Medical Aspects of Renal Stones

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1 REVIEW ARTICLE JIACM 2008; 9(4): Medical Aspects of Renal Stones KK Malhotra Abstract There is a high prevalence of renal stones in the general population. Renal stone disease happens to be one of the major causes of chronic kidney disease and chronic renal failure. Investigations of renal stone patients should be carried out with the aim of finding the composition of renal stones, cause of stone formation, functional status of kidneys, presence/absence of obstruction in the urinary tract. Calcium calculi are most frequent type of stones occurring in 70-88% of cases. Lesser in frequency are struvite stones (6-20%), and uric acid stones (6-17%. Important clinical states associated with calcium stones are idiopathic hypercalciuria, primary hyperparathyroidism, hyperuricosuria, renal tubular acidosis, hypocitraturia, and hyperoxaluria. Medical treatment should be based on specific clinical disease of patients and observed metabolic abnormalities. Medical prophylaxis is effective in up to 80% of patients with recurrent stones. Introduction There is a high prevalence of renal stones in the general population. It has been estimated that about 5% of American women and 12% of men develop kidney stones sometime in their life 1. The figures for India are not known. Renal stones happen to be one of the major causes of chronic kidney disease and chronic renal failure. The disease is neglected many-a-times by the patients. They visit doctors mostly at the time of acute episodes; subsequent follow-up and long-term management is mostly inadequate. Pathogenesis of renal stones broader view There are two basic aspects in the pathogenesis of renal stones:- a) Increased urinary excretion of stone forming elements like calcium, phosphorus, uric acid, oxalate, and cystine; b) Physio-chemical changes which influence stone formation like ph of urine, stone matrix, and protective substances in the urine. For a stone to form within the urinary tract, urine must be supersaturated for precipitating crystalline component. Thus, a major consideration is the state of saturation within the urine. Solute load is important, but since urine is a complex solution, other factors influence saturation. These include ionic strength, complexation, and ph. Normally urine has presence of inorganic and organic substances which inhibit crystallisation of elements which lead to stone formation. These agents can modify nucleation, crystallisation, and aggregation (Table I) 2. ph of the urine can also influence stone formation. Table I: Renal stones - crystallisation inhibitors in urine 2. Nucleation Growth Aggregation Citrate No Yes Yes Glycosaminoglycans Yes Yes Yes Tamm-horsfall protein No No Yes Uropontin Yes Yes Yes Nephrocalcin Yes Yes Yes Calgranulin? Yes Yes Uronic acid rich protein Yes Yes? Investigations in renal calculus disease It is important to investigate the aetiology in patients with renal stones. This helps understand the life history of this disease and its management. The main objectives in investigation are to find out the composition of stones, cause of stone formation, functional status of kidney, presence/absence of obstruction in urinary tract, and evidence of possible urinary infection. Imaging The initial investigation in renal stone is to document the presence of stone. This is best done by various imaging techniques. Plain X-ray of abdomen (KUB) is the usual test done in evaluating such patients. More than 90% of renal calculi are sufficiently radio-opaque to be detected. However, radioluscent and small stones are * Senior Consultant, Department of Nephrology, Pushpawati Singhania Research Institute, Press Enclave Marg, Sheikh Sarai-II, New Delhi

2 missed in a considerable number of patients. Ultrasonography is a simple technique and is widely available these days. This is a non-invasive investigation; however, it is operator dependent and its sensitivity is similar to KUB. Intravenous urography is the standard investigation for evaluating obstruction in patients with renal stones. It provides good structural and functional information and detects radioluscent stones. This investigation is however, more expensive and requires administration of a dye. CT scan of kidneys is a new approach for evaluating suspected renal and ureteric calculi. It is superior to radiography and ultrasonograpy but is more costly. Radionuclide studies of the kidney with DTPA (diethylenetriamine pentaacetic acid) renal scan are helpful in assessing patients