A “renal-centric” approach to detect TA-TMA. Because TA-TMA is unlikely to occur without alterations in renal function or blood pressure, careful routine monitoring of these parameters in the context of HSCT can aid in the differential diagnosis. This includes close attention to creatinine (and its dependence on muscle mass), other potentially more reliable measures of GFR (ie, cystatin C), urinalysis findings, and blood pressure readings. Evidence for proteinuria should be quantified by a first-morning spot urine protein-to-creatinine ratio (> 0.2 mg/mg is elevated). Patients with elevated LDH, abnormal renal findings or elevated blood pressure or a combination should be carefully screened for TA-TMA according to current guidelines and clinical findings. In the presence of diagnostic uncertainty, the benefit of tissue diagnosis, especially renal biopsy, should be carefully weighed against procedural risks. Potential therapeutic interventions to consider for patients with TA-TMA include calcineurin inhibitor withdrawal, plasma exchange, and rituximab. Patients without TA-TMA should be assessed for other causes of renal dysfunction or hypertension, including, but not limited to, BK virus and medication exposure (eg, steroids, calcineurin inhibitors, chemotherapeutic agents, or antimicrobials).