Teach me surgery for exams Detailed comparison table between, Bh, CA prostate, prostatitis - definition, causes and risk factors, pathogenesis, staging, types, signs and symptoms, investigations, management, complications,

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Here is your complete exam-ready comparison table, synthesized from Bailey & Love's Short Practice of Surgery (28th ed), Robbins & Kumar Basic Pathology, and Campbell Walsh Wein Urology.

Prostate Disorders: Comprehensive Comparison Table for Surgery Exams

1. DEFINITION

Feature	BPH (Benign Prostatic Hyperplasia)	Carcinoma of Prostate (CA Prostate)	Prostatitis
Definition	Non-malignant stromal and glandular proliferation of the prostate, predominantly in the transitional zone, causing bladder outflow obstruction (BOO)	Malignant neoplasm of the prostate, almost always adenocarcinoma, typically arising in the peripheral zone	Inflammatory condition of the prostate - may be bacterial (acute/chronic) or non-bacterial (chronic pelvic pain syndrome)
Key distinction	Benign, obstructive	Malignant, potentially metastatic	Infective/inflammatory

2. CAUSES AND RISK FACTORS

Feature	BPH	CA Prostate	Prostatitis
Primary cause	Androgen-dependent growth (DHT-mediated); hormonal imbalance with age	Multifactorial: androgens, heredity, environmental factors, acquired somatic mutations	Bacterial infection (acute): E. coli, S. aureus, Streptococcus faecalis, Neisseria gonorrhoeae, Chlamydia
Hormonal	Testosterone levels fall with age but estrogen relatively rises; DHT synthesized in prostate by 5α-reductase type 2 remains driver; estrogen acts synergistically with DHT	Androgens drive growth; androgen receptor amplifications drive castration-resistant disease	Not hormonal
Age	>50 years; frequency rises progressively - 50% histological evidence by age 60, 90% by 8th decade	>65 years; incidence at autopsy: 20% in 50s rising to 70% in 70-80s	Any age; acute form common and underdiagnosed
Genetics	Metabolic syndrome, hereditary factors	First-degree relative: 2x risk; BRCA2 mutations, DNA mismatch repair gene variants; MYC amplification	-
Race	-	African American men die at >2x rate of European American men; low incidence in Japan, China, India	-
Diet/environment	Metabolic syndrome	Western diet (charred red meats, animal fats), carcinogens, estrogens, oxidants	Haematogenous spread from distant focus; secondary to acute UTI
Castration	Does NOT occur in males castrated before puberty	Regresses with castration (androgen-dependent initially)	-

3. PATHOGENESIS

Feature	BPH	CA Prostate	Prostatitis
Molecular mechanism	DHT (10x more potent than testosterone) binds nuclear androgen receptors → growth factors → stromal cell proliferation + decreased epithelial cell death	TMPRSS2-ETS gene rearrangement (most common); PTEN deletion; MYC amplification; late-stage: TP53 loss, RB deletion, androgen receptor amplification	Bacterial invasion via haematogenous or ascending urinary route
Key enzyme	5α-reductase type 2 (converts testosterone → DHT)	5α-reductase relevant; androgen receptor mutations drive castration-resistant disease	-
Zone affected	Transitional zone (periurethral)	Peripheral zone (70% of cases)	Diffuse; seminal vesicles and posterior urethra also involved
Estrogen role	With aging, estrogen levels remain unchanged or rise (peripheral androgen conversion) → synergistic DHT effect	Estrogens implicated as environmental carcinogens	-
Precursor lesion	None	High-grade prostatic intraepithelial neoplasia (HGPIN) - found in ~80% of specimens; shares molecular changes with invasive cancer	-
Result	Compression of urethra → BOO → bladder hypertrophy/trabeculation → hydronephrosis	Local invasion, lymphatic spread, haematogenous spread (bone)	Tissue inflammation → possible abscess formation

4. TYPES

Feature	BPH	CA Prostate	Prostatitis
Classification	By lobe: Lateral lobes (most common), Middle lobe (projects into bladder - worst obstruction), Posterior lobe (least common)	By clinical stage: Latent/microscopic (incidental autopsy), Incidental (TURP specimen T1a/T1b, PSA-detected T1c), Early localised (T2), Locally advanced (T3-T4), Metastatic (T0/T1→occult, T2/T3/T4→evident)	Type I: Acute bacterial prostatitis; Type II: Chronic bacterial prostatitis; Type III: Chronic abacterial prostatitis/Chronic Pelvic Pain Syndrome (CPPS) - MOST COMMON; Type IV: Asymptomatic inflammatory prostatitis
Histological types (CA)	-	Adenocarcinoma (vast majority); Transitional cell carcinoma; Squamous cell carcinoma (rare)	Granulomatous prostatitis (BCG-induced, fungal in immunocompromised, or nonspecific foreign-body reaction)

