Is HRT advice just a bid to save face?
Renal stone disease can encompass a variety of conditions of the kidney including ureteric and bladder stones Professor Robert Unwin, Professor Giovambattista Capasso, Dr William Robertson and Mr Simon Choong give an overview
Renal stone disease is a disorder whose prevalence has been increasing in most countries over the past century. It is more common in affluent, industrialised countries than in poorer countries. In the UK about 8 per cent of men and 4 per cent of women will form at least one stone by age 60-70.
Diet and lifestyle appear to be key determinants of stone risk in a population. Epidemiological studies have shown populations that consume diets rich in meat, fish and poultry have a higher risk of stones than more vegetarian populations. A low intake of fluid will also raise the risk of forming stones by increasing the concentration of stone-forming salts and acids in urine.
If the patient is left with no preventive treatment after their first stone, 40 per cent will return within three years with at least one more stone; by 10 years after the first episode this figure rises to 75 per cent of patients and by 25 years virtually everyone will have formed at least one more stone.
The rate of recurrence has actually increased since the introduction of the minimally invasive techniques of extracorporeal shockwave lithotripsy (ESWL) (see below) and percutaneous nephrolithotomy (PCNL) during the past two decades. ESWL, in particular, carries with it the risk of stone fragments being left behind in the kidney where they may eventually form 'new' stones. However, the advantages of these techniques over open and major surgery far outweigh their disadvantages.
The different types of renal stones and their treatments are outlined in the box on the right. The first step in medical management is to carry out a full metabolic screen.
To do this, patients need to be referred to a specialised stone clinic. They should be studied at home on their normal 'free' home diet at least one month after any procedure for removing a stone.
The NSAID diclofenac (100mg per rectum is easiest) is generally very effective and widely used, but care should be taken to avoid repeated use in elderly patients, or in patients with pre-existing renal impairment (especially if they are also taking an ACE inhibitor), and in those who have become dehydrated as a result of nausea and vomiting. Pethidine can be used to supplement diclofenac if pain relief is not adequate.
The majority of patients (>90 per cent) will have dipstick-positive microscopic or macroscopic haematuria. If there is no dipstick haematuria, a non-urological cause of the pain is much more likely.
Direct referral to a urologist can be made in cases that are strongly suggestive of renal colic. Although a stone in the region of a kidney, bladder or ureter might be visible on a plain abdominal X-ray (a KUB), some stones are lucent and not all calcific densities may be renal tract stones.
A renal ultrasound scan is prone to false negatives in the kidney and is not a good method for localising a stone in the ureter, as it provides no dynamic information, and the presence or absence of a dilated renal pelvis does not (confidently) predict an obstructed system, as even a non-dilated system can be obstructed. So the diagnosis should be confirmed by an intravenous urogram (IVU) or a non-contrast CT scan. The injection of intravenous contrast does carry a small risk of an adverse reaction.
CT scans have the advantage of not requiring intravenous contrast and they can also detect radio-lucent stones composed of urate or cystine, and can demonstrate non-urological pathology in the abdomen or pelvis.
The management of renal colic depends on symptoms, the size and site of a stone, the level of any obstruction and evidence of urine infection (including fever and rigors). Note that leucocyte positivity on dipstick testing can be misleading in patients with a history of recurrent stones, persisting stone fragments or with nephrocalcinosis, and so culture confirmation is needed before longer-term antibiotics can be prescribed.
Emergency intervention is required to relieve obstruction in the presence of infection or kidney function can be permanently lost. Either a percutaneous nephrostomy tube is inserted directly through the kidney into the renal pelvis under local anaesthesia, or a JJ stent is inserted up the ureter via a cystoscope under general anaesthesia.
Both before and following these procedures, patients are given intravenous antibiotics (once blood and urine cultures are taken), and these may be continued for up to two weeks if there has been a temperature spike. Stones measuring <4mm in="" diameter="" have="" a="">95 per cent chance of passing spontaneously. Between 4-6mm the likelihood of spontaneous passage is down to about 50 per cent, and with stones >6mm it is <10 per="" cent.="" a="" conservative="" approach="" is="" therefore="" common="" in="" the="" presence="" of="" a="" small="" stone,="" as="" long="" as="" pain="" relief="" is="" adequate="" and="" there="" are="" no="" signs="" of="">10>
Extracorporeal shockwave lithotripsy
ESWL can be used to shatter a stone in the kidney or ureter. It is an outpatient procedure and usually requires only a rectal suppository of diclofenac, further oral analgesia, or occasionally an intramuscular injection of pethidine.
Different types of lithotripters exist, but they all produce shockwaves external to the patient that can be focused on the stone and use a USS or X-ray to localise the stone and bring it into the shockwave focus, either by moving the shockwave generator itself or the supporting table and patient.
