* - URIC ACID STONES VIRTUALLY NEVER DEVELOP UNLESS URINARY PH IS < 5.5. CYSTINE STONE MORE LIKELY IN ACIDIC URINE, CAL PHOSPHATE & STRUVATE STONE ONLY IN ALKALINE URINE, CAL OXLATE IN EITHER URINE PH.
* - SUBSTANCES THAT INCREASE CHANCES OF STONE FORMATION : GRAPE JUICE ( BY 30-50% ), VIT C, HIGH ANIMAL PROTEIN INTAKE, HIGH CALCIUM & SODIUM INTAKE
* - ORANGE JUICE PREVENTS STONE FORMATION
* Systemic illnesses that may increase the risk for kidney stone formation or otherwise affect the clinical course include primary hyperparathyroidism, renal tubular acidosis, cystinuria, gout, diabetes mellitus, inflammatory bowel disease, renal insufficiency, sarcoidosis, and medullary sponge kidney.
Anatomic abnormalities or surgery of the urinary tract that may predispose to or complicate stone formation are presence of horseshoe kidney, previous urinary diversion, obstruction of the ureteropelvic junction, solitary kidney, previous renal or ureteral surgery, previous kidney disease, history of urinary tract infection and/or pyelonephritis, family history of urolithiasis, and previous stone formation.
* A complete drug history is crucial because many medications predispose to urolithiasis. These include carbonic anhydrase inhibitors (topirimate), ephedrine, guaifenesin, calcium with vitamin D, triamterene, indinavir, or sulfadiazine.
Indications for urgent intervention include presence of infection with urinary tract obstruction, often indicated by fever, urosepsis, intractable pain and/or vomiting, impending acute renal failure, obstruction in a solitary or transplanted kidney, and bilateral obstructing stones. Acute obstruction must be treated urgently, for once a stone passes into the ureter, obstruction may cause reduced glomerular filtration rate and renal blood flow.
In a randomized controlled trial, ureteral catheters, ureteral stents, and percutaneous nephrostomy tubes were equally effective for urinary tract decompression. Pending bladder and renal pelvic urine culture and sensitivity, broad spectrum antibiotics should be prescribed initially.
Parenteral narcotics have traditionally been prescribed for acute renal colic, but nonsteroidal anti-inflammatory drugs (NSAIDs), such as ketorolac and diclofenac, are also effective. NSAIDs should be avoided in patients with poor renal function or a history of gastrointestinal bleeding.
Detailed metabolic evaluation should be postponed until after the acute stone event has resolved. Factors suggesting a metabolic cause include family history of urolithiasis; bilateral stone disease; presence of inflammatory bowel disease, chronic diarrhea, or malabsorption; history of bariatric surgery; medical conditions associated with urolithiasis, such as primary hyperparathyroidism, gout, or renal tubular acidosis; nephrocalcinosis; osteoporosis or pathologic skeletal fractures; pediatric urolithiasis; and stones formed from cystine, uric acid, or calcium phosphate.
When a comprehensive metabolic evaluation is indicated, it should include analysis of stone composition, cystine screen, and two 24-hour urine collections for volume, pH, calcium, oxalate, citrate, uric acid, phosphate, sodium, potassium, magnesium, ammonium, chloride, sulfate, and creatinine. Blood tests should include serum calcium, bicarbonate, creatinine, chloride, potassium, magnesium, phosphate, uric acid, and blood urea nitrogen. Cystinuric patients should undergo this evaluation plus 24-hour measurement of cystine, and hypercalcemic patients should also have measurement of intact parathyroid hormone and 1,25 dihydroxyvitamin D.
A relatively recent treatment is medical expulsive therapy or use of drugs to facilitate spontaneous passage of ureteral calculi. These may include calcium channel blockers (nifedipine), steroids, and alpha-adrenergic blockers.
"The rationale for using alpha blockers is based on the presence of large numbers of alpha-1 adrenoceptors in the distal ureter," the authors conclude. "These blockers inhibit basal ureteral tone and peristaltic frequency and decrease the intensity of ureteral contractions."