5. STAGING

Feature	BPH	CA Prostate	Prostatitis
Staging system	No formal staging; graded by IPSS (International Prostate Symptom Score)	TNM Staging	No formal staging
T1a	-	Incidental tumour <5% of TURP specimen; usually well/moderately differentiated	-
T1b	-	Incidental tumour >5% of TURP specimen	-
T1c	-	Impalpable tumour found following raised PSA investigation	-
T2a	-	Suspicious nodule on DRE confined within capsule, involving ONE lobe	-
T2b	-	Tumour involves BOTH lobes, confined within capsule	-
T3	-	Extracapsular extension; may involve seminal vesicles	-
T4	-	Invades adjacent structures (bladder neck, external sphincter, rectum, levator ani, pelvic wall)	-
Gleason Grading	-	Grades 1-5 based on glandular pattern; combined Gleason Score = primary + secondary grade. Score 6-7 = most commonly detected treatable cancers. Score 8-10 = high risk. Underpins risk stratification (low/intermediate/high risk)	-
Risk stratification (CA)	-	Low risk: PSA <10, Gleason ≤6, T1-T2a; Intermediate risk: PSA 10-20 OR Gleason 7 OR T2b; High risk: PSA >20 OR Gleason ≥8 OR T3-T4	-

6. SIGNS AND SYMPTOMS

Feature	BPH	CA Prostate	Prostatitis
Onset	Gradual, progressive	Often silent until advanced; may present with incidental finding	Acute: sudden; Chronic: insidious
Obstructive LUTS (voiding symptoms)	Hesitancy; poor flow (not improved by straining); intermittent stream; terminal dribbling; sensation of incomplete emptying; straining to void	Same as BPH if locally advanced	Acute: dysuria, urinary retention possible
Irritative LUTS (storage symptoms)	Frequency; urgency; urge incontinence; nocturia	Same if locally advanced	Frequency, urgency, dysuria
Pain	Suprapubic discomfort in retention	Bone pain (metastases - lumbar spine, pelvis, femoral head common); perineal pain	Acute: perineal heaviness, rectal irritation, pain on defecation; severe perineal and rectal pain in abscess; Chronic: perigenital pain, testicular pain, prostatic pain exacerbated by intercourse
Systemic symptoms	None	Anaemia, weight loss (advanced disease)	Acute: fever (up to 39°C), rigors, chills, myalgia, malaise - may resemble influenza; bacteraemia if DRE performed on acutely inflamed prostate
DRE findings	Uniformly enlarged, smooth, firm, rubbery prostate; loss of median sulcus	Hard, nodular, irregular prostate; loss of normal anatomy; fixed; one lobe may be more affected	Acute: tender, hot, swollen prostate; one lobe may be more swollen; possibly fluctuant (abscess); DRE CONTRAINDICATED in acute prostatitis (risk of bacteraemia)
Haematuria	Can occur (increased vascularity at base of bladder)	Haematuria if bladder neck invaded	Rare
Urethral discharge	Absent	Absent	Rare in acute prostatitis
Spinal cord compression	-	Can occur with vertebral metastases	-

7. INVESTIGATIONS

Feature	BPH	CA Prostate	Prostatitis
Urinalysis	Glucose, leukocyte esterase, blood; MSU for culture and cytology	Haematuria if advanced; cytology	Pus cells, threads in initial voided sample; urine culture (positive in bacterial type)
PSA	Moderately raised (proportional to prostate size); free:total PSA ratio >25% (benign pattern)	Markedly raised; free:total PSA ratio <15% suspicious for malignancy; PSA >20 = high risk	Markedly raised in acute bacterial prostatitis (non-specific)
Uroflowmetry	Peak flow rate <10 mL/s (for voided volume >200 mL) = low; 10-15 = equivocal; >15 = normal	Only if obstructive symptoms present	Not primary investigation
Post-void residual (PVR)	Measured by USS; >250 mL = high-pressure chronic retention	-	-
Blood tests	Serum creatinine, electrolytes, haemoglobin	PSA, Alkaline phosphatase (bone mets), FBC, LFTs	FBC (leucocytosis), CRP, blood cultures (if septic)
TRUS (Transrectal USS)	Prostate volume measurement; guides biopsy	TRUS-guided biopsy (12-core systematic); can show local T3 extension; 4 sequences for mpMRI	Aids diagnosis of prostatic abscess
mpMRI (Multiparametric MRI)	If PSA 4-10 ng/mL before biopsy decision	Gold standard for local staging and targeting biopsy; PI-RADS v2 scoring - score ≥3 suspicious; four sequences: T1W, T2W, diffusion-weighted (DWI), dynamic contrast-enhanced (DCE)	MRI aids diagnosis of prostatic abscess
Bone scan	Not indicated	For staging - detects skeletal metastases (most commonly lumbar spine, pelvis, femoral head, ribs, skull)	-
Prostate biopsy	Not required for diagnosis	TRUS-guided or transperineal; antibiotic cover; fusion biopsy (mpMRI + TRUS) increasing in use	CONTRAINDICATED in acute - can cause sepsis; used in granulomatous prostatitis to exclude cancer
Pressure-flow urodynamics	Indicated in: suspected neuropathy, dominant irritative symptoms, doubtful history, post-BPH surgery recurrence, young (<50) or elderly (>80), high residual	-	-
Expressed prostatic secretions (EPS)	-	-	>10 WBC/HPF = inflammation; bacteria on culture in bacterial types; three-glass urine test (Meares-Stamey test)
CT scan	-	Lymph node staging, distant metastases	If abscess suspected
IPSS questionnaire	Guides symptom severity and treatment threshold	-	-

