Renal Calculus | Expert Homeopathy

Renal Calculus


Etiology:
Urinary calculus is composed of urinary salts or crystalloids cemented together by colloid substances e.g, mucin and fibrin. The normal urine is super-saturated with urinary salts. They are held in solution by the protective action of the normal colloid & citric acid. When the solute status of the crystalloid is altered, the urinary salts precipitate to form urinary stones. The status of the solute can be disturbed by the following factors:

A] Increase in urinary salts:-
Oxaluria, cystinuria, and hypercalcinuria cases are likely to develop stones. The excessive salts may be due to endogenous breakdown or excessive intake. Therefore cause and disturbed metabolism may be responsible for stone formation.
Hypercalcinuria is secondary to decalcification of boned in parathyroid adenoma. Excessive intake of Vitamin D may lead to urinary stones.

B] High concentration of urine altered urinary solutes and colloids:-
In hot climates, the concentration of solutes will rise due to excessive perspiration. This leads to a relative increase in urinary salts. It has been postulated that any reduction of the urinary colloids which absorb solutes or excess mucoproteins that may chelate calcium predisposes to the formation of an insoluble complex. This is supported by the fact that renal stones are more prevalent in the dry northern states of India.

C] Diminished protective action of colloid or abnormal colloid and citric acid:-
Infection: Infection favors the formation of urinary stones. Both clinical and experimental stone formation is common when urine is infected with urea-splitting streptococcus, staphylococcus, or proteus. The predominant organisms found in the nucleus of urinary calculi are staphylococcus and E. Coli.
Infection disturbs the colloid content of the urine. In urinary infection, abnormal mucin and fibrine are formed which are the cementing substances.
Infection precipitates the earthy salts e.g calcium ammonium and magnesium phosphates by liberating ammonia from urea by urea splitting micro-organisms. This leads to phosphate stone.

Diatetic: Deficiency of Vitamin A perhaps lowers the resistance of renal epithelium and causes desquamation of epithelium. These desquamated cells from the nidus of stone on which salts are deposited. Vitamin A is deficient in the diet of patients with low economic status.

Stasis: Inadequate  urinary drainage causes stasis of free flow of urine and stones are prone to occur:

Prolonged immobilization: From any cause e.g paraplegia, the urinary drainage is inadequate for the neurogenic bladder causing stasis of urine. These patients are prone to have an increased output of calcium in urine due to skeletal decalcification. This combined with the mechanical effects of recumbency on renal drainage favors the formation of Calcium phosphate stones.

Hyperparathyroidism: Although a rare cause but in multiple renal calculi(bilateral) and recurrent calculi. This cause should be accounted for. Hyperparathyroidism produces a large increase in calcium removal in urine. It has been partly remarked that these patients pass their skeleton in urine. A parathyroid adenoma must be removed before the urinary calculi are treated or removed.

Decreased urinary output of citrate: The urinary citrate keeps the relatively insoluble calcium phosphate and carbonate into solution The excretion of citrate is under hormonal control and decreased during menstruation.


Classification of renal stones:
Primary stone: Without any infection i.e, sterile urine and reaction of urine is acid e.t oxalate stone, uric acid stone, urate stone, cystine stone.

Secondary Stone: They have formed secondary to infection of the urine any tract and when the reaction of urine is alkaline e.g, phosphate stone.


Clinical features:
Age: Males between 30 and 50 years of age are a common victim

Sex: M: F=4:3
The symptoms are not stereotype and sometimes the diagnosis remains obscure until a radiological examination is done.

Quiescent calculus/silent stone: A patient with renal calculus or calculi may be symptomless. The patient may report uremia when renal parenchyma has been damaged grossly or secondary infection supervene.

Pain: Pain is the common presenting feature. Fixed renal pain is located in the renal angle and in the upper outer quadrant of the abdomen. It is worse on movement.

Ureteric colic: It is an agonizing pain passing from the loin to groin, commencing on suddenly, causing the patient to draw up his knees and roll about. It often shoots to the testicle in the male or labia majora in females, along the distribution of the genito-crural nerve. The corresponding testis is often drawn up due to the cremasteric reflex. This is often accompanied by vomiting and a lot of sweating. Strangury may occur if the stone is intramural ureter. The pulse quickens and the temperature may be subnormal.

Hematuria: Sometimes the hematuria is the leading only symptom. Hematuria occurs in small amounts during or after an attack of pain. Rarely hematuria may be profuse.

Pyuria: Infection of the kidney is liable to supervene and the number of pus cells in the urine even in absence of infection.

Frequency of micturition: During the attack of pain micturition may be frequent, but a small quantity of urine is passed at a time.


Investigation:
Urine examination:- Reveals pus cells, R.B.C, urinary crystals, and a trace of albumin.

Radiography:-
  • St. Xray K.U.B after proper preparation of bowel with laxatives.
  • U.S.G of K.U.B helpful in the diagnosis of stone, growth, hydronephrosis.
I.V.U ( excretory urogram):- May show a negative shadow due to filling defect in a nonopaque calculus. It is of value in confirming that the opacity is intrarenal in determining in which part of the kidney the stone is situated and also shows the function of the kidneys.

Cystoscopy:- The corresponding ureteric orifice may be congested and blood or hazy urine may be seen coming out from the affected side. The urinary efflux may be absent when the stone blocks the ureter.

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