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Renal Calculus (Urolithiasis) - Complete 10-Mark Answer

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Definition

• More common in males than females (2:1 ratio)
• Peak incidence: 4th to 6th decade of life
• Lifetime risk: ~9% in men, ~5% in women
• Strong familial tendency - runs in families

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Diagram 1 - Sites of Calculi & Urinary Obstruction

Calculi can lodge at: (1) pelviureteric junction (PUJ), (2) pelvic brim where ureter crosses iliac vessels, (3) vesicoureteric junction (VUJ) - the narrowest point.

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Etiopathogenesis (How Stones Form)

1. Concentration of solute - dehydration raises all mineral concentrations
2. Changes in urine pH - acidic urine favors uric acid/cystine stones; alkaline urine favors calcium phosphate and struvite stones
3. Bacterial infections - urea-splitting organisms raise urine pH and release ammonia
4. Absence of inhibitors - citrate, magnesium, pyrophosphate normally prevent crystal aggregation; low citrate = stone-prone
5. Nidus formation - bacteria, desquamated epithelial cells (e.g., in vitamin A deficiency) act as seeds for crystal deposition

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Types of Renal Stones

Memory trick - "CSUC": Calcium (80%), Struvite (10%), Uric acid (7%), Cystine (2%)

Causes of Hypercalciuria (most common predisposing factor):

• Absorptive - gut absorbs too much calcium (most common)
• Renal - kidney fails to reabsorb calcium - excretes excess
• Resorptive - hyperparathyroidism causes bone breakdown releasing calcium
• Immobilization, sarcoidosis, vitamin D excess, malignancy

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Clinical Features (Symptoms)

The Classic Presentation - Renal Colic

• Sudden, severe, colicky flank pain radiating to groin ("loin to groin" pain)
• Pain waxes and wanes but position changes do NOT relieve it (differentiates from musculoskeletal)
• Nausea and vomiting (visceral response to ureteric distension)
• Hematuria - either visible (gross) or on dipstick (microscopic) - present in >80%
• Dysuria and urinary frequency - when stone is near vesicoureteric junction

Danger Signs (Emergency):

• Fever + obstruction = Pyonephrosis/urosepsis - SURGICAL EMERGENCY
• Anuria = bilateral obstruction or obstruction of a solitary kidney

Chronic/Asymptomatic Stones:

• Detected incidentally on imaging (e.g., during hematuria workup)
• Staghorn calculi may present with recurrent UTIs and flank dull ache

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Investigations

1. Urine Examination

• Dipstick/microscopy: Hematuria (>80%), pyuria if infected
• Urine culture: Identify infecting organism
• 24-hour urine: pH, calcium, oxalate, uric acid, citrate, creatinine, sodium - for metabolic workup

2. Blood Tests

• Serum calcium, phosphate, uric acid - identify metabolic cause
• Serum creatinine + eGFR - assess renal function
• CBC - leukocytosis suggests infection
• Parathyroid hormone (PTH) - if hypercalcemia present

3. Imaging

• Gold standard - sensitivity ~97%, specificity ~97%
• Detects ALL stone types (including radiolucent uric acid stones)
• Shows stone size, location, degree of hydronephrosis, and secondary signs

• Quick and cheap
• Shows only radiopaque stones (85% of stones)
• Uric acid stones are INVISIBLE on plain X-ray

• No radiation - ideal for pregnant women and children
• Shows hydronephrosis and large stones well
• Misses small ureteric stones

• Older technique but still used in some centers
• Shows anatomy and degree of obstruction

Diagram 2 - Staghorn Calculus on X-ray KUB

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Management

A. Immediate/Emergency Management (Acute Renal Colic)

1. Pain relief (first priority):
   • IV NSAIDs (Ketorolac) - first line; reduces ureteral spasm
   • IV Opioids (Morphine) - if NSAIDs contraindicated
2. IV fluids for hydration
3. If infection + obstruction = EMERGENCY decompression:
   • Cystoscopic ureteral stent placement, OR
   • Percutaneous nephrostomy - to drain the obstructed kidney
   • Then treat infection; plan definitive stone removal later