8. MANAGEMENT

Feature	BPH	CA Prostate	Prostatitis
Conservative / Watchful waiting	Active surveillance if IPSS mild and no complications	Active surveillance for low-risk, elderly, or comorbid patients; counselling regarding impotence/incontinence risk	Supportive care (NSAIDS, stool softeners)
Medical - Alpha blockers	α1-adrenergic blockers (tamsulosin, alfuzosin, doxazosin) - relax prostatic smooth muscle, rapid symptom relief	Not indicated	-
Medical - 5α-reductase inhibitors	Finasteride, dutasteride - inhibit DHT formation; best for glands >35-40 mL; take 3-6 months for effect; combination therapy (α-blocker + 5α-RI) best for large glands	Not primary treatment	-
Medical - Androgen ablation (hormonal therapy)	-	Surgical (bilateral orchidectomy) or medical (GnRH agonists: leuprorelin, goserelin; anti-androgens: bicalutamide, flutamide); combined androgen blockade; coupled with radiotherapy for T3 disease; docetaxel chemotherapy for metastatic disease in fit patients	-
Antibiotics	-	-	Acute: trimethoprim, ciprofloxacin, or aminoglycoside - prolonged and rigorous course to prevent recurrence; Chronic: ciprofloxacin or trimethoprim (good prostatic penetration) for 4-6 weeks; Chlamydia: tetracycline/azithromycin
Surgical - TURP	Gold standard surgical treatment; indicated when medical therapy fails, acute/chronic retention, recurrent UTI, bladder stones, haematuria, renal impairment	TURP for locally advanced disease causing outflow obstruction (with or without hormone therapy)	Transurethral resection (unroofing) to drain prostatic abscess
Surgical - Open prostatectomy	For very large glands (>80-100 g); Millin's retropubic or transvesical approach	Radical prostatectomy (retropubic or laparoscopic/robotic) for localised T1/T2 disease in men <70 years	-
Radical radiotherapy	-	External beam radiotherapy (EBRT) or brachytherapy; alternative to radical prostatectomy for intermediate/high-risk localised disease	-
Minimally invasive	HIFU, laser therapy (HoLEP), transurethral electrovaporization, radiofrequency ablation, UroLift	HIFU for localised disease	TRUS-guided or perineal needle drainage (abscess)
Catheterisation	Urethral catheter (acute retention); suprapubic catheter for chronic retention or prostatic abscess; avoid urethral catheter in prostatitis	Suprapubic if outflow obstruction with active disease	Suprapubic catheterisation preferred in urinary retention caused by acute prostatitis
Metastatic disease (CA)	-	Androgen ablation (symptomatic relief >2/3 patients); docetaxel chemotherapy; bone-targeted therapy (zoledronic acid, denosumab); palliative radiotherapy to painful bone mets; spinal cord compression: urgent surgical decompression or radiotherapy	-

