Renal Stones (Calculi)

-Some of the chemicals found in urine are able to crystallize, and in a concentrated form, these chemicals can precipitate into a solid deposit attached to the kidney or ureter walls. These crystals can grow through a process of accretion to form a kidney stone.

-They are caused by underlying metabolic conditions such as renal tubular acidosis, Dent's disease, hyperparathyroidism, and medullary sponge kidney. So, patients with recurrent kidney stones should be screened for these disorders (24-hr urine for volume, magnesium, sodium, uric acid, calcium, citrate, oxalate and phosphate). There’s a strong relationship between Crohn's disease and stone formation, too. Also, high protein intake is therefore associated with decreased bone density as well as stones. Protein -> uric acid, the most available alkaline base to balance the acid from protein is calcium phosphate (hydroxyapatite) from the bones (buffering). The kidney filters the liberated calcium which may then crystallize in urine with oxalate (partly from metabolic processes, partly from diet) or phosphate ions, depending on the condition. The acid load is associated with decreased urinary citrate excretion; citrate competes with oxalate for calcium and can thereby prevent stones.

-Many small stones are passed in urine with no symptoms, but if they grow to
sufficient size, they can cause obstruction of the ureter with a subsequent dilation
of the upper ureter and renal pelvis as well as spasm of muscle trying to move the
stone, which can cause severe pain and bleeding (hematuria and pyuria). Patients also produce low amounts of urine (oliguria) due to obstruction of the free flow of urine in the ureters or bladder. Azotemia (of the postrenal type, obviously!) is common too. The BUN:Cr in postrenal azotemia is normal (the increased nephron tubular pressure causes increased reabsorption of BUN, elevating it abnormally relative to creatinine).

-Obtaining the Specimen: Most kidney stones do not require surgery and will pass on their own. Surgery is necessary when the pain is persistent and severe, in renal failure, and kidney infection. It may also be advisable if the stone fails to pass or move after 30 days. Finding a significant stone before it passes into the ureter allows physicians to fragment it surgically before it causes any severe problems. In most of these cases, non-invasive extracorporeal shockwave lithotripsy (ESWL) will be used. Otherwise some form of invasive procedure is required; with approaches including ureteroscopic fragmentation using laser, ultrasonic or mechanical (pneumatic, shockwave) forms of energy. Percutaneous nephrolithotomy or rarely open surgery may ultimately be necessary for large or complicated stones or stones which fail other less invasive attempts at treatment.

-Stones are of different types based on the kind of crystal of which they’re formed. They should be analyzed in the lab for their chemical makeup which will determine treatment choices and preventive measures. Confirmation is achieved through radiological studies (X-Ray, CT scan, ultrasound…) to visualize the stone.

        *Calcium Oxalate: Most stones are of this type (80% of cases). Consumption of low-calcium diets is linked to a higher risk for stones. This is related to the role of calcium in binding ingested oxalate in the GIT. As the amount of calcium intake decreases, the amount of oxalate in the blood available for absorption increases; this oxalate is then excreted in greater amounts into the urine. There, oxalate is a very strong promoter of calcium oxalate precipitation, and even stronger than calcium. Restricting oxalate intake is only helpful in those patients who are absorbing excess oxalate which is a minority of patients as most oxalate excreted in the urine is actually made by the liver. 
     
        *Calcium Phosphate: The second most commonly encountered type of stones. Mostly associated with parahyperthyroidisim and renal tubular acidosis.

        *Uric Acid: 5-10% of cases. Associated with hyperuricosuria (with or without hyperuricemia), and acid/base metabolism disorders in which urine becomes extremely acidic, allowing for uric acid precipitation. The presence of (1) radiolucent stone, (2) persistent acidic urine, and (3) uric acid crystals in fresh samples; support the diagnosis of uric acid urolithiasis.

       *Struvite (Magnesium Ammonium Phosphate): It’s caused by urea-splitting bacteria (i.e. UTIs) that raise urine pH to neutral/alkaline values, allowing struvite to precipitate forming stones.
          
        *Cystine: This is uniquely associated with people suffering from cystinuria (possibly due to Fanconi's syndrome).

        *Drug-Induced Stones: Some drugs have the ability to crystallize as well (e.g. Indinavir, Sulfadiazine, and Triamterene).

-Culture of a urine sample to exclude urine infection (either as a differential cause of the patient's pain, or secondary to the presence of a stone) is always a smart move.