The most likely diagnosis is thin glomerular basement membrane (GBM) disease, an inherited type IV collagen abnormality that causes thinning of the GBM and results in hematuria. The disorder may affect up to 5% of the population, and 30% to 50% of patients report a family history of hematuria. The disease is characterized by microscopic or macroscopic hematuria that may be first discovered in young adults. Diagnosis is usually based on the history of persistent hematuria, normal kidney function, and positive family history of hematuria without kidney failure; biopsy is not typically required. Long-term prognosis for kidney function is excellent, with rare progression to chronic kidney disease (CKD).

Fabry disease is a rare X-linked inherited disorder in which there is deficiency of α-galactosidase A (an enzyme in the glycosphingolipid pathway) that leads to progressive deposit of globotriaosylceramide (Gb3) in lysosomes. This disorder may present as CKD in young adulthood. Other associated clinical features include premature coronary artery disease, severe neuropathic pain, telangiectasias, and angiokeratomas. Because Fabry disease is X-linked and this patient has no other clinical findings of this disorder, it is not a likely diagnostic consideration.

Hereditary nephritis (also known as Alport syndrome), also a heritable disorder of type IV collagen, is a rare cause of end-stage kidney disease with a prevalence of 0.4% among adult U.S. patients. Most cases are X-linked (80%) and are associated with sensorineural hearing loss and lenticonus (conical deformation of the lens), with proteinuria, hypertension, and kidney failure developing over time. The remaining cases are autosomal recessive (15%) or autosomal dominant (5%) and may also be associated with hearing loss. Female carriers variably develop kidney disease depending on activity of the X chromosome in somatic renal cells. The prevalence of this disorder and the patient's gender make this a less likely possibility.

Tuberous sclerosis complex (TSC) results from mutations in genes coding for proteins that have a tumor-suppressing effect. Disruption of these gene products allows abnormal cell proliferation in different tissues, including the skin, brain, lung, liver, and kidney. Mild TSC may be detected in adulthood. Renal angiomyolipomas are a characteristic kidney lesion in TSC and occur in 75% of patients on imaging. The lack of evidence of other lesions suggestive of TSC and her normal kidney ultrasound make this an unlikely diagnosis in this patient.