9. COMPLICATIONS

Feature	BPH	CA Prostate	Prostatitis
Urinary	Acute urinary retention (AUR); chronic urinary retention (high-pressure or low-pressure); recurrent UTI; bladder stones	Urinary retention (locally advanced); ureteric obstruction → bilateral hydronephrosis → anuria	Urinary retention (acute prostatitis); recurrent UTI (chronic prostatitis)
Renal	Bilateral hydronephrosis; chronic kidney disease; uraemia; post-obstructive diuresis after catheterisation	Bilateral hydronephrosis (trigone invasion)	-
Bladder	Trabeculation; diverticulum formation; bladder stones; detrusor decompensation	Bladder neck invasion	-
Haematuria	Secondary to increased vascularity	Secondary to tumour invasion	-
Infective	Recurrent UTI; ascending infection	-	Epididymo-orchitis (spread from acute prostatitis); bacteraemia/septicaemia; prostatic abscess; recurrent UTI (chronic)
Metastatic (CA)	-	Bone metastases (osteosclerotic/osteoblastic - distinguishes from other primary tumours which give lytic mets); pathological fractures; spinal cord compression; lymphoedema (pelvic lymph nodes)	-
Post-surgical	TURP syndrome (hyponatraemia from glycine absorption); retrograde ejaculation (90%); incontinence (rare); erectile dysfunction; urethral stricture; haemorrhage	Radical prostatectomy: impotence (nerve damage), urinary incontinence, anastomotic stricture; radiotherapy: radiation proctitis, cystitis, erectile dysfunction	-
Psychosexual	Reduced sexual function due to medications/surgery	Significant (treatment-related)	Chronic prostatitis/CPPS: psychosexual dysfunction, reduced quality of life

QUICK EXAM MEMORY AID

Feature	BPH	CA Prostate	Prostatitis
Zone	Transitional	Peripheral (70%)	Diffuse
Age peak	>50 years	>65 years	Any age
DRE	Smooth, rubbery, enlarged	Hard, nodular, irregular	Tender, hot (DO NOT perform in acute)
PSA	Mildly elevated	Markedly elevated	Very high (acute, non-specific)
Key investigation	Uroflowmetry + PVR + PSA	mpMRI + TRUS biopsy + bone scan	Urine culture + EPS (3-glass test)
Key enzyme	5α-reductase type 2	5α-reductase / androgen receptor	N/A
Grading	IPSS score	Gleason score (1-5 each; combined score)	NIH Classification (Types I-IV)
Gold standard surgery	TURP	Radical prostatectomy (T1/T2)	TURP for abscess drainage
Bone mets	No	Yes - osteoblastic (sclerotic)	No
Key drug class	Alpha-blockers + 5α-RI	GnRH agonists + anti-androgens	Fluoroquinolones (ciprofloxacin)
Contraindication	-	PSA screening not population-wide	DRE in acute prostatitis (bacteraemia risk)

Sources: Bailey and Love's Short Practice of Surgery, 28th Edition - Robbins & Kumar Basic Pathology - Campbell Walsh Wein Urology, 3-Volume Set

Teach me RCC, Wilms tumor, in detail - comparison table with same headings

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RCC vs Wilms Tumor: Comprehensive Comparison Table for Surgery Exams

Sources: Robbins & Kumar Basic Pathology - Smith & Tanagho's General Urology (19th ed) - Campbell Walsh Wein Urology - National Kidney Foundation Primer on Kidney Diseases

1. DEFINITION

Feature	Renal Cell Carcinoma (RCC)	Wilms Tumor (Nephroblastoma)
Definition	Malignant neoplasm derived from renal tubular epithelium, located predominantly in the cortex; the most common primary malignant renal neoplasm in adults	Malignant embryonal neoplasm of the kidney derived from metanephric blastema; the most common solid renal tumor of childhood
Histological origin	Renal tubular epithelium (proximal tubule for clear cell and papillary; intercalated cells for chromophobe)	Metanephric blastema - triphasic: blastemal, epithelial (tubular/glomeruloid), and stromal elements
Eponym	Grawitz tumor (historical); "hypernephroma" (outdated)	Wilms tumor = nephroblastoma
Biological behavior	Malignant; notorious for late presentations, paraneoplastic syndromes, IVC extension	Malignant; chemosensitive and radiosensitive; one of the great success stories of pediatric oncology

2. CAUSES AND RISK FACTORS

Feature	RCC	Wilms Tumor
Age	6th-7th decade; most common from 50-70 years	Peak: 3rd year of life; 90% diagnosed before age 7; rare in adults
Sex	Males 2x more than females	No sex predilection
Genetic/Hereditary	VHL disease (clear cell - bilateral, multiple); familial papillary RCC (MET mutations); Hereditary leiomyomatosis RCC syndrome; Birt-Hogg-Dube syndrome	WT1 gene mutations (chromosome 11p13); ~1% familial (autosomal dominant); Knudson two-hit hypothesis applies
Syndromes	Von Hippel-Lindau disease (40-60% develop bilateral clear cell RCC); tuberous sclerosis; acquired cystic disease (dialysis patients - 30-fold increased risk)	WAGR syndrome (Wilms, Aniridia, Genitourinary malformations, mental Retardation); Beckwith-Wiedemann syndrome (overgrowth, hemihypertrophy - WT2 locus, 11p15); isolated hemihypertrophy; trisomy 18; isolated aniridia
Environmental	Smoking (most important modifiable risk factor); hypertension; obesity; occupational cadmium exposure; analgesic nephropathy; dialysis/acquired polycystic kidneys	-
Congenital anomalies	-	Hypospadias, cryptorchidism, renal fusion in 4.5-7.5% (unilateral) to 13.4% (bilateral disease)
Race	-	Anaplastic subtype more common in African-American children

