Case 14.2 – Renal Calculi

The patient is suddenly aware of pain in the loin, which radiates anteroinferiorly to the groin and often into the testis or labium, in the sensory distribution of the first lumbar nerve. The pain steadily increases in intensity to reach a peak in a few minutes. The patient is restless, and generally tries unsuccessfully to obtain relief by changing position or pacing the room. Frequency, dysuria and haematuria may occur. The pain is usually constant during attacks, although slight fluctuations in severity may occur. Subsequent to an attack of renal colic there may be intermittent or constant dull ache in the loin or back.

History of previous renal colic (family history of renal calculi)

Distension of the renal pelvis seems to be responsible for the development of renal colic. The rise in pelvic pressure due to a ureteric calculus can result from various mechanisms such as increased diuresis, inflammatory oedema around the stone and increased frequency of ureteric contractions. Prostaglandins can play an important role in these mechanisms, therefore inhibition of prostaglandin synthesis by drugs such as non-steroidal anti-inflammatory drugs could contribute to the lowering of pelvic pressure and distension, and thus to the relief of renal colic.

Renal calculi consist of aggregates of crystals containing small amounts of proteins and glycoprotein that can lodge anywhere along the course of the urinary tract. Human urine is often saturated to the limit with uric acid, phosphates and calcium oxalate. Normally due to the secretion of various protective compounds – proteins, glycosaminoglycans, pyrophosphate and citrate – and natural mechanisms that control the pH of urine, these substances remain suspended in solution. If the protective compounds are overwhelmed or immunity becomes depressed, the substances may crystallize and the crystals may begin to clump together, eventually forming calculi.

Four basic kinds of renal calculi:

• Calcium (most commonly as oxalate but also as phosphate)
• Uric acid
• Struvite (composed of magnesium ammonium phosphate, these are often associated with infection e.g. staghorn calculi)
• Cystine (rare, tend to occur at a younger age)

About 90% of all calculi contain calcium as the chief constituent. In Europe, 80% of calculi are calcium oxalate.

Environmental and dietary:

• Low urine volumes, high ambient temperatures, low fluid intake
• Diet: high protein intake, high sodium, low calcium
• High sodium excretion, High urate excretion
• High oxalate excretion, Low citrate excretion

Acquired causes:

• Hypercalcaemia of any cause e.g. hyperparathyroidism, malignancy etc.
• Ileal disease or resection (leads to increased oxalate absorption and urinary excretion)
• Renal tubular acidosis type I

Congenital and inherited causes:

• Familial hypercalciuria
• Renal tubular acidosis type I
• Medullary sponge kidney (distal) 70% will develop calculi
• Cystinuria
• Primary hyperoxaluria

The classic patient with renal colic is writhing in pain, pacing about, and unable to lie still, in contrast to a patient with peritoneal irritation, who remains motionless to minimize discomfort. There may be pallor, sweating and often vomiting. Fever is not part of the presentation of uncomplicated nephrolithiasis. The most common finding in ureterolithiasis is loin tenderness due to the dilatation and spasm of the ureter from transient obstruction as the calculus passes from the kidney to the bladder. Abdominal examination is usually unremarkable. Bowel sounds may be decreased, a reflection of mild ileus.

Urinalysis:

• Haematuria present in 80 – 90% of cases
• Pyuria in a patient with ureterolithiasis should prompt a careful search for signs of infected hydronephrosis
• Urine pH >7 suggests urea-splitting organisms and struvite calculi. pH <5 suggests uric acid calculi

• Obtain intravenous access to facilitate delivery of analgesic and antiemetic medications
• Analgesia should be provided promptly. IV morphine. Indomethacin suppository (the pain of renal colic is mediated by prostaglandin E2)
• Antiemetics should be administered as necessary
• Intravenous hydration if the patient is considered clinically dehydrated
• Bloods collected for - full blood count (elevated WBC suggests infected hydronephrosis), electrolytes (hypokalaemia and decreased serum HCO₃⁻ level suggests underlying distal [type1] renal tubular acidosis), creatinine (serum level is the major predictor of contrast-induced nephrotoxicity), uric acid, phosphorus, calcium (if elevated check PTH)
• Occasionally, a patient may require urinary catheterization to relieve retention due to extreme pain or an obstructing bladder neck calculus
• Strain the urine for calculus collection
• If, after analgesics, the patient is pain-free he could be discharged from the ED and undergo imaging in 2-3 weeks depending on symptoms
• If the pain persists after analgesia then imaging becomes necessary. KUB (kidney, ureters, bladder) has low (40-50%) sensitivity and specificity for ureterolithiasis. CT KUB is the imaging technique of choice for suspected calculi in the urinary tract

Consider the use of MET – active medical expulsive therapy – in any patient with a reasonable probability of calculus passage. It is probably most useful in calculi 3 – 10mm in size as those ≤ 3mm have an 85% chance of passing spontaneously. Overall, MET is associated with a 65% greater likelihood of calculus passage. The calcium blocker nifedipine relaxes ureteral smooth muscle and enhances calculus passage. Alpha-1 selective blockers, such as tamsulosin also relax musculature of the ureter and lower urinary tract.

CT KUB should be arranged if not already performed and further management determined pending result.

A 24 hour urine analysis for urea, creatinine clearance, sodium, calcium, oxalate; magnesium and citrate (both important chemical inhibitors of calculus formation esp. citrate), pH (some stones are Ph dependent e.g. uric acid and struvite) should be performed if:

• Initial presentation with multiple calculi
• Initial presentation before the age of 30
• Family history of calculi
• Solitary kidney
• Bilateral calculi
• More than one calculus in the past year

Recommend measures to prevent calcium calculus formation:

• Fluid: at least 2 litres output per day (intake 3-4 litres), intake distributed throughout the day (esp. before bed)
• Sodium: restrict intake
• Protein: moderate intake, not high
• Calcium: plenty in diet (because calcium forms an insoluble salt with dietary oxalate, lowering oxalate absorption and excretion). Avoid supplements away from meals (increase calcium excretion without reducing oxalate excretion)
• Oxalate: avoid foods that are rich in oxalates (e.g. rhubarb, spinach, beets, peanuts, chocolate, sweet potatoes)
• Drugs: thiazide diuretics - reduce calcium excretion, valuable in recurrent calculi-formers and patients with hypercalciuria. Allopurinol - if urate excretion high. Avoid Vitamin D supplements as they increase calcium absorption and excretion

Calculus in the renal pelvis or kidney:

• Extracorporeal shock-wave lithotripsy (ESWL) - shock waves generated outside the body are focused to the calculus, breaking it into smaller pieces which can pass easily down the ureter. Limited by the size and location of the calculus
• Percutaneous nephrolithotomy - allows fragmentation and removal of large calculi from the kidney and ureter
• Open surgery (very rarely)

Calculus in the upper ureter:

• ESWL
• Ureteroscopic destruction – laser or mechanical
• Laparoscopic removal (rarely)
• Open surgery (very rarely)

Calculus in the lower ureter:

• ESWL
• Ureteroscopic destruction
• Dormier basket extraction

Calculus in the bladder:

• Cystoscopic destruction – calculus punch
• Open removal (suprapubic cystostomy)