. Teratomas often have both cystic and solid components. Mixed cancers generally have diverse morphological characteristics. Histopathology
Seminoma comprises sheets or clusters of polygonal cells distinguished by translucent or eosinophilic cytoplasm and spherical nuclei containing one or two nucleoli. A lymphocytic infiltration is commonly detected within the tumor.
Teratoma comprises tissues that mimic either undeveloped fetal tissues or mature adult tissues.
Embryonal carcinoma comprises anaplastic cells distinguished by large vesicular nuclei featuring prominent nucleoli. The tumors may manifest in solid sheets or form glandular structures.
The yolk sac tumor comprises small, somewhat pleomorphic cells that display various architectural configurations, primarily reticular and microcystic.
Choriocarcinoma has a mixture of syncytiotrophoblastic and cytotrophoblastic cells. Profuse bleeding and necrosis often transpire. Germ cell cancers may comprise entirely one subtype or a mixture of multiple kinds.
Prognosis: Excellent, with 5-year survival rates of 98% in the majority of countries. This indicates the high sensitivity of germ cell cancers to modern platinum-based chemotherapy protocols.
TNM 7 pathological staging of testicular germ cell
tumours
Primary tumour (T)
pT1: tumour limited to the testis without lymphovascular invasion.
pT2: tumour limited to the testis with lymphovascular invasion or
tumour extending through the tunica albuginea with involvement of the
tunica vaginalis.
pT3: tumour invades the spermatic cord with or without lymphovascular
invasion.
pT4: tumour invades the scrotum with or without lymphovascular
invasio
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Pathology - Non-germ cell tumors of the testis
Testicular lymphomas • Approximately 5% of all testicular tumors. • Predominantly observed in older males. The testis is typically substituted by a substantial gray or tan mass that may extend into the cord. The predominant histological type is diffuse large B-cell lymphoma).Prognosis for survival is typically unfavorable.
Leydig cell tumor • A sex-cord stromal neoplasm comprising approximately 3% of all testicular tumors. • Can manifest at any age. • Prepubertally, they typically exhibit indicators of precocious puberty resulting from androgen production. • Post-puberty, they exhibit a testicular mass. Macroscopically, these tumors are well-defined, frequently exhibiting a brown cut surface. Histologically, they consist of sheets or nests of polygonal cells characterized by eosinophilic cytoplasm and round nuclei containing a single nucleolus. Reinke's crystals, characterized by their rhomboid shape and intracytoplasmic location, may be observed. • Most Leydig cell tumors exhibit benign characteristics; however, approximately 10% demonstrate malignant behavior. • Histological analysis is not consistently dependable in forecasting aggressive tumor behavior; nonetheless, concerning indicators include tumor size exceeding 5 cm, necrosis, vascular invasion, cellular pleomorphism, and elevated mitotic activity
Sertoli cell tumor • A sex-cord stromal neoplasm constituting approximately 1% of all testicular tumors. • Predominantly manifests as a testicular mass in young and middle-aged males. Macroscopically, they typically present as solid yellow or white tumors. Histologically, they consist of oval cells that create hollow or solid tubular structures. Approximately 10% of tumors are malignant; analogous histological parameters are employed to anticipate malignant behavior as with Leydig cell tumors.
Testicular lymphomas • Approximately 5% of all testicular tumors. • Predominantly observed in older males. The testis is typically substituted by a substantial gray or tan mass that may extend into the cord. The predominant histological type is diffuse large B-cell lymphoma).Prognosis for survival is typically unfavorable.