of obstructive nephropathy with deranged renal functions and in deciding about surgical management of such cases. MRI gives a good localisation of stones but is fairly expensive and is not a popular investigation with clinicians. Urine analysis and urine culture Urine analysis is a simple and helpful investigation in evaluation of renal stones. It may show crystals, red blood cells, and/or pus cells in urine. Glycosuria may be found in suspected/diagnosed cases of diabetes. Urine culture should be done during the initial evaluation and subsequent treatment. Stone analysis It is important to know the chemical composition of urinary stone to understand the aetiology and plan appropriate treatment. Chemical analysis of stones is a simple test but is not an accurate method. Better methods are optical crystallography, and X-ray diffraction/infrared spectroscopy. The frequency of types of kidney stones by analysis is shown in Table II 2. Chemical analysis of urinary stones reported in Indian series have demonstrated a very high incidence of calcium oxalate 3. X-ray diffraction studies of upper urinary calculi done recently in Northern India have shown that calcium oxalate monohydrate is the predominant stone in the studied population. These stones are hard to break and seem to have a different metabolic origin from those consisting of calcium oxalate dihydrate 4. Table II: Types of kidney stones by analysis 2. Type of stone Frequency (%) Risk factors Calcium Oxalate Hypercalciuria, hyperoxaluria, hyperuricosuria, hypocitraturia, hypomagnesuria, low urine volume Phosphate 6-20 Primary hyperparathyroidism, (brushite-calh[po 4 ], RTA Milk alkali syndrome 2H 2 O, Apatite-Ca 5 (PO 4 ) 3. OH) Mixed Non-calcium MgNH 4 PO 4 6H 2 O(struvite) 6-20 Urinary tract infection with and Ca10 [PO 4 ] 6.CO3 urease producing bacteria (Carbonate apatite) Uric acid 6-17 Gout, hyperuricaemia, chronic diarrhoea, low urine ph Cystine Cystinuria Miscellaneous 1-4 Biochemical investigations There are some biochemical investigations which should be done in all patients of renal calculi. These are serum calcium, phosphorus, uric acid, and renal function tests. In patients having special problems like recurrent stone formation, positive family history, and presence of risk factors for stone formation, additional studies are needed. These are 24-hour urine for calcium, phosphorus, uric acid, oxalate, citrate, and cystine. Investigations for special clinical situations like hyperparathyroidism, gout, renal tubular acidosis should also be included. The cause of renal stones can be found in 80-90% of cases with detailed metabolic and biochemical investigations 5. An aetiological study of nephrolithiasis in north Indian children have shown that an underlying metabolic disorder can be demonstrated in about 50% of such children 6. One should try to distinguish between metabolic active or inactive stones by clinical and laboratory investigations. Metabolic active stones are those that have been formed within the past year, grown on X-ray within the past year, or resulted in passage of documented gravel. Otherwise, they are considered metabolically inactive. Metabolically active stone should undergo detailed metabolic investigations. This helps in proper management of such Journal, Indian Academy of Clinical Medicine Vol. 9, No. 4 October-December,

3 patients and prevent recurrence of disease. Medical prophylaxis is cost-effective in patients with metabolic active stone disease. Calcium calculi, hypercalciuria Hypercalciuria is a fairly common abnormality in patients of urinary calculus disease. This can result from various mechanisms: a) Absorptive hypercalciuria There is increased absorption of calcium from the gut resulting in increased circulating calcium and causing increased renal filtered load. Its exact mechanism is unknown but seems to be inherited in an autosomal dominant fashion; b) Renal hypercalciuria There is increased excretion of calcium in the urine resulting from impaired tubular absorption of calcium; c) Resorptive hypercalciuria In this condition there is increased resorption of bone. The classical example is primary hyperparathyroidism. Conditions associated with hypercalciuria and calcium stones Primary hyperparathyroidism In primary hyperparathyroidism one sees calcium phospate stones as well as calcium oxalate stones and a mixture of the two. Recent estimates of prevalence of stones among patients of hyperparathyroidism average around 20 per cent. Hypercalciuria and hypercalcaemia are screening tests for this