RENAL CALCULI AND NEPHROCALCINOSIS

Renal (nephrolithiasis) and ureteral stones (urolithiasis) are very common world-wide, with a lifetime risk of about 10%, and in many patients it is a recurrent problem. The male: female ratio is 2 : 1. Prevalence of stone disease is much higher in the Middle East due to a higher oxalate and lower calcium containing diet (see below) and increased risk of dehydration in hot climates.

Aetiology

Most stones are composed of calcium oxalate and/or calcium phosphate. Other types are uric acid, magnesium ammonium phosphate (struvite) and cystine stones. Stone formation occurs when normally soluble material, e.g. calcium, supersaturates the urine and begins the process of crystal forma-tion. In normal urine, inhibitors of crystal formation also prevent stone formation.

Calcium stones

Hypercalciuria Increased urinary calcium excretion is the most common metabolic abnormality in calcium stone-formers. Causes of hypercalciuria are:

■ Hypercalcaemia of which the most common cause (p. 648) leading to stone formation is primary hyperparathyroidism

■ Excessive dietary intake of calcium

■ Excessive resorption of calcium from bone, e.g. with prolonged immobilization

■ Idiopathic hypercalciuria, in which there is increased absorption of calcium from the gut and in turn increased urinary excretion. Serum calcium levels are normal.

Primary renal disease, such as medullary sponge kidney and polycystic renal disease, is also associated with calcium stones. The alkaline urine seen in the renal tubular acidoses favours the precipitation of calcium phosphate.

Hyperoxaluria Increased oxalate excretion favours the formation of calcium oxalate, even if calcium excretion is normal. The main causes are:

■ Dietary hyperoxaluria: A high dietary intake of oxalate-rich foods (e.g. spinach, rhubarb and tea) results in hyperoxaluria. Low dietary calcium intake can also result in hyperoxaluria via decreased intestinal binding of oxalate (by calcium) and the resulting increased oxalate absorption and urinary excretion.

■ Enteric hyperoxaluria: Chronic intestinal malabsorption of any cause leads to reduced levels of intestinal calcium for oxalate binding (see above). Dehydration secondary to fluid loss from the gut also plays a part in stone formation.

■ Primary hyperoxaluria: This is a rare autosomal recessive enzyme defi-ciency resulting in high levels of endogenous oxalate production. There is widespread calcium oxalate crystal deposition in the kidneys, and later in other tissues (myocardium, tissues and bone). CKD develops in the late teens or early 20s.

Uric acid stones

These are associated with hyperuricaemia (p. 293) with or without clinical gout. Patients with ileostomies are also at risk of developing urate stones, as loss of bicarbonate from gastrointestinal secretions results in the production of an acid urine and reduced solubility of uric acid.

Infection-induced stones

UTI with organisms that produce urease (Proteus, Klebsiella and Pseu-domonas spp.) is associated with stones containing ammonium, magnesium and calcium. Urease hydrolyses urea to ammonia and this raises the urine pH. An alkaline urine and high ammonia concentration favour stone forma-tion. These stones are often large and fill the pelvicalyceal system, producing the typical radiopaque staghorn calculus.

Cystine stones

These occur with cystinuria, an autosomal recessive condition affecting cystine and dibasic amino acid transport (lysine, ornithine and arginine) in the epithelial cells of renal tubules and the gastrointestinal tract. Excessive urinary excretion of cystine, the least soluble of the amino acids, leads to the formation of crystals and calculi.

Clinical features

Most people with urinary tract calculi are asymptomatic; pain is the most common symptom (Table 9.6). Large staghorn renal calculi cause loin pain. Ureteric stones cause renal colic, a severe intermittent pain lasting for hours. The pain is felt anywhere between the loin and the groin, and may radiate into the scrotum or labium or into the tip of the penis. Nausea, vomiting and sweating are common. Haematuria often occurs. There will be features of acute pyelonephritis or Gram-negative septicaemia if there is associated infection in an obstructed urinary system. Bladder stones present with urinary

Table 9.6 Clinical features of urinary tract calculi
Asymptomatic
Pain
Haematuria
Urinary tract infection
Urinary tract obstruction

frequency and haematuria. Urethral stones may cause bladder outflow obstruction, resulting in anuria and painful bladder distension.