Leydig cell tumor • A sex-cord stromal neoplasm comprising approximately 3% of all testicular tumors. • Can manifest at any age. • Prepubertally, they typically exhibit indicators of precocious puberty resulting from androgen production. • Post-puberty, they exhibit a testicular mass. Macroscopically, these tumors are well-defined, frequently exhibiting a brown cut surface. Histologically, they consist of sheets or nests of polygonal cells characterized by eosinophilic cytoplasm and round nuclei containing a single nucleolus. Reinke's crystals, characterized by their rhomboid shape and intracytoplasmic location, may be observed. • Most Leydig cell tumors exhibit benign characteristics; however, approximately 10% demonstrate malignant behavior. • Histological analysis is not consistently dependable in forecasting aggressive tumor behavior; nonetheless, concerning indicators include tumor size exceeding 5 cm, necrosis, vascular invasion, cellular pleomorphism, and elevated mitotic activity
Sertoli cell tumor • A sex-cord stromal neoplasm constituting approximately 1% of all testicular tumors. • Predominantly manifests as a testicular mass in young and middle-aged males. Macroscopically, they typically present as solid yellow or white tumors. Histologically, they consist of oval cells that create hollow or solid tubular structures. Approximately 10% of tumors are malignant; analogous histological parameters are employed to anticipate malignant behavior as with Leydig cell tumors.
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Pathology - Paratesticular disorders
Epididymal cyst • Benign cystic lesion of the epididymis. • Typically manifests as a tiny paratesticular swelling that may exhibit tenderness. • Macroscopically, it presents as a thin-walled translucent cystic lesion. • Histologically, the cyst is lined by a thin, attenuated layer of non-descript epithelial cells.
Epididymitis • Typically arises from an ascending infection originating in the lower urinary tract. In males under 35 years, the etiology is typically a sexually transmitted infection, such as Chlamydia trachomatis or Neisseria gonorrhoeae. In males over 35 years, the predominant cause is Escherichia coli.
Varicocele • A chronic abnormal enlargement of the pampiniform venous plexus within the spermatic cord. • More prevalent on the left side due to the drainage of the testicular vein into the renal vein. • Typically manifests as nodularity on the lateral aspect of the scrotum. • May induce a dull ache, particularly after extended periods of standing or towards the day's conclusion. • May lead to male subfertility due to elevated blood flow, which increases scrotal warmth and hinders spermatogenesis.
Hydrocele • An abnormal accumulation of fluid in the interstitial space between the two layers of the tunica vaginalis. • A prevalent etiology of scrotal swelling. • Typically induced by trauma or a response to an underlying ailment such as epididymitis, orchitis, or a neoplasm.
Adenomatoid tumor • The predominant benign neoplasm of the paratesticular region. • Can manifest in the epididymis, spermatic cord, and tunica albuginea. • Predominantly observed in young people. • Grossly, they appear as small, solid, firm grey/white tumors often measuring less than 3 cm. • Histologically, they consist of dilated tubular structures lined with attenuated mesothelial cells.
Paratesticular sarcomas • Infrequent yet well-documented paratesticular neoplasms. The two predominant varieties are well-differentiated liposarcoma in adults and embryonal rhabdomyosarcoma in children and adolescents.
Epididymal cyst • Benign cystic lesion of the epididymis. • Typically manifests as a tiny paratesticular swelling that may exhibit tenderness. • Macroscopically, it presents as a thin-walled translucent cystic lesion. • Histologically, the cyst is lined by a thin, attenuated layer of non-descript epithelial cells.
Epididymitis • Typically arises from an ascending infection originating in the lower urinary tract. In males under 35 years, the etiology is typically a sexually transmitted infection, such as Chlamydia trachomatis or Neisseria gonorrhoeae. In males over 35 years, the predominant cause is Escherichia coli.
Varicocele • A chronic abnormal enlargement of the pampiniform venous plexus within the spermatic cord. • More prevalent on the left side due to the drainage of the testicular vein into the renal vein. • Typically manifests as nodularity on the lateral aspect of the scrotum. • May induce a dull ache, particularly after extended periods of standing or towards the day's conclusion. • May lead to male subfertility due to elevated blood flow, which increases scrotal warmth and hinders spermatogenesis.
Hydrocele • An abnormal accumulation of fluid in the interstitial space between the two layers of the tunica vaginalis. • A prevalent etiology of scrotal swelling. • Typically induced by trauma or a response to an underlying ailment such as epididymitis, orchitis, or a neoplasm.
Adenomatoid tumor • The predominant benign neoplasm of the paratesticular region. • Can manifest in the epididymis, spermatic cord, and tunica albuginea. • Predominantly observed in young people. • Grossly, they appear as small, solid, firm grey/white tumors often measuring less than 3 cm. • Histologically, they consist of dilated tubular structures lined with attenuated mesothelial cells.