3. PATHOGENESIS

Feature	RCC	Wilms Tumor
Key molecular event	Clear cell: Loss/inactivation of both VHL alleles (chromosome 3p25) → accumulation of HIF → overexpression of VEGF → intense angiogenesis; also histone methylation gene mutations (epigenomic changes); MYC amplification; Papillary: Activating MET gene mutations/amplification (chromosome 7q) → tyrosine kinase signalling → proximal tubule growth; Chromophobe: Multiple whole-chromosome losses → extreme hypoploidy	Two-hit hypothesis (Knudson & Strong, 1972): Familial = prezygotic mutation (germline WT1) + postzygotic event; Sporadic = two postzygotic mutations in same cell. WT1 gene (chromosome 11p13) mutations only in 5-10% of sporadic cases; other genes: IGF1, H19, p57 (Beckwith-Wiedemann); WT2 locus (11p15)
Precursor lesion	None recognized (incidental small tumors may represent precursors)	Nephrogenic rests (NRs): Perilobar NRs (associated with Beckwith-Wiedemann, bilateral tumors) and Intralobar NRs (associated with WAGR syndrome, aniridia). NRs may remain dormant, involute, or progress to Wilms tumor
Angiogenesis	Central to clear cell RCC pathogenesis - VHL loss → HIF → VEGF; basis for anti-VEGF/mTOR targeted therapy	Secondary importance
Anaplasia	Not classified this way	Anaplasia (5% of tumors): extreme nuclear atypia, hyperdiploidy, complex translocations; linked to p53 mutations; more common with age and in African-Americans; diffuse anaplasia = worst prognosis
Effect of spread	IVC extension (renal vein → IVC → right heart) - characteristic; lymphatic spread; haematogenous to lung and bone	Direct extension through renal capsule; haematogenous (renal vein → IVC); lymphatic spread (25% regional nodes); lungs 85-95%, liver 10-15% most common metastatic sites

4. TYPES

Feature	RCC	Wilms Tumor
Main types	1. Clear Cell RCC (65%): Most common; VHL mutation; yellow-orange cut surface (lipid-rich); clear cytoplasm; highly vascular; worst prognosis among subtypes; 2. Papillary RCC (10-15%): MET mutations; papillary growth pattern; frequently bilateral and multifocal; less orange (lower lipid); 3. Chromophobe RCC (5%): Least common; from collecting duct intercalated cells; eosinophilic pale cells; prominent cell membranes; peri-nuclear haloes; most favorable prognosis; Other: Collecting duct carcinoma; medullary carcinoma (sickle cell disease); translocation-associated RCC (children, TFE3 gene, Xp11.2)	Favorable histology (majority): Blastemal, epithelial (tubular/glomeruloid structures), stromal - classic triphasic pattern; all without anaplasia; Unfavorable histology: (1) Focal anaplasia (intermediate prognosis); (2) Diffuse anaplasia (worst prognosis); (3) Clear cell sarcoma of kidney (CCSK) - bones mets most common; (4) Rhabdoid tumor of kidney (RTK) - most aggressive; brain metastases; INI1 gene loss
Laterality	Usually unilateral; papillary type can be bilateral	Usually unicentric, either kidney equally; bilateral in 5% of cases; stage V = bilateral disease
Benign renal tumors (for contrast)	Oncocytoma (3-7%), Angiomyolipoma (1-2%), Papillary adenoma	Mesoblastic nephroma (most common neonatal renal tumor - benign hamartoma; cannot be distinguished from Wilms preoperatively)