Renal stones up to 25mm in diameter can be treated successfully by ESWL. The stone is broken into smaller fragments, which then pass down the ureter and into the bladder. The larger the stone, the more likely it is that fragments will get stuck in the ureter, causing obstruction and severe pain.
Overall, the rate of stone clearance by ESWL is around 90 per cent, but clearance rates vary between <60 per="" cent="" for="" lower="" pole="" stones="" and="">90 per cent for upper pole stones, depending on the anatomy of the pelvi-calyceal system.
Types and causes of renal stone disease
The salts and acids that make up kidney stones do so because of their relative insolubility in urine. Stones are generally a mixture, but the most common component is usually the most insoluble: calcium oxalate. Once formed, it is almost impossible to re-dissolve. Its solubility is independent of urine pH over the normal range.
In contrast, the solubilities of other common stone constituents such as cystine, uric acid, calcium phosphate and magnesium ammonium phosphate, do depend on urine pH and are potentially more amenable to treatment.
When pure, these stones are lucent on plain X-ray. There is often an important dietary component and patients may be glucose intolerant, hyperlipidaemic and hypertensive,
ie stone disease is increasingly part of the panoply of cardiovascular risk.
Dietary advice is important to limit meat protein, including white meat and fish intake, in order to make the urine less acidic (pH ~5), as urate precipitates at low pH (<5.4), but="" is="" soluble="" at="" more="" alkaline="" ph="" (ph="">6.2).
Dietary sodium tends to parallel meat consumption and tends to promote urinary calcium excretion.
These can be the most difficult to manage and will recur, often rapidly, so careful and regular follow-up is essential. They are the result of cystinuria (to be distinguished from cystinosis), in which there is a high urinary cystine content due to an inherited defect.
At high urinary concentration and low urine pH cysteine molecules combine to form the insoluble cystine. Therapy is difficult, but must include a high fluid intake, particularly at the end the day, because of the normal overnight rise in urine concentration and fall in urine pH.
These occur in the setting of hyperoxaluria, which is often found in patients with the most common form of calcium stones, calcium oxalate, and can be diet-related. Calcium oxalate precipitation, is relatively pH-insensitive and depends primarily on the presence and amount of oxalate in the urine.
Hyperoxaluria can result from chronic inflammatory bowel disease or surgical resection of the bowel, leading to steatorrhoea and calcium binding to fat rather than oxalate. Indeed, restricting dietary calcium will increase intestinal oxalate absorption and the risk of calcium oxalate stones, and is no longer recommended.
Renal tubular acidosis and stones
The form most commonly associated with nephrocalcinosis and renal stones is known as distal or 'classical' (type I) renal tubular acidosis (dRTA). This can be primary and inherited, or secondary to autoimmune diseases such as Sjgren's syndrome, or to micro-anatomical defects, such as medullary sponge kidney.
Potassium supplements can boost citrate excretion. The patients may also be hypercalciuric so a thiazide diuretic may be tried (bendrofluazide 10mg/day).
For most cases, all that can be offered is close monitoring and regular follow-up to identify and deal
pre-emptively with any new or enlarging stones.
In patients with chronic urinary tract infection, especially if the urinary tract is infected by a urea-splitting, ammonia-producing micro-organism such as Proteus, large struvite stones will occur. These are made up of magnesium ammonium phosphate, and precipitate at urine pH >7.0, which is typical of infected urine, and often form staghorn casts of the renal pelvis and upper ureter.
These can be extremely difficult to eradicate by antibiotics alone, unless all infected stone material is successfully removed at surgery.
Non-infected, ammonium-rich stones can be due to chronic diuretic or laxative abuse, and eating disorders. Chronic potassium deficiency stimulates renal ammonium production and urinary excretion; magnesium is lost, which is a urinary stone inhibitor. Both magnesium ammonium phosphate and calcium phosphate stones will re-dissolve at pH <>
Calcium excretion is an obvious and important risk factor. The causes are, together or separately, increased intestinal absorption, increased bone resorption and renal leak of calcium. In most cases the actual cause is never clearly defined, and so it is often called idiopathic hypercalciuria.
Thiazide diuretics reduce calcium excretion but can increase uric acid and glucose and decrease potassium levels. Use of bisphosphonates is less well tried and tested.
Robert Unwin professor of nephrology and physiology, Royal Free and University College Medical School, London
Giovambattista Capasso professor of nephrology, second university of Naples
William Robertson clinical scientist and head of urinary stone management
Simon Choong consultant urologist and director of the stone unit, Royal Free and University College Medical School, London5.4),>60>4mm>