Paratesticular sarcomas • Infrequent yet well-documented paratesticular neoplasms. The two predominant varieties are well-differentiated liposarcoma in adults and embryonal rhabdomyosarcoma in children and adolescents.
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Pathology - Benign prostatic hyperplasia
Definition: Enlargement of the prostate gland resulting from a rise in cellular proliferation. Epidemiology • Extremely prevalent. • Symptomatic illness impacts approximately 3% of men aged 45–49, increasing to roughly 25% by age 80. Histological evidence is observed in 90% of men by the age of 80.
Aetiology • Ambiguous.
Pathogenesis • Androgens play a pivotal role in the pathogenesis of benign prostatic hyperplasia (BPH), particularly through elevated local concentrations of dihydrotestosterone in the prostate. • Contemporary evidence indicates that heightened estrogen levels in the bloodstream, which increase with age, activate androgen receptors in prostate tissue and promote hyperplasia. Presentation: Frequency, urgency, nocturia, hesitancy, diminished flow, and terminal dribbling, generally referred to as lower urinary tract symptoms (LUTS). • Certain individuals exhibit urinary tract infection, acute urine retention, or renal failure.
Macroscopy The prostate exhibits nodular enlargement, typically affecting the transition zone. • The association between prostate size and symptom severity is weak.
Histopathology • There is a proliferation of both epithelial and stromal components of the prostate, resulting in the formation of nodules. • The ratio of epithelial to stromal components varies significantly among instances, with some being primarily epithelial and others mostly stromal.
Complications • Urinary retention. • Recurrent urinary tract infections. • Uroliths. • Obstructive nephropathy
Definition: Enlargement of the prostate gland resulting from a rise in cellular proliferation. Epidemiology • Extremely prevalent. • Symptomatic illness impacts approximately 3% of men aged 45–49, increasing to roughly 25% by age 80. Histological evidence is observed in 90% of men by the age of 80.
Aetiology • Ambiguous.
Pathogenesis • Androgens play a pivotal role in the pathogenesis of benign prostatic hyperplasia (BPH), particularly through elevated local concentrations of dihydrotestosterone in the prostate. • Contemporary evidence indicates that heightened estrogen levels in the bloodstream, which increase with age, activate androgen receptors in prostate tissue and promote hyperplasia. Presentation: Frequency, urgency, nocturia, hesitancy, diminished flow, and terminal dribbling, generally referred to as lower urinary tract symptoms (LUTS). • Certain individuals exhibit urinary tract infection, acute urine retention, or renal failure.
Macroscopy The prostate exhibits nodular enlargement, typically affecting the transition zone. • The association between prostate size and symptom severity is weak.
Histopathology • There is a proliferation of both epithelial and stromal components of the prostate, resulting in the formation of nodules. • The ratio of epithelial to stromal components varies significantly among instances, with some being primarily epithelial and others mostly stromal.
Complications • Urinary retention. • Recurrent urinary tract infections. • Uroliths. • Obstructive nephropathy
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Pathology - Reflux nephropathy
Definition: Renal scarring linked to vesicoureteric reflux (VUR), a congenital condition characterized by the retrograde flow of urine from the bladder into the upper urinary tract.
Epidemiology: A significant contributor to chronic kidney disease, accounting for around 30% of cases in pediatric populations and 10% in adults.
Aetiology: Vesicoureteral Reflux (VUR). It is important to note that not all cases of vesicoureteral reflux (VUR) are complicated by reflux nephropathy (RN).
Pathogenesis • Believed to be caused by the reflux of contaminated urine into the kidney. Intra-renal reflux typically occurs near the poles of the kidneys, where compound papillae are located. Compound papillae exhibit increased susceptibility to reflux due to the papillary ducts opening at less oblique angles onto a flat or concave surface. The immediate inflammatory reaction to the infection results in kidney scarring. • The loss of adequate nephron mass leads to the progression of renal disease.
Presentation • Patients commonly have hypertension and/or proteinuria. • When renal scarring is substantial, biochemical indicators of renal failure become apparent.