Differential diagnosis

Bleeding within the kidney, e.g. after renal biopsy, can produce clots that lodge temporarily in the ureter and produce ureteric colic. Pain may also occur from sloughed necrotic renal papillae (p. 382). Pain from an ectopic pregnancy or leaking aortic aneurysm may be mistaken for renal colic.

Investigations

These include a mid-stream specimen of urine for culture and measurement of serum urea, electrolytes, creatinine and calcium levels. A plain abdominal X-ray (KUB: kidney, ureters and bladder) may show a radiopaque stone in the line of the renal tract. Unenhanced helical (spiral) CT is the best diagnostic test available; a normal CT scan during an episode of pain excludes calculus disease as the cause of the pain. A detailed history may reveal possible aetiological factors for stone formation, e.g. vitamin D consumption (leading to hypercalcaemia), gouty arthritis, recurrent UTIs, intestinal resection. A further work-up to look for underlying metabolic risk factors is indicated in all patients other than the elderly with a single episode (Table 9.7).

Management

Initial treatment A strong analgesic, e.g. diclofenac 75 mg by intravenous infusion is given to relieve the pain of renal colic. Patients are managed at home if there is no evidence of sepsis and they are able to take oral medica-tions and fluids. Most small ureteric stones (<5 mm) will pass spontaneously. Indications for intervention include persistent pain, infection above the site of obstruction, and failure of the stone to pass down the ureter. The options for stone removal include the following:

■ Extracorporeal shock wave lithotripsy (ESWL) will fragment most stones which then pass spontaneously.

■ Endoscopy (ureteroscopy) with a YAG laser is used for larger stones.

■ Open surgery is rarely needed.

Table 9.7 Investigations to identify the cause of stone formation

Urine

Chemical analysis of any stone passed

MSU for culture and sensitivity

24-h urine collection for calcium, oxalate, uric acid

Screen for cystinuria (purple colour of urine after addition of sodium nitroprusside)

Blood

Serum urea and electrolytes Serum calcium Serum urate

Plasma bicarbonate (low in renal tubular acidosis)

Radiography

CT scan will normally have been performed at diagnosis Imaging is also to look for a primary renal disease

MSU, mid-stream urine specimen.

Prevention of recurrence Further treatment depends on the type of stone and any underlying condition identified during screening investigations (Table 9.7). For prevention of all stones, whatever the cause, a high intake of fluid (to produce a urine volume of 2-2.5 L/day) must be maintained, particularly during the summer months. This is the mainstay of treatment when no metabolic or renal abnormality has been identified (‘idiopathic stone formers').

■ Idiopathic hypercalciuria. Patients should be encouraged to consume a normal calcium diet and avoid foods containing large amounts of oxalate. A water softener may be helpful for patients who live in hard water areas. Thiazide diuretics, e.g. bendroflumethiazide 2.5 mg daily, reduce urinary calcium excretion and are used if hypercalciuria persists.

■ Mixed infective stones. Meticulous control of bacteriuria, if necessary with long-term, low-dose, prophylactic antibiotics and a high fluid intake helps to prevent recurrent stone formation.

■ Uric acid stones are prevented by the long-term use of the xanthine oxidase inhibitor, allopurinol, which allows the excretion of the more soluble precursor compound, hypoxanthine, in preference to uric acid. Oral sodium bicarbonate supplements to maintain an alkaline urine, and hence increased solubility of uric acid, are an alternative approach in those patients unable to tolerate allopurinol.

■ Cystine stones. A very high fluid intake (5 L of water in 24 hours) is needed to maintain solubility of cystine in the urine. An alternative is D-penicillamine, which chelates cystine, forming a more soluble complex.

Nephrocalcinosis

Nephrocalcinosis is diffuse renal parenchymal calcification that is detectable radiologically. The causes are listed in Table 9.8. It is typically painless and hypertension and renal impairment commonly occur. Treatment is of the underlying cause.

Ebook Essentials of Kumar and Clark's Clinical Medicine, 5e

1. Ethics and communication

Ethics and communication

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Infectious diseases

3. Gastroenterology and nutrition

Gastroenterology and nutrition

4. Liver, biliary tract and pancreatic disease

Liver, biliary tract and pancreatic disease
LIVER BIOCHEMISTRY AND LIVER FUNCTION TESTS
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HEPATITIS
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