Renal stone or calculus or lithiasis is one of the most common diseases of the urinary tract. It occurs more frequently in men than in women and in whites than in blacks. It is rare in children. It shows a familial predisposition.

                       Urinary calculus is a stone-like body composed of urinary salts bound together by a colloid matrix of organic materials. It consists of a nucleus around which concentric layers of urinary salts are deposited.



(1)         Hyperexcretion of relatively insoluble urinary constituents such as oxalates, calcium, uric acid, cystine and certain drugs (such as magnesium trisilicate in the treatment of peptic ulcer).

(2)         Physiological changes in urine such as Urinary pH (which is influenced by diet and medicines), Colloid content, Decreased concentration of crystalloids, Urinary magnesium/calcium ratio.


        Either there is an increase in the crystalloid level or a fall in the colloid level, urinary stones may be formed.

        If there is any modification of the colloids e. g. they lose their solvent action or adhesive property, urinary stones may develop.



        The desquamated cells form nidus for stone formation. This is more applicable to bladder stones.


        Infection disturbs the colloid content of the urine, also causes abnormality in the colloids (which may cause the crystalloid to be precipitated).

        Infection also changes urinary pH and also causes increase in concentration of crystalloids.

(7)         URINARY STASIS

        It causes a shift of the pH of the urine to the alkaline side, predisposes urinary infection, and allows the crystalloids to precipitate.


        Due to overproduction of parathormone the bones become decalcified and calcium concentration in the urine is increased. This extra calcium may be deposited in the renal tubules or in the pelvis to form renal calculus.

(9)         Prolonged immobilisation










(a)         Low urine volumes

(b)        High ambient temperatures

(c)         Low fluid intake

(d)        Diet

(e)         High protein intake

(f)           High sodium

(g)        Low calcium

(h)        High sodium excretion

(i)           High oxalate excretion

(j)           High urate excretion

(k)         Low citrate excretion


(a)         Hypercalcemia of any cause

(b)        Ileal disease or resection (leading to increased oxalate absorption and urinary excretion)

(c)         Renal tubular acidosis type I



(a)         Familial hypercalciuria

(b)        Medullary sponge kidney

(c)         Cystinuria

(d)        Renal tubular acidosis type I

Primary hyperoxaluria


Types of renal calculi

      Basically the renal stones can be divided into two major groups

I. Primary stones

II. Secondary stones.


            They appear in apparently healthy urinary tract without any antecedent inflammation.

(a)   Calcium oxalate

(b)  Uric acid calculi

(c)   Cystine calculi

(d)  Xanthine calculi

(e)   Indigo calculi


            They are usually formed as the result of inflammation.

(a)   Triple phosphate calculus

(b)  Mixed stones


The size and position of the stone usually govern the development of secondary pathologic changes in the urinary tract.


(a)   Obstruction.

(b)  Infection

(c)   The epithelium of the pelvis and calyces in relation to the stone gradually loses lustre, becomes rough and thickened. Parenchymal ischaemia may be caused by local pressure due to stone.

(d)  Metaplasia


(a)   Compensatory hypertrophy

(b)  Stone formation may be bilateral

(c)   Infection of the opposite kidney

(d)  Calculus anuria



(a)   Quiescent calculus

(b)  Pain

        Fixed renal pain

        Ureteric colic

        Referred pain

(c)   Hydronephrosis (a lump in the loin and a dull ache)

(d)  Haematuria

(e)   Pyuria




                                    The usual distribution of renal pain



(a)   Tenderness at the 'renal angle' posteriorly.

(b)  Muscle rigidity over the kidney

(c)   Swelling in the flank when there is hydronephrosis or pyonephrosis associated with renal calculus.

(d)  Abdominal distension and diminished peristalsis may accompany ureteric colic.

SPECIAL Investigations

(a)   Blood examination

(b)  Urinalysis

(c)   Radiography

        Straight X-ray

        Excretory urogram

(d)  Ultrasonography

(e)   Computed tomography

(f)     Renal Scan

(g)  Cystoscopy

(h)  stone analysis


Recurrence may be classified into two varieties

(a)   False recurrence which means a tiny stone was overlooked at the time of operation.

(b)  True recurrence. The various measures which should be adopted to prevent such recurrence are divided into two categories - (i) General measures and (ii) Specific measures.