5. STAGING

Feature	RCC (TNM Staging)	Wilms Tumor (NWTS Staging)
System used	TNM (UICC/AJCC)	National Wilms Tumor Study (NWTS) staging - based on surgical and pathologic findings
Stage I / T1	T1a: ≤4 cm, confined to kidney; T1b: 4-7 cm, confined to kidney	Stage I: Tumor limited to kidney, completely excised; no capsule penetration; no renal sinus vessel involvement; no rupture; no residual tumor
Stage II / T2	T2a: 7-10 cm, confined to kidney; T2b: >10 cm, confined to kidney	Stage II: Tumor extends beyond kidney but completely removed; capsule penetrated OR renal sinus invasion OR local spillage/biopsy pre-removal; no residual tumor; no lymph node involvement
Stage III / T3	T3a: Invades renal vein/its branches, perinephric fat, renal sinus fat (not adrenal, not beyond Gerota's fascia); T3b: Extends into IVC below diaphragm; T3c: Extends into IVC above diaphragm or into IVC wall	Stage III: Residual non-haematogenous tumor in abdomen - any of: (a) regional LN involvement; (b) diffuse peritoneal contamination/rupture; (c) peritoneal implants; (d) positive margins; (e) unresectable; (f) tumour thrombus transected
Stage IV / T4	T4: Invades beyond Gerota's fascia (including ipsilateral adrenal gland); M1: Distant metastases	Stage IV: Haematogenous metastases (lung, liver, bone, brain) or lymph node metastases outside the abdominopelvic region
Stage V	N1: Any regional LN metastasis	Stage V: Bilateral renal involvement at diagnosis - stage each kidney separately
Fuhrman Nuclear Grade	Used for clear cell RCC (Grades 1-4 based on nuclear size, shape, nucleolar prominence); higher grade = worse prognosis	Histology (favorable vs unfavorable) more important than nuclear grade

6. SIGNS AND SYMPTOMS

Feature	RCC	Wilms Tumor
Classic triad	Painless hematuria + flank pain + palpable abdominal mass (all three present in only 10% of cases)	Asymptomatic abdominal mass (most common presentation - often discovered by parents or on routine examination)
Hematuria	Most frequent symptom (>50% of cases); typically intermittent, painless macroscopic hematuria with persistent microscopic hematuria	Present in up to 30%; less common than in adult RCC
Abdominal mass	Palpable in advanced disease; usually smooth, does not cross midline	Most common presenting sign; smooth, firm, usually does not cross midline (vs neuroblastoma which crosses midline); may be enormous
Pain	Dull flank/loin pain; acute pain if haemorrhage into tumor	Abdominal pain and distension
Hypertension	Can occur (renal vein occlusion, renin production)	Present in 25-60% of cases - due to elevated renin levels
Fever	Paraneoplastic (pyrexia of unknown origin) - PUO is a classic presentation of RCC	Fever in some cases
Paraneoplastic syndromes	Polycythaemia (5-10% - EPO production); Hypercalcaemia (PTHrP); Hypertension; Cushing syndrome (ACTH); Stauffer syndrome (non-metastatic hepatic dysfunction - liver function abnormality that resolves after nephrectomy); Feminisation/Masculinisation; Anaemia (most common)	Hypertension (renin); coagulopathy (10%); anaemia (subcapsular haemorrhage)
Varicocoele	Left-sided varicocoele that does not empty on lying down = IVC/renal vein obstruction by RCC	-
Bone pain	Metastatic bone disease	Less common; bone mets mainly with clear cell sarcoma of kidney variant
Metastatic presentation	Lung (commonest - cannon ball metastases), bone, brain, liver; RCC is the "great imitator" - may present with symptoms from metastases before primary is found	Lungs (85-95%), liver (10-15%), regional lymph nodes (25%); bone and brain uncommon