Macroscopy • The renal poles have regions of coarse cortical scarring. Histopathology: The scarred regions exhibit characteristics of chronic pyelonephritis, including tubular atrophy and interstitial fibrosis, accompanied by a mononuclear inflammatory cell infiltrate. Some tubules are collapsed, while others may be dilated and filled with proteinaceous material, a condition referred to as 'thyroidization.' • Remaining glomeruli exhibit hypertrophy and subsequent glomerulosclerosis.
This constellation of characteristics is not exclusive to reflux nephropathy and may also be observed in other situations, including obstructive nephropathy. The differentiation between the two is typically achievable, depending on the clinical presentation and the scarring pattern.
Complications • Recurrent urinary tract infections. • Renal calculi. • Chronic kidney disease
Definition: Renal scarring linked to vesicoureteric reflux (VUR), a congenital condition characterized by the retrograde flow of urine from the bladder into the upper urinary tract.
Epidemiology: A significant contributor to chronic kidney disease, accounting for around 30% of cases in pediatric populations and 10% in adults.
Aetiology: Vesicoureteral Reflux (VUR). It is important to note that not all cases of vesicoureteral reflux (VUR) are complicated by reflux nephropathy (RN).
Pathogenesis • Believed to be caused by the reflux of contaminated urine into the kidney. Intra-renal reflux typically occurs near the poles of the kidneys, where compound papillae are located. Compound papillae exhibit increased susceptibility to reflux due to the papillary ducts opening at less oblique angles onto a flat or concave surface. The immediate inflammatory reaction to the infection results in kidney scarring. • The loss of adequate nephron mass leads to the progression of renal disease.
Presentation • Patients commonly have hypertension and/or proteinuria. • When renal scarring is substantial, biochemical indicators of renal failure become apparent.
Macroscopy • The renal poles have regions of coarse cortical scarring. Histopathology: The scarred regions exhibit characteristics of chronic pyelonephritis, including tubular atrophy and interstitial fibrosis, accompanied by a mononuclear inflammatory cell infiltrate. Some tubules are collapsed, while others may be dilated and filled with proteinaceous material, a condition referred to as 'thyroidization.' • Remaining glomeruli exhibit hypertrophy and subsequent glomerulosclerosis.
This constellation of characteristics is not exclusive to reflux nephropathy and may also be observed in other situations, including obstructive nephropathy. The differentiation between the two is typically achievable, depending on the clinical presentation and the scarring pattern.
Complications • Recurrent urinary tract infections. • Renal calculi. • Chronic kidney disease
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Pathology - Anti-glomerular Basement Membrane Disease
Definition: A severe kidney illness induced by the production of autoantibodies against the glomerular basement membrane.
Epidemiology • Rare. The peak incidence occurs in adults aged 20 to 40 years.
Aetiology: Autoantibodies against the C-terminal region of type IV collagen.
Pathogenesis • Autoantibodies bind to the glomerular basement membrane, causing an autoimmune attack on the glomeruli.
Presentation: ARF caused by significant acute glomerular damage. Some individuals may experience pulmonary hemorrhage if the autoantibody also reacts with the alveolar basement membrane.
Light microscopy • Glomeruli exhibit segmental, necrotizing glomerulonephritis, with breaks in the glomerular basement membrane and production of crescents in the Bowman's space. • Unaffected segments of the glomeruli appear normal. • A lymphoplasmacytic immune cell infiltrate is found in the interstitium of afflicted glomeruli. immune fluorescence • IgG and C3 exhibit strong linear staining in the glomerular basement membrane. • Linear staining may also be observed in tubular basement membranes.
Electron microscopy • There are no immunological deposits present.
Prognosis: Prompt immunosuppressive therapy can limit disease activity, although renal damage may be irreversible.
Definition: A severe kidney illness induced by the production of autoantibodies against the glomerular basement membrane.
Epidemiology • Rare. The peak incidence occurs in adults aged 20 to 40 years.
Aetiology: Autoantibodies against the C-terminal region of type IV collagen.
Pathogenesis • Autoantibodies bind to the glomerular basement membrane, causing an autoimmune attack on the glomeruli.