General measures.

The general measures or advises which should be given to the patient regardless of the type of stone are:

      Fluid intake should he high at all times. Fluids should be taken at bed time so that nocturia will occur. This will prevent dehydration.

      Avoidance of milk, cheese and great deal of calcium should be advised. If renal function is satisfactory, sodium cellulose phosphate 5 g T.D.S. with meals should be prescribed to reduce calcium absorption.

      Urine should be kept acid all the time. Alkalies should be prohibited or used in lesser quantities in those patients who are suffering from peptic ulcer.

      Vitamin D should be stopped or used in very low quantity.

      Patients with hyperuricemia should avoid red meats, offal and fish, which are rich in purines, and should receive treatment with allopurinol.

      Eggs, meat and fish are high in sulphur containing proteins and should be restricted in patients with cystinuria.

The following investigations are appropriate in bilateral and recurrent stone formers:

  • Serum calcium, measured fasting on three occasions to exclude hyperparathyroidism
  • Serum uric acid
  • Urinary urate, calcium and phosphate in a 24 hour collection. The urine should also be screened for cystine.
  • Analysis of any stone passed.

Specific measures.

(A) Calcium stone disease

   (a) Non-idiopathic Calcium stone disease

         Specific treatmcnt of metabolic defect in calcium (e.g. hyperparathyroidism, increased vitamin D, sarcoidosis) or oxalate (primary hyperoxaluria or acquired disease secondary to enteric disorder).

   (b) Idiopathic Calcium stone disease

        Low urinary volume, hypercalciuria, hyperoxaluria, hyperuricosuria .and hypocitraturia and low urinary magnesium are all responsible for stone formation.

        Fluid intake

         A low urinary volume will increase the risk of crystal formation. The aim should be to maintain the urine volume at least a minimum of 1.5 to 2 litres/day.


         Western diet with increased intake of animal protein and carbohydrate is associated with increased urinary calcium, oxalate, phosphate and hypocitraturia compared with controls and thus represents a potent risk of stone formation. So patients should be advised to restrict this type of diet.

         Dietary intake of calcium should also be restricted. However it has been shown that calcium binds oxalate in the gut preventing its uptake, so low calcium intake will increase the amount of oxalate available for absorption creating an increased risk of oxalate crystallisation. So in mild hyperoxaluria, a high calcium diet is required, together with a diet avoiding oxalate-rich foods (e.g. tea and chocholate).

         A mega dose of vitamin C should be avoided.

         No excess stone risk has been shown related to dietary intake of sodium, sucrose or cola.

        Indomethacin 20 mg T.D.S. has been found to reduce calcium secretion. This may help in preventing further stone formation.

(B) Infection stones

        Infection stones consist of magnesium ammonium phosphate (Struvite) with varying admixtures of calcium phosphate (apatite).

        In general, Struvite stones may partially dissolve in the presence of sterile urine, so long term low-dose treatment with antibiotics is appropriate even when urine culture is initially sterile.

(C) Oxalate stones

        Foods high in oxalate should be eliminated from the diet. These are strawberrys, plums, spinach, asparagus etc. These may be used in low quantities or with milk or cream, in which case the oxalates are precipitated as insoluble calcium salts in the intestine and are not absorbed.

        Pyridoxine in large doses may be helpful.

        Thiazides are useful agents which decrease both urinary calcium and oxalate.

(D) Phosphate calculi

        Phosphates in the diet should also be restricted.

        Aluminium gel 40 ml T.D.S. and at bed time is also very useful to prevent the recurrence of phosphate calculi.

(E) Uric acid calculi

        A low-purine diet should be prescribed for the uric acid stone former. Red meat, fish and liver are rich in purine.

(F) Cystine calculi

        Sulphur containing proteins such as meat, fish and eggs should be restricted.

        Carbohydrates and fats may be increased in the diet along with low sulphur content proteins.

        Intake of fluids must be increased to dilute cystine in the urine.

        Fluid must be taken at night just before going to bed.

        Urine should be kept alkaline.

        Penicillamine may be prescribed to prevent recurrence of cystine calculi. This usually reduces the amount of cystine in the urine.

        Pyridoxine 50 mg daily should also be given. This not only ceases stone formation but it may also dissolve some stones.