Gross & microscopic appearance	Pathologic basis of disease	Clinical correlation	
Gross:
•	Hydronephrosis: dilation of renal pelvis & calyces.
•	Thin renal parenchyma between enlarged calyces.
•	Stones that develop in the renal pelvis & calyces can grow to conform to the contour of these structures & have the shape of a staghorn.
•	Staghorn calculus are almost always associated with a concomitant infection.

Microscopic:
•	Kidney shows atrophy of tubules.
•	Obliteration of glomeruli.

Types of stones:
•	Calcium oxalate (60%): hypercalcemia & hypercalciuria.
•	Struvite stones (15%): composed of mangesium ammonium phosphate; associated with infection by urea splitting bacteria that convert urea to ammonia.
•	Uric acid stones: may or may not form in presence of hyperuricemia or hyperuricosuria.	Causes of urinary tract obstruction:
•	Congenital anomalies: urethral valves, urethral strictures, bladder neck obstruction, severe vesicoureteral reflux.
•	Urinary calculi
•	Prostatic hypertrophy or carcinoma
•	Tumors
•	Inflammation: prostatitis, ureteritis, urethritis, retroperitoneal fibrosis.
•	Sloughed papillae or blood clots
•	Normal pregnancy
•	Functional disorders: neurogenic bladder

Obstruction:
•	Sudden & complete: causes rapid progression of urine production & atrophy of renal parenchyma; if both kidneys are involved, renal failure quickly follows.
•	Subtotal & intermittent: GFR is not suppressed & progressive dilation ensues. 

Stages of Hydronephrosis:
•	1st stage: hypertrophy of muscle to overcome obstruction.
•	2nd stage: increasing pressure dilates pelvis.
•	3rd stage: cortex thin & renal tissue reduced; pelvis greatly distended.

Site of obstruction:
•	Unilateral obstruction: pelvic-ureteric junction, pelvic brim, entrance to bladder.
•	Bilateral: in or around bladder or urethra.

Sequels:
•	Infection: takes the form of a chronic pyelonephritis; it exacerbates the whole process & a vicious cycle is set up.
•	Calculus formation: combination of stasis & infection causes precipitation of phosphates & a stone is produced.

Sites of formation:
•	Precipitates form in the collecting tubules & pass into the renal pelvis where they enlarge.
•	Deposits are formed in the lymphatics of the renal papillae & are extruded into the renal pelvis.

Predisposing factors:
•	Urinary pH: urate & oxalate stones form in an acid urine; phosphate stones in alkaline urine.
•	Dehydration: causing increased urinary concentration.
•	Stasis: obstruction to urine flow encourages salt precipitation.
•	Renal disease: infection & tumors encourage stone formation.
•	Metabolic factors: 	Urinary tract obstruction:
•	Inability to concentrate urine
•	Polyuria
•	Acquired distal tubular acidosis
•	Salt wasting
•	Renal calculi
•	Tubulointerstitial nephritis, atrophy & hypertension

Nephrolithiasis:
•	Extreme flank pain radiating to groin
•	Hematuria
•	Dysuria
•	Frequency
•	Renal colic: obstruction, ulceration, bleeding & pain.

Effects & complications:
•	Passage of small stone: colic, injury to ureter, stricture & subsequent impaction of stone.
•	Passage of larger stone: impaction at lower ends of ureter or at pelvic brim leads to stasis, hydronephrosis & infection.