Presentation: ARF caused by significant acute glomerular damage. Some individuals may experience pulmonary hemorrhage if the autoantibody also reacts with the alveolar basement membrane.
Light microscopy • Glomeruli exhibit segmental, necrotizing glomerulonephritis, with breaks in the glomerular basement membrane and production of crescents in the Bowman's space. • Unaffected segments of the glomeruli appear normal. • A lymphoplasmacytic immune cell infiltrate is found in the interstitium of afflicted glomeruli. immune fluorescence • IgG and C3 exhibit strong linear staining in the glomerular basement membrane. • Linear staining may also be observed in tubular basement membranes.
Electron microscopy • There are no immunological deposits present.
Prognosis: Prompt immunosuppressive therapy can limit disease activity, although renal damage may be irreversible.
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Pathology - Acute tubular injury
Definition: Acute renal impairment resulting from damage to renal tubules.
Epidemiology • A prevalent etiology of acute renal failure (ARF).
Aetiology • Ischemia resulting from extended hypoperfusion. • Nephrotoxins including pharmaceuticals, radiological contrast agents, uric acid, hemoglobin, myoglobin, and ethylene glycol.
Pathogenesis: Tubular epithelial cells have high metabolic activity and are highly susceptible to injury from ischemia or toxins.
Presentation: ARF. Macroscopy • The kidneys exhibit hypertrophy, with a mass exceeding 200 grams. The renal cortex exhibits a pale appearance on the sliced surface.
Histopathology:The affected tubules exhibit dilation, accompanied by the flattening of tubular epithelial cells and the disappearance of the brush boundary. Casts of desquamated necrotic epithelial cells may be observed in the lumen of distal tubules. • The interstitial compartment is enlarged due to edema, although there is no substantial infiltration of inflammatory cells. • Indicators of the underlying etiology may be evident, such as birefringent oxalate crystals in cases of ethylene glycol poisoning or pigmented casts in rhabdomyolysis.
Prognosis: Typically linked to a serious circulatory abnormality and a significant death rate.
Definition: Acute renal impairment resulting from damage to renal tubules.
Epidemiology • A prevalent etiology of acute renal failure (ARF).
Aetiology • Ischemia resulting from extended hypoperfusion. • Nephrotoxins including pharmaceuticals, radiological contrast agents, uric acid, hemoglobin, myoglobin, and ethylene glycol.
Pathogenesis: Tubular epithelial cells have high metabolic activity and are highly susceptible to injury from ischemia or toxins.
Presentation: ARF. Macroscopy • The kidneys exhibit hypertrophy, with a mass exceeding 200 grams. The renal cortex exhibits a pale appearance on the sliced surface.
Histopathology:The affected tubules exhibit dilation, accompanied by the flattening of tubular epithelial cells and the disappearance of the brush boundary. Casts of desquamated necrotic epithelial cells may be observed in the lumen of distal tubules. • The interstitial compartment is enlarged due to edema, although there is no substantial infiltration of inflammatory cells. • Indicators of the underlying etiology may be evident, such as birefringent oxalate crystals in cases of ethylene glycol poisoning or pigmented casts in rhabdomyolysis.
Prognosis: Typically linked to a serious circulatory abnormality and a significant death rate.
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Pathology - IgA nephropathy
Definition: A glomerulopathy characterized by IgA deposition in glomeruli, either dominant or co-dominant.
Epidemiology: • The most prevalent glomerulopathy worldwide. The cause of IgAN is unknown, although it can reoccur in transplanted kidneys, indicating a systemic issue. One suggestion is that an aberrant mucosal immune system creates a kind of IgA that is resistant to breakdown, enters the circulation, and deposits in glomeruli.
Pathogenesis: • Deposition of IgA in the mesangium affects glomerular function, causing blood and protein leaks into urine.
Presentation: Haematuria (microscopic or macroscopic) with proteinuria. Light microscopy shows that IgAN can cause glomeruli alterations ranging from modest mesangial enlargement to focal and diffuse proliferative lesions, with the possibility of crescents in severe cases. immune fluorescence • The mesangial region of the glomeruli has dominant or co-dominant IgA staining, as defined. Electron microscopy reveals immunological deposits in mesangial regions of glomeruli.
