Please refer the DTPA / EC scan page on this web site for introduction to relevant aspects of structure and function of the urinary system.
DMSA stands for 'dimercaptosuccinic acid'. It is very avidly absorbed by the cells of renal tubules from the surrounding blood vessels. Upon entering these cells, DMSA further binds with proteins within the cells and gets 'trapped'. Very little (~15%) DMSA circulating in the blood filters across the glomerular membrane in healthy kidneys (which is in contrast with DTPA and EC). Also, normally no other organs take up DMSA to any appreciable degree.
Thus, DMSA is very good for imaging the functional cortex of the kidney as there are no distracting signals coming from urine within the kidney.
Before injection, DMSA is combined with radioactive pertechnetate.
In most organs of the human body, a minor injury heals completely and the injured cells are replaced by completely functional cells. However, if the injury at a site is very severe or if the same site sustains multiple minor injuries, some of the dead cells are replaced by non-functional fibrous bands, which are known as 'scar tissue'. E.g., when we have a small and superficial cut on the skin, it heals so well that after a few weeks we can't even recognize the site. In contrast, if the cut is deep, or if the site of skin experiences constant friction, we either develop a visible scar or the skin hardens. While injury to the skin is because of very tangible causes e.g., physical cause (like sharp object or blunt trauma), heat or some kind of chemical, internal organs (like kidneys) are well protected by external agents, but they get 'injured' by infections, toxins or inflammation.
In a large organ, small scars could go unnoticed, and might have no immediate consequence. However, presence of a scar alerts us about the presence of an injuring agent, which if not countered could cause more extensive scarring. Extensive scarring of any organ reduces its function, and as alluded to above, such scar tissue cannot regain normal function.
A ureter is a thin elongated hollow tube that carries urine from kidney to the urinary bladder. The lower most part of the ureter passes through the wall of the urinary bladder to reach into its cavity. The urinary bladder wall largely consists of muscles that continuously squeeze the ureter from outside resulting in a valve-like action that allows for flow of urine in only one direction, i.e., from ureter into the urinary bladder. However, in some cases, this valve like action is weak, and whenever the urinary bladder contracts (e.g., while urinating), because of increased pressure, some urine flows back into the ureter. This abnormal backward / upward (retrograde) flow of urine is known as 'vesicoureteric reflux' (VUR). Although, VUR could be diagnosed in adults, if significant, it is usually diagnosed in childhood itself because of propensity to cause urinary tract infections accompanied by fever ('febrile UTI').
Important structural manifestations or VUR include widening and spring-like appearance (tortuosity) of the ureter, and widening of renal pelvis. In more severe cases, the renal cortex could also become thin. However, all of these manifestations could be because of causes other than VUR.
In presence of VUR (especially severe cases), some portion of urine keeps on shuttling between the urinary bladder and ureter/kidney, which in turn increases the risk of harmful bacteria reaching up to the kidneys and colonizing the cells of renal tubules and their surroundings. The resulting inflammation is called 'pyelonephritis'. Recurrent or long-standing episodes of pyelonephritis cause cortical scarring. In very severe cases of VUR, refluxed urine exerts back pressure on the kidney cortex (not unlike in PUJ obstruction explained in the write up on DTPA scan), which can reduce blood supply and cause uniform damage to the kidney independent of infection and inflammation. The (largely irreversible) damage caused by VUR to the affected kidney is known as 'reflux nephropathy'.
Many cases of VUR resolve spontaneously with increasing age (say, typically by the age of 5 years). If VUR is not accompanied by infection or if suspected cortical scars remain stable for long time, surgical treatment might not be warranted (which is best determined by the treating paediatrician, nephrologist, urologist or paediatric surgeon). The radiographic study to diagnose and establish severity of VUR called micturating cystourethrography (MCUG) is an invasive procedure. Thus, if a single baseline DMSA scan or serial DMSA scans convincingly exclude presence of scarring and also provide evidence of a healthy kidney on the same side as VUR, surgical treatment and repeat MCUG tests could be avoided. Also, probability of developing new scars in previously healthy kidney decreases as the child ages.
The primary consequence of reflux nephropathy is that it reduces function of the affected kidney. However, if the other kidney is perfectly healthy, it takes over some of the function and enlarges in size ('compensatory hypertrophy / function'). So, overall function of both kidneys combined could still be largely preserved and compatible with a healthy life. However, a secondary of reflux nephropathy is that the affected kidney (especially if shrunken), could cause hypertension (increased blood pressure) in childhood that could continue into the adulthood. Hypertension in turn puts further strain on the only normally functioning kidney that is already burdened. This could turn into a vicious cycle that results in reduced function of the previously normally functioning kidney as well. Hence, it is of utmost importance to suspect, diagnose and treat severe VUR and/or reflux nephropathy.
In summary, DMSA is a very helpful tool in establishing the need for further work up / follow up for VUR, and to determine course of action in confirmed cases of VUR / reflux nephropathy.
There are no remarkable expected risks or side effects.
For additional information, please visit the following links.