Kidney stones, also called renal calculi, are solid concretions (crystal aggregations) of dissolved minerals in urine; calculi typically form inside the kidneys or bladder. The terms nephrolithiasis and urolithiasis refer to the presence of calculi in the kidneys and urinary tract, respectively.
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.
Renal calculi can vary in size from as small as grains of sand to as large as a golf ball.
Most calculi originate within the kidney and proceed distally, creating various degrees of urinary obstruction as they become lodged in narrow areas, including the ureteropelvic junction, pelvic brim, and ureterovesical junction. Location and quality of pain are related to position of the stone within the urinary tract. Severity of pain is related to the degree of obstruction, presence of ureteral spasm, and presence of any associated infection.
- Hyperexcretion of relatively insoluble rinary constituents such as oxalates, calcium, uric acid, cystine and certain drugs (such as magnesium trisilicate in the treatment of peptic ulcer).
- 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.
- ALTERED URINARY CRYSTALLOIDS AND COLLOIDS.
- 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.
- DECREASED URINARY OUTPUT OF CITRATE.
- VITAMIN A DEFICIENCY.
- The desquamated cells form nidus for stone formation. This is more applicable to bladder stones.
- URINARY INFECTION.
- 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.
- 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.
- Prolonged immobilisation.
- NIDUS OF STONE FORMATION.
ENVIRONMENTAL AND DIETARY FACTORS
- Low urine volumes.
- High ambient temperatures.
- Low fluid intake.
- High protein intake.
- High sodium.
- Low calcium.
- High sodium excretion.
- High oxalate excretion.
- High urate excretion.
- Low citrate excretion.
OTHER MEDICAL CONDITIONS
- Hypercalcemia of any cause
- Ileal disease or resection (leading to increased oxalate absorption and urinary excretion)
- Renal tubular acidosis type I
CONGENITAL AND INHERITED CONDITIONS
- Familial hypercalciuria
- Medullary sponge kidney
- Renal tubular acidosis type I
- Primary hyperoxaluria
Types of renal calculi
Basically the renal stones can be divided into two major groups
- Primary stones
- Secondary stones.
They appear in apparently healthy urinary tract without any antecedent inflammation.
· Calcium oxalate.
- Uric acid calculi.
- Cystine calculi.
- Xanthine calculi.
- Indigo calculi.
They are usually formed as the result of inflammation.
- Triple phosphate calculus.
- Mixed stones.
· Colicky pain: “loin to groin”. Often described as “the worst pain […] ever experienced”.
· Hematuria: blood in the urine, due to minor damage to inside wall of kidney, ureter and/or urethra.
· Pyuria: pus (white blood cells) in the urine.
· Dysuria: burning on urination when passing stones (rare). More typical of infection.
· Oliguria: reduced urinary volume caused by obstruction of the bladder or urethra by stone, or extremely rarely, simultaneous obstruction of both ureters by a stone.
· Abdominal distension.
· Nausea/vomiting: embryological link with intestine – stimulates the vomiting center.
· Fever and chills.
· Postrenal azotemia: when kidney stone blocks ureter.
· frequency in micturation: Defined as an increase in number of voids per day (>than 5 times), but not an increase of total urine output per day (2500 ml). That would be called polyuria.
· loss of appetite.
· loss of weight.
- Blood examination.
- Straight X-ray.
- Excretory urogram.
- Computed tomography.
- Renal Scan.
- Stone analysis.
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.
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.