Most published data on KUS in patients with NS assess patients with congenital NS and are thus not generalizable to the broader idiopathic NS population. The remaining available literature is largely underpowered. One study of 11 patients under one year of age with NS showed parenchymal hyperechogenicity, a subcapsular hypoechoic band, and loss of corticomedullary differentiation as the most frequent findings, though no finding was specific to any one disease process.[11] Another study of 15 patients showed similar findings.[12] Only three patients out of either cohort had biopsy-confirmed MCD. In their case-control study, Atalabi, et al, showed largely no difference in Doppler indices between nephrotic syndrome patients (n = 53) and matched controls (n = 57); they also showed no correlation of Doppler ultrasound endpoints to serum albumin or creatinine levels.[13] Finally, a retrospective study of pediatric patients with known increased kidney echogenicity showed that 20% of patients with this KUS finding presented with NS (24 of 119 patients), but ultimately this nonspecific finding was most commonly associated with glomerulonephritis and not NS.[14]
In Gershen’s 1994 study of 43 children with nephrotic syndrome, nephromegaly was the most common finding (42%), followed by increased kidney echogenicity (35%).[4] Ultrasound technology has advanced since that study was published, and yet, even with the increased detail and sensitivity of modern imaging, our study similarly showed that nephromegaly (35.8%) and increased echogenicity (39.6%) were the two most common abnormal findings on KUS, neither anomaly being clinically impactful. While Gershen, et al, found no correlation between nephromegaly and incidence of steroid resistance, they did report that echogenic kidneys were associated with steroid resistance.[4] However our data did not find any sonographic findings associated with increased frequency of steroid resistance. Nor did our data identify any ultrasound findings that prompted a deviation in management of these patients from the standard of care for presumed MCD.
At our institution the current gross charge for a dedicated KUS is $903.00. In aggregate, the cost of the 46 kidney ultrasounds obtained for our participants exceeded $40,000 with very limited clinical benefit. If KUS has no diagnostic relevance in this population, in that it will not change management or alter outcomes, then this is an unnecessary added cost placed on the shoulders of families. Our data supports omitting a KUS from the initial work up of patients with idiopathic NS secondary to presumed minimal change disease. There are indeed several scenarios in which KUS would be warranted: if there is evidence of systemic disease, a reduction in kidney function, or presence of nephritic symptoms, for example. However, those who had KUS did not have statistically higher rates of hypertension, hematuria, or decreased kidney function, meaning imaging was ordered indiscriminately of these risk factors for secondary causes of NS. Institutions should work to educate emergency, hospital medicine, and even renal clinicians on the specific indications for KUS and its limited utility in the workup of presumed MCD with the goal of preserving resources and eliminating unnecessary, low-value tests.