Prognosis: • Approximately one-third of patients acquire progressive renal disease.
• Clinical characteristics such as proteinuria, hypertension, and renal function might indicate progression. The Oxford classification of IgAN identifies four histological characteristics that predict the outcome: mesangial hypercellularity, segmental glomerulosclerosis, endocapillary hypercellularity, and tubular atrophy/interstitial fibrosis.
Definition: A glomerulopathy characterized by IgA deposition in glomeruli, either dominant or co-dominant.
Epidemiology: • The most prevalent glomerulopathy worldwide. The cause of IgAN is unknown, although it can reoccur in transplanted kidneys, indicating a systemic issue. One suggestion is that an aberrant mucosal immune system creates a kind of IgA that is resistant to breakdown, enters the circulation, and deposits in glomeruli.
Pathogenesis: • Deposition of IgA in the mesangium affects glomerular function, causing blood and protein leaks into urine.
Presentation: Haematuria (microscopic or macroscopic) with proteinuria. Light microscopy shows that IgAN can cause glomeruli alterations ranging from modest mesangial enlargement to focal and diffuse proliferative lesions, with the possibility of crescents in severe cases. immune fluorescence • The mesangial region of the glomeruli has dominant or co-dominant IgA staining, as defined. Electron microscopy reveals immunological deposits in mesangial regions of glomeruli.
Prognosis: • Approximately one-third of patients acquire progressive renal disease.
• Clinical characteristics such as proteinuria, hypertension, and renal function might indicate progression. The Oxford classification of IgAN identifies four histological characteristics that predict the outcome: mesangial hypercellularity, segmental glomerulosclerosis, endocapillary hypercellularity, and tubular atrophy/interstitial fibrosis.
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Pathology- Acute drug-induced interstitial nephritis
Definition: Renal impairment resulting from a hypersensitivity reaction to a medication.
Epidemiology • Rare.
Aetiology • Nonsteroidal anti-inflammatory drugs (NSAIDs). • Antimicrobials. • Diuretics. • Allopurinol. • Proton pump inhibitors.
Pathogenesis: A hypersensitive reaction to the offending medication induces tubulointerstitial inflammation and tubular destruction. The usual presentation is acute respiratory failure accompanied by fever and rash. Numerous patients have eosinophilia, eosinophiluria, and elevated serum IgE levels. • Patients with NSAID-induced conditions may exhibit significant proteinuria. • Typically, symptoms manifest within days of initiating the medication, although in other instances, they may not appear until many months of exposure.
Macroscopy • The kidneys exhibit swelling, pallor, and increased weight.
Histopathology • The interstitium exhibits expansion due to edema and a heterogeneous inflammatory cell infiltrate, prominently including eosinophils, which may lead to the formation of eosinophilic microabscesses. • Lymphocytes are additionally observed infiltrating the tubules, a condition referred to as 'tubulitis.'
Prognosis: The discontinuation of the causative medication typically leads to full recovery.
Definition: Renal impairment resulting from a hypersensitivity reaction to a medication.
Epidemiology • Rare.
Aetiology • Nonsteroidal anti-inflammatory drugs (NSAIDs). • Antimicrobials. • Diuretics. • Allopurinol. • Proton pump inhibitors.
Pathogenesis: A hypersensitive reaction to the offending medication induces tubulointerstitial inflammation and tubular destruction. The usual presentation is acute respiratory failure accompanied by fever and rash. Numerous patients have eosinophilia, eosinophiluria, and elevated serum IgE levels. • Patients with NSAID-induced conditions may exhibit significant proteinuria. • Typically, symptoms manifest within days of initiating the medication, although in other instances, they may not appear until many months of exposure.
Macroscopy • The kidneys exhibit swelling, pallor, and increased weight.
Histopathology • The interstitium exhibits expansion due to edema and a heterogeneous inflammatory cell infiltrate, prominently including eosinophils, which may lead to the formation of eosinophilic microabscesses. • Lymphocytes are additionally observed infiltrating the tubules, a condition referred to as 'tubulitis.'
Prognosis: The discontinuation of the causative medication typically leads to full recovery.