7. INVESTIGATIONS

Feature	RCC	Wilms Tumor
Urinalysis	Haematuria (micro or macro)	Haematuria (up to 30%); urinalysis
Blood tests	FBC (polycythaemia or anaemia); U&E, creatinine; LFTs (Stauffer syndrome); calcium (hypercalcaemia); ESR (raised); LDH; alkaline phosphatase (bone mets)	FBC (anaemia); LFTs (if liver mets); coagulation screen; U&E
Ultrasound	First-line investigation; characterises solid vs cystic; can detect IVC extension; low sensitivity for small lesions; hyperechoic or isoechoic mass	First-line investigation for abdominal mass; identifies intrarenal origin, contralateral kidney, vascular involvement; US can confirm hydronephrosis, rule out cystic kidney
CT scan (contrast-enhanced multiphasic)	Gold standard for diagnosis, staging, and surgical planning; shows enhancement pattern (clear cell = avid enhancement in corticomedullary phase + washout; papillary = hypoenhancing all phases); renal vein/IVC involvement; LN status; adrenal involvement	Primary staging investigation for Wilms; CT abdomen with contrast; contralateral kidney assessment; hepatic invasion assessment (false-positive rate high for right-sided tumors); 7% bilateral cases missed on CT
MRI	For IVC thrombus extent (especially supradiaphragmatic extension, intracardiac); complex cyst characterisation; used when CT is contraindicated	Defines IVC/intracardiac extension of tumour thrombus; distinguishes nephrogenic rests from Wilms tumour; requires sedation in children
Chest X-ray / CT chest	CXR for lung metastases ("cannon ball"); CT chest for staging	CXR: initial examination for lung mets; CT chest: controversial in low-risk patients - may be done with abdominal CT in high-risk
Bone scan	For bone metastases (bone pain, raised ALP)	Only if clear cell sarcoma of kidney (CCSK) suspected - CCSK is the Wilms variant with bone metastases
IVU/IVP	Now largely replaced by CT; historically showed distorted pelvicalyceal system, filling defects	-
Tumour markers	No specific tumour marker; EPO (if polycythaemia); calcium	Catecholamines (VMA, HVA) and MIBG scan used to EXCLUDE neuroblastoma (not a Wilms marker); no specific marker for Wilms
Biopsy	Percutaneous biopsy for small renal masses before ablative therapy or active surveillance; not routinely done before nephrectomy for typical lesion	Usually avoided pre-operatively (avoid tumour spill); indicated only for tumours deemed too large/unsafe for primary resection when pre-operative chemo/RT planned; needle aspiration used in some centres; avoid spillage at surgery
Bosniak Classification	For cystic renal masses: I-II = benign; IIF = follow-up; III-IV = surgical resection	-

8. MANAGEMENT

Feature	RCC	Wilms Tumor
Principle	Surgery is mainstay; targeted therapy for metastatic disease; RCC is resistant to conventional chemo and radiotherapy	Multimodality: surgery + chemotherapy + (radiotherapy for stages III-IV); extremely chemosensitive and radiosensitive
Radical nephrectomy	Standard for T1b-T3 disease; includes kidney, Gerota's fascia, ipsilateral adrenal (if involved), regional lymph nodes; open or laparoscopic/robotic	Radical nephrectomy via transabdominal incision - standard for unilateral resectable disease; lymph node biopsy (renal hilum + para-aortic) for staging; avoid spillage; lymph node dissection not proven beneficial
Partial nephrectomy (nephron-sparing)	For T1a tumours (≤4 cm) and in specific circumstances (solitary kidney, bilateral disease, hereditary RCC, impaired contralateral function); equivalent oncological outcomes for small tumours	Renal-sparing surgery for bilateral tumours after pre-operative chemotherapy (favorable histology); preserves renal function
IVC thrombus surgery	IVC thrombectomy required for T3b/c (infra- or supradiaphragmatic IVC extension); may require cardiopulmonary bypass for intracardiac extension	Tumor extending into IVC should be removed unless total obstruction; cardiopulmonary bypass may be needed for intracardiac extension
Bilateral RCC	Nephron-sparing surgery where possible; staged approaches; ablative techniques	Pre-operative chemotherapy then bilateral renal-sparing surgery; biopsy for staging first if pre-op chemo planned
Pre-operative chemotherapy	Not standard in RCC (radio/chemo-resistant)	European approach (SIOP): Pre-op chemo → staged surgery → post-op chemo; American approach (NWTS/COG): Surgery first then chemo; pre-op chemo in USA only for bilateral/unresectable tumours
Post-operative chemotherapy	Not standard; targeted therapy used for metastatic disease	Stage I (favorable histology): Vincristine + Actinomycin D (EE-4A regimen); Stage I (anaplastic) + Stage II (favorable): Vincristine + Actinomycin D; Stage III-IV (favorable histology): Vincristine + Actinomycin D + Doxorubicin (DD-4A regimen); Unfavorable histology / advanced: Add cyclophosphamide, etoposide; modified regimens
Radiotherapy	RCC is radioresistant; palliative RT for bone/brain mets only	Radiosensitive tumor; whole abdominal RT for stage III/IV favorable histology, focal anaplasia stages II-IV, CCSK all stages, rhabdoid tumor all stages; NOT required for stage I-II favorable histology; doses reduced from historical 2000cGy to 1000cGy for stage III
Targeted therapy (metastatic RCC)	Anti-VEGF/VEGFR: Sunitinib (first-line), Pazopanib, Sorafenib, Axitinib, Cabozantinib; mTOR inhibitors: Everolimus, Temsirolimus; Immunotherapy (immune checkpoint inhibitors): Nivolumab (anti-PD-1), Ipilimumab (anti-CTLA4) - combination now standard first-line for advanced disease; Pembrolizumab; Cytoreductive nephrectomy before systemic therapy in selected fit patients	Not relevant (systemic chemotherapy as above)
Surveillance/active monitoring	Small renal masses (<3 cm) in elderly/comorbid patients: active surveillance with serial imaging	Nephrogenic rests: regular ultrasound surveillance; bilateral stage V: individualized follow-up
Metastasectomy	Surgical resection of solitary/limited metastases (especially lung) may be curative in selected patients; RCC has unique biology - occasional spontaneous regression; solitary brain mets: resection + radiosurgery	Not a standard approach