B. Medical Expulsive Therapy (MET) - For Small Stones <10mm

• Tamsulosin (alpha-1 blocker) - relaxes smooth muscle of ureter, promotes stone passage
• High fluid intake (>2 liters/day)
• Most stones <5mm pass spontaneously within 4-6 weeks
• Patient must be observed with re-imaging if no evidence of passage

C. Interventional / Surgical Treatment

D. Prevention (Long-term Medical Management)

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Complications of Renal Calculus

1. Hydronephrosis - progressive dilatation of collecting system due to obstruction
2. Pyelonephritis / Pyonephrosis - infected, obstructed kidney - life-threatening
3. Urosepsis - systemic sepsis from infected obstructed kidney
4. Chronic kidney disease (CKD) - from repeated obstruction and infection
5. Renal atrophy / loss of kidney - end-stage untreated obstruction
6. Squamous cell carcinoma of renal pelvis - rare, associated with chronic staghorn calculi
7. Steinstrasse - "stone street" - multiple stone fragments blocking ureter after ESWL

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Key Points for Exam Memory

• Commonest stone = Calcium oxalate (80%); radiopaque
• Radiolucent stone = Uric acid (appears on CT but not X-ray)
• Staghorn calculus = Struvite (from Proteus UTI); fills entire renal pelvis
• Most dangerous complication = Pyonephrosis (infected obstructed kidney)
• Gold standard imaging = Non-contrast CT (NCCT KUB)
• MET drug = Tamsulosin (alpha-blocker)
• ESWL for stones <2cm; PCNL for stones >2cm or staghorn
• Pain of renal colic is NOT relieved by position change (unlike musculoskeletal)

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Renal Cell Carcinoma (RCC) / Adenocarcinoma of the Kidney

Complete 10-Mark Surgery Exam Answer

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Definition

• 80-90% of all primary malignant neoplasms of the kidney
• 2-3% of all cancers in adults
• Male : Female ratio = 2:1
• Peak age: 6th to 7th decade (55-75 years)

It is also called Grawitz tumor, hypernephroma, or clear cell carcinoma (for the most common subtype).

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Etiology / Risk Factors

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Pathology

Gross Appearance

• Located in the renal cortex, usually upper pole
• Characteristically solitary, well-circumscribed, rounded mass
• Bulges out of the renal contour, often compressing normal parenchyma
• Cut surface: bright yellow-orange (due to high lipid content) with areas of hemorrhage, necrosis, and cystic change
• Has a pseudocapsule of compressed renal tissue

Diagram 1 - Gross Pathology of Clear Cell RCC

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Histological Types

Diagram 2 - Histology of RCC Subtypes (H&E stain)

Molecular Pathogenesis of Clear Cell RCC (most important for exams):

1. VHL gene (Tumor suppressor) on chromosome 3p25 is mutated/lost
2. VHL protein normally degrades HIF (Hypoxia Inducible Factor)
3. Without VHL → HIF accumulates even in normal oxygen conditions
4. HIF stimulates VEGF (Vascular Endothelial Growth Factor) → rich tumor vascularity
5. This is why RCC is highly vascular and why anti-VEGF drugs work in RCC treatment

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Spread of RCC

1. Local Spread

• Through the renal capsule into perinephric fat
• Into the renal sinus and collecting system

2. Venous Extension (Characteristic of RCC!)

• RCC has a special tendency to grow into the renal vein as a tumor thrombus
• Can extend into the Inferior Vena Cava (IVC) and even up to the right atrium
• This is a unique hallmark of RCC

3. Lymphatic Spread

• To para-aortic and paracaval lymph nodes

4. Hematogenous Spread (Most common route)

• Lungs - "Cannonball metastases" (large round deposits on CXR) - most common site
• Bones - osteolytic; pathological fractures; bone pain
• Liver
• Brain
• Opposite kidney
• Adrenal gland

Special feature: RCC is famous for late metastases - solitary lung or bone metastases may appear years after nephrectomy. Even then, surgical removal of the metastasis can be curative!

