Urolithiasis and urinary outflow obstructions

1. Urolithiasis (Kidney Stones)

Overview

• Frequent disease with familial predisposition; men > women.
• Main cause: ↑ urinary concentration of stone constituents > solubility → supersaturation → precipitation.
• Stones in renal pelvis → usually asymptomatic.
• Stones passing into ureter → colic pain (renal/ureteric colic), bleeding, ascending infection, hydronephrosis.

2. Types of Renal Stones

A) Calcium stones (~75 %) — most common

• Composition: Ca²⁺-oxalate ± Ca²⁺-phosphate.
• Radio-opaque.
• Three pathways:
  1. Hypercalcemia
     • Hyperparathyroidism (primary)
     • Diffuse bone disease — sarcoidosis, multiple myeloma, immobilization
     • → followed by hypercalciuria
  2. Hypercalciuria (with normal serum Ca²⁺)
     • Absorptive hypercalciuria — ↑ gut absorption of Ca²⁺
     • Renal hypercalciuria — impaired tubular reabsorption of Ca²⁺
  3. Hyperoxaluria
     • Diet rich in oxalate (vegetarians, spinach, rhubarb)
     • Enteric hyperoxaluria (Crohn, short bowel)

B) Struvite / Triple stones (~15 %)

• Composition: Mg²⁺-NH₄-PO₄³⁻ (magnesium-ammonium-phosphate).
• Radio-opaque.
• Caused by urea-splitting bacteria — Proteus, Klebsiella, Staphylococcus saprophyticus.
  • Convert urea → NH₃ → alkaline urine.
  • NH₄⁺ binds Mg²⁺ + PO₄³⁻ → precipitation.
• Large branching “staghorn calculi” filling renal pelvis + calyces.
• Common in chronic UTI patients.

C) Uric acid stones (~6–7 %)

• Associated with gout, leukemia, tumor lysis syndrome (↑ uric acid).
• Precipitate when urine pH < 5.5 (acidic).
• Radiolucent (not visible on plain X-ray; visible on CT).
• Prevention/treatment: alkalinize urine (potassium citrate).

D) Cysteine stones (~1–2 %)

• Genetic defect in renal tubular transport of dibasic amino acids (cystinuria).
• Children/young adults.
• May form staghorn-like stones.

Stone summary table

Stone	%	Cause	Urine pH	X-ray
Calcium oxalate / phosphate	75 %	Hypercalcemia / hypercalciuria / hyperoxaluria	Variable	Radio-opaque
Struvite	15 %	Urea-splitting bacteria (Proteus)	Alkaline	Radio-opaque; staghorn
Uric acid	6–7 %	Gout, tumor lysis	Acidic < 5.5	Radiolucent
Cysteine	1–2 %	Cystinuria (AR)	Acidic	Faintly opaque

3. Urinary Outflow Obstruction — Hydronephrosis

Definition

• Dilation of renal pelvis + calyces with accompanying parenchymal atrophy caused by urinary outflow obstruction.

Causes

• Congenital: ureteropelvic junction obstruction, posterior urethral valves.
• Acquired:
  • Stones (urolithiasis)
  • Tumors: BPH, prostate carcinoma, bladder carcinoma
  • Inflammation: prostatitis, urethritis, scarring
  • Pregnancy (uterine compression)
  • Neurogenic bladder

Pathogenesis

• Even with complete obstruction, glomerular filtration persists initially.
• Continued filtration into obstructed system → dilation of calyces + pelvis.
• ↑ Intrapelvic pressure → compression of renal vasculature → arterial insufficiency + venous stasis.
• Eventually GFR diminishes; interstitial inflammation → fibrosis.

Morphology

• Below ureters (urethra, bladder) → bilateral hydronephrosis → renal failure.
• At/above ureters → unilateral:
  • Subtotal / intermittent: enlarged kidney; parenchyma compressed + atrophied.
  • Complete + sudden: GFR compromised early; renal function may cease with only slight dilation.

Clinical course

• Bilateral + complete → anuria.
• Bilateral + incomplete → polyuria (tubular concentration defect).
• Unilateral → often silent (contralateral kidney compensates).
• Reversibility: removal within weeks → reversible; irreversible with time + fibrosis.

💡 High-yield: Stones: calcium oxalate (75 %) = most common (hypercalcemia / hypercalciuria / hyperoxaluria); struvite (15 %) = Proteus + alkaline urine → staghorn; uric acid (7 %) = acidic urine + radiolucent (gout, tumor lysis); cystine (1–2 %) = cystinuria. Symptoms = colic pain + hematuria. Hydronephrosis = obstruction → calyceal dilation + parenchymal atrophy. Bilateral complete → anuria; bilateral incomplete → polyuria; unilateral → silent. Reversible early, irreversible if chronic.