9. COMPLICATIONS

Feature	RCC	Wilms Tumor
Local complications	IVC extension → Budd-Chiari-like syndrome; IVC occlusion; pulmonary embolism from tumour thrombus; renal vein thrombosis	Tumour rupture/spillage (upstages to Stage III, risk of abdominal recurrence); haemorrhage; bowel obstruction from mass effect
Metastatic	Lung metastases (cannon-ball); bone metastases (pathological fractures, hypercalcaemia); brain metastases; adrenal metastases; liver metastases; contra-lateral kidney	Lung (85-95%) - must assess with CXR/CT; liver (10-15%); bone (mainly CCSK variant); brain (mainly rhabdoid variant)
Paraneoplastic	Polycythaemia; hypercalcaemia; Cushing syndrome; Stauffer syndrome; hypertension; peripheral neuropathy; amyloidosis	Hypertension (renin-mediated); coagulopathy
Post-nephrectomy	Renal insufficiency (especially with partial nephrectomy/solitary kidney); haemorrhage; adjacent organ injury; lymphocele; urine leak (partial nephrectomy); port-site recurrence (laparoscopic)	Renal failure (especially bilateral tumor requiring bilateral nephrectomy); need for dialysis/transplant
Treatment-related (Wilms)	-	Short-term: Bone marrow suppression (chemo); infection; nausea/vomiting; hepatotoxicity (actinomycin D); cardiotoxicity (doxorubicin); radiation pneumonitis/hepatitis; Long-term: Renal failure; congestive heart failure (doxorubicin); restrictive lung disease (radiation); growth disturbances (RT to spine); Secondary malignancies (higher risk)
Prognosis	Localised disease (stage I/II): 5-year survival ~90%; Stage III: 60%; Stage IV (metastatic): 10-20% (improving with targeted therapy/immunotherapy)	Extremely good overall: 4-year survival favorable histology ~90%; stage I favorable: near 100%; bilateral (stage V): 82% 3-year survival; worst prognosis: rhabdoid tumor (no improvement with doxorubicin), diffuse anaplasia

QUICK EXAM MEMORY AID

Feature	RCC	Wilms Tumor
Who gets it	Adults 50-70 years; male:female = 2:1	Children, peak 3 years; no sex predilection
Common presentation	Haematuria (>50%); incidental finding on imaging	Asymptomatic abdominal mass (parents find it)
Classic triad	Haematuria + flank pain + mass (only 10% have all 3)	Not a triad - just mass
Key gene	VHL (chromosome 3p25) - clear cell	WT1 (chromosome 11p13)
Key syndrome	Von Hippel-Lindau	WAGR, Beckwith-Wiedemann
Most common type	Clear cell (65%) - yellow/orange, avid enhancement	Favorable histology (no anaplasia) - triphasic
IVC extension	T3b (below diaphragm), T3c (above) - characteristic	Assess with MRI; remove if possible
Diagnosis	CT multiphasic (gold standard)	CT abdomen; CXR for lungs; MRI for IVC
Biopsy	Before ablation or surveillance for small masses	Avoided pre-op (risk of spill); only if too big to resect
Surgery	Radical or partial nephrectomy	Radical nephrectomy via transabdominal incision
Chemo sensitive?	NO - resistant to chemotherapy	YES - vincristine, actinomycin D, doxorubicin
Radio sensitive?	NO - palliative only	YES - but minimized in stages I-II
Targeted therapy	Anti-VEGF (sunitinib), anti-PD-1 (nivolumab)	Not used
Neuroblastoma DDx	-	Neuroblastoma crosses midline; displaces kidney down ("drooping lily"); calcification; VMA/catecholamines raised
Prognosis	Good if localised; poor if metastatic	Excellent overall ~90% cure rate
Varicocoele clue	Left varicocoele not emptying on lying down = renal vein/IVC obstruction by RCC	-
Paraneoplastic	EPO → polycythaemia; PTHrP → hypercalcaemia; Stauffer syndrome (hepatic dysfunction)	Renin → hypertension

Sources: Robbins & Kumar Basic Pathology - Smith & Tanagho's General Urology (19th Ed) - Campbell Walsh Wein Urology (3-Vol Set) - National Kidney Foundation Primer on Kidney Diseases (8th Ed)

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