condition. Diagnosis can be confirmed by intact PTH assays. Ultrasound, CT scanning, MRI, and nuclear imaging studies have all been done to identify the likely site of PTH secretion. Bone disease and peptic ulcer are frequent clinical associations. Therapy for primary hyperparathyroidism is surgical removal of the hyperplastic gland. The appropriateness of surgery increases in patients with recurrent stones, diminished bone density, and more elevated serum calcium concentrations. Idiopathic hypercalciuria This condition needs special mention in renal stone disease. It is characterised by excretion of more than 300 mg of calcium in urine/day in presence of normal serum calcium. The diagnosis requires exclusion of other causes of normocalcaemic hypercalciuria; these are sarcoidosis, renal tubular acidosis, hyperthyroidism, malignant tumours, immobilisation, and Paget s disease. The exact pathogenesis of the condition is not understood. It is currently thought that there may be increased intestinal absorption of calcium due to increased levels of calciferol and decreased tubular absorption of calcium. It is being considered that the above pathophysiological changes are due to a genetic defect 7. Additional studies are however, needed to further clarify the precise role of kidney, intestine, bone, PTH, and calciferol in the pathogenesis. The treatment advocated comprises of a low calcium diet, use of cellulose phosphate which reduces absorption of calcium from intestine, and thiazide diuretics which reduce excretion of calcium by tubules. Hyperuricosuria About 25% patients of calcium renal stones have hyperuricosuria. Seed crystals of sodium hydrogen urate/ uric acid initiate calcium oxalate precipitation from a metastable solution. Reduction of new stone formation during allopurinol administration is the most compelling evidence for a role of hyperuricosuria in calcium oxalate stone disease 8. Renal tubular acidosis Stones in renal tubular acidosis result from a combination of hypercalciuria, hypocitraturia, and alkaline urine. Most stones in this condition are composed of calcium phosphate. Supplemental alkali in the form of potassium citrate is required to correct the metabolic acidosis and hypocalaemia. Doses for adults should range between 1-3 meq of alkali/kg body weight. Hypocitraturia This is found in 22-28% of cases. Levels of citrate are less than 500 mg/day in males and less than 350 mg/day in females in this condition. It may occur as an isolated abnormality, or be associated with some other stone risk factors such as hypercalciuria. The mechanism of stone formation involves binding of calcium in the urine resulting in lower supersaturation of calcium salts. In addition, citrate has a direct inhibitory effect on crystallisation of calcium salts. Treatment lies in correction of the underlying disorder that reduces citrate such as acidosis or hypocalcaemia. 284 Journal, Indian Academy of Clinical Medicine Vol. 9, No. 4 October-December, 2008

4 Hyperoxaluria This is defined as urinary excretion of oxalate in excess of 45 mg/day. On the basis of the mechanism it is classified as follows: (a) Enteric hyperoxaluria this results from increased intestinal absorption due to ileal disease or short bowel syndrome. A study from North India has shown that absence of Oxalobacter formigenes can lead to significant risk of absorptive hyperoxaluria and resultant oxalate stone episode 9 ; (b) Increased ingestion (oxalate gluttons) - Increased ingestion of certain food stuffs like spinach, rhubarb, beets, chocolate, nuts, strawberry, and soya foods are known to increase urinary oxalate concentration; (c) Primary hyperoxaluria This is an inborn error of metabolism. Uric acid stones They account for 5-10% of all renal stones. They are more frequent in gouty patients. In a study of gouty patients, Malhotra et al 10 found renal calculi in 66% of their cases. The chances of stone formation increase with increasing serum uric acid levels and urine excretion rates. The management of uric acid stone involves treatment with low protein/purine diet, large amount of fluids (more than 3 l/day), and alkalisation of urine. Allopurinol should be used if stones recur despite fluid and alkalies, and when uric acid excretion is above 1,000 mg/day, or if patients have gout. Cystine stones Cystinuria is a hereditary disorder of amino acid transport involving the intestinal epithelia and renal tubule cells. As a result of renal tubular transport disorder, abnormally large amounts of cystine are excreted in urine. The solubility of