Renal stone

- flank pain, hematuria, pyelonephritis, previous stone passage.
- costovertebral tenderness
- red cells in urine
- stone visualized on urography, ultrasonography, or spiral CT scan.

If the stone acutely obstructs the ureteropelvic junction or a calix, moderate to severe Renal pain will be noted, often accompanied by nausea, vomiting, and ileus. Hematuria is common. Staghorn calculi which may form a cast of all calices and the pelvis. Symptoms of infection , if present, will be exacerbated.
Laboratory:
Leukocytosis is to be expected. Urinalysis may reveal red and white blood cells and bacteria. A pH of 7,6 or higher implies the presence of urea-splitting organisms. A pH below 5,5 is compatible with the formation of uric acid or cystine stones. If the pH is fixed between 6 and 7, Renal tubular acidosis should be considered as a cause of nephrocalcinosis. A 24 hours urine collection for calcium may reveal hypercalciuria, which occurs with hyperparathyroidism and idiopathic hypercalciuria.
Imaging:
90% of calculi are radiopaque: calcium, cystine.
Nonopaque stone will be seen as radiolucent defect in the opaque contrast media.
Stone analysis:
Stone chemical composition should be analyzed.
Treatment:
- a high fluid intake 3-4L/d
specific:
* calcium stone formers, stop vitamin D suplements.
* oral orthophosphates are effective in decreasing urine calcium and increasing inhibitor activity
* thiazide diuretics, decreasing the calcium/oxalate content in urine by 50%.
* antibiotics
* percutaneous nephrostomy and percutaneous nephrolithotomy
* pulverization by means of ultrasonic, electrohydraulic, or laser probes passed through the nephrostomy tract may also be useful.
* residual infection stones may be dissolved by percutaneous irrigation with hemiacidrin
* extracorporeal shock wave lithotripsy/ eswl
* open surgical removal of stones