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Clinical Features

Classic Triad (seen in only 10% of cases today):

1. Painless hematuria (most common presenting symptom, >50% cases)
2. Loin/flank pain (dull ache)
3. Palpable flank/abdominal mass

Today most RCCs are detected incidentally on imaging done for other reasons.

Other Features:

• Constitutional symptoms: fever, weight loss, malaise, anorexia (advanced disease)
• Varicocele (usually right-sided): sudden-onset, non-reducing varicocele = RCC until proven otherwise (IVC or renal vein obstruction by tumor thrombus prevents drainage of testicular vein)
• Bilateral lower limb edema - IVC thrombus extension

Paraneoplastic Syndromes (PNS) - Very Important!

PNS may disappear after nephrectomy and return with metastases - a useful marker of recurrence.

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Investigations

1. Blood Tests

• CBC: anemia (common) or polycythemia
• ESR: elevated (most common PNS)
• Serum calcium: hypercalcemia (PTHrP)
• LDH: elevated in advanced disease; used for risk stratification
• Liver function tests (ALP elevated = bone/liver metastasis)
• Serum creatinine / eGFR: renal function assessment

2. Urine Tests

• Urinalysis: hematuria (micro or macro)
• Urine cytology: not helpful (unlike TCC/urothelial cancer)

3. Imaging

• First investigation for a renal mass
• Differentiates solid from cystic lesion
• Solid enhancement = suspicious for malignancy

• Investigation of choice for diagnosis AND staging
• Key finding: contrast enhancement >15 Hounsfield Units (HU) = significant; confirms RCC
• Shows: tumor size, local extension, venous involvement, lymph nodes, adrenal glands, opposite kidney
• IVC thrombus is well shown

• Superior to CT for assessing IVC thrombus level and vein wall invasion
• Used when CT is contraindicated (e.g., allergy to contrast, pregnancy)

• Cannonball metastases on CXR
• CT chest for staging

• If alkaline phosphatase elevated, bone pain, or hypercalcemia

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Staging - TNM Classification

• Vein wall invasion (worse than mere tumor thrombus)
• Lymph node involvement
• Sarcomatoid differentiation
• High WHO/ISUP nuclear grade

• 10 cm size

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Management

A. Localized Disease (Surgical - Primary Treatment)

• Removal of: kidney + Gerota's fascia + perinephric fat + ipsilateral adrenal gland + regional lymph nodes
• Can be done open, laparoscopic, or robotic
• For tumors >7 cm or involving renal sinus

• Preferred for tumors <4 cm
• Also indicated for: bilateral tumors, tumor in solitary kidney, renal insufficiency, 4-7 cm well-selected tumors
• Oncological outcomes equal to radical nephrectomy for T1 tumors

• If tumor thrombus extends into IVC, the thrombus must be surgically removed at the same time as nephrectomy
• May require cardiopulmonary bypass for supradiaphragmatic thrombus

• Radiofrequency ablation (RFA)
• Cryotherapy

B. Metastatic Disease

• Removing the primary tumor even in metastatic disease to improve response to systemic therapy

RCC is one of the few cancers where immunotherapy has worked for decades (old IL-2/IFN-α, now checkpoint inhibitors).

• Surgical removal of isolated lung or bone metastases can be curative in selected patients.

• Not effective against the primary tumor
• Used for palliative treatment of bone or brain metastases

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Prognosis Summary

• Organ-confined disease (T1-T2): 70-95% 5-year survival with surgery
• Metastatic disease: 10% 5-year survival
• RCC can have very long latency - metastases can appear 10-20 years after nephrectomy

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Key Exam Points (Quick Recall)

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