cystine in urine is approximately 300 mg/l. Renal stones begin to form from the first to fourth decade. Calculi tend to occur as staghorns or as multiple and bilateral separate stones and are visible on X-ray because of the density of the sulphur in the cystine molecule. Lowering urinary cystine concentration by increasing urine volume reduces the likelihood of precipitation and forms one of the basis of treatment. Dietary restriction of methionine has also been recommended. Pharmacological therapy is required when patients fail to respond to diet, fluid, and alkali therapy. Drug therapy increases cystine solubility by creating a thiol-cystine disulphide which is more soluble than cystine. These thiolcontaining drugs may also reduce cystine excretion in addition to increasing cystine solubility. D-penicillamine and tiopronin are the most commonly used drugs but they have significant side-effects. Captopril, a thiol, has been reported to reduce stone formation with cystinuria and is well-tolerated. Treatment of large cystine stones can be difficult. The stones are difficult to fragment by extracorporeal shock wave lithotripsy and percutaneous lithotripsy. Struvite stones Struvite (MgNH 4 PO 4.6H 2 O) stones form in the renal pelvis and calyces only when the urinary tract is infected by a urea-splitting bacteria, usually proteus species. Struvite stones tend to branch and enlarge, and their growth is rapid. Often, they fill the renal collecting systems and assume a staghorn configuration. Kidneys are often damaged by obstruction and infection. The preferred treatment of struvite staghorn stone is surgical removal. Untreated calculi ultimately require nephrectomy in 50% of cases. Medical treatment Medical treatment should be based on the specific clinical condition in a given patient as also the observed metabolic abnormalities. These have been discussed under individual stone headings. Medical prophylaxis is effective in upto 80% of patients with recurrent stones. Prospective clinical trials lasting for more than 3 years have shown that selective treatments have a distinctive benefit for idiopathic calcium oxalate stones 11. Three prospective trials of potassium citrate salts have been performed and it has shown fewer recurrences of stones as compared to controls. Thiazide diuretics have shown therapeutic benefit in treating stone recurrence. Diet has long been thought to be an important risk factor for stones. Excessive intake of animal protein, salt, oxalate, and calcium have all been implicated by epidemiological or pathophysiological studies as possible contributors to calcium stone formation 12. There is however, notable lack of prospective trials of dietary manipulations in such patients. The existing data has failed to show any Journal, Indian Academy of Clinical Medicine Vol. 9, No. 4 October-December,

5 convincing results with diet therapy. References 1. Coe FL, Evan A, Worcester E. Kidney stone disease. J Clin Invest 2005; 115: Agarwal AK. Urinary Stones. Ed. Mandal AK. In: Textbook of Nephrology for the Asian-Pacific Physician. New Delhi. Jaypee Brothers Medical Publisher, 2004; 2nd edition: Malhotra KK, Ahuja MMS, Singh SM, Bapna BC. A correlative study of urinary calculus disease. Ind Jr Med Sci 1968; 22: Ahlawat R, Goel MC, Elhence A. Upper urinary tract stone analysis using X-ray diffraction: results from a tertiary referral centre in Northern India. Urol Res 2001; 29: Pak CYC, Resnik MI. Medical therapy and new approaches to management of urolithiasis. Urol Clin North Am 2000; 27: Hari P, Bagga A, Vasudev V, Singh M, Srivastava RN. Aetiology of nephrolithiasis in Northern Indian children. Pediatr Nephrol 1995; 9: Coe FL, Parks JH, Moore ES. Familial idiopathic hypercalciuria. N Engl J Med 1979; 300: Coe FL, Raisen L. Allopurinol treatment of uric acid disorders in calcium stone formers. Lancet 1973; 1: Kumar R, Mukherjee M, Bhandari M et al. Role of Oxalobacter formigenes in calcium oxalate stone disease. A study from North India. Eur Urol 2002; 41: Malhotra KK, Kathpalia SC, Goulatia RK. Urolithiasis and Nephropathy in Gout. J Assoc Phys India 1973; 21: Barcelo P, Wuhl O, Servitage E et al. Randomised doubleblind study of potassium citrate in idiopathic hypocitraturic calcium nephrolithiasis. J Urol 1993; 150: Borghi L et al. Comparison of two diets for the prevention of recurrent stones in idiopathic hypercalciuria. N Eng J Med 2002; 346: Telma 286 Journal, Indian Academy of Clinical Medicine Vol. 9, No. 4 October-December, 2008

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