Nephro Flash Vol-3, No-3, 2017

Renal colic describes the pain arising from obstruction of the ureter, although ureteric colic would be a more accurate term. The pain is caused by spasm of the ureter around the stone, causing obstruction and distension of the ureter, pelvicalyceal 1 system and renal capsule.

Although the most common cause is a stone, the term “renal colic” actually refers to a collection of symptoms attributed to the kidney and ureter. There are other intrinsic or occasionally extrinsic causes such as lymphadenopathy, although extrinsic causes tend to present with milder and more chronic discomfort. Other common intrinsic causes are blood clots (from upper tract bleeding) or sloughed renal papilla (which can occur in sickle cell disease, diabetes, or long term use of 1 analgesics). The underlying cause of acute flank pain is not always a urinary stone and other important conditions can mimic this. A thorough history, examination and investigations are important to 1 determine further management.

Uric acid nephrolithiasis is typically found in individuals with a low urine pH and a normal concentration of urinary uric acid. Patients with a history of gout are at greater risk of forming uric acid stones, as are patients with obesity, diabetes or the complete metabolic syndrome. The unifying renal tubular abnormality of these disorders appears to be the excretion of 1 abnormally acidic urine. Gout is an inflammatory disease characterized by hyperuricemia that leads to acute arthritis with monosodium urate crystal deposition and is associated with 1 uric acid kidney stones. The association between gout and an increased prevalance of uric acid stones appears logical. Clinically gout is caused by an elevated level of serum uric acid that leads to deposition of crystals in the joints and tissues, and intuitively an increase in uric acid excretion. However, this paradigm is not consistent with the observation that approximately 90% of patients with hyperuricemia and gout have a defect in uric acid excretion. Patients with gout form kidney stones due to a persistently low urinary pH, which favours formation of the relatively insoluble 1 uric acid rather than the more soluble urate. Excessively acidic urine is found in patients with complete metabolic syndrome, as well as those with only type 2 diabetes and/or obesity. Renal tubular insulin resistance has been implicated as a causative 1 factor in excretion of overly acidic urine.