Renal colic

Introduction

The risk of kidney stones is about 1 in 10 for men and 1 in 35 for women. Between 4% and 8% of the Australian population suffer from kidney stones at any given time. The rate is about four to five times higher in ‘stone belt’ areas. It occurs most frequently between the ages of 20 and 50 years, with a male:female ratio of approximately 3:1. About 50% of patients experience only a single episode, but the remaining 50% have recurrent episodes within 5 years.

Most calculi are believed to originate in the collecting system (renal calyces and pelvis) before passing into the ureter. Supersaturation with stone-forming substances (calcium, phosphate, oxalate, cystine or urate), combined with a decrease in urine volume and lack of chemicals that inhibit stone formation (such as magnesium, citrate and pyrophosphate) result in the production of a calculus. In addition to this, infection with urea-splitting organisms that produce an alkaline urinary pH frequently contribute to the growth of ‘struvites’ or triple phosphate (calcium, magnesium and ammonium phosphate) stones.

Less commonly, mixed stones occur via nucleation with sodium hydrogen, urate, uric acid and hydroxyapatite crystals, providing a core to which calcium and oxalate ions adhere (heterogeneous nucleation).

Approximately 75% of all stones are calcium based, consisting of calcium oxalate, calcium phosphate or a mixture of the two. Ten percent are uric acid based, 1% are cystine based and the remainder are primarily struvite.

Predisposing factors for stone formation include dehydration and low fluid intake, hypertension, prolonged immobilization, strong family history of nephrolithiasis, hyperparathyroidism, peptic ulcer disease (hyperexcretion of calcium), small bowel disease such as Crohn disease or ulcerative colitis (hyperoxaluria) and gout (hyperuricaemia). Myeloproliferative disorders, malignancy, glycogen storage disorders, renal tubular acidosis and the use of certain medications (calcium supplements, acetazolamide, vitamins C and D and antacids) may also be conducive to nephrolithiasis.

Persistent obstruction of the ureter leads to hydronephrosis of the urinary tract and may precipitate renal failure. Common sites of obstruction are the ureteropelvic junction, pelvic brim and vesicoureteric junction.

Pathophysiology of pain

The mechanisms implicated in the production of the pain associated with renal colic are an increase in renal pelvic pressure, ureteric spasm, local inflammatory effects at the level of the calculus and increased peristalsis and pressure proximal to the calculus.

Acute obstruction of the upper urinary tract from a calculus results in increased pressure in the renal pelvis, which, in turn, induces the synthesis and secretion of renal prostaglandins, in particular PGE2, which promotes a diuresis by causing dilatation of the afferent arteriole, thus further elevating renal pelvic pressure. Acute obstruction and renal capsular tension are believed to be the cause of the constant ache in the costovertebral angle.

In experiments utilizing isolated ureteric smooth muscle, prostaglandins have also been shown to increase phasic and tonic contractile activity, resulting in ureteric spasm and